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Case scenarioStavros, a 35-year-old male with focal epilepsy, presents to the pharmacy to collect his medicines. He appears tired and mentions he has been having more frequent breakthrough seizures lately. As you chat, he reveals he recently started lorazepam 1 mg twice daily for generalised anxiety disorder (GAD), prescribed by his new GP. Stavros has been missing doses of his anti-seizure medicine, carbamazepine, as he feels it worsens his drowsiness and confusion. |
Dr Ming S Soh PhD, BPharm (Hons)[/caption]
Epilepsy is a chronic neurological condition characterised by a persistent tendency to produce seizures.1,2 According to the International League Against Epilepsy (ILAE), epilepsy is diagnosed when an individual experiences at least two unprovoked seizures more than 24 hours apart, one unprovoked seizure with a high probability (≥60%) of recurrence, or when an epilepsy syndrome is identified.3 Seizures result from abnormal, excessive electrical discharges in the brain, and vary in type, severity and frequency.4 While most seizures are brief, lasting seconds to minutes, they can become prolonged and continuous (i.e. status epilepticus), which requires urgent, intensive medical intervention.4 Globally, epilepsy affects around 50 million people.5,6 It can affect individuals across all age groups, races and ethnicities, and can significantly disrupt quality of life.7,8 Epilepsy is often associated with neurobiological, cognitive, psychological and social sequelae.1,2
Management of epilepsy primarily involves antiseizure medicines (ASM), administered as monotherapy or polytherapy depending on the patient’s response.8,9 In some cases, surgery, dietary therapy or neurostimulation may be considered.9 Treatment complexity, adverse drug reactions and non-adherence to medicines can hinder seizure control and prevent optimal outcomes.8
Learning OutcomesAfter reading this article, pharmacists should be able to:
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In practice, pharmacists provide therapeutic drug monitoring (hospital setting), Home Medicines Reviews (HMR), MedsChecks and patient counselling, and they support the management of common comorbidities such as depression, anxiety and cognitive impairments, which can complicate treatment.6,8,9

Globally, the pooled incidence rate of epilepsy is estimated at 50–61.4 cases per 100,000 person-years.2,10,11 However, incidence varies by region and income level. In high-income countries, rates typically range from 40–70 per 100,000 person-years, while in low- and middle-income countries, incidence can reach 100–190 per 100,000 person-years, reflecting disparities in healthcare access, diagnostic capacity and exposure to risk factors.2,10 The highest incidence of epilepsy occurs in childhood, reflecting the higher seizure susceptibility of the developing brain.12
In Australia, the lifetime risk of developing epilepsy is estimated to be up to 4%, while approximately 0.6–1% of the population is living with epilepsy at any given time.13,14 Modelled data estimates that prevalence peaks in males aged 60–64 (8.54 per 1,000), and in females aged 50–54 (9.57 per 1,000).15 National surveillance data indicates that prevalence generally remains high into older age groups, largely due to increased rates of stroke, neurodegenerative diseases and brain tumours.2,14,15
Disparities are pronounced among Aboriginal and Torres Strait Islander people, who experience twice the prevalence of epilepsy compared to non-Aboriginal and Torres Strait Islander people.14,16 Aboriginal and Torres Strait Islander people also face higher rates of hospitalisation, reduced access to specialist care and ASM, and significantly elevated epilepsy-related mortality.16 The disability-adjusted life years for Aboriginal and Torres Strait Islander people with epilepsy are double those of non-Aboriginal and Torres Strait Islander people.16
Epilepsy has a multifactorial aetiology. The ILAE classifies epilepsy aetiologies into six main categories: genetic, structural, infectious, metabolic, immune and unknown (see Figure 1).17,18 Genetic mutations generally affect neuronal excitability, especially ion channels, and are linked to specific epilepsy syndromes.18–20 Structural causes include brain malformations, trauma, stroke and tumours. Infections like meningitis or encephalitis can provoke seizures through inflammation. Metabolic causes arise from systemic or inherited metabolic disorders that disrupt brain chemistry or energy production. Autoimmune responses, where the body’s immune system attacks brain tissue, can also lead to seizures. Unknown causes refer to cases where no clear aetiology can be identified despite thorough investigation. Neurodegenerative causes are increasingly recognised as important contributors to epilepsy.18 Despite structured classifications, many overlap. For example, an infection such as encephalitis may lead to structural brain damage.18 Risk factors include family history, perinatal insults, head trauma, brain infections, febrile seizures and socioeconomic disparities, which can influence both the likelihood of developing epilepsy as well as its clinical progression.21

Epilepsy involves several interconnected mechanisms that predominate in different seizure types and epilepsy syndromes and are targeted by specific ASM.
Neuronal hyperexcitability is increased neuronal responsiveness due to ion-channel dysfunction, resulting in spontaneous, excessive neuronal firing. This is a key mechanism underlying all seizure types, but is not the sole pathophysiological mechanism.4,22,23
Hypersynchrony is the abnormal synchronisation of neuronal activity which facilitates seizure propagation across brain regions, particularly in generalised epilepsies such as absence and tonic-clonic seizures.1,4,12,18
Excitatory/inhibitory neurotransmitter imbalance refers to the disruption of glutamate and gamma-aminobutyric acid (GABA) neurotransmission, shifting networks toward hyperexcitability and is central to both focal and generalised epilepsy.4,17
Neuroinflammation refers to the immune activation and cytokine release (e.g. IL-1 beta, TNF-alpha) that can enhance excitability, and are implicated in structural focal epilepsies, post-stroke epilepsy and autoimmune epilepsies. Anti-inflammatory and immunomodulatory therapies may be used in selected cases.4,24
mTOR pathway dysregulation is the abnormal mTOR signalling that alters synaptic plasticity, contributing to epileptogenesis, most notably in tuberous sclerosis complex–associated epilepsy, where mTOR inhibitors such as everolimus are used as targeted therapy.18
Oxidative stress is the excess reactive oxygen species that can damage neurons and lower seizure thresholds, contributing to seizures in metabolic and neurodegenerative epilepsies.24
Mitochondrial dysfunction refers to impaired energy metabolism, which reduces neuronal resilience and is characteristic of mitochondrial epilepsies and some childhood epileptic encephalopathies.24
Synaptic reorganisation refers to structural changes, including aberrant axon sprouting and new excitatory circuit formation, and are commonly seen in temporal lobe epilepsy following brain injury or prolonged seizures.4
Recognising underlying epileptogenic mechanisms aids interpretation of seizure type/classification and guides appropriate ASM selection.
Focal seizures (formerly known as partial)
Focal seizures originate in a specific area of one cerebral hemisphere. Depending on the brain area affected, they may present with localised motor activity like rhythmic jerking or muscle stiffening, sensory changes such as tingling or visual distortions, or autonomic signs, including flushing and gastrointestinal discomfort.12 Awareness may or may not be impaired during these seizures.25 Some focal seizures begin with an aura, such as déjà vu or intense emotions, during which a person remains alert. First-line treatment includes carbamazepine, lamotrigine or levetiracetam, where selection is guided by contraindications and other patient-specific factors.26
Generalised seizures
Generalised seizures involve widespread electrical activity across both cerebral hemispheres and typically include tonic-clonic, absence, myoclonic and atonic seizures.12,25
Tonic-clonic seizures (formerly known as grand mal)
Tonic-clonic seizures are characterised by a sudden loss of consciousness, muscle stiffening followed by rhythmic jerking, and a post-seizure phase with confusion, agitation or fatigue. They can sometimes be fatal due to associated complications. Some tonic-clonic seizures begin as focal seizures with preserved awareness, but progress to loss of consciousness as they generalise across both hemispheres of the brain.12 First-line treatment is sodium valproate, unless contraindicated or otherwise inappropriate for the patient (e.g. individuals of childbearing potential).26
Absence seizures (formerly known as petit mal)
Absence seizures are typically characterised by brief episodes of staring or unresponsiveness, and are often unnoticed or mistaken for daydreaming.12,25 First-line treatment includes ethosuximide or sodium valproate where selection is guided by contraindications and other patient-specific factors.26
Myoclonic seizures
Myoclonic seizures present as sudden and brief muscle jerks.12,25 First-line treatment is sodium valproate unless contraindicated or otherwise inappropriate (e.g. individuals of childbearing potential).26
Atonic seizures
Atonic seizures result in a sudden loss of muscle tone, leading to falls.12,25
For further information, see Australian Medicines Handbook: Epilepsy.26
Diagnosis of epilepsy involves detailed clinical history, neurological examination and supportive investigations.12,17 Electroencephalogram (EEG) is central for detecting epileptiform discharges, while neuroimaging techniques such as computed tomography (CT) and magnetic resonance imaging (MRI) can help identify structural causes.12 In complex cases, additional tools including positron emission tomography (PET)/single photon emission computed tomography (SPECT), magnetoencephalography (MEG) and genetic testing can support diagnosis and guide treatment. The advanced neuroimaging modalities are especially useful for presurgical evaluations in specialised centres.12 Neuropsychological assessments can also provide insight into cognitive impacts.1 ILAE classification recommends a structured, three-level diagnostic approach, identifying seizure type, epilepsy type and specific epilepsy syndrome, while integrating aetiology at each stage to inform treatment decisions.3 Syncope, psychogenic non-epileptic seizures, transient ischaemic attacks, migraine auras and sleep disorders can mimic epileptic seizures but differ in aetiology and treatment.12,27
Prognosis varies widely, depending on seizure type, aetiology, age of onset and treatment response.12 Many patients can achieve seizure control with ASM, and some enter long-term remission. However, around one-third of patients develop drug-resistant epilepsy, unresponsive to two or more ASM.12 Early age of onset, especially in infancy, and epilepsy with structural lesions such as hippocampal sclerosis, are often linked to poorer outcomes.28,29 Sudden unexpected death in epilepsy remains a serious risk,30 particularly in patients with uncontrolled generalised tonic-clonic seizures and early-onset syndromes such as Dravet syndrome (severe infantile-onset developmental epileptic encephalopathy), which has a 3–5-fold higher mortality risk than the general epilepsy population.31 Early diagnosis and individualised treatment strategies improve outcomes.
The primary aim is to achieve seizure freedom with minimal side effects, improving quality of life. Treatment recommendations follow a stepwise approach, guided by seizure classification, epilepsy type, underlying aetiology, side effect profile, cost, potential for measuring serum drug concentration, pharmacokinetics and patient-specific factors such as age, pregnancy, medicine interactions and comorbidities.17,26,32,33
Initial management involves monotherapy with an appropriate ASM. Dose is generally started low and titrated slowly to achieve seizure control. If control is not achieved with maximally tolerated doses of a single agent, a second agent may be added. The second agent may be considered for monotherapy if the patient and prescriber are willing to gradually withdraw the first agent. If two agents do not promote seizure control, the second agent may be withdrawn gradually and replaced with a third.34
Treatment with an ASM should never be ceased abruptly.34
Key treatment considerations
For further information, see Therapeutic Guidelines: Neurology.34
Evidence is limited for cannabis-derived products. Cannabidiol is approved for specific syndromes but requires specialist oversight.33,34
Non-pharmacological management includes surgery following EEG/MRI evaluation, vagus nerve and deep brain stimulation, ketogenic diet and gene therapy. Yoga, meditation and acupuncture have limited evidence for use.17,31–35
One of the most common challenges during epilepsy treatment is adherence. Missed doses or abrupt discontinuation can trigger recurrent seizures which significantly increase mortality risk.33 Medicine interactions are another significant concern, particularly with older ASM such as phenytoin and carbamazepine, which are enzyme inducers and can alter the efficacy of other medicines.33 Patients should be informed that some medicines can lower their seizure threshold. These include theophylline, pethidine, certain antidepressants (uncommon), and some antipsychotics. Some important medicine interactions are shown in Table 1.

Treatment complications range from mild to severe. Common side effects include fatigue, dizziness, cognitive issues such as memory or attention difficulties, and abdominal upset including pain, nausea and vomiting.33
More serious but less frequent reactions include liver and renal toxicity, bone marrow suppression and skin reactions.26 Long-term use of certain ASM including carbamazepine and phenytoin may also reduce bone density, increasing fracture risk.12,33 Additionally, some ASM including levetiracetam and topiramate can worsen mood disorders, contributing to anxiety and depression.26,33
Age also influences management.32,33 Children often require weight-based dosing and closer monitoring due to variable metabolism, while older adults are more susceptible to adverse effects and medicine interactions due to comorbidities and declining organ function.34
To manage these risks, routine monitoring, including liver and renal function tests, therapeutic drug monitoring, bone health assessments and mental health screening, is essential.
Epilepsy treatment requires regular follow-up to assess seizure control, treatment efficacy and adverse effects. Monitoring for drugs with narrow therapeutic index should also be considered. Treatment plans should be reviewed annually, or sooner, to discuss any changes in seizure occurrence.
Patients in Australia can access further advice and support through multiple channels, including:
Epilepsy Action Australia – education, telehealth and resources
Epilepsy Foundation – seizure management and support services
National Epilepsy Support Service/Epilepsy Smart Australia – 1300 761 487 Monday to Friday, from 9 am to 5 pm (AEST).
Pharmacists support epilepsy management across both community and hospital settings. Hospital pharmacists contribute by implementing therapeutic drug monitoring, especially for ASM with narrow therapeutic windows, collaborating with multidisciplinary teams to optimise treatment plans, monitoring for adverse drug reactions, and managing complex cases involving polytherapy or comorbidities. Community pharmacists can provide ongoing support and medicines counselling, and conduct MedsChecks, detect side effects early, and address mental health concerns. Together, pharmacists provide personalised care that can help improve seizure control, enhance treatment safety and reduce mortality.
With appropriate treatment, many people with epilepsy can achieve good seizure control and lead full, active lives. However, outcomes depend on early intervention, consistent follow-up, monitoring and personalised care. Pharmacist involvement helps reduce complications, improves medicine adherence and supports overall wellbeing.
Case scenario continuedYou recognise that emotional stress, non-adherence and adverse effects are likely precipitating Stavros’ seizures. Concomitant use of lorazepam and carbamazepine contributes to additive CNS depression, causing sedation. As Stavros prefers pharmacological treatment for GAD, you call his GP and suggest sertraline 50 mg daily, noting that carbamazepine may reduce sertraline concentrations via enzyme induction, and clinical response should be monitored. You recommend ceasing lorazepam and encourage cognitive behavioural therapy. The GP reviews Stavros and he returns with a cessation plan for lorazepam and a prescription for sertraline. You counsel on treatment expectations and the importance of adherence. A month later, Stavros returns, feeling alert with no recent seizures. |
DR Ming S Soh PhD, BPharm (Hons) is a Research Fellow at the Florey Institute of Neuroscience and Mental Health, University of Melbourne, with expertise in preclinical models of genetic epilepsy and therapeutic development.
Fisher RS, van Emde Boas W, Blume W, et al. Epileptic seizures and epilepsy: definitions proposed by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE). Epilepsia. 2005;46(4):470–472.
Beghi E. The epidemiology of epilepsy. Neuroepidemiology. 2020;54(2):185–191.
Scheffer IE, Berkovic S, Capovilla G, et al. ILAE classification of the epilepsies: position paper of the ILAE commission for classification and terminology. Epilepsia. 2017;58(4):512–521.
Scharfman HE. The neurobiology of epilepsy. Curr Neurol Neurosci Rep. 2007;7(4):348–354.
World Health Organization. Epilepsy. 2022. Available from: www.who.int/news-room/fact-sheets/detail/epilepsy
Petrides M, Peletidi A, Nena E, et al. The role of pharmacists in enhancing epilepsy care: a systematic review of community and outpatient interventions. J Pharm Policy Pract. 2025;18(1):2487046.
Zack MM. National and state estimates of the numbers of adults and children with active epilepsy—United States, 2015. MMWR Morb Mortal Wkly Rep. 2017;66.
Bacci JL, Zaraa S, Stergachis A, et al. Community pharmacists’ role in caring for people living with epilepsy: a scoping review. Epilepsy Behav. 2021;117:107850.
Reis TM, Campos M, Nagai MM, et al. Contributions of pharmacists in the treatment of epilepsy: a systematic review. Am J Pharm Benefits. 2016;8(3):e55–e60.
Bell GS, Sander JW. The epidemiology of epilepsy: the size of the problem. Seizure. 2001;10(4):306–316.
Fiest KM, Sauro KM, Wiebe S, et al. Prevalence and incidence of epilepsy: a systematic review and meta-analysis of international studies. Neurology. 2017;88(3):296–303.
Stafstrom CE, Carmant L. Seizures and epilepsy: an overview for neuroscientists. Cold Spring Harb Perspect Med. 2015;5(6):a022426.
Mohanannair Geethadevi G, Chen Z, et al. Impact of epilepsy on productivity and quality of life: the Australian epilepsy project. Neurology. 2025;105(5):e214011.
Australian Institute of Health and Welfare. Epilepsy in Australia. Canberra: AIHW; 2022. Available from: www.aihw.gov.au/reports/chronic-disease/epilepsy-in-australia/contents/about
Foster E, Chen Z, Zomer E, et al. The costs of epilepsy in Australia: a productivity-based analysis. Neurology. 2020;95(24):e3221–e3231.
Keenan NF, Aitchison SG, Jetté N, et al. Epilepsy in the Indigenous peoples in Canada, Australia, New Zealand, and the USA: a systematic scoping review. Lancet Glob Health. 2025;13(4):e656–e668.
Vera-González A. Pathophysiological mechanisms underlying the etiologies of seizures and epilepsy. In: Czuczwar SJ, editor. Epilepsy. Brisbane: Exon Publications; 2022. p. 1–13.
Balestrini S, Arzimanoglou A, Blümcke I, et al. The aetiologies of epilepsy. Epileptic Disord. 2021;23(1):1–16.
Perucca P, Bahlo M, Berkovic SF. The genetics of epilepsy. Annu Rev Genomics Hum Genet. 2020;21(1):205–230.
Scheffer IE, Berkovic SF. The genetics of human epilepsy. Trends Pharmacol Sci. 2003;24(8):428–433.
Bhalla D, Godet B, Druet-Cabanac M, Preux P-M. Etiologies of epilepsy: a comprehensive review. Expert Rev Neurother. 2011;11(6):861–876.
Reid CA. Preface: ion channels and genetic epilepsy. J Neurochem. 2024;168(12):3829–3830.
Oyrer J, Maljevic S, Scheffer IE, et al. Ion channels in genetic epilepsy: from genes and mechanisms to disease-targeted therapies. Pharmacol Rev. 2018;70(1):142–173.
Fabisiak T, Patel M. Crosstalk between neuroinflammation and oxidative stress in epilepsy. Front Cell Dev Biol. 2022;10:976953.
Fisher RS, Cross JH, French JA, et al. Operational classification of seizure types by the International League Against Epilepsy: position paper of the ILAE commission for classification and terminology. Epilepsia. 2017;58(4):522–530.
Buckley N, editor. Australian medicines handbook. Adelaide: Australian Medicines Handbook Pty Ltd; 2025. Available from: https://amhonline.amh.net.au/
Cook M. Differential diagnosis of epilepsy. In: Shorvon S, Perucca E, Engel J Jr, editors. The treatment of epilepsy. 4th ed. Hoboken (NJ): John Wiley & Sons; 2015. p. 24–37.
Semah F, Picot M-C, Adam C, et al. Is the underlying cause of epilepsy a major prognostic factor for recurrence? Neurology. 1998;51(5):1256–1262.
Nickels K. Earlier is not always better: outcomes when epilepsy occurs in early life versus adolescence. Epilepsy Curr. 2020;20(1):27–29.
Devinsky O, Hesdorffer DC, Thurman DJ, et al. Sudden unexpected death in epilepsy: epidemiology, mechanisms, and prevention. Lancet Neurol. 2016;15(10):1075–1088.
Cooper MS, McIntosh A, Crompton DE, et al. Mortality in Dravet syndrome. Epilepsy Res. 2016;128:43–47.
Perucca E. General principles of medical management. In: Shorvon S, Perucca E, Engel J Jr, editors. The treatment of epilepsy. 4th ed. Hoboken (NJ): John Wiley & Sons; 2015. p. 110–123.
Perucca P, Scheffer IE, Kiley M. The management of epilepsy in children and adults. Med J Aust. 2018;208(5):226–233.
Therapeutic Guidelines Limited. eTG complete. Melbourne: Therapeutic Guidelines; 2025. Available from: www.tg.org.au
Baxendale S. Complementary and alternative treatments for epilepsy. In: Shorvon S, Perucca E, Engel J Jr, editors. The treatment of epilepsy. Hoboken (NJ): John Wiley & Sons; 2015. p. 298–310.
Johannessen SI, Johannessen Landmark C. Antiepileptic drug interactions: principles and clinical implications. Curr Neuropharmacol. 2010;8(3):254–267.
Buchanan N. Medications which may lower seizure threshold. Aust Prescr. 2001;24(1):8–9.
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[post_content] => New avenues for nurse prescribing have the potential to reshape frontline care. For pharmacists, it’s a live example of how scope expansion translates into real impact.
Nurse prescribing is entering a new phase in Australia, and pharmacists should be paying close attention.
While nurse practitioners and endorsed midwives have been able to prescribe Pharmaceutical Benefits Schedule (PBS) subsidised medicines since 2010, a new pathway will soon expand prescribing to a broader group of experienced nurses.
‘A lot of people wouldn't even know that nurses are already prescribing medications that are funded on the PBS,’ said Denise Lyons, President of the Australian Primary Health Care Nurses Association. ‘But there are more than 3,000 nurse practitioners and endorsed midwives in Australia now who are already prescribing.’
Under a new registration standard which came into effect in September last year, suitably qualified registered nurses will be able to prescribe medicines in Schedules 2, 3, 4 and 8 in partnership with an authorised prescriber.
‘It took until this year for universities to start the course that enables registered nurses to meet [the new standard],’ Ms Lyons said. ‘Most are 6-month postgraduate courses … So it will probably be around July 2026 that we will see the first [wave] of nurses completing the educational requirement.’
For pharmacists, this shift offers a live view of how prescribing reform is built – through legislation, governance, defined scope and, crucially, access to the PBS.
What’s changing?
The new framework is deliberately cautious. To become a designated RN prescriber, a nurse must:
‘Pharmacists and nurses are often people's first point of contact with the healthcare system, and it's really good if we can work to the top of our scope and do what we know we can do, with the right guardrails in place.' denise lyons
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[post_content] => Case scenario
Sarah, a 42-year-old woman, presents to the pharmacy reporting a small lump near the anus, occasional bright red bleeding on toilet paper after bowel movements, anal itching and discomfort. She mentions feeling embarrassed to seek advice and has been self-managing with sitz baths. She reports a history of chronic constipation with frequent training during defecation. She is not taking any regular medicines and requests an over-the-counter product to relieve her symptoms. You take the time to explore Sarah’s symptoms in more detail, to help identify any red flags that would require immediate referral. You ask about the duration, severity and other symptoms such as fatigue, unintentional weight loss and changes in bowel habits, all of which she denies.
Learning objectivesAfter reading this article, pharmacists should be able to:
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Anal fissures and haemorrhoids are commonly encountered, but their epidemiology is not well documented. Haemorrhoids represent the most frequent reason for proctology consultations, followed by anal fissures.1 Haemorrhoids are estimated to affect up to 40% of adults in the general population, although many individuals are asymptomatic.2 Anal fissures occur in approximately 10–15% of the population.3

An anal fissure is a longitudinal tear in the anal canal, most often occurring in the posterior midline, just below the dentate line.4 Anal fissures are typically classified as primary or secondary, depending on the cause. Primary fissures are usually benign and caused by local trauma, such as the passage of hard stools, prolonged diarrhoea, vaginal delivery, repeated injury or anal penetration.4 Secondary fissures, which are often multiple and located off the midline, are uncommon, accounting for less than 1% of cases.5 They result from underlying conditions like previous anal surgery, inflammatory bowel disease (e.g. Crohn’s disease), colorectal malignancy, infections (e.g. HIV/AIDS), or dermatological conditions (e.g. psoriasis).6 Anal fissures are further described as acute or chronic, with chronic fissures lasting more than 6 weeks.7
[caption id="attachment_31774" align="alignright" width="200"]
DR Amy Page (she/her) PhD, MClinPharm, GradDipBiostat, GCertHProfEd, GAICD, GStat, FSHPA, FPS is a consultant pharmacist, biostatistician, and the director of the Centre for Optimisation of Medicines at UWA’s School of Allied Health.[/caption]
Anal fissures are often mistaken for haemorrhoids because of their overlapping symptoms. Haemorrhoids differ in that they are normal vascular cushions within the anal canal that maintain continence. Although part of normal anatomy, the term ‘haemorrhoid’ is commonly used when these vascular anal cushions, containing a rich arteriovenous network, become enlarged or displaced.8 Haemorrhoids may be classified as internal (located above the dentate line) or external (located below the dentate line). Factors such as constipation, straining during bowel movements and a low-fibre diet are commonly considered to increase the risk of haemorrhoids.9,10 However, the causal relationship between these factors and the development of haemorrhoids remains unclear. A possible genetic component that predisposes to smooth muscle, epithelial and connective tissue dysfunction, may contribute to haemorrhoids.11
It is important to note that certain medicines can contribute to or worsen constipation as an adverse effect, thereby aggravating haemorrhoids and anal fissures.9,10 Common examples include opioids, anticholinergics, and iron and calcium supplements.12 Regular medication review should be incorporated into comprehensive care to identify opportunities for deprescribing and prevent inappropriate prescribing cascades, with further guidance available in the new deprescribing guidelines.13
The symptoms of haemorrhoids may include rectal bleeding, anal pruritus, prolapse, faecal seepage and mucus discharge.7
Internal haemorrhoids are usually painless because the columnar epithelium is insensitive to touch and temperature.8 In contrast, external haemorrhoids are pain sensitive and may become thrombosed, often following straining during defecation.8
Anal fissures, by comparison, typically cause severe tearing pain that is provoked by defecation.4 A key distinguishing feature is that the pain of an anal fissure typically occurs during or immediately after defecation.

For diagnostic purposes, medical practitioners perform a physical examination with the individual lying on their side, gently parting the buttocks to inspect the posterior midline.4 Several other anorectal disorders may present with similar symptoms to anal fissures and haemorrhoids. Differential diagnoses include anal fistula and solitary rectal ulcer syndrome, which can often be distinguished based on their clinical appearance through careful physical examination. An anal fistula typically presents as a draining skin punctum.14 It is an abnormal hollow tract, most often arising from infection of an anal gland.15 Solitary rectal ulcer syndrome may present with anal pain, rectal bleeding, constipation, mucus discharge, excessive straining and a sensation of incomplete evacuation. Despite its name, the condition does not always involve an ulcer. Diagnosis requires a combination of endoscopic and histopathological findings, together with the individual’s reported symptoms.16
Haemorrhoids
[caption id="attachment_31775" align="alignright" width="200"]
Hui Wen Quek (she/her) BPharm(Hons), GradCertAppPharmPrac is a pharmacist and PhD candidate at the University of Western Australia (UWA).[/caption]
Non-pharmacological treatment options
First-line management for haemorrhoids usually involves lifestyle measures, which include ensuring adequate fluid and fibre intake, reducing prolonged time on the toilet and avoiding excessive straining, the use of sitz baths, and maintaining anal hygiene.10 In practice, dietary and lifestyle modifications are usually recommended as a conservative and preventive measure for haemorrhoids.17
Pharmacological treatment options
Over-the-counter therapies for internal haemorrhoids include ointments and suppositories that contain emollients, mild astringents, local anaesthetics and/or corticosteroids.8 These preparations temporarily relieve itching and discomfort. Prolonged use of topical corticosteroids is not recommended, as it increases the risk of local infections such as candidiasis.8 Similarly, prolonged use of anaesthetic-containing products should be avoided due to potential adverse effects, including skin sensitisation and dermatitis.8
Outpatient procedures and surgery
For individuals who do not respond to conservative measures, other treatment options for haemorrhoids include outpatient procedures and surgery.10 Outpatient procedures include rubber band ligation, infrared coagulation, bipolar probe, heater probe, sclerotherapy and cryotherapy.10 These are generally reserved for people with grade I or grade II haemorrhoids.10 Surgery can be considered for people who do not respond to or cannot tolerate outpatient procedures, as well as those with large external haemorrhoids, or combined internal and external haemorrhoids with prolapse.10
A recent meta-analysis found that surgical treatments, compared with conservative treatments, offer greater symptom relief, quicker recovery and lower recurrence rates.18 However, they do carry risks of procedure-related complications. In contrast, conservative treatments are safer and less invasive, but tend to provide slower symptom improvement and have higher recurrence rates.18 Therefore, treatment decisions should be individualised, taking into account symptom severity, individual preferences and risk tolerance.
Anal fissures
The primary aim of treatment for anal fissures is to reduce anal sphincter spasm, improve blood flow and promote healing.6 First-line management is usually non-operative and includes increasing dietary fibre, use of sitz baths and applying glyceryl trinitrate 0.2% ointment, three times daily for up to 4 weeks to relieve pain.19 Headache is a common adverse effect of glyceryl trinitrate due to systemic absorption, which could limit its use.20 Other topical agents used in clinical practice include lidocaine and hydrocortisone, although these are less effective than a combination of fibre intake and warm sitz baths.4
Botulinum toxin injections may also be considered and can achieve good healing rates.6,19 However, botulinum toxin may cause temporary reduced control of wind or bowel motions, which usually resolves as the effect of the injection wears off.4 Due to these adverse effects and the invasive nature of the procedure, botulinum toxin is generally reserved as a second-line therapy.4 If these treatment options are unsuccessful, surgical treatment may be required.6
Secondary or chronic anal fissures warrant additional investigation and multidisciplinary management is advised, especially when malignancy is suspected or confirmed.4
Pharmacists play a key role in recognising the symptoms of haemorrhoids and anal fissures, providing timely advice and suggesting a suitable course of action. Pharmacists can also educate individuals on first-line management strategies and provide lifestyle advice where appropriate to prevent recurrence. In addition, pharmacists can advocate for the safe use of over-the-counter treatments, advise on appropriate duration of use and counsel individuals on potential adverse effects.
Referral to a medical practitioner is advisable for individuals who21:
Anal fissures and haemorrhoids are common conditions encountered in primary care and can greatly impact quality of life. Pharmacists play a critical role in early management and referral, helping prevent complications and improve outcomes.
Case scenario continuedYou identify that Sarah has haemorrhoids and provide lifestyle advice, including increasing fluid and dietary fibre intake, avoiding prolonged straining during bowel movements and practising good anal hygiene. For symptomatic relief, you suggest a topical ointment containing cinchocaine 0.5% and zinc oxide 20%, to be applied as needed. You also advise her to consult her general practitioner if she experiences persistent bleeding, ongoing pain or worsening prolapse. With your support and advice, Sarah feels more confident in managing her condition effectively while reducing the risk of recurrence. |
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Hui Wen Quek (she/her) BPharm(Hons), GradCertAppPharmPrac is a pharmacist and PhD candidate at the University of Western Australia (UWA).
DR Amy Page (she/her) PhD, MClinPharm, GradDipBiostat, GCertHProfEd, GAICD, GStat, FSHPA, FPS is a consultant pharmacist, biostatistician, and the director of the Centre for Optimisation of Medicines at UWA’s School of Allied Health.
Manisha Pillai (she/her) BPharm
Higuero T. Update on the management of anal fissure. J Visc Surg. 2015;152(2 Suppl):S37–S43.
Riss S, Weiser FA, Schwameis K, Riss T, Mittlböck M, Steiner G, et al. The prevalence of hemorrhoids in adults. Int J Colorectal Dis. 2012;27(2):215–220.
Vitton V, Bouchard D, Guingand M, Higuero T. Treatment of anal fissures: results from a national survey on French practice. Clin Res Hepatol Gastroenterol. 2022;46(4):101821.
Schlichtemeier S, Engel A. Anal fissure. Aust Prescr. 2016;39(1):14–17.
Zaghiyan KN, Fleshner P. Anal fissure. Clin Colon Rectal Surg. 2011;24(1):22–30.
Newman M, Collie M. Anal fissure: diagnosis, management, and referral in primary care. Br J Gen Pract. 2019;69(685):409–410.
Lyle V, Young C. Anal fissures: an update on treatment options. Aust J Gen Pract. 2024;53:33–35.
Therapeutic Guidelines Limited. Haemorrhoids. Melbourne: Therapeutic Guidelines Limited; 2022. Available from: https://www.tg.org.au
Lohsiriwat V. Hemorrhoids: from basic pathophysiology to clinical management. World J Gastroenterol. 2012;18(17):2009–2017.
Sandler RS, Peery AF. Rethinking what we know about hemorrhoids. Clin Gastroenterol Hepatol. 2019;17(1):8–15.
Zheng T, Ellinghaus D, Juzenas S, Cossais F, Burmeister G, Mayr G, et al. Genome-wide analysis of 944 133 individuals provides insights into the etiology of haemorrhoidal disease. Gut. 2021;70(8):1538–1549.
Therapeutic Guidelines Limited. Functional constipation in adults. Melbourne: Therapeutic Guidelines Limited; 2022. Available from: https://www.tg.org.au
Quek HW, Reus X, Lee K, Etherton-Beer C, Page A; Guideline Development Group. Deprescribing in older people: a clinical practice guideline. Perth (WA): The University of Western Australia; 2025.
Stewart D. Anal fissure: clinical manifestations, diagnosis, prevention. UpToDate. 2025. Available from: https://www.uptodate.com/contents/anal-fissure-clinical-manifestations-diagnosis-prevention
Therapeutic Guidelines Limited. Anorectal abscess and fistula. Melbourne: Therapeutic Guidelines Limited; 2022. Available from: https://www.tg.org.au
Sadeghi A, Biglari M, Forootan M, Adibi P. Solitary rectal ulcer syndrome: a narrative review. Middle East J Dig Dis. 2019;11(3):129–134.
Lohsiriwat V. Treatment of hemorrhoids: a coloproctologist's view. World J Gastroenterol. 2015;21(31):9245–9252.
Quan L, Bai X, Cheng F, Chen J, Ma H, Wang P, et al. Comparison of efficacy and safety between surgical and conservative treatments for hemorrhoids: a meta-analysis. BMC Gastroenterol. 2025;25(1):492.
Therapeutic Guidelines Limited. Anal fissure. Melbourne: Therapeutic Guidelines Limited; 2022. Available from: https://www.tg.org.au
Australian Medicines Handbook Pty Ltd. Glyceryl trinitrate (rectal). Adelaide: Australian Medicines Handbook Pty Ltd; 2025. Available from: https://amhonline.amh.net.au/
Allen S. Haemorrhoids and anal fissures. S Afr Pharm J. 2008;75(5):36.
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[post_content] => Community pharmacies are often the first place people turn when something feels ‘off’. But as pharmacists know, many requests for over-the-counter medicines are more complex than they may initially seem.
AP took a look at some presentations which might signal hidden red flags.
‘I just want a multivitamin’
When people present to community pharmacies, they often arrive with a solution already in mind. For example, ‘I need a strong painkiller,’ ‘I just want a multivitamin,’ or ‘What do you have for nerve pain?’
Nearly always, consistent with professional standards, these invite an open ended question to uncover the rationale for the request
Gauri Godbole FPS[/caption]
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[post_content] => Case scenario
During peak hour, 19-year-old Enzo and his mother arrive to collect a new prescription for melatonin MR 2 mg. The pharmacy is highly stimulating: background music blares, customers converse loudly nearby, staff assist others in a cramped space, and general noise amplifies the chaos. While processing Enzo’s prescription and attempting to deliver verbal instructions, you observe Enzo avoiding eye contact, fidgeting intensely, and appearing overwhelmed, with reduced capacity to process verbal or non-verbal cues due to sensory overload.
Learning objectivesAfter reading this article, pharmacists should be able to:
|
Yvette Anderson (she/her) BPharm, MPS, CredPharm (MMR), ANZCAP (MentalHth, Paeds), CPGx, GradCert Autism[/caption]
Neurodevelopmental disorders (NDDs) arise from differences in brain development and typically affect cognition, communication, behaviour and occupational functioning. Common NDDs include attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), referred to as autism in this article, and intellectual developmental disorder (IDD).1 Autism is characterised by persistent social interaction and communication difficulties and restricted behavioural patterns.2 Symptoms begin in early childhood; however, diagnosis can occur at any age.3 Autism affects how the brain processes information, shaping how autistic people see, understand and respond to the world around them, with marked variability in presentation, day-to-day functioning and support needs.3,4
In Australia, autism prevalence has increased due to evolving diagnostic practices and awareness,5 meaning pharmacists now routinely engage with autistic individuals as part of everyday practice.
The challenge and opportunity for pharmacy is to shift from a medical model of crisis response, treatments and cures to a neuro-affirming social model that helps autistic individuals thrive, not just survive.
A neuro-affirming social model conceptualises neurodevelopmental differences as natural variations within human diversity and rejects deficit-based assumptions that frame these differences as disorders.6 Rather than ‘correcting’ individual traits, this approach provides reasonable adjustments while supporting autonomy, community participation and wellbeing, alongside awareness of diagnostic criteria, comorbidities, communication styles, lived realities and the impact of misinformation.6 The shift to a neuro-affirming social model calls for reducing systemic and environmental barriers, while still addressing health needs.6,7
For pharmacists, it means making practice adjustments in the way that the profession engages with and provides support for autistic individuals.
According to the Australian Bureau of Statistics, approximately 290,900 Australians (1.1%) are reported to have had an autism diagnosis in 2022.5 A recent estimate by Autism Spectrum Australia (Aspect) suggested at least 1 in 40 Australians are autistic.7
Rising prevalence reflects improved awareness and diagnostic practices rather than a true increase in incidence, including better recognition in historically underdiagnosed groups such as females and older adults.7 Autism prevalence peaks in children and adolescents, particularly those aged 10–14 years, and is markedly lower in adults, acknowledging limited adult data.5,8,9
Autism prevalence rates may appear to vary among ethnic and cultural groups, reflecting inequities such as access to healthcare, effective communication, diagnostic practices and cultural perceptions.10
Prevalence remains higher in males than females, with 1.6% of males identified compared with 0.7% of females, and the greatest disparity is seen in children aged 5–9 years.5 Autism in females is frequently underdiagnosed, as characteristics may manifest differently, be masked (e.g. forced eye contact, rehearsed social scripts, suppressing stimming or copying peers), or fail to align with historically male-centred diagnostic criteria, leading to misdiagnosis as mood or personality disorders.11,12 Masking may occur due to a desire to fit in, fear of stigma or bullying, previous negative reactions to autistic behaviours, and expectations of how females are ‘supposed’ to behave.12 Increasing awareness of the under-recognition of autism in females and gender-diverse individuals, and the social drivers of masking, is anticipated to influence future prevalence estimates.4,5,11
There is no single cause of autism, and despite extensive research, aetiology remains incompletely understood. Current evidence indicates autism arises from a complex interaction between genetic susceptibility and environmental influences on neurodevelopment.13
Family history is one of the strongest predictors of autism.13,14 Researchers have identified hundreds of genes, with approximately 10–20% of cases associated with rare genetic variants arising from mutations in sperm or egg cells.14 Autism is considered polygenic, meaning overall risk typically reflects the cumulative effect of multiple inherited variants, each contributing a small effect.14
The expression of genetic susceptibility is known to be influenced by prenatal, perinatal and postnatal environmental factors.13 Environmental factors appear most relevant during the prenatal period.14 Modest associations have been reported between autism likelihood and maternal factors such as hypertension, gestational diabetes, obesity, alcohol and substance use, poor antenatal care, and infection or fever during pregnancy.15
Imprecise and inconsistent associations have been reported for folate status, exposure to some air pollutants, and the use of some medicines.15–17 Importantly, these findings are largely derived from observational studies and are subject to confounding. While some prenatal medicine exposures show more consistent associations with autism, there is no clear evidence that associations between autism and other environmental and medicine exposures represent a causal relationship, and any contribution to autism risk remains limited and uncertain.14,17

Autism is diagnosed according to Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR) criteria: ‘persistent deficits in social communication and social interaction across multiple contexts’, with the presence of ‘restricted, repetitive patterns of behaviour, interests or activities’.2
‘Symptoms must be present in the early development period’, although they may only become fully apparent later in life.
‘Symptoms cause clinically significant impairment in social, occupational or other important areas of functioning’ and ‘these disturbances are not better explained by IDD’ although both can co-occur.2 The DSM-5-TR also specifies severity levels (1–3) to indicate the degree of support required.2
In Australia, individuals may pursue an autism diagnosis through public or private pathways.18 Both are typically lengthy and necessitate a degree of health literacy and English proficiency. Diagnostic assessments may be conducted by a multidisciplinary team, including paediatricians, psychiatrists, psychologists, speech pathologists and occupational therapists.4 Multiple appointments may be needed, drawing on input from family, carers or teachers.18,19
Barriers to diagnosis include limited awareness of early signs among caregivers and clinicians, long wait times and out-of-pocket costs for specialist assessment, socioeconomic and geographic disparities, and bias in recognising diverse presentations.11,20,21 Limited health literacy and the complexity of navigating multidisciplinary assessments and National Disability Insurance Scheme requirements further impede access.21 In some communities, stigma, fear of labelling, and differing cultural interpretations of behaviour may delay help-seeking.22
A best-practice diagnostic approach should promote cultural safety and sensitivity, acknowledge variations in health literacy, address socioeconomic barriers, and be grounded in person-centred care.
Autism is a spectrum, with each individual having a unique mix of strengths, challenges, interests, needs and way of interacting with the world. Autism advocate Dr Stephen Shore states, ‘If you have met one autistic person, you have met one autistic person’.23
Beyond the core featuresComorbid NDDs, and psychiatric and medical conditions can create significant challenges for autistic individuals in relation to diagnosis, selection of appropriate interventions, medicines and support services.1,24
Comorbid NDDs among autistic individuals include ADHD, developmental coordination disorder (dyspraxia), IDD, and specific learning disorders such as dyslexia, dysgraphia and dyscalculia.25 Psychiatric comorbidities are also prevalent, including anxiety, depression, obsessive-compulsive disorder, and post-traumatic stress disorder.26 These conditions can intensify social and sensory challenges, increase vulnerability to stress, and impair emotional regulation and executive functioning.
Autistic individuals experience higher rates and severity of mental and physical health comorbidities than neurotypical individuals. Neurodivergent mental health outcomes are influenced by the interaction between individual differences and environmental and societal factors.25–28 Diagnostic overshadowing, whereby mental health symptoms are erroneously attributed to autism, should be avoided.29 Comorbid conditions warrant assessment and treatment according to the same clinical standards applied to neurotypical individuals, with adaptations made to accommodate the communication, sensory and support needs of autistic people. Neurodivergent individuals experience the full range of medical comorbidities seen in the general population; however, research indicates higher prevalence of certain conditions, including gastrointestinal disorders (e.g. irritable bowel syndrome, chronic constipation), sleep disturbances, epilepsy, and immune or metabolic disorders.30 These conditions may worsen fatigue, concentration and mood regulation, while motor difficulties may contribute to musculoskeletal pain, reduced physical activity and secondary health issues.31
Physical health conditions may be underdiagnosed when the clinical focus is limited to behavioural or psychological symptoms.29
Recognising the complex interconnections between physical, psychiatric and NDD health is paramount. Pharmacists can play a vital role in this process. Effective care relies on health professionals working collaboratively to identify how comorbid conditions, treatment burden and medicines may influence behaviour, cognition and developmental outcomes.
Autism is a lifelong NDD for which there is no curative treatment.4 Clinical care focuses on supporting health, functioning and community participation, addressing comorbidities, and optimising quality of life, while recognising and respecting the individual strengths, capabilities and perspectives of autistic individuals.3
Supports and interventions are individualised and typically involve a multidisciplinary team to address evolving needs.10 Allied health professionals may include speech pathologists to support communication, occupational therapists to address sensory processing and daily living skills, and psychologists to support emotional regulation and mental health. Physiotherapists may support gross motor skills, while dietitians support feeding and nutritional adequacy, alongside specialist educational support and therapy (e.g. play therapy, art therapy).3 Effective management relies on coordinated care, regular goal review and clear communication between the autistic individual, families and carers, and the multidisciplinary team.24
There is no evidence to support the use of medicines, exclusion diets or other biological treatment for the core features of autism.32,33 To support comorbidities, psychotropic medicines, antiepileptics and sleep agents may be used short term and under specific circumstances. Off-label use is common and requires careful assessment of risk-benefit balance, adverse effects, formulation choice, monitoring, cumulative treatment burden, and very careful consideration if the medicine is being prescribed as a chemical restraint.4

Autism is subject to persistent myths that pharmacists may encounter. The most damaging is the long-debunked claim that vaccines cause autism.14 The retracted 1998 Lancet study by Andrew Wakefield that claimed a link between the measles, mumps, rubella (MMR) vaccine and autism was a small, flawed study (with only 12 participants) and was exposed for unethical processes, methodological misconduct, and undisclosed conflicts of interest.14 Despite retraction, its claims were (and continue to be) amplified, eroding trust in public health and fuelling vaccine hesitancy. A Cochrane review published in 2021 found no credible evidence of an association between MMR and MMRV vaccines and autism.34
Two medicines made headlines in 2025: paracetamol and leucovorin (folinic acid or calcium folinate) claimed as a cause and treatment of autism respectively. Antenatal paracetamol exposure was alleged to increase autism and ADHD risk; however, major studies have not demonstrated a causal relationship.9 Stronger evidence from a large Swedish population-based cohort of 2,480,797 children born between 1995 and 2019 found no association between paracetamol use during pregnancy and autism, ADHD or IDD in sibling-controlled analysis.16 Cerebral folate deficiency (CFD) has been reported in a subset of autistic individuals, related to impaired folate transport into the brain, and may be associated with symptoms of speech difficulties, seizures and IDD, often within early childhood.35,36 Leucovorin, a folinic acid derivative, has been investigated as a potential treatment for autistic children with CFD. Leucovorin can bypass impaired folate transport, increasing central nervous system folate availability.36 Although some small-scale trials indicate potential minor behavioural improvements, supporting evidence remains limited, inconsistent, and not independently replicated.15,37
As medicines experts, pharmacists are well placed to counter common myths. Responses should prioritise empathetic, respectful communication and the provision of clear, evidence-based information and resources.
Accessibility, strong communication skills, medicines expertise, understanding of health system navigation and ability to synthesise information, position pharmacists to provide continuity of care for autistic individuals. Pharmacists can serve as an integrative link within multidisciplinary teams, supporting autistic individuals and their families across the healthcare continuum.
Effective communication underpins person-centred pharmacy practice. Pharmacists supporting autistic individuals should adapt both verbal and non-verbal communication to meet diverse needs.38 Autism can influence communication and sensory processing in unique ways, with some individuals experiencing sensory sensitivities to sound, light, smell, touch and visual stimuli.3,4,33 Some autistic individuals regulate sensory input through stimming (self-stimulatory behaviour), which may present as repetitive movements or sounds such as fidgeting, rocking or hand-flapping.39 Flexibility, empathy and understanding of sensory needs ensure equitable access to healthcare and fosters the relationship between patient and pharmacist. Verbal communication with autistic individuals should be clear and structured. Pharmacists should use straightforward, unambiguous language and present information in small, logical steps, allowing time for processing and response. Offering a calm, quiet space can both minimise sensory overload and facilitate a more comfortable environment for communication.38,40
Non-verbal communication requires equal attention. Eye contact, facial expressions and gestures can carry unintended meaning for autistic individuals. Some avoid eye contact as a coping mechanism, not as disinterest.38 Pharmacists should avoid assumptions and focus on open, calm body language and a reassuring tone. Visual supports can reinforce verbal explanations to provide ongoing reference, especially for individuals who process visual information more effectively than spoken language.40
A person-centred approach requires pharmacists to recognise, respond and adapt to the communication preferences of each autistic individual. If a caregiver or support worker is present, collaboration should occur while directing communication towards the patient whenever possible.40 Empathy, flexibility and inclusive communication techniques ensure care that is respectful and accessible and upholds an individual’s dignity and autonomy.
By adopting inclusive, neuro-affirming approaches, pharmacists strengthen equity, accessibility and person-centredness within healthcare. In doing so, they uphold the profession’s commitment to compassionate, evidence-based practice and help ensure autistic Australians receive the respect, understanding and tailored support needed to achieve optimal health and wellbeing.
Case scenario continuedEnzo’s mother discloses Enzo’s autism diagnosis and requests a quiet area and slower, step-by-step instructions. You offer a consultation room with dimmed lights, minimal visual clutter and no background noise. Enzo settles, visibly calmer. In this adapted space, you employ person-centred strategies: a soft, steady voice; paced delivery; short, simple sentences; pauses after each point for processing; confirming understanding via yes/no questions or thumbs-up signals; and a clear, written handout with bullet points, icons (e.g. clock for bedtime), and appropriate font. Enzo engages, maintaining partial eye contact and nodding, while his mother clarifies. These modifications demonstrate empathy, flexibility and equitable care, minimising distress, enhancing information access and supporting Enzo’s autonomy. |
Yvette Anderson (she/her) BPharm, MPS, CredPharm (MMR), ANZCAP (MentalHth, Paeds), CPGx, GradCert Autism is an accredited clinical pharmacist with over 20 years’ experience across aged care, consultancy, community pharmacy and hospital pharmacy. In 2020, she launched The Spectrum Pharmacist to increase awareness, promote inclusion, and provide education and support for neurodevelopmental disorders.
Victor Senescall (he/him) BPharm (Hons)
Merck Manual Professional Version. Overview of learning disorders. 2024. Available from: www.merckmanuals.com/professional/pediatrics/learning-and-developmental-disorders/overview-of-learning-disorders?query=neurodevelopment%20disorders
American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 5th ed. Washington (DC): American Psychiatric Publishing; 2022.
Merck Manual Professional Version. Autism spectrum disorder. 2025. Available from: www.merckmanuals.com/professional/pediatrics/learning-and-developmental-disorders/autism-spectrum-disorder
Therapeutic Guidelines. Autism spectrum disorder. Melbourne: Therapeutic Guidelines; 2021.
Australian Bureau of Statistics. Autism in Australia 2022. 2024. Available from: www.abs.gov.au/articles/autism-australia-2022
Bertilsdotter Rosqvist H, Pearson A, Pavlopoulou G, et al. The social model in autism research. Autism. 2025;29(9):2201–2204.
Autism Spectrum Australia. At least 1 in 40 Australians are autistic: new estimate by Aspect on World Autism Understanding Day. 2024. Available from: www.aspect.org.au/news/at-least-1-in-40-australians-are-autistic
Therapeutic Guidelines. Autism spectrum disorder. eTG complete. Melbourne: Therapeutic Guidelines; 2021.
Trollor J, Arnold S, Walker SE. Australian Longitudinal Study of Autism in Adulthood (ALSAA): final report. Brisbane: Autism CRC; 2022.
Rasheed Z. Autism in Australia: understanding, challenges, and support. Int J Health Sci. 2023;17(5):1–4.
Lai M-C, Amestoy A, Bishop S, et al. Improving autism identification and support for individuals assigned female at birth: clinical suggestions and research priorities. Lancet Child Adolesc Health. 2023;7(12):897–908.
National Autistic Society. Masking. 2026. Available from: www.autism.org.uk/advice-and-guidance/topics/behaviour/masking
Ostrowski J, Religioni U, Gellert B, et al. Autism spectrum disorders: etiology, epidemiology, and challenges for public health. Med Sci Monit. 2024;30.
Australian Academy of Health and Medical Sciences. Autism: an evidence brief. 2025. Available from: https://aahms.org/policy/evidence-brief-on-autism
Love C, Sominsky L, O'Hely M, et al. Prenatal environmental risk factors for autism spectrum disorder and their potential mechanisms. BMC Med. 2024;22.
Ahlqvist VH, Sjöqvist H, Dalman C, et al. Acetaminophen use during pregnancy and children's risk of autism, ADHD, and intellectual disability. JAMA. 2024;331(14):1205–1214.
de Lara I, Wagner P, Matheus G, et al. Association of prenatal exposure to antiseizure medication with risk of autism: a systematic review and meta-analysis. Seizure. 2025;130:41–47.
Government of South Australia Office for Autism. Pathways for assessment and diagnosis. 2023. Available from: www.officeforautism.sa.gov.au/autism/pathways-for-diagnosis
Autism Awareness Australia. Understanding and accessing the NDIS. 2024. Available from: www.autismawareness.com.au/navigating-autism/understanding-and-accessing-the-ndis-for-autism
Estrin GL, Milner V, Spain D, et al. Barriers to autism spectrum disorder diagnosis for young women and girls: a systematic review. Rev J Autism Dev Disord. 2021;8(4):454–470.
Allen-Meares P, Lowry B, Estrella ML, et al. Health literacy barriers in the health care system: barriers and opportunities for the profession. Health Soc Work. 2020;45(1):62–64.
Khalil A, Yatcilla J, Christie N, et al. A systematic review of help-seeking barriers for racial-ethnic minority caregivers accessing autism diagnostic and intervention services. J Racial Ethn Health Disparities. 2025.
Flannery KA, Wisner-Carlson R. Autism and education. Child Adolesc Psychiatr Clin N Am. 2020;29(2).
Autism Awareness Australia. Navigating the health system. 2024. Available from: www.autismawareness.com.au/navigating-autism/navigating-the-health-system-for-autism
Bonti E, Zerva IK, Koundourou C, et al. The high rates of comorbidity among neurodevelopmental disorders: reconsidering the clinical utility of distinct diagnostic categories. J Pers Med. 2024;14(3):300.
Lai M-C, Kassee C, Besney R, et al. Prevalence of co-occurring mental health diagnoses in the autism population: a systematic review and meta-analysis. Lancet Psychiatry. 2019;6(10):819–829.
Mazurek MO, Sadikova E, Cheak-Zamora N, et al. Health care needs, experiences, and perspectives of autistic adults. Autism Adulthood. 2023;5(1):51–62.
Barlattani T, D'Amelio C, Cavatassi A, et al. Autism spectrum disorders and psychiatric comorbidities: a narrative review. J Psychopathol. 2023;29(1):3–24.
Blair J. Diagnostic overshadowing: see beyond the diagnosis. 2017. Available from: www.intellectualdisability.info/changing-values/diagnostic-overshadowing-see-beyond-the-diagnosis
Al-Beltagi M. Autism medical comorbidities. World J Clin Pediatr. 2021;10(3):15–28.
Sung Y-S, Loh SC, Lin L-Y. Physical activity and motor performance: a comparison between young children with and without autism spectrum disorder. Neuropsychiatr Dis Treat. 2021;17:3743–3751.
Turner M. The role of drugs in the treatment of autism. Aust Prescr. 2020;43:185–190.
Mayo Clinic. Autism spectrum disorder. 2025. Available from: www.mayoclinic.org/diseases-conditions/autism-spectrum-disorder/diagnosis-treatment/drc-20352934
Di Pietrantonj C, Rivetti A, Marchione P, et al. Vaccines for measles, mumps, rubella, and varicella in children. Cochrane Database Syst Rev. 2021;(11):CD004407.
Wong A, Frye RE, Ohnemus-Kawamura B, et al. Cerebral folate deficiency. 2019. Available from: https://rarediseases.org/rare-diseases/cerebral-folate-deficiency/
Ramaekers VTH, Quadros EV. Cerebral folate deficiency syndrome: early diagnosis, intervention and treatment strategies. Nutrients. 2022;14(15):3096.
Sheppeard A. What is leucovorin, and can it cure autism? 2025. Available from: www.medicalrepublic.com.au/what-is-leucovorin-and-can-it-cure-autism/120175
Norris JE, Milton D, Heasman B. Adapting communication with autistic service users: a participatory study. Autism. 2024.
National Autistic Society. Repeated movements and behaviour (stimming). 2026. Available from: www.autism.org.uk/advice-and-guidance/topics/about-autism/repeated-movements-and-behaviour-stimming
National Autistic Society. Autism and communication. 2024. Available from: www.autism.org.uk/advice-and-guidance/topics/about-autism/autism-and-communication
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Case scenarioStavros, a 35-year-old male with focal epilepsy, presents to the pharmacy to collect his medicines. He appears tired and mentions he has been having more frequent breakthrough seizures lately. As you chat, he reveals he recently started lorazepam 1 mg twice daily for generalised anxiety disorder (GAD), prescribed by his new GP. Stavros has been missing doses of his anti-seizure medicine, carbamazepine, as he feels it worsens his drowsiness and confusion. |
Dr Ming S Soh PhD, BPharm (Hons)[/caption]
Epilepsy is a chronic neurological condition characterised by a persistent tendency to produce seizures.1,2 According to the International League Against Epilepsy (ILAE), epilepsy is diagnosed when an individual experiences at least two unprovoked seizures more than 24 hours apart, one unprovoked seizure with a high probability (≥60%) of recurrence, or when an epilepsy syndrome is identified.3 Seizures result from abnormal, excessive electrical discharges in the brain, and vary in type, severity and frequency.4 While most seizures are brief, lasting seconds to minutes, they can become prolonged and continuous (i.e. status epilepticus), which requires urgent, intensive medical intervention.4 Globally, epilepsy affects around 50 million people.5,6 It can affect individuals across all age groups, races and ethnicities, and can significantly disrupt quality of life.7,8 Epilepsy is often associated with neurobiological, cognitive, psychological and social sequelae.1,2
Management of epilepsy primarily involves antiseizure medicines (ASM), administered as monotherapy or polytherapy depending on the patient’s response.8,9 In some cases, surgery, dietary therapy or neurostimulation may be considered.9 Treatment complexity, adverse drug reactions and non-adherence to medicines can hinder seizure control and prevent optimal outcomes.8
Learning OutcomesAfter reading this article, pharmacists should be able to:
|
In practice, pharmacists provide therapeutic drug monitoring (hospital setting), Home Medicines Reviews (HMR), MedsChecks and patient counselling, and they support the management of common comorbidities such as depression, anxiety and cognitive impairments, which can complicate treatment.6,8,9

Globally, the pooled incidence rate of epilepsy is estimated at 50–61.4 cases per 100,000 person-years.2,10,11 However, incidence varies by region and income level. In high-income countries, rates typically range from 40–70 per 100,000 person-years, while in low- and middle-income countries, incidence can reach 100–190 per 100,000 person-years, reflecting disparities in healthcare access, diagnostic capacity and exposure to risk factors.2,10 The highest incidence of epilepsy occurs in childhood, reflecting the higher seizure susceptibility of the developing brain.12
In Australia, the lifetime risk of developing epilepsy is estimated to be up to 4%, while approximately 0.6–1% of the population is living with epilepsy at any given time.13,14 Modelled data estimates that prevalence peaks in males aged 60–64 (8.54 per 1,000), and in females aged 50–54 (9.57 per 1,000).15 National surveillance data indicates that prevalence generally remains high into older age groups, largely due to increased rates of stroke, neurodegenerative diseases and brain tumours.2,14,15
Disparities are pronounced among Aboriginal and Torres Strait Islander people, who experience twice the prevalence of epilepsy compared to non-Aboriginal and Torres Strait Islander people.14,16 Aboriginal and Torres Strait Islander people also face higher rates of hospitalisation, reduced access to specialist care and ASM, and significantly elevated epilepsy-related mortality.16 The disability-adjusted life years for Aboriginal and Torres Strait Islander people with epilepsy are double those of non-Aboriginal and Torres Strait Islander people.16
Epilepsy has a multifactorial aetiology. The ILAE classifies epilepsy aetiologies into six main categories: genetic, structural, infectious, metabolic, immune and unknown (see Figure 1).17,18 Genetic mutations generally affect neuronal excitability, especially ion channels, and are linked to specific epilepsy syndromes.18–20 Structural causes include brain malformations, trauma, stroke and tumours. Infections like meningitis or encephalitis can provoke seizures through inflammation. Metabolic causes arise from systemic or inherited metabolic disorders that disrupt brain chemistry or energy production. Autoimmune responses, where the body’s immune system attacks brain tissue, can also lead to seizures. Unknown causes refer to cases where no clear aetiology can be identified despite thorough investigation. Neurodegenerative causes are increasingly recognised as important contributors to epilepsy.18 Despite structured classifications, many overlap. For example, an infection such as encephalitis may lead to structural brain damage.18 Risk factors include family history, perinatal insults, head trauma, brain infections, febrile seizures and socioeconomic disparities, which can influence both the likelihood of developing epilepsy as well as its clinical progression.21

Epilepsy involves several interconnected mechanisms that predominate in different seizure types and epilepsy syndromes and are targeted by specific ASM.
Neuronal hyperexcitability is increased neuronal responsiveness due to ion-channel dysfunction, resulting in spontaneous, excessive neuronal firing. This is a key mechanism underlying all seizure types, but is not the sole pathophysiological mechanism.4,22,23
Hypersynchrony is the abnormal synchronisation of neuronal activity which facilitates seizure propagation across brain regions, particularly in generalised epilepsies such as absence and tonic-clonic seizures.1,4,12,18
Excitatory/inhibitory neurotransmitter imbalance refers to the disruption of glutamate and gamma-aminobutyric acid (GABA) neurotransmission, shifting networks toward hyperexcitability and is central to both focal and generalised epilepsy.4,17
Neuroinflammation refers to the immune activation and cytokine release (e.g. IL-1 beta, TNF-alpha) that can enhance excitability, and are implicated in structural focal epilepsies, post-stroke epilepsy and autoimmune epilepsies. Anti-inflammatory and immunomodulatory therapies may be used in selected cases.4,24
mTOR pathway dysregulation is the abnormal mTOR signalling that alters synaptic plasticity, contributing to epileptogenesis, most notably in tuberous sclerosis complex–associated epilepsy, where mTOR inhibitors such as everolimus are used as targeted therapy.18
Oxidative stress is the excess reactive oxygen species that can damage neurons and lower seizure thresholds, contributing to seizures in metabolic and neurodegenerative epilepsies.24
Mitochondrial dysfunction refers to impaired energy metabolism, which reduces neuronal resilience and is characteristic of mitochondrial epilepsies and some childhood epileptic encephalopathies.24
Synaptic reorganisation refers to structural changes, including aberrant axon sprouting and new excitatory circuit formation, and are commonly seen in temporal lobe epilepsy following brain injury or prolonged seizures.4
Recognising underlying epileptogenic mechanisms aids interpretation of seizure type/classification and guides appropriate ASM selection.
Focal seizures (formerly known as partial)
Focal seizures originate in a specific area of one cerebral hemisphere. Depending on the brain area affected, they may present with localised motor activity like rhythmic jerking or muscle stiffening, sensory changes such as tingling or visual distortions, or autonomic signs, including flushing and gastrointestinal discomfort.12 Awareness may or may not be impaired during these seizures.25 Some focal seizures begin with an aura, such as déjà vu or intense emotions, during which a person remains alert. First-line treatment includes carbamazepine, lamotrigine or levetiracetam, where selection is guided by contraindications and other patient-specific factors.26
Generalised seizures
Generalised seizures involve widespread electrical activity across both cerebral hemispheres and typically include tonic-clonic, absence, myoclonic and atonic seizures.12,25
Tonic-clonic seizures (formerly known as grand mal)
Tonic-clonic seizures are characterised by a sudden loss of consciousness, muscle stiffening followed by rhythmic jerking, and a post-seizure phase with confusion, agitation or fatigue. They can sometimes be fatal due to associated complications. Some tonic-clonic seizures begin as focal seizures with preserved awareness, but progress to loss of consciousness as they generalise across both hemispheres of the brain.12 First-line treatment is sodium valproate, unless contraindicated or otherwise inappropriate for the patient (e.g. individuals of childbearing potential).26
Absence seizures (formerly known as petit mal)
Absence seizures are typically characterised by brief episodes of staring or unresponsiveness, and are often unnoticed or mistaken for daydreaming.12,25 First-line treatment includes ethosuximide or sodium valproate where selection is guided by contraindications and other patient-specific factors.26
Myoclonic seizures
Myoclonic seizures present as sudden and brief muscle jerks.12,25 First-line treatment is sodium valproate unless contraindicated or otherwise inappropriate (e.g. individuals of childbearing potential).26
Atonic seizures
Atonic seizures result in a sudden loss of muscle tone, leading to falls.12,25
For further information, see Australian Medicines Handbook: Epilepsy.26
Diagnosis of epilepsy involves detailed clinical history, neurological examination and supportive investigations.12,17 Electroencephalogram (EEG) is central for detecting epileptiform discharges, while neuroimaging techniques such as computed tomography (CT) and magnetic resonance imaging (MRI) can help identify structural causes.12 In complex cases, additional tools including positron emission tomography (PET)/single photon emission computed tomography (SPECT), magnetoencephalography (MEG) and genetic testing can support diagnosis and guide treatment. The advanced neuroimaging modalities are especially useful for presurgical evaluations in specialised centres.12 Neuropsychological assessments can also provide insight into cognitive impacts.1 ILAE classification recommends a structured, three-level diagnostic approach, identifying seizure type, epilepsy type and specific epilepsy syndrome, while integrating aetiology at each stage to inform treatment decisions.3 Syncope, psychogenic non-epileptic seizures, transient ischaemic attacks, migraine auras and sleep disorders can mimic epileptic seizures but differ in aetiology and treatment.12,27
Prognosis varies widely, depending on seizure type, aetiology, age of onset and treatment response.12 Many patients can achieve seizure control with ASM, and some enter long-term remission. However, around one-third of patients develop drug-resistant epilepsy, unresponsive to two or more ASM.12 Early age of onset, especially in infancy, and epilepsy with structural lesions such as hippocampal sclerosis, are often linked to poorer outcomes.28,29 Sudden unexpected death in epilepsy remains a serious risk,30 particularly in patients with uncontrolled generalised tonic-clonic seizures and early-onset syndromes such as Dravet syndrome (severe infantile-onset developmental epileptic encephalopathy), which has a 3–5-fold higher mortality risk than the general epilepsy population.31 Early diagnosis and individualised treatment strategies improve outcomes.
The primary aim is to achieve seizure freedom with minimal side effects, improving quality of life. Treatment recommendations follow a stepwise approach, guided by seizure classification, epilepsy type, underlying aetiology, side effect profile, cost, potential for measuring serum drug concentration, pharmacokinetics and patient-specific factors such as age, pregnancy, medicine interactions and comorbidities.17,26,32,33
Initial management involves monotherapy with an appropriate ASM. Dose is generally started low and titrated slowly to achieve seizure control. If control is not achieved with maximally tolerated doses of a single agent, a second agent may be added. The second agent may be considered for monotherapy if the patient and prescriber are willing to gradually withdraw the first agent. If two agents do not promote seizure control, the second agent may be withdrawn gradually and replaced with a third.34
Treatment with an ASM should never be ceased abruptly.34
Key treatment considerations
For further information, see Therapeutic Guidelines: Neurology.34
Evidence is limited for cannabis-derived products. Cannabidiol is approved for specific syndromes but requires specialist oversight.33,34
Non-pharmacological management includes surgery following EEG/MRI evaluation, vagus nerve and deep brain stimulation, ketogenic diet and gene therapy. Yoga, meditation and acupuncture have limited evidence for use.17,31–35
One of the most common challenges during epilepsy treatment is adherence. Missed doses or abrupt discontinuation can trigger recurrent seizures which significantly increase mortality risk.33 Medicine interactions are another significant concern, particularly with older ASM such as phenytoin and carbamazepine, which are enzyme inducers and can alter the efficacy of other medicines.33 Patients should be informed that some medicines can lower their seizure threshold. These include theophylline, pethidine, certain antidepressants (uncommon), and some antipsychotics. Some important medicine interactions are shown in Table 1.

Treatment complications range from mild to severe. Common side effects include fatigue, dizziness, cognitive issues such as memory or attention difficulties, and abdominal upset including pain, nausea and vomiting.33
More serious but less frequent reactions include liver and renal toxicity, bone marrow suppression and skin reactions.26 Long-term use of certain ASM including carbamazepine and phenytoin may also reduce bone density, increasing fracture risk.12,33 Additionally, some ASM including levetiracetam and topiramate can worsen mood disorders, contributing to anxiety and depression.26,33
Age also influences management.32,33 Children often require weight-based dosing and closer monitoring due to variable metabolism, while older adults are more susceptible to adverse effects and medicine interactions due to comorbidities and declining organ function.34
To manage these risks, routine monitoring, including liver and renal function tests, therapeutic drug monitoring, bone health assessments and mental health screening, is essential.
Epilepsy treatment requires regular follow-up to assess seizure control, treatment efficacy and adverse effects. Monitoring for drugs with narrow therapeutic index should also be considered. Treatment plans should be reviewed annually, or sooner, to discuss any changes in seizure occurrence.
Patients in Australia can access further advice and support through multiple channels, including:
Epilepsy Action Australia – education, telehealth and resources
Epilepsy Foundation – seizure management and support services
National Epilepsy Support Service/Epilepsy Smart Australia – 1300 761 487 Monday to Friday, from 9 am to 5 pm (AEST).
Pharmacists support epilepsy management across both community and hospital settings. Hospital pharmacists contribute by implementing therapeutic drug monitoring, especially for ASM with narrow therapeutic windows, collaborating with multidisciplinary teams to optimise treatment plans, monitoring for adverse drug reactions, and managing complex cases involving polytherapy or comorbidities. Community pharmacists can provide ongoing support and medicines counselling, and conduct MedsChecks, detect side effects early, and address mental health concerns. Together, pharmacists provide personalised care that can help improve seizure control, enhance treatment safety and reduce mortality.
With appropriate treatment, many people with epilepsy can achieve good seizure control and lead full, active lives. However, outcomes depend on early intervention, consistent follow-up, monitoring and personalised care. Pharmacist involvement helps reduce complications, improves medicine adherence and supports overall wellbeing.
Case scenario continuedYou recognise that emotional stress, non-adherence and adverse effects are likely precipitating Stavros’ seizures. Concomitant use of lorazepam and carbamazepine contributes to additive CNS depression, causing sedation. As Stavros prefers pharmacological treatment for GAD, you call his GP and suggest sertraline 50 mg daily, noting that carbamazepine may reduce sertraline concentrations via enzyme induction, and clinical response should be monitored. You recommend ceasing lorazepam and encourage cognitive behavioural therapy. The GP reviews Stavros and he returns with a cessation plan for lorazepam and a prescription for sertraline. You counsel on treatment expectations and the importance of adherence. A month later, Stavros returns, feeling alert with no recent seizures. |
DR Ming S Soh PhD, BPharm (Hons) is a Research Fellow at the Florey Institute of Neuroscience and Mental Health, University of Melbourne, with expertise in preclinical models of genetic epilepsy and therapeutic development.
Fisher RS, van Emde Boas W, Blume W, et al. Epileptic seizures and epilepsy: definitions proposed by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE). Epilepsia. 2005;46(4):470–472.
Beghi E. The epidemiology of epilepsy. Neuroepidemiology. 2020;54(2):185–191.
Scheffer IE, Berkovic S, Capovilla G, et al. ILAE classification of the epilepsies: position paper of the ILAE commission for classification and terminology. Epilepsia. 2017;58(4):512–521.
Scharfman HE. The neurobiology of epilepsy. Curr Neurol Neurosci Rep. 2007;7(4):348–354.
World Health Organization. Epilepsy. 2022. Available from: www.who.int/news-room/fact-sheets/detail/epilepsy
Petrides M, Peletidi A, Nena E, et al. The role of pharmacists in enhancing epilepsy care: a systematic review of community and outpatient interventions. J Pharm Policy Pract. 2025;18(1):2487046.
Zack MM. National and state estimates of the numbers of adults and children with active epilepsy—United States, 2015. MMWR Morb Mortal Wkly Rep. 2017;66.
Bacci JL, Zaraa S, Stergachis A, et al. Community pharmacists’ role in caring for people living with epilepsy: a scoping review. Epilepsy Behav. 2021;117:107850.
Reis TM, Campos M, Nagai MM, et al. Contributions of pharmacists in the treatment of epilepsy: a systematic review. Am J Pharm Benefits. 2016;8(3):e55–e60.
Bell GS, Sander JW. The epidemiology of epilepsy: the size of the problem. Seizure. 2001;10(4):306–316.
Fiest KM, Sauro KM, Wiebe S, et al. Prevalence and incidence of epilepsy: a systematic review and meta-analysis of international studies. Neurology. 2017;88(3):296–303.
Stafstrom CE, Carmant L. Seizures and epilepsy: an overview for neuroscientists. Cold Spring Harb Perspect Med. 2015;5(6):a022426.
Mohanannair Geethadevi G, Chen Z, et al. Impact of epilepsy on productivity and quality of life: the Australian epilepsy project. Neurology. 2025;105(5):e214011.
Australian Institute of Health and Welfare. Epilepsy in Australia. Canberra: AIHW; 2022. Available from: www.aihw.gov.au/reports/chronic-disease/epilepsy-in-australia/contents/about
Foster E, Chen Z, Zomer E, et al. The costs of epilepsy in Australia: a productivity-based analysis. Neurology. 2020;95(24):e3221–e3231.
Keenan NF, Aitchison SG, Jetté N, et al. Epilepsy in the Indigenous peoples in Canada, Australia, New Zealand, and the USA: a systematic scoping review. Lancet Glob Health. 2025;13(4):e656–e668.
Vera-González A. Pathophysiological mechanisms underlying the etiologies of seizures and epilepsy. In: Czuczwar SJ, editor. Epilepsy. Brisbane: Exon Publications; 2022. p. 1–13.
Balestrini S, Arzimanoglou A, Blümcke I, et al. The aetiologies of epilepsy. Epileptic Disord. 2021;23(1):1–16.
Perucca P, Bahlo M, Berkovic SF. The genetics of epilepsy. Annu Rev Genomics Hum Genet. 2020;21(1):205–230.
Scheffer IE, Berkovic SF. The genetics of human epilepsy. Trends Pharmacol Sci. 2003;24(8):428–433.
Bhalla D, Godet B, Druet-Cabanac M, Preux P-M. Etiologies of epilepsy: a comprehensive review. Expert Rev Neurother. 2011;11(6):861–876.
Reid CA. Preface: ion channels and genetic epilepsy. J Neurochem. 2024;168(12):3829–3830.
Oyrer J, Maljevic S, Scheffer IE, et al. Ion channels in genetic epilepsy: from genes and mechanisms to disease-targeted therapies. Pharmacol Rev. 2018;70(1):142–173.
Fabisiak T, Patel M. Crosstalk between neuroinflammation and oxidative stress in epilepsy. Front Cell Dev Biol. 2022;10:976953.
Fisher RS, Cross JH, French JA, et al. Operational classification of seizure types by the International League Against Epilepsy: position paper of the ILAE commission for classification and terminology. Epilepsia. 2017;58(4):522–530.
Buckley N, editor. Australian medicines handbook. Adelaide: Australian Medicines Handbook Pty Ltd; 2025. Available from: https://amhonline.amh.net.au/
Cook M. Differential diagnosis of epilepsy. In: Shorvon S, Perucca E, Engel J Jr, editors. The treatment of epilepsy. 4th ed. Hoboken (NJ): John Wiley & Sons; 2015. p. 24–37.
Semah F, Picot M-C, Adam C, et al. Is the underlying cause of epilepsy a major prognostic factor for recurrence? Neurology. 1998;51(5):1256–1262.
Nickels K. Earlier is not always better: outcomes when epilepsy occurs in early life versus adolescence. Epilepsy Curr. 2020;20(1):27–29.
Devinsky O, Hesdorffer DC, Thurman DJ, et al. Sudden unexpected death in epilepsy: epidemiology, mechanisms, and prevention. Lancet Neurol. 2016;15(10):1075–1088.
Cooper MS, McIntosh A, Crompton DE, et al. Mortality in Dravet syndrome. Epilepsy Res. 2016;128:43–47.
Perucca E. General principles of medical management. In: Shorvon S, Perucca E, Engel J Jr, editors. The treatment of epilepsy. 4th ed. Hoboken (NJ): John Wiley & Sons; 2015. p. 110–123.
Perucca P, Scheffer IE, Kiley M. The management of epilepsy in children and adults. Med J Aust. 2018;208(5):226–233.
Therapeutic Guidelines Limited. eTG complete. Melbourne: Therapeutic Guidelines; 2025. Available from: www.tg.org.au
Baxendale S. Complementary and alternative treatments for epilepsy. In: Shorvon S, Perucca E, Engel J Jr, editors. The treatment of epilepsy. Hoboken (NJ): John Wiley & Sons; 2015. p. 298–310.
Johannessen SI, Johannessen Landmark C. Antiepileptic drug interactions: principles and clinical implications. Curr Neuropharmacol. 2010;8(3):254–267.
Buchanan N. Medications which may lower seizure threshold. Aust Prescr. 2001;24(1):8–9.
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[post_content] => New avenues for nurse prescribing have the potential to reshape frontline care. For pharmacists, it’s a live example of how scope expansion translates into real impact.
Nurse prescribing is entering a new phase in Australia, and pharmacists should be paying close attention.
While nurse practitioners and endorsed midwives have been able to prescribe Pharmaceutical Benefits Schedule (PBS) subsidised medicines since 2010, a new pathway will soon expand prescribing to a broader group of experienced nurses.
‘A lot of people wouldn't even know that nurses are already prescribing medications that are funded on the PBS,’ said Denise Lyons, President of the Australian Primary Health Care Nurses Association. ‘But there are more than 3,000 nurse practitioners and endorsed midwives in Australia now who are already prescribing.’
Under a new registration standard which came into effect in September last year, suitably qualified registered nurses will be able to prescribe medicines in Schedules 2, 3, 4 and 8 in partnership with an authorised prescriber.
‘It took until this year for universities to start the course that enables registered nurses to meet [the new standard],’ Ms Lyons said. ‘Most are 6-month postgraduate courses … So it will probably be around July 2026 that we will see the first [wave] of nurses completing the educational requirement.’
For pharmacists, this shift offers a live view of how prescribing reform is built – through legislation, governance, defined scope and, crucially, access to the PBS.
What’s changing?
The new framework is deliberately cautious. To become a designated RN prescriber, a nurse must:
‘Pharmacists and nurses are often people's first point of contact with the healthcare system, and it's really good if we can work to the top of our scope and do what we know we can do, with the right guardrails in place.' denise lyons
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[post_content] => Case scenario
Sarah, a 42-year-old woman, presents to the pharmacy reporting a small lump near the anus, occasional bright red bleeding on toilet paper after bowel movements, anal itching and discomfort. She mentions feeling embarrassed to seek advice and has been self-managing with sitz baths. She reports a history of chronic constipation with frequent training during defecation. She is not taking any regular medicines and requests an over-the-counter product to relieve her symptoms. You take the time to explore Sarah’s symptoms in more detail, to help identify any red flags that would require immediate referral. You ask about the duration, severity and other symptoms such as fatigue, unintentional weight loss and changes in bowel habits, all of which she denies.
Learning objectivesAfter reading this article, pharmacists should be able to:
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Anal fissures and haemorrhoids are commonly encountered, but their epidemiology is not well documented. Haemorrhoids represent the most frequent reason for proctology consultations, followed by anal fissures.1 Haemorrhoids are estimated to affect up to 40% of adults in the general population, although many individuals are asymptomatic.2 Anal fissures occur in approximately 10–15% of the population.3

An anal fissure is a longitudinal tear in the anal canal, most often occurring in the posterior midline, just below the dentate line.4 Anal fissures are typically classified as primary or secondary, depending on the cause. Primary fissures are usually benign and caused by local trauma, such as the passage of hard stools, prolonged diarrhoea, vaginal delivery, repeated injury or anal penetration.4 Secondary fissures, which are often multiple and located off the midline, are uncommon, accounting for less than 1% of cases.5 They result from underlying conditions like previous anal surgery, inflammatory bowel disease (e.g. Crohn’s disease), colorectal malignancy, infections (e.g. HIV/AIDS), or dermatological conditions (e.g. psoriasis).6 Anal fissures are further described as acute or chronic, with chronic fissures lasting more than 6 weeks.7
[caption id="attachment_31774" align="alignright" width="200"]
DR Amy Page (she/her) PhD, MClinPharm, GradDipBiostat, GCertHProfEd, GAICD, GStat, FSHPA, FPS is a consultant pharmacist, biostatistician, and the director of the Centre for Optimisation of Medicines at UWA’s School of Allied Health.[/caption]
Anal fissures are often mistaken for haemorrhoids because of their overlapping symptoms. Haemorrhoids differ in that they are normal vascular cushions within the anal canal that maintain continence. Although part of normal anatomy, the term ‘haemorrhoid’ is commonly used when these vascular anal cushions, containing a rich arteriovenous network, become enlarged or displaced.8 Haemorrhoids may be classified as internal (located above the dentate line) or external (located below the dentate line). Factors such as constipation, straining during bowel movements and a low-fibre diet are commonly considered to increase the risk of haemorrhoids.9,10 However, the causal relationship between these factors and the development of haemorrhoids remains unclear. A possible genetic component that predisposes to smooth muscle, epithelial and connective tissue dysfunction, may contribute to haemorrhoids.11
It is important to note that certain medicines can contribute to or worsen constipation as an adverse effect, thereby aggravating haemorrhoids and anal fissures.9,10 Common examples include opioids, anticholinergics, and iron and calcium supplements.12 Regular medication review should be incorporated into comprehensive care to identify opportunities for deprescribing and prevent inappropriate prescribing cascades, with further guidance available in the new deprescribing guidelines.13
The symptoms of haemorrhoids may include rectal bleeding, anal pruritus, prolapse, faecal seepage and mucus discharge.7
Internal haemorrhoids are usually painless because the columnar epithelium is insensitive to touch and temperature.8 In contrast, external haemorrhoids are pain sensitive and may become thrombosed, often following straining during defecation.8
Anal fissures, by comparison, typically cause severe tearing pain that is provoked by defecation.4 A key distinguishing feature is that the pain of an anal fissure typically occurs during or immediately after defecation.

For diagnostic purposes, medical practitioners perform a physical examination with the individual lying on their side, gently parting the buttocks to inspect the posterior midline.4 Several other anorectal disorders may present with similar symptoms to anal fissures and haemorrhoids. Differential diagnoses include anal fistula and solitary rectal ulcer syndrome, which can often be distinguished based on their clinical appearance through careful physical examination. An anal fistula typically presents as a draining skin punctum.14 It is an abnormal hollow tract, most often arising from infection of an anal gland.15 Solitary rectal ulcer syndrome may present with anal pain, rectal bleeding, constipation, mucus discharge, excessive straining and a sensation of incomplete evacuation. Despite its name, the condition does not always involve an ulcer. Diagnosis requires a combination of endoscopic and histopathological findings, together with the individual’s reported symptoms.16
Haemorrhoids
[caption id="attachment_31775" align="alignright" width="200"]
Hui Wen Quek (she/her) BPharm(Hons), GradCertAppPharmPrac is a pharmacist and PhD candidate at the University of Western Australia (UWA).[/caption]
Non-pharmacological treatment options
First-line management for haemorrhoids usually involves lifestyle measures, which include ensuring adequate fluid and fibre intake, reducing prolonged time on the toilet and avoiding excessive straining, the use of sitz baths, and maintaining anal hygiene.10 In practice, dietary and lifestyle modifications are usually recommended as a conservative and preventive measure for haemorrhoids.17
Pharmacological treatment options
Over-the-counter therapies for internal haemorrhoids include ointments and suppositories that contain emollients, mild astringents, local anaesthetics and/or corticosteroids.8 These preparations temporarily relieve itching and discomfort. Prolonged use of topical corticosteroids is not recommended, as it increases the risk of local infections such as candidiasis.8 Similarly, prolonged use of anaesthetic-containing products should be avoided due to potential adverse effects, including skin sensitisation and dermatitis.8
Outpatient procedures and surgery
For individuals who do not respond to conservative measures, other treatment options for haemorrhoids include outpatient procedures and surgery.10 Outpatient procedures include rubber band ligation, infrared coagulation, bipolar probe, heater probe, sclerotherapy and cryotherapy.10 These are generally reserved for people with grade I or grade II haemorrhoids.10 Surgery can be considered for people who do not respond to or cannot tolerate outpatient procedures, as well as those with large external haemorrhoids, or combined internal and external haemorrhoids with prolapse.10
A recent meta-analysis found that surgical treatments, compared with conservative treatments, offer greater symptom relief, quicker recovery and lower recurrence rates.18 However, they do carry risks of procedure-related complications. In contrast, conservative treatments are safer and less invasive, but tend to provide slower symptom improvement and have higher recurrence rates.18 Therefore, treatment decisions should be individualised, taking into account symptom severity, individual preferences and risk tolerance.
Anal fissures
The primary aim of treatment for anal fissures is to reduce anal sphincter spasm, improve blood flow and promote healing.6 First-line management is usually non-operative and includes increasing dietary fibre, use of sitz baths and applying glyceryl trinitrate 0.2% ointment, three times daily for up to 4 weeks to relieve pain.19 Headache is a common adverse effect of glyceryl trinitrate due to systemic absorption, which could limit its use.20 Other topical agents used in clinical practice include lidocaine and hydrocortisone, although these are less effective than a combination of fibre intake and warm sitz baths.4
Botulinum toxin injections may also be considered and can achieve good healing rates.6,19 However, botulinum toxin may cause temporary reduced control of wind or bowel motions, which usually resolves as the effect of the injection wears off.4 Due to these adverse effects and the invasive nature of the procedure, botulinum toxin is generally reserved as a second-line therapy.4 If these treatment options are unsuccessful, surgical treatment may be required.6
Secondary or chronic anal fissures warrant additional investigation and multidisciplinary management is advised, especially when malignancy is suspected or confirmed.4
Pharmacists play a key role in recognising the symptoms of haemorrhoids and anal fissures, providing timely advice and suggesting a suitable course of action. Pharmacists can also educate individuals on first-line management strategies and provide lifestyle advice where appropriate to prevent recurrence. In addition, pharmacists can advocate for the safe use of over-the-counter treatments, advise on appropriate duration of use and counsel individuals on potential adverse effects.
Referral to a medical practitioner is advisable for individuals who21:
Anal fissures and haemorrhoids are common conditions encountered in primary care and can greatly impact quality of life. Pharmacists play a critical role in early management and referral, helping prevent complications and improve outcomes.
Case scenario continuedYou identify that Sarah has haemorrhoids and provide lifestyle advice, including increasing fluid and dietary fibre intake, avoiding prolonged straining during bowel movements and practising good anal hygiene. For symptomatic relief, you suggest a topical ointment containing cinchocaine 0.5% and zinc oxide 20%, to be applied as needed. You also advise her to consult her general practitioner if she experiences persistent bleeding, ongoing pain or worsening prolapse. With your support and advice, Sarah feels more confident in managing her condition effectively while reducing the risk of recurrence. |
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Hui Wen Quek (she/her) BPharm(Hons), GradCertAppPharmPrac is a pharmacist and PhD candidate at the University of Western Australia (UWA).
DR Amy Page (she/her) PhD, MClinPharm, GradDipBiostat, GCertHProfEd, GAICD, GStat, FSHPA, FPS is a consultant pharmacist, biostatistician, and the director of the Centre for Optimisation of Medicines at UWA’s School of Allied Health.
Manisha Pillai (she/her) BPharm
Higuero T. Update on the management of anal fissure. J Visc Surg. 2015;152(2 Suppl):S37–S43.
Riss S, Weiser FA, Schwameis K, Riss T, Mittlböck M, Steiner G, et al. The prevalence of hemorrhoids in adults. Int J Colorectal Dis. 2012;27(2):215–220.
Vitton V, Bouchard D, Guingand M, Higuero T. Treatment of anal fissures: results from a national survey on French practice. Clin Res Hepatol Gastroenterol. 2022;46(4):101821.
Schlichtemeier S, Engel A. Anal fissure. Aust Prescr. 2016;39(1):14–17.
Zaghiyan KN, Fleshner P. Anal fissure. Clin Colon Rectal Surg. 2011;24(1):22–30.
Newman M, Collie M. Anal fissure: diagnosis, management, and referral in primary care. Br J Gen Pract. 2019;69(685):409–410.
Lyle V, Young C. Anal fissures: an update on treatment options. Aust J Gen Pract. 2024;53:33–35.
Therapeutic Guidelines Limited. Haemorrhoids. Melbourne: Therapeutic Guidelines Limited; 2022. Available from: https://www.tg.org.au
Lohsiriwat V. Hemorrhoids: from basic pathophysiology to clinical management. World J Gastroenterol. 2012;18(17):2009–2017.
Sandler RS, Peery AF. Rethinking what we know about hemorrhoids. Clin Gastroenterol Hepatol. 2019;17(1):8–15.
Zheng T, Ellinghaus D, Juzenas S, Cossais F, Burmeister G, Mayr G, et al. Genome-wide analysis of 944 133 individuals provides insights into the etiology of haemorrhoidal disease. Gut. 2021;70(8):1538–1549.
Therapeutic Guidelines Limited. Functional constipation in adults. Melbourne: Therapeutic Guidelines Limited; 2022. Available from: https://www.tg.org.au
Quek HW, Reus X, Lee K, Etherton-Beer C, Page A; Guideline Development Group. Deprescribing in older people: a clinical practice guideline. Perth (WA): The University of Western Australia; 2025.
Stewart D. Anal fissure: clinical manifestations, diagnosis, prevention. UpToDate. 2025. Available from: https://www.uptodate.com/contents/anal-fissure-clinical-manifestations-diagnosis-prevention
Therapeutic Guidelines Limited. Anorectal abscess and fistula. Melbourne: Therapeutic Guidelines Limited; 2022. Available from: https://www.tg.org.au
Sadeghi A, Biglari M, Forootan M, Adibi P. Solitary rectal ulcer syndrome: a narrative review. Middle East J Dig Dis. 2019;11(3):129–134.
Lohsiriwat V. Treatment of hemorrhoids: a coloproctologist's view. World J Gastroenterol. 2015;21(31):9245–9252.
Quan L, Bai X, Cheng F, Chen J, Ma H, Wang P, et al. Comparison of efficacy and safety between surgical and conservative treatments for hemorrhoids: a meta-analysis. BMC Gastroenterol. 2025;25(1):492.
Therapeutic Guidelines Limited. Anal fissure. Melbourne: Therapeutic Guidelines Limited; 2022. Available from: https://www.tg.org.au
Australian Medicines Handbook Pty Ltd. Glyceryl trinitrate (rectal). Adelaide: Australian Medicines Handbook Pty Ltd; 2025. Available from: https://amhonline.amh.net.au/
Allen S. Haemorrhoids and anal fissures. S Afr Pharm J. 2008;75(5):36.
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[post_content] => Community pharmacies are often the first place people turn when something feels ‘off’. But as pharmacists know, many requests for over-the-counter medicines are more complex than they may initially seem.
AP took a look at some presentations which might signal hidden red flags.
‘I just want a multivitamin’
When people present to community pharmacies, they often arrive with a solution already in mind. For example, ‘I need a strong painkiller,’ ‘I just want a multivitamin,’ or ‘What do you have for nerve pain?’
Nearly always, consistent with professional standards, these invite an open ended question to uncover the rationale for the request
Gauri Godbole FPS[/caption]
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[post_content] => Case scenario
During peak hour, 19-year-old Enzo and his mother arrive to collect a new prescription for melatonin MR 2 mg. The pharmacy is highly stimulating: background music blares, customers converse loudly nearby, staff assist others in a cramped space, and general noise amplifies the chaos. While processing Enzo’s prescription and attempting to deliver verbal instructions, you observe Enzo avoiding eye contact, fidgeting intensely, and appearing overwhelmed, with reduced capacity to process verbal or non-verbal cues due to sensory overload.
Learning objectivesAfter reading this article, pharmacists should be able to:
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Yvette Anderson (she/her) BPharm, MPS, CredPharm (MMR), ANZCAP (MentalHth, Paeds), CPGx, GradCert Autism[/caption]
Neurodevelopmental disorders (NDDs) arise from differences in brain development and typically affect cognition, communication, behaviour and occupational functioning. Common NDDs include attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), referred to as autism in this article, and intellectual developmental disorder (IDD).1 Autism is characterised by persistent social interaction and communication difficulties and restricted behavioural patterns.2 Symptoms begin in early childhood; however, diagnosis can occur at any age.3 Autism affects how the brain processes information, shaping how autistic people see, understand and respond to the world around them, with marked variability in presentation, day-to-day functioning and support needs.3,4
In Australia, autism prevalence has increased due to evolving diagnostic practices and awareness,5 meaning pharmacists now routinely engage with autistic individuals as part of everyday practice.
The challenge and opportunity for pharmacy is to shift from a medical model of crisis response, treatments and cures to a neuro-affirming social model that helps autistic individuals thrive, not just survive.
A neuro-affirming social model conceptualises neurodevelopmental differences as natural variations within human diversity and rejects deficit-based assumptions that frame these differences as disorders.6 Rather than ‘correcting’ individual traits, this approach provides reasonable adjustments while supporting autonomy, community participation and wellbeing, alongside awareness of diagnostic criteria, comorbidities, communication styles, lived realities and the impact of misinformation.6 The shift to a neuro-affirming social model calls for reducing systemic and environmental barriers, while still addressing health needs.6,7
For pharmacists, it means making practice adjustments in the way that the profession engages with and provides support for autistic individuals.
According to the Australian Bureau of Statistics, approximately 290,900 Australians (1.1%) are reported to have had an autism diagnosis in 2022.5 A recent estimate by Autism Spectrum Australia (Aspect) suggested at least 1 in 40 Australians are autistic.7
Rising prevalence reflects improved awareness and diagnostic practices rather than a true increase in incidence, including better recognition in historically underdiagnosed groups such as females and older adults.7 Autism prevalence peaks in children and adolescents, particularly those aged 10–14 years, and is markedly lower in adults, acknowledging limited adult data.5,8,9
Autism prevalence rates may appear to vary among ethnic and cultural groups, reflecting inequities such as access to healthcare, effective communication, diagnostic practices and cultural perceptions.10
Prevalence remains higher in males than females, with 1.6% of males identified compared with 0.7% of females, and the greatest disparity is seen in children aged 5–9 years.5 Autism in females is frequently underdiagnosed, as characteristics may manifest differently, be masked (e.g. forced eye contact, rehearsed social scripts, suppressing stimming or copying peers), or fail to align with historically male-centred diagnostic criteria, leading to misdiagnosis as mood or personality disorders.11,12 Masking may occur due to a desire to fit in, fear of stigma or bullying, previous negative reactions to autistic behaviours, and expectations of how females are ‘supposed’ to behave.12 Increasing awareness of the under-recognition of autism in females and gender-diverse individuals, and the social drivers of masking, is anticipated to influence future prevalence estimates.4,5,11
There is no single cause of autism, and despite extensive research, aetiology remains incompletely understood. Current evidence indicates autism arises from a complex interaction between genetic susceptibility and environmental influences on neurodevelopment.13
Family history is one of the strongest predictors of autism.13,14 Researchers have identified hundreds of genes, with approximately 10–20% of cases associated with rare genetic variants arising from mutations in sperm or egg cells.14 Autism is considered polygenic, meaning overall risk typically reflects the cumulative effect of multiple inherited variants, each contributing a small effect.14
The expression of genetic susceptibility is known to be influenced by prenatal, perinatal and postnatal environmental factors.13 Environmental factors appear most relevant during the prenatal period.14 Modest associations have been reported between autism likelihood and maternal factors such as hypertension, gestational diabetes, obesity, alcohol and substance use, poor antenatal care, and infection or fever during pregnancy.15
Imprecise and inconsistent associations have been reported for folate status, exposure to some air pollutants, and the use of some medicines.15–17 Importantly, these findings are largely derived from observational studies and are subject to confounding. While some prenatal medicine exposures show more consistent associations with autism, there is no clear evidence that associations between autism and other environmental and medicine exposures represent a causal relationship, and any contribution to autism risk remains limited and uncertain.14,17

Autism is diagnosed according to Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR) criteria: ‘persistent deficits in social communication and social interaction across multiple contexts’, with the presence of ‘restricted, repetitive patterns of behaviour, interests or activities’.2
‘Symptoms must be present in the early development period’, although they may only become fully apparent later in life.
‘Symptoms cause clinically significant impairment in social, occupational or other important areas of functioning’ and ‘these disturbances are not better explained by IDD’ although both can co-occur.2 The DSM-5-TR also specifies severity levels (1–3) to indicate the degree of support required.2
In Australia, individuals may pursue an autism diagnosis through public or private pathways.18 Both are typically lengthy and necessitate a degree of health literacy and English proficiency. Diagnostic assessments may be conducted by a multidisciplinary team, including paediatricians, psychiatrists, psychologists, speech pathologists and occupational therapists.4 Multiple appointments may be needed, drawing on input from family, carers or teachers.18,19
Barriers to diagnosis include limited awareness of early signs among caregivers and clinicians, long wait times and out-of-pocket costs for specialist assessment, socioeconomic and geographic disparities, and bias in recognising diverse presentations.11,20,21 Limited health literacy and the complexity of navigating multidisciplinary assessments and National Disability Insurance Scheme requirements further impede access.21 In some communities, stigma, fear of labelling, and differing cultural interpretations of behaviour may delay help-seeking.22
A best-practice diagnostic approach should promote cultural safety and sensitivity, acknowledge variations in health literacy, address socioeconomic barriers, and be grounded in person-centred care.
Autism is a spectrum, with each individual having a unique mix of strengths, challenges, interests, needs and way of interacting with the world. Autism advocate Dr Stephen Shore states, ‘If you have met one autistic person, you have met one autistic person’.23
Beyond the core featuresComorbid NDDs, and psychiatric and medical conditions can create significant challenges for autistic individuals in relation to diagnosis, selection of appropriate interventions, medicines and support services.1,24
Comorbid NDDs among autistic individuals include ADHD, developmental coordination disorder (dyspraxia), IDD, and specific learning disorders such as dyslexia, dysgraphia and dyscalculia.25 Psychiatric comorbidities are also prevalent, including anxiety, depression, obsessive-compulsive disorder, and post-traumatic stress disorder.26 These conditions can intensify social and sensory challenges, increase vulnerability to stress, and impair emotional regulation and executive functioning.
Autistic individuals experience higher rates and severity of mental and physical health comorbidities than neurotypical individuals. Neurodivergent mental health outcomes are influenced by the interaction between individual differences and environmental and societal factors.25–28 Diagnostic overshadowing, whereby mental health symptoms are erroneously attributed to autism, should be avoided.29 Comorbid conditions warrant assessment and treatment according to the same clinical standards applied to neurotypical individuals, with adaptations made to accommodate the communication, sensory and support needs of autistic people. Neurodivergent individuals experience the full range of medical comorbidities seen in the general population; however, research indicates higher prevalence of certain conditions, including gastrointestinal disorders (e.g. irritable bowel syndrome, chronic constipation), sleep disturbances, epilepsy, and immune or metabolic disorders.30 These conditions may worsen fatigue, concentration and mood regulation, while motor difficulties may contribute to musculoskeletal pain, reduced physical activity and secondary health issues.31
Physical health conditions may be underdiagnosed when the clinical focus is limited to behavioural or psychological symptoms.29
Recognising the complex interconnections between physical, psychiatric and NDD health is paramount. Pharmacists can play a vital role in this process. Effective care relies on health professionals working collaboratively to identify how comorbid conditions, treatment burden and medicines may influence behaviour, cognition and developmental outcomes.
Autism is a lifelong NDD for which there is no curative treatment.4 Clinical care focuses on supporting health, functioning and community participation, addressing comorbidities, and optimising quality of life, while recognising and respecting the individual strengths, capabilities and perspectives of autistic individuals.3
Supports and interventions are individualised and typically involve a multidisciplinary team to address evolving needs.10 Allied health professionals may include speech pathologists to support communication, occupational therapists to address sensory processing and daily living skills, and psychologists to support emotional regulation and mental health. Physiotherapists may support gross motor skills, while dietitians support feeding and nutritional adequacy, alongside specialist educational support and therapy (e.g. play therapy, art therapy).3 Effective management relies on coordinated care, regular goal review and clear communication between the autistic individual, families and carers, and the multidisciplinary team.24
There is no evidence to support the use of medicines, exclusion diets or other biological treatment for the core features of autism.32,33 To support comorbidities, psychotropic medicines, antiepileptics and sleep agents may be used short term and under specific circumstances. Off-label use is common and requires careful assessment of risk-benefit balance, adverse effects, formulation choice, monitoring, cumulative treatment burden, and very careful consideration if the medicine is being prescribed as a chemical restraint.4

Autism is subject to persistent myths that pharmacists may encounter. The most damaging is the long-debunked claim that vaccines cause autism.14 The retracted 1998 Lancet study by Andrew Wakefield that claimed a link between the measles, mumps, rubella (MMR) vaccine and autism was a small, flawed study (with only 12 participants) and was exposed for unethical processes, methodological misconduct, and undisclosed conflicts of interest.14 Despite retraction, its claims were (and continue to be) amplified, eroding trust in public health and fuelling vaccine hesitancy. A Cochrane review published in 2021 found no credible evidence of an association between MMR and MMRV vaccines and autism.34
Two medicines made headlines in 2025: paracetamol and leucovorin (folinic acid or calcium folinate) claimed as a cause and treatment of autism respectively. Antenatal paracetamol exposure was alleged to increase autism and ADHD risk; however, major studies have not demonstrated a causal relationship.9 Stronger evidence from a large Swedish population-based cohort of 2,480,797 children born between 1995 and 2019 found no association between paracetamol use during pregnancy and autism, ADHD or IDD in sibling-controlled analysis.16 Cerebral folate deficiency (CFD) has been reported in a subset of autistic individuals, related to impaired folate transport into the brain, and may be associated with symptoms of speech difficulties, seizures and IDD, often within early childhood.35,36 Leucovorin, a folinic acid derivative, has been investigated as a potential treatment for autistic children with CFD. Leucovorin can bypass impaired folate transport, increasing central nervous system folate availability.36 Although some small-scale trials indicate potential minor behavioural improvements, supporting evidence remains limited, inconsistent, and not independently replicated.15,37
As medicines experts, pharmacists are well placed to counter common myths. Responses should prioritise empathetic, respectful communication and the provision of clear, evidence-based information and resources.
Accessibility, strong communication skills, medicines expertise, understanding of health system navigation and ability to synthesise information, position pharmacists to provide continuity of care for autistic individuals. Pharmacists can serve as an integrative link within multidisciplinary teams, supporting autistic individuals and their families across the healthcare continuum.
Effective communication underpins person-centred pharmacy practice. Pharmacists supporting autistic individuals should adapt both verbal and non-verbal communication to meet diverse needs.38 Autism can influence communication and sensory processing in unique ways, with some individuals experiencing sensory sensitivities to sound, light, smell, touch and visual stimuli.3,4,33 Some autistic individuals regulate sensory input through stimming (self-stimulatory behaviour), which may present as repetitive movements or sounds such as fidgeting, rocking or hand-flapping.39 Flexibility, empathy and understanding of sensory needs ensure equitable access to healthcare and fosters the relationship between patient and pharmacist. Verbal communication with autistic individuals should be clear and structured. Pharmacists should use straightforward, unambiguous language and present information in small, logical steps, allowing time for processing and response. Offering a calm, quiet space can both minimise sensory overload and facilitate a more comfortable environment for communication.38,40
Non-verbal communication requires equal attention. Eye contact, facial expressions and gestures can carry unintended meaning for autistic individuals. Some avoid eye contact as a coping mechanism, not as disinterest.38 Pharmacists should avoid assumptions and focus on open, calm body language and a reassuring tone. Visual supports can reinforce verbal explanations to provide ongoing reference, especially for individuals who process visual information more effectively than spoken language.40
A person-centred approach requires pharmacists to recognise, respond and adapt to the communication preferences of each autistic individual. If a caregiver or support worker is present, collaboration should occur while directing communication towards the patient whenever possible.40 Empathy, flexibility and inclusive communication techniques ensure care that is respectful and accessible and upholds an individual’s dignity and autonomy.
By adopting inclusive, neuro-affirming approaches, pharmacists strengthen equity, accessibility and person-centredness within healthcare. In doing so, they uphold the profession’s commitment to compassionate, evidence-based practice and help ensure autistic Australians receive the respect, understanding and tailored support needed to achieve optimal health and wellbeing.
Case scenario continuedEnzo’s mother discloses Enzo’s autism diagnosis and requests a quiet area and slower, step-by-step instructions. You offer a consultation room with dimmed lights, minimal visual clutter and no background noise. Enzo settles, visibly calmer. In this adapted space, you employ person-centred strategies: a soft, steady voice; paced delivery; short, simple sentences; pauses after each point for processing; confirming understanding via yes/no questions or thumbs-up signals; and a clear, written handout with bullet points, icons (e.g. clock for bedtime), and appropriate font. Enzo engages, maintaining partial eye contact and nodding, while his mother clarifies. These modifications demonstrate empathy, flexibility and equitable care, minimising distress, enhancing information access and supporting Enzo’s autonomy. |
Yvette Anderson (she/her) BPharm, MPS, CredPharm (MMR), ANZCAP (MentalHth, Paeds), CPGx, GradCert Autism is an accredited clinical pharmacist with over 20 years’ experience across aged care, consultancy, community pharmacy and hospital pharmacy. In 2020, she launched The Spectrum Pharmacist to increase awareness, promote inclusion, and provide education and support for neurodevelopmental disorders.
Victor Senescall (he/him) BPharm (Hons)
Merck Manual Professional Version. Overview of learning disorders. 2024. Available from: www.merckmanuals.com/professional/pediatrics/learning-and-developmental-disorders/overview-of-learning-disorders?query=neurodevelopment%20disorders
American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 5th ed. Washington (DC): American Psychiatric Publishing; 2022.
Merck Manual Professional Version. Autism spectrum disorder. 2025. Available from: www.merckmanuals.com/professional/pediatrics/learning-and-developmental-disorders/autism-spectrum-disorder
Therapeutic Guidelines. Autism spectrum disorder. Melbourne: Therapeutic Guidelines; 2021.
Australian Bureau of Statistics. Autism in Australia 2022. 2024. Available from: www.abs.gov.au/articles/autism-australia-2022
Bertilsdotter Rosqvist H, Pearson A, Pavlopoulou G, et al. The social model in autism research. Autism. 2025;29(9):2201–2204.
Autism Spectrum Australia. At least 1 in 40 Australians are autistic: new estimate by Aspect on World Autism Understanding Day. 2024. Available from: www.aspect.org.au/news/at-least-1-in-40-australians-are-autistic
Therapeutic Guidelines. Autism spectrum disorder. eTG complete. Melbourne: Therapeutic Guidelines; 2021.
Trollor J, Arnold S, Walker SE. Australian Longitudinal Study of Autism in Adulthood (ALSAA): final report. Brisbane: Autism CRC; 2022.
Rasheed Z. Autism in Australia: understanding, challenges, and support. Int J Health Sci. 2023;17(5):1–4.
Lai M-C, Amestoy A, Bishop S, et al. Improving autism identification and support for individuals assigned female at birth: clinical suggestions and research priorities. Lancet Child Adolesc Health. 2023;7(12):897–908.
National Autistic Society. Masking. 2026. Available from: www.autism.org.uk/advice-and-guidance/topics/behaviour/masking
Ostrowski J, Religioni U, Gellert B, et al. Autism spectrum disorders: etiology, epidemiology, and challenges for public health. Med Sci Monit. 2024;30.
Australian Academy of Health and Medical Sciences. Autism: an evidence brief. 2025. Available from: https://aahms.org/policy/evidence-brief-on-autism
Love C, Sominsky L, O'Hely M, et al. Prenatal environmental risk factors for autism spectrum disorder and their potential mechanisms. BMC Med. 2024;22.
Ahlqvist VH, Sjöqvist H, Dalman C, et al. Acetaminophen use during pregnancy and children's risk of autism, ADHD, and intellectual disability. JAMA. 2024;331(14):1205–1214.
de Lara I, Wagner P, Matheus G, et al. Association of prenatal exposure to antiseizure medication with risk of autism: a systematic review and meta-analysis. Seizure. 2025;130:41–47.
Government of South Australia Office for Autism. Pathways for assessment and diagnosis. 2023. Available from: www.officeforautism.sa.gov.au/autism/pathways-for-diagnosis
Autism Awareness Australia. Understanding and accessing the NDIS. 2024. Available from: www.autismawareness.com.au/navigating-autism/understanding-and-accessing-the-ndis-for-autism
Estrin GL, Milner V, Spain D, et al. Barriers to autism spectrum disorder diagnosis for young women and girls: a systematic review. Rev J Autism Dev Disord. 2021;8(4):454–470.
Allen-Meares P, Lowry B, Estrella ML, et al. Health literacy barriers in the health care system: barriers and opportunities for the profession. Health Soc Work. 2020;45(1):62–64.
Khalil A, Yatcilla J, Christie N, et al. A systematic review of help-seeking barriers for racial-ethnic minority caregivers accessing autism diagnostic and intervention services. J Racial Ethn Health Disparities. 2025.
Flannery KA, Wisner-Carlson R. Autism and education. Child Adolesc Psychiatr Clin N Am. 2020;29(2).
Autism Awareness Australia. Navigating the health system. 2024. Available from: www.autismawareness.com.au/navigating-autism/navigating-the-health-system-for-autism
Bonti E, Zerva IK, Koundourou C, et al. The high rates of comorbidity among neurodevelopmental disorders: reconsidering the clinical utility of distinct diagnostic categories. J Pers Med. 2024;14(3):300.
Lai M-C, Kassee C, Besney R, et al. Prevalence of co-occurring mental health diagnoses in the autism population: a systematic review and meta-analysis. Lancet Psychiatry. 2019;6(10):819–829.
Mazurek MO, Sadikova E, Cheak-Zamora N, et al. Health care needs, experiences, and perspectives of autistic adults. Autism Adulthood. 2023;5(1):51–62.
Barlattani T, D'Amelio C, Cavatassi A, et al. Autism spectrum disorders and psychiatric comorbidities: a narrative review. J Psychopathol. 2023;29(1):3–24.
Blair J. Diagnostic overshadowing: see beyond the diagnosis. 2017. Available from: www.intellectualdisability.info/changing-values/diagnostic-overshadowing-see-beyond-the-diagnosis
Al-Beltagi M. Autism medical comorbidities. World J Clin Pediatr. 2021;10(3):15–28.
Sung Y-S, Loh SC, Lin L-Y. Physical activity and motor performance: a comparison between young children with and without autism spectrum disorder. Neuropsychiatr Dis Treat. 2021;17:3743–3751.
Turner M. The role of drugs in the treatment of autism. Aust Prescr. 2020;43:185–190.
Mayo Clinic. Autism spectrum disorder. 2025. Available from: www.mayoclinic.org/diseases-conditions/autism-spectrum-disorder/diagnosis-treatment/drc-20352934
Di Pietrantonj C, Rivetti A, Marchione P, et al. Vaccines for measles, mumps, rubella, and varicella in children. Cochrane Database Syst Rev. 2021;(11):CD004407.
Wong A, Frye RE, Ohnemus-Kawamura B, et al. Cerebral folate deficiency. 2019. Available from: https://rarediseases.org/rare-diseases/cerebral-folate-deficiency/
Ramaekers VTH, Quadros EV. Cerebral folate deficiency syndrome: early diagnosis, intervention and treatment strategies. Nutrients. 2022;14(15):3096.
Sheppeard A. What is leucovorin, and can it cure autism? 2025. Available from: www.medicalrepublic.com.au/what-is-leucovorin-and-can-it-cure-autism/120175
Norris JE, Milton D, Heasman B. Adapting communication with autistic service users: a participatory study. Autism. 2024.
National Autistic Society. Repeated movements and behaviour (stimming). 2026. Available from: www.autism.org.uk/advice-and-guidance/topics/about-autism/repeated-movements-and-behaviour-stimming
National Autistic Society. Autism and communication. 2024. Available from: www.autism.org.uk/advice-and-guidance/topics/about-autism/autism-and-communication
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Case scenarioStavros, a 35-year-old male with focal epilepsy, presents to the pharmacy to collect his medicines. He appears tired and mentions he has been having more frequent breakthrough seizures lately. As you chat, he reveals he recently started lorazepam 1 mg twice daily for generalised anxiety disorder (GAD), prescribed by his new GP. Stavros has been missing doses of his anti-seizure medicine, carbamazepine, as he feels it worsens his drowsiness and confusion. |
Dr Ming S Soh PhD, BPharm (Hons)[/caption]
Epilepsy is a chronic neurological condition characterised by a persistent tendency to produce seizures.1,2 According to the International League Against Epilepsy (ILAE), epilepsy is diagnosed when an individual experiences at least two unprovoked seizures more than 24 hours apart, one unprovoked seizure with a high probability (≥60%) of recurrence, or when an epilepsy syndrome is identified.3 Seizures result from abnormal, excessive electrical discharges in the brain, and vary in type, severity and frequency.4 While most seizures are brief, lasting seconds to minutes, they can become prolonged and continuous (i.e. status epilepticus), which requires urgent, intensive medical intervention.4 Globally, epilepsy affects around 50 million people.5,6 It can affect individuals across all age groups, races and ethnicities, and can significantly disrupt quality of life.7,8 Epilepsy is often associated with neurobiological, cognitive, psychological and social sequelae.1,2
Management of epilepsy primarily involves antiseizure medicines (ASM), administered as monotherapy or polytherapy depending on the patient’s response.8,9 In some cases, surgery, dietary therapy or neurostimulation may be considered.9 Treatment complexity, adverse drug reactions and non-adherence to medicines can hinder seizure control and prevent optimal outcomes.8
Learning OutcomesAfter reading this article, pharmacists should be able to:
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In practice, pharmacists provide therapeutic drug monitoring (hospital setting), Home Medicines Reviews (HMR), MedsChecks and patient counselling, and they support the management of common comorbidities such as depression, anxiety and cognitive impairments, which can complicate treatment.6,8,9

Globally, the pooled incidence rate of epilepsy is estimated at 50–61.4 cases per 100,000 person-years.2,10,11 However, incidence varies by region and income level. In high-income countries, rates typically range from 40–70 per 100,000 person-years, while in low- and middle-income countries, incidence can reach 100–190 per 100,000 person-years, reflecting disparities in healthcare access, diagnostic capacity and exposure to risk factors.2,10 The highest incidence of epilepsy occurs in childhood, reflecting the higher seizure susceptibility of the developing brain.12
In Australia, the lifetime risk of developing epilepsy is estimated to be up to 4%, while approximately 0.6–1% of the population is living with epilepsy at any given time.13,14 Modelled data estimates that prevalence peaks in males aged 60–64 (8.54 per 1,000), and in females aged 50–54 (9.57 per 1,000).15 National surveillance data indicates that prevalence generally remains high into older age groups, largely due to increased rates of stroke, neurodegenerative diseases and brain tumours.2,14,15
Disparities are pronounced among Aboriginal and Torres Strait Islander people, who experience twice the prevalence of epilepsy compared to non-Aboriginal and Torres Strait Islander people.14,16 Aboriginal and Torres Strait Islander people also face higher rates of hospitalisation, reduced access to specialist care and ASM, and significantly elevated epilepsy-related mortality.16 The disability-adjusted life years for Aboriginal and Torres Strait Islander people with epilepsy are double those of non-Aboriginal and Torres Strait Islander people.16
Epilepsy has a multifactorial aetiology. The ILAE classifies epilepsy aetiologies into six main categories: genetic, structural, infectious, metabolic, immune and unknown (see Figure 1).17,18 Genetic mutations generally affect neuronal excitability, especially ion channels, and are linked to specific epilepsy syndromes.18–20 Structural causes include brain malformations, trauma, stroke and tumours. Infections like meningitis or encephalitis can provoke seizures through inflammation. Metabolic causes arise from systemic or inherited metabolic disorders that disrupt brain chemistry or energy production. Autoimmune responses, where the body’s immune system attacks brain tissue, can also lead to seizures. Unknown causes refer to cases where no clear aetiology can be identified despite thorough investigation. Neurodegenerative causes are increasingly recognised as important contributors to epilepsy.18 Despite structured classifications, many overlap. For example, an infection such as encephalitis may lead to structural brain damage.18 Risk factors include family history, perinatal insults, head trauma, brain infections, febrile seizures and socioeconomic disparities, which can influence both the likelihood of developing epilepsy as well as its clinical progression.21

Epilepsy involves several interconnected mechanisms that predominate in different seizure types and epilepsy syndromes and are targeted by specific ASM.
Neuronal hyperexcitability is increased neuronal responsiveness due to ion-channel dysfunction, resulting in spontaneous, excessive neuronal firing. This is a key mechanism underlying all seizure types, but is not the sole pathophysiological mechanism.4,22,23
Hypersynchrony is the abnormal synchronisation of neuronal activity which facilitates seizure propagation across brain regions, particularly in generalised epilepsies such as absence and tonic-clonic seizures.1,4,12,18
Excitatory/inhibitory neurotransmitter imbalance refers to the disruption of glutamate and gamma-aminobutyric acid (GABA) neurotransmission, shifting networks toward hyperexcitability and is central to both focal and generalised epilepsy.4,17
Neuroinflammation refers to the immune activation and cytokine release (e.g. IL-1 beta, TNF-alpha) that can enhance excitability, and are implicated in structural focal epilepsies, post-stroke epilepsy and autoimmune epilepsies. Anti-inflammatory and immunomodulatory therapies may be used in selected cases.4,24
mTOR pathway dysregulation is the abnormal mTOR signalling that alters synaptic plasticity, contributing to epileptogenesis, most notably in tuberous sclerosis complex–associated epilepsy, where mTOR inhibitors such as everolimus are used as targeted therapy.18
Oxidative stress is the excess reactive oxygen species that can damage neurons and lower seizure thresholds, contributing to seizures in metabolic and neurodegenerative epilepsies.24
Mitochondrial dysfunction refers to impaired energy metabolism, which reduces neuronal resilience and is characteristic of mitochondrial epilepsies and some childhood epileptic encephalopathies.24
Synaptic reorganisation refers to structural changes, including aberrant axon sprouting and new excitatory circuit formation, and are commonly seen in temporal lobe epilepsy following brain injury or prolonged seizures.4
Recognising underlying epileptogenic mechanisms aids interpretation of seizure type/classification and guides appropriate ASM selection.
Focal seizures (formerly known as partial)
Focal seizures originate in a specific area of one cerebral hemisphere. Depending on the brain area affected, they may present with localised motor activity like rhythmic jerking or muscle stiffening, sensory changes such as tingling or visual distortions, or autonomic signs, including flushing and gastrointestinal discomfort.12 Awareness may or may not be impaired during these seizures.25 Some focal seizures begin with an aura, such as déjà vu or intense emotions, during which a person remains alert. First-line treatment includes carbamazepine, lamotrigine or levetiracetam, where selection is guided by contraindications and other patient-specific factors.26
Generalised seizures
Generalised seizures involve widespread electrical activity across both cerebral hemispheres and typically include tonic-clonic, absence, myoclonic and atonic seizures.12,25
Tonic-clonic seizures (formerly known as grand mal)
Tonic-clonic seizures are characterised by a sudden loss of consciousness, muscle stiffening followed by rhythmic jerking, and a post-seizure phase with confusion, agitation or fatigue. They can sometimes be fatal due to associated complications. Some tonic-clonic seizures begin as focal seizures with preserved awareness, but progress to loss of consciousness as they generalise across both hemispheres of the brain.12 First-line treatment is sodium valproate, unless contraindicated or otherwise inappropriate for the patient (e.g. individuals of childbearing potential).26
Absence seizures (formerly known as petit mal)
Absence seizures are typically characterised by brief episodes of staring or unresponsiveness, and are often unnoticed or mistaken for daydreaming.12,25 First-line treatment includes ethosuximide or sodium valproate where selection is guided by contraindications and other patient-specific factors.26
Myoclonic seizures
Myoclonic seizures present as sudden and brief muscle jerks.12,25 First-line treatment is sodium valproate unless contraindicated or otherwise inappropriate (e.g. individuals of childbearing potential).26
Atonic seizures
Atonic seizures result in a sudden loss of muscle tone, leading to falls.12,25
For further information, see Australian Medicines Handbook: Epilepsy.26
Diagnosis of epilepsy involves detailed clinical history, neurological examination and supportive investigations.12,17 Electroencephalogram (EEG) is central for detecting epileptiform discharges, while neuroimaging techniques such as computed tomography (CT) and magnetic resonance imaging (MRI) can help identify structural causes.12 In complex cases, additional tools including positron emission tomography (PET)/single photon emission computed tomography (SPECT), magnetoencephalography (MEG) and genetic testing can support diagnosis and guide treatment. The advanced neuroimaging modalities are especially useful for presurgical evaluations in specialised centres.12 Neuropsychological assessments can also provide insight into cognitive impacts.1 ILAE classification recommends a structured, three-level diagnostic approach, identifying seizure type, epilepsy type and specific epilepsy syndrome, while integrating aetiology at each stage to inform treatment decisions.3 Syncope, psychogenic non-epileptic seizures, transient ischaemic attacks, migraine auras and sleep disorders can mimic epileptic seizures but differ in aetiology and treatment.12,27
Prognosis varies widely, depending on seizure type, aetiology, age of onset and treatment response.12 Many patients can achieve seizure control with ASM, and some enter long-term remission. However, around one-third of patients develop drug-resistant epilepsy, unresponsive to two or more ASM.12 Early age of onset, especially in infancy, and epilepsy with structural lesions such as hippocampal sclerosis, are often linked to poorer outcomes.28,29 Sudden unexpected death in epilepsy remains a serious risk,30 particularly in patients with uncontrolled generalised tonic-clonic seizures and early-onset syndromes such as Dravet syndrome (severe infantile-onset developmental epileptic encephalopathy), which has a 3–5-fold higher mortality risk than the general epilepsy population.31 Early diagnosis and individualised treatment strategies improve outcomes.
The primary aim is to achieve seizure freedom with minimal side effects, improving quality of life. Treatment recommendations follow a stepwise approach, guided by seizure classification, epilepsy type, underlying aetiology, side effect profile, cost, potential for measuring serum drug concentration, pharmacokinetics and patient-specific factors such as age, pregnancy, medicine interactions and comorbidities.17,26,32,33
Initial management involves monotherapy with an appropriate ASM. Dose is generally started low and titrated slowly to achieve seizure control. If control is not achieved with maximally tolerated doses of a single agent, a second agent may be added. The second agent may be considered for monotherapy if the patient and prescriber are willing to gradually withdraw the first agent. If two agents do not promote seizure control, the second agent may be withdrawn gradually and replaced with a third.34
Treatment with an ASM should never be ceased abruptly.34
Key treatment considerations
For further information, see Therapeutic Guidelines: Neurology.34
Evidence is limited for cannabis-derived products. Cannabidiol is approved for specific syndromes but requires specialist oversight.33,34
Non-pharmacological management includes surgery following EEG/MRI evaluation, vagus nerve and deep brain stimulation, ketogenic diet and gene therapy. Yoga, meditation and acupuncture have limited evidence for use.17,31–35
One of the most common challenges during epilepsy treatment is adherence. Missed doses or abrupt discontinuation can trigger recurrent seizures which significantly increase mortality risk.33 Medicine interactions are another significant concern, particularly with older ASM such as phenytoin and carbamazepine, which are enzyme inducers and can alter the efficacy of other medicines.33 Patients should be informed that some medicines can lower their seizure threshold. These include theophylline, pethidine, certain antidepressants (uncommon), and some antipsychotics. Some important medicine interactions are shown in Table 1.

Treatment complications range from mild to severe. Common side effects include fatigue, dizziness, cognitive issues such as memory or attention difficulties, and abdominal upset including pain, nausea and vomiting.33
More serious but less frequent reactions include liver and renal toxicity, bone marrow suppression and skin reactions.26 Long-term use of certain ASM including carbamazepine and phenytoin may also reduce bone density, increasing fracture risk.12,33 Additionally, some ASM including levetiracetam and topiramate can worsen mood disorders, contributing to anxiety and depression.26,33
Age also influences management.32,33 Children often require weight-based dosing and closer monitoring due to variable metabolism, while older adults are more susceptible to adverse effects and medicine interactions due to comorbidities and declining organ function.34
To manage these risks, routine monitoring, including liver and renal function tests, therapeutic drug monitoring, bone health assessments and mental health screening, is essential.
Epilepsy treatment requires regular follow-up to assess seizure control, treatment efficacy and adverse effects. Monitoring for drugs with narrow therapeutic index should also be considered. Treatment plans should be reviewed annually, or sooner, to discuss any changes in seizure occurrence.
Patients in Australia can access further advice and support through multiple channels, including:
Epilepsy Action Australia – education, telehealth and resources
Epilepsy Foundation – seizure management and support services
National Epilepsy Support Service/Epilepsy Smart Australia – 1300 761 487 Monday to Friday, from 9 am to 5 pm (AEST).
Pharmacists support epilepsy management across both community and hospital settings. Hospital pharmacists contribute by implementing therapeutic drug monitoring, especially for ASM with narrow therapeutic windows, collaborating with multidisciplinary teams to optimise treatment plans, monitoring for adverse drug reactions, and managing complex cases involving polytherapy or comorbidities. Community pharmacists can provide ongoing support and medicines counselling, and conduct MedsChecks, detect side effects early, and address mental health concerns. Together, pharmacists provide personalised care that can help improve seizure control, enhance treatment safety and reduce mortality.
With appropriate treatment, many people with epilepsy can achieve good seizure control and lead full, active lives. However, outcomes depend on early intervention, consistent follow-up, monitoring and personalised care. Pharmacist involvement helps reduce complications, improves medicine adherence and supports overall wellbeing.
Case scenario continuedYou recognise that emotional stress, non-adherence and adverse effects are likely precipitating Stavros’ seizures. Concomitant use of lorazepam and carbamazepine contributes to additive CNS depression, causing sedation. As Stavros prefers pharmacological treatment for GAD, you call his GP and suggest sertraline 50 mg daily, noting that carbamazepine may reduce sertraline concentrations via enzyme induction, and clinical response should be monitored. You recommend ceasing lorazepam and encourage cognitive behavioural therapy. The GP reviews Stavros and he returns with a cessation plan for lorazepam and a prescription for sertraline. You counsel on treatment expectations and the importance of adherence. A month later, Stavros returns, feeling alert with no recent seizures. |
DR Ming S Soh PhD, BPharm (Hons) is a Research Fellow at the Florey Institute of Neuroscience and Mental Health, University of Melbourne, with expertise in preclinical models of genetic epilepsy and therapeutic development.
Fisher RS, van Emde Boas W, Blume W, et al. Epileptic seizures and epilepsy: definitions proposed by the International League Against Epilepsy (ILAE) and the International Bureau for Epilepsy (IBE). Epilepsia. 2005;46(4):470–472.
Beghi E. The epidemiology of epilepsy. Neuroepidemiology. 2020;54(2):185–191.
Scheffer IE, Berkovic S, Capovilla G, et al. ILAE classification of the epilepsies: position paper of the ILAE commission for classification and terminology. Epilepsia. 2017;58(4):512–521.
Scharfman HE. The neurobiology of epilepsy. Curr Neurol Neurosci Rep. 2007;7(4):348–354.
World Health Organization. Epilepsy. 2022. Available from: www.who.int/news-room/fact-sheets/detail/epilepsy
Petrides M, Peletidi A, Nena E, et al. The role of pharmacists in enhancing epilepsy care: a systematic review of community and outpatient interventions. J Pharm Policy Pract. 2025;18(1):2487046.
Zack MM. National and state estimates of the numbers of adults and children with active epilepsy—United States, 2015. MMWR Morb Mortal Wkly Rep. 2017;66.
Bacci JL, Zaraa S, Stergachis A, et al. Community pharmacists’ role in caring for people living with epilepsy: a scoping review. Epilepsy Behav. 2021;117:107850.
Reis TM, Campos M, Nagai MM, et al. Contributions of pharmacists in the treatment of epilepsy: a systematic review. Am J Pharm Benefits. 2016;8(3):e55–e60.
Bell GS, Sander JW. The epidemiology of epilepsy: the size of the problem. Seizure. 2001;10(4):306–316.
Fiest KM, Sauro KM, Wiebe S, et al. Prevalence and incidence of epilepsy: a systematic review and meta-analysis of international studies. Neurology. 2017;88(3):296–303.
Stafstrom CE, Carmant L. Seizures and epilepsy: an overview for neuroscientists. Cold Spring Harb Perspect Med. 2015;5(6):a022426.
Mohanannair Geethadevi G, Chen Z, et al. Impact of epilepsy on productivity and quality of life: the Australian epilepsy project. Neurology. 2025;105(5):e214011.
Australian Institute of Health and Welfare. Epilepsy in Australia. Canberra: AIHW; 2022. Available from: www.aihw.gov.au/reports/chronic-disease/epilepsy-in-australia/contents/about
Foster E, Chen Z, Zomer E, et al. The costs of epilepsy in Australia: a productivity-based analysis. Neurology. 2020;95(24):e3221–e3231.
Keenan NF, Aitchison SG, Jetté N, et al. Epilepsy in the Indigenous peoples in Canada, Australia, New Zealand, and the USA: a systematic scoping review. Lancet Glob Health. 2025;13(4):e656–e668.
Vera-González A. Pathophysiological mechanisms underlying the etiologies of seizures and epilepsy. In: Czuczwar SJ, editor. Epilepsy. Brisbane: Exon Publications; 2022. p. 1–13.
Balestrini S, Arzimanoglou A, Blümcke I, et al. The aetiologies of epilepsy. Epileptic Disord. 2021;23(1):1–16.
Perucca P, Bahlo M, Berkovic SF. The genetics of epilepsy. Annu Rev Genomics Hum Genet. 2020;21(1):205–230.
Scheffer IE, Berkovic SF. The genetics of human epilepsy. Trends Pharmacol Sci. 2003;24(8):428–433.
Bhalla D, Godet B, Druet-Cabanac M, Preux P-M. Etiologies of epilepsy: a comprehensive review. Expert Rev Neurother. 2011;11(6):861–876.
Reid CA. Preface: ion channels and genetic epilepsy. J Neurochem. 2024;168(12):3829–3830.
Oyrer J, Maljevic S, Scheffer IE, et al. Ion channels in genetic epilepsy: from genes and mechanisms to disease-targeted therapies. Pharmacol Rev. 2018;70(1):142–173.
Fabisiak T, Patel M. Crosstalk between neuroinflammation and oxidative stress in epilepsy. Front Cell Dev Biol. 2022;10:976953.
Fisher RS, Cross JH, French JA, et al. Operational classification of seizure types by the International League Against Epilepsy: position paper of the ILAE commission for classification and terminology. Epilepsia. 2017;58(4):522–530.
Buckley N, editor. Australian medicines handbook. Adelaide: Australian Medicines Handbook Pty Ltd; 2025. Available from: https://amhonline.amh.net.au/
Cook M. Differential diagnosis of epilepsy. In: Shorvon S, Perucca E, Engel J Jr, editors. The treatment of epilepsy. 4th ed. Hoboken (NJ): John Wiley & Sons; 2015. p. 24–37.
Semah F, Picot M-C, Adam C, et al. Is the underlying cause of epilepsy a major prognostic factor for recurrence? Neurology. 1998;51(5):1256–1262.
Nickels K. Earlier is not always better: outcomes when epilepsy occurs in early life versus adolescence. Epilepsy Curr. 2020;20(1):27–29.
Devinsky O, Hesdorffer DC, Thurman DJ, et al. Sudden unexpected death in epilepsy: epidemiology, mechanisms, and prevention. Lancet Neurol. 2016;15(10):1075–1088.
Cooper MS, McIntosh A, Crompton DE, et al. Mortality in Dravet syndrome. Epilepsy Res. 2016;128:43–47.
Perucca E. General principles of medical management. In: Shorvon S, Perucca E, Engel J Jr, editors. The treatment of epilepsy. 4th ed. Hoboken (NJ): John Wiley & Sons; 2015. p. 110–123.
Perucca P, Scheffer IE, Kiley M. The management of epilepsy in children and adults. Med J Aust. 2018;208(5):226–233.
Therapeutic Guidelines Limited. eTG complete. Melbourne: Therapeutic Guidelines; 2025. Available from: www.tg.org.au
Baxendale S. Complementary and alternative treatments for epilepsy. In: Shorvon S, Perucca E, Engel J Jr, editors. The treatment of epilepsy. Hoboken (NJ): John Wiley & Sons; 2015. p. 298–310.
Johannessen SI, Johannessen Landmark C. Antiepileptic drug interactions: principles and clinical implications. Curr Neuropharmacol. 2010;8(3):254–267.
Buchanan N. Medications which may lower seizure threshold. Aust Prescr. 2001;24(1):8–9.
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[post_content] => New avenues for nurse prescribing have the potential to reshape frontline care. For pharmacists, it’s a live example of how scope expansion translates into real impact.
Nurse prescribing is entering a new phase in Australia, and pharmacists should be paying close attention.
While nurse practitioners and endorsed midwives have been able to prescribe Pharmaceutical Benefits Schedule (PBS) subsidised medicines since 2010, a new pathway will soon expand prescribing to a broader group of experienced nurses.
‘A lot of people wouldn't even know that nurses are already prescribing medications that are funded on the PBS,’ said Denise Lyons, President of the Australian Primary Health Care Nurses Association. ‘But there are more than 3,000 nurse practitioners and endorsed midwives in Australia now who are already prescribing.’
Under a new registration standard which came into effect in September last year, suitably qualified registered nurses will be able to prescribe medicines in Schedules 2, 3, 4 and 8 in partnership with an authorised prescriber.
‘It took until this year for universities to start the course that enables registered nurses to meet [the new standard],’ Ms Lyons said. ‘Most are 6-month postgraduate courses … So it will probably be around July 2026 that we will see the first [wave] of nurses completing the educational requirement.’
For pharmacists, this shift offers a live view of how prescribing reform is built – through legislation, governance, defined scope and, crucially, access to the PBS.
What’s changing?
The new framework is deliberately cautious. To become a designated RN prescriber, a nurse must:
‘Pharmacists and nurses are often people's first point of contact with the healthcare system, and it's really good if we can work to the top of our scope and do what we know we can do, with the right guardrails in place.' denise lyons
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[post_content] => Case scenario
Sarah, a 42-year-old woman, presents to the pharmacy reporting a small lump near the anus, occasional bright red bleeding on toilet paper after bowel movements, anal itching and discomfort. She mentions feeling embarrassed to seek advice and has been self-managing with sitz baths. She reports a history of chronic constipation with frequent training during defecation. She is not taking any regular medicines and requests an over-the-counter product to relieve her symptoms. You take the time to explore Sarah’s symptoms in more detail, to help identify any red flags that would require immediate referral. You ask about the duration, severity and other symptoms such as fatigue, unintentional weight loss and changes in bowel habits, all of which she denies.
Learning objectivesAfter reading this article, pharmacists should be able to:
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Anal fissures and haemorrhoids are commonly encountered, but their epidemiology is not well documented. Haemorrhoids represent the most frequent reason for proctology consultations, followed by anal fissures.1 Haemorrhoids are estimated to affect up to 40% of adults in the general population, although many individuals are asymptomatic.2 Anal fissures occur in approximately 10–15% of the population.3

An anal fissure is a longitudinal tear in the anal canal, most often occurring in the posterior midline, just below the dentate line.4 Anal fissures are typically classified as primary or secondary, depending on the cause. Primary fissures are usually benign and caused by local trauma, such as the passage of hard stools, prolonged diarrhoea, vaginal delivery, repeated injury or anal penetration.4 Secondary fissures, which are often multiple and located off the midline, are uncommon, accounting for less than 1% of cases.5 They result from underlying conditions like previous anal surgery, inflammatory bowel disease (e.g. Crohn’s disease), colorectal malignancy, infections (e.g. HIV/AIDS), or dermatological conditions (e.g. psoriasis).6 Anal fissures are further described as acute or chronic, with chronic fissures lasting more than 6 weeks.7
[caption id="attachment_31774" align="alignright" width="200"]
DR Amy Page (she/her) PhD, MClinPharm, GradDipBiostat, GCertHProfEd, GAICD, GStat, FSHPA, FPS is a consultant pharmacist, biostatistician, and the director of the Centre for Optimisation of Medicines at UWA’s School of Allied Health.[/caption]
Anal fissures are often mistaken for haemorrhoids because of their overlapping symptoms. Haemorrhoids differ in that they are normal vascular cushions within the anal canal that maintain continence. Although part of normal anatomy, the term ‘haemorrhoid’ is commonly used when these vascular anal cushions, containing a rich arteriovenous network, become enlarged or displaced.8 Haemorrhoids may be classified as internal (located above the dentate line) or external (located below the dentate line). Factors such as constipation, straining during bowel movements and a low-fibre diet are commonly considered to increase the risk of haemorrhoids.9,10 However, the causal relationship between these factors and the development of haemorrhoids remains unclear. A possible genetic component that predisposes to smooth muscle, epithelial and connective tissue dysfunction, may contribute to haemorrhoids.11
It is important to note that certain medicines can contribute to or worsen constipation as an adverse effect, thereby aggravating haemorrhoids and anal fissures.9,10 Common examples include opioids, anticholinergics, and iron and calcium supplements.12 Regular medication review should be incorporated into comprehensive care to identify opportunities for deprescribing and prevent inappropriate prescribing cascades, with further guidance available in the new deprescribing guidelines.13
The symptoms of haemorrhoids may include rectal bleeding, anal pruritus, prolapse, faecal seepage and mucus discharge.7
Internal haemorrhoids are usually painless because the columnar epithelium is insensitive to touch and temperature.8 In contrast, external haemorrhoids are pain sensitive and may become thrombosed, often following straining during defecation.8
Anal fissures, by comparison, typically cause severe tearing pain that is provoked by defecation.4 A key distinguishing feature is that the pain of an anal fissure typically occurs during or immediately after defecation.

For diagnostic purposes, medical practitioners perform a physical examination with the individual lying on their side, gently parting the buttocks to inspect the posterior midline.4 Several other anorectal disorders may present with similar symptoms to anal fissures and haemorrhoids. Differential diagnoses include anal fistula and solitary rectal ulcer syndrome, which can often be distinguished based on their clinical appearance through careful physical examination. An anal fistula typically presents as a draining skin punctum.14 It is an abnormal hollow tract, most often arising from infection of an anal gland.15 Solitary rectal ulcer syndrome may present with anal pain, rectal bleeding, constipation, mucus discharge, excessive straining and a sensation of incomplete evacuation. Despite its name, the condition does not always involve an ulcer. Diagnosis requires a combination of endoscopic and histopathological findings, together with the individual’s reported symptoms.16
Haemorrhoids
[caption id="attachment_31775" align="alignright" width="200"]
Hui Wen Quek (she/her) BPharm(Hons), GradCertAppPharmPrac is a pharmacist and PhD candidate at the University of Western Australia (UWA).[/caption]
Non-pharmacological treatment options
First-line management for haemorrhoids usually involves lifestyle measures, which include ensuring adequate fluid and fibre intake, reducing prolonged time on the toilet and avoiding excessive straining, the use of sitz baths, and maintaining anal hygiene.10 In practice, dietary and lifestyle modifications are usually recommended as a conservative and preventive measure for haemorrhoids.17
Pharmacological treatment options
Over-the-counter therapies for internal haemorrhoids include ointments and suppositories that contain emollients, mild astringents, local anaesthetics and/or corticosteroids.8 These preparations temporarily relieve itching and discomfort. Prolonged use of topical corticosteroids is not recommended, as it increases the risk of local infections such as candidiasis.8 Similarly, prolonged use of anaesthetic-containing products should be avoided due to potential adverse effects, including skin sensitisation and dermatitis.8
Outpatient procedures and surgery
For individuals who do not respond to conservative measures, other treatment options for haemorrhoids include outpatient procedures and surgery.10 Outpatient procedures include rubber band ligation, infrared coagulation, bipolar probe, heater probe, sclerotherapy and cryotherapy.10 These are generally reserved for people with grade I or grade II haemorrhoids.10 Surgery can be considered for people who do not respond to or cannot tolerate outpatient procedures, as well as those with large external haemorrhoids, or combined internal and external haemorrhoids with prolapse.10
A recent meta-analysis found that surgical treatments, compared with conservative treatments, offer greater symptom relief, quicker recovery and lower recurrence rates.18 However, they do carry risks of procedure-related complications. In contrast, conservative treatments are safer and less invasive, but tend to provide slower symptom improvement and have higher recurrence rates.18 Therefore, treatment decisions should be individualised, taking into account symptom severity, individual preferences and risk tolerance.
Anal fissures
The primary aim of treatment for anal fissures is to reduce anal sphincter spasm, improve blood flow and promote healing.6 First-line management is usually non-operative and includes increasing dietary fibre, use of sitz baths and applying glyceryl trinitrate 0.2% ointment, three times daily for up to 4 weeks to relieve pain.19 Headache is a common adverse effect of glyceryl trinitrate due to systemic absorption, which could limit its use.20 Other topical agents used in clinical practice include lidocaine and hydrocortisone, although these are less effective than a combination of fibre intake and warm sitz baths.4
Botulinum toxin injections may also be considered and can achieve good healing rates.6,19 However, botulinum toxin may cause temporary reduced control of wind or bowel motions, which usually resolves as the effect of the injection wears off.4 Due to these adverse effects and the invasive nature of the procedure, botulinum toxin is generally reserved as a second-line therapy.4 If these treatment options are unsuccessful, surgical treatment may be required.6
Secondary or chronic anal fissures warrant additional investigation and multidisciplinary management is advised, especially when malignancy is suspected or confirmed.4
Pharmacists play a key role in recognising the symptoms of haemorrhoids and anal fissures, providing timely advice and suggesting a suitable course of action. Pharmacists can also educate individuals on first-line management strategies and provide lifestyle advice where appropriate to prevent recurrence. In addition, pharmacists can advocate for the safe use of over-the-counter treatments, advise on appropriate duration of use and counsel individuals on potential adverse effects.
Referral to a medical practitioner is advisable for individuals who21:
Anal fissures and haemorrhoids are common conditions encountered in primary care and can greatly impact quality of life. Pharmacists play a critical role in early management and referral, helping prevent complications and improve outcomes.
Case scenario continuedYou identify that Sarah has haemorrhoids and provide lifestyle advice, including increasing fluid and dietary fibre intake, avoiding prolonged straining during bowel movements and practising good anal hygiene. For symptomatic relief, you suggest a topical ointment containing cinchocaine 0.5% and zinc oxide 20%, to be applied as needed. You also advise her to consult her general practitioner if she experiences persistent bleeding, ongoing pain or worsening prolapse. With your support and advice, Sarah feels more confident in managing her condition effectively while reducing the risk of recurrence. |
[cpd_submit_answer_button]
Hui Wen Quek (she/her) BPharm(Hons), GradCertAppPharmPrac is a pharmacist and PhD candidate at the University of Western Australia (UWA).
DR Amy Page (she/her) PhD, MClinPharm, GradDipBiostat, GCertHProfEd, GAICD, GStat, FSHPA, FPS is a consultant pharmacist, biostatistician, and the director of the Centre for Optimisation of Medicines at UWA’s School of Allied Health.
Manisha Pillai (she/her) BPharm
Higuero T. Update on the management of anal fissure. J Visc Surg. 2015;152(2 Suppl):S37–S43.
Riss S, Weiser FA, Schwameis K, Riss T, Mittlböck M, Steiner G, et al. The prevalence of hemorrhoids in adults. Int J Colorectal Dis. 2012;27(2):215–220.
Vitton V, Bouchard D, Guingand M, Higuero T. Treatment of anal fissures: results from a national survey on French practice. Clin Res Hepatol Gastroenterol. 2022;46(4):101821.
Schlichtemeier S, Engel A. Anal fissure. Aust Prescr. 2016;39(1):14–17.
Zaghiyan KN, Fleshner P. Anal fissure. Clin Colon Rectal Surg. 2011;24(1):22–30.
Newman M, Collie M. Anal fissure: diagnosis, management, and referral in primary care. Br J Gen Pract. 2019;69(685):409–410.
Lyle V, Young C. Anal fissures: an update on treatment options. Aust J Gen Pract. 2024;53:33–35.
Therapeutic Guidelines Limited. Haemorrhoids. Melbourne: Therapeutic Guidelines Limited; 2022. Available from: https://www.tg.org.au
Lohsiriwat V. Hemorrhoids: from basic pathophysiology to clinical management. World J Gastroenterol. 2012;18(17):2009–2017.
Sandler RS, Peery AF. Rethinking what we know about hemorrhoids. Clin Gastroenterol Hepatol. 2019;17(1):8–15.
Zheng T, Ellinghaus D, Juzenas S, Cossais F, Burmeister G, Mayr G, et al. Genome-wide analysis of 944 133 individuals provides insights into the etiology of haemorrhoidal disease. Gut. 2021;70(8):1538–1549.
Therapeutic Guidelines Limited. Functional constipation in adults. Melbourne: Therapeutic Guidelines Limited; 2022. Available from: https://www.tg.org.au
Quek HW, Reus X, Lee K, Etherton-Beer C, Page A; Guideline Development Group. Deprescribing in older people: a clinical practice guideline. Perth (WA): The University of Western Australia; 2025.
Stewart D. Anal fissure: clinical manifestations, diagnosis, prevention. UpToDate. 2025. Available from: https://www.uptodate.com/contents/anal-fissure-clinical-manifestations-diagnosis-prevention
Therapeutic Guidelines Limited. Anorectal abscess and fistula. Melbourne: Therapeutic Guidelines Limited; 2022. Available from: https://www.tg.org.au
Sadeghi A, Biglari M, Forootan M, Adibi P. Solitary rectal ulcer syndrome: a narrative review. Middle East J Dig Dis. 2019;11(3):129–134.
Lohsiriwat V. Treatment of hemorrhoids: a coloproctologist's view. World J Gastroenterol. 2015;21(31):9245–9252.
Quan L, Bai X, Cheng F, Chen J, Ma H, Wang P, et al. Comparison of efficacy and safety between surgical and conservative treatments for hemorrhoids: a meta-analysis. BMC Gastroenterol. 2025;25(1):492.
Therapeutic Guidelines Limited. Anal fissure. Melbourne: Therapeutic Guidelines Limited; 2022. Available from: https://www.tg.org.au
Australian Medicines Handbook Pty Ltd. Glyceryl trinitrate (rectal). Adelaide: Australian Medicines Handbook Pty Ltd; 2025. Available from: https://amhonline.amh.net.au/
Allen S. Haemorrhoids and anal fissures. S Afr Pharm J. 2008;75(5):36.
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[post_content] => Community pharmacies are often the first place people turn when something feels ‘off’. But as pharmacists know, many requests for over-the-counter medicines are more complex than they may initially seem.
AP took a look at some presentations which might signal hidden red flags.
‘I just want a multivitamin’
When people present to community pharmacies, they often arrive with a solution already in mind. For example, ‘I need a strong painkiller,’ ‘I just want a multivitamin,’ or ‘What do you have for nerve pain?’
Nearly always, consistent with professional standards, these invite an open ended question to uncover the rationale for the request
Gauri Godbole FPS[/caption]
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[post_content] => Case scenario
During peak hour, 19-year-old Enzo and his mother arrive to collect a new prescription for melatonin MR 2 mg. The pharmacy is highly stimulating: background music blares, customers converse loudly nearby, staff assist others in a cramped space, and general noise amplifies the chaos. While processing Enzo’s prescription and attempting to deliver verbal instructions, you observe Enzo avoiding eye contact, fidgeting intensely, and appearing overwhelmed, with reduced capacity to process verbal or non-verbal cues due to sensory overload.
Learning objectivesAfter reading this article, pharmacists should be able to:
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Yvette Anderson (she/her) BPharm, MPS, CredPharm (MMR), ANZCAP (MentalHth, Paeds), CPGx, GradCert Autism[/caption]
Neurodevelopmental disorders (NDDs) arise from differences in brain development and typically affect cognition, communication, behaviour and occupational functioning. Common NDDs include attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), referred to as autism in this article, and intellectual developmental disorder (IDD).1 Autism is characterised by persistent social interaction and communication difficulties and restricted behavioural patterns.2 Symptoms begin in early childhood; however, diagnosis can occur at any age.3 Autism affects how the brain processes information, shaping how autistic people see, understand and respond to the world around them, with marked variability in presentation, day-to-day functioning and support needs.3,4
In Australia, autism prevalence has increased due to evolving diagnostic practices and awareness,5 meaning pharmacists now routinely engage with autistic individuals as part of everyday practice.
The challenge and opportunity for pharmacy is to shift from a medical model of crisis response, treatments and cures to a neuro-affirming social model that helps autistic individuals thrive, not just survive.
A neuro-affirming social model conceptualises neurodevelopmental differences as natural variations within human diversity and rejects deficit-based assumptions that frame these differences as disorders.6 Rather than ‘correcting’ individual traits, this approach provides reasonable adjustments while supporting autonomy, community participation and wellbeing, alongside awareness of diagnostic criteria, comorbidities, communication styles, lived realities and the impact of misinformation.6 The shift to a neuro-affirming social model calls for reducing systemic and environmental barriers, while still addressing health needs.6,7
For pharmacists, it means making practice adjustments in the way that the profession engages with and provides support for autistic individuals.
According to the Australian Bureau of Statistics, approximately 290,900 Australians (1.1%) are reported to have had an autism diagnosis in 2022.5 A recent estimate by Autism Spectrum Australia (Aspect) suggested at least 1 in 40 Australians are autistic.7
Rising prevalence reflects improved awareness and diagnostic practices rather than a true increase in incidence, including better recognition in historically underdiagnosed groups such as females and older adults.7 Autism prevalence peaks in children and adolescents, particularly those aged 10–14 years, and is markedly lower in adults, acknowledging limited adult data.5,8,9
Autism prevalence rates may appear to vary among ethnic and cultural groups, reflecting inequities such as access to healthcare, effective communication, diagnostic practices and cultural perceptions.10
Prevalence remains higher in males than females, with 1.6% of males identified compared with 0.7% of females, and the greatest disparity is seen in children aged 5–9 years.5 Autism in females is frequently underdiagnosed, as characteristics may manifest differently, be masked (e.g. forced eye contact, rehearsed social scripts, suppressing stimming or copying peers), or fail to align with historically male-centred diagnostic criteria, leading to misdiagnosis as mood or personality disorders.11,12 Masking may occur due to a desire to fit in, fear of stigma or bullying, previous negative reactions to autistic behaviours, and expectations of how females are ‘supposed’ to behave.12 Increasing awareness of the under-recognition of autism in females and gender-diverse individuals, and the social drivers of masking, is anticipated to influence future prevalence estimates.4,5,11
There is no single cause of autism, and despite extensive research, aetiology remains incompletely understood. Current evidence indicates autism arises from a complex interaction between genetic susceptibility and environmental influences on neurodevelopment.13
Family history is one of the strongest predictors of autism.13,14 Researchers have identified hundreds of genes, with approximately 10–20% of cases associated with rare genetic variants arising from mutations in sperm or egg cells.14 Autism is considered polygenic, meaning overall risk typically reflects the cumulative effect of multiple inherited variants, each contributing a small effect.14
The expression of genetic susceptibility is known to be influenced by prenatal, perinatal and postnatal environmental factors.13 Environmental factors appear most relevant during the prenatal period.14 Modest associations have been reported between autism likelihood and maternal factors such as hypertension, gestational diabetes, obesity, alcohol and substance use, poor antenatal care, and infection or fever during pregnancy.15
Imprecise and inconsistent associations have been reported for folate status, exposure to some air pollutants, and the use of some medicines.15–17 Importantly, these findings are largely derived from observational studies and are subject to confounding. While some prenatal medicine exposures show more consistent associations with autism, there is no clear evidence that associations between autism and other environmental and medicine exposures represent a causal relationship, and any contribution to autism risk remains limited and uncertain.14,17

Autism is diagnosed according to Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR) criteria: ‘persistent deficits in social communication and social interaction across multiple contexts’, with the presence of ‘restricted, repetitive patterns of behaviour, interests or activities’.2
‘Symptoms must be present in the early development period’, although they may only become fully apparent later in life.
‘Symptoms cause clinically significant impairment in social, occupational or other important areas of functioning’ and ‘these disturbances are not better explained by IDD’ although both can co-occur.2 The DSM-5-TR also specifies severity levels (1–3) to indicate the degree of support required.2
In Australia, individuals may pursue an autism diagnosis through public or private pathways.18 Both are typically lengthy and necessitate a degree of health literacy and English proficiency. Diagnostic assessments may be conducted by a multidisciplinary team, including paediatricians, psychiatrists, psychologists, speech pathologists and occupational therapists.4 Multiple appointments may be needed, drawing on input from family, carers or teachers.18,19
Barriers to diagnosis include limited awareness of early signs among caregivers and clinicians, long wait times and out-of-pocket costs for specialist assessment, socioeconomic and geographic disparities, and bias in recognising diverse presentations.11,20,21 Limited health literacy and the complexity of navigating multidisciplinary assessments and National Disability Insurance Scheme requirements further impede access.21 In some communities, stigma, fear of labelling, and differing cultural interpretations of behaviour may delay help-seeking.22
A best-practice diagnostic approach should promote cultural safety and sensitivity, acknowledge variations in health literacy, address socioeconomic barriers, and be grounded in person-centred care.
Autism is a spectrum, with each individual having a unique mix of strengths, challenges, interests, needs and way of interacting with the world. Autism advocate Dr Stephen Shore states, ‘If you have met one autistic person, you have met one autistic person’.23
Beyond the core featuresComorbid NDDs, and psychiatric and medical conditions can create significant challenges for autistic individuals in relation to diagnosis, selection of appropriate interventions, medicines and support services.1,24
Comorbid NDDs among autistic individuals include ADHD, developmental coordination disorder (dyspraxia), IDD, and specific learning disorders such as dyslexia, dysgraphia and dyscalculia.25 Psychiatric comorbidities are also prevalent, including anxiety, depression, obsessive-compulsive disorder, and post-traumatic stress disorder.26 These conditions can intensify social and sensory challenges, increase vulnerability to stress, and impair emotional regulation and executive functioning.
Autistic individuals experience higher rates and severity of mental and physical health comorbidities than neurotypical individuals. Neurodivergent mental health outcomes are influenced by the interaction between individual differences and environmental and societal factors.25–28 Diagnostic overshadowing, whereby mental health symptoms are erroneously attributed to autism, should be avoided.29 Comorbid conditions warrant assessment and treatment according to the same clinical standards applied to neurotypical individuals, with adaptations made to accommodate the communication, sensory and support needs of autistic people. Neurodivergent individuals experience the full range of medical comorbidities seen in the general population; however, research indicates higher prevalence of certain conditions, including gastrointestinal disorders (e.g. irritable bowel syndrome, chronic constipation), sleep disturbances, epilepsy, and immune or metabolic disorders.30 These conditions may worsen fatigue, concentration and mood regulation, while motor difficulties may contribute to musculoskeletal pain, reduced physical activity and secondary health issues.31
Physical health conditions may be underdiagnosed when the clinical focus is limited to behavioural or psychological symptoms.29
Recognising the complex interconnections between physical, psychiatric and NDD health is paramount. Pharmacists can play a vital role in this process. Effective care relies on health professionals working collaboratively to identify how comorbid conditions, treatment burden and medicines may influence behaviour, cognition and developmental outcomes.
Autism is a lifelong NDD for which there is no curative treatment.4 Clinical care focuses on supporting health, functioning and community participation, addressing comorbidities, and optimising quality of life, while recognising and respecting the individual strengths, capabilities and perspectives of autistic individuals.3
Supports and interventions are individualised and typically involve a multidisciplinary team to address evolving needs.10 Allied health professionals may include speech pathologists to support communication, occupational therapists to address sensory processing and daily living skills, and psychologists to support emotional regulation and mental health. Physiotherapists may support gross motor skills, while dietitians support feeding and nutritional adequacy, alongside specialist educational support and therapy (e.g. play therapy, art therapy).3 Effective management relies on coordinated care, regular goal review and clear communication between the autistic individual, families and carers, and the multidisciplinary team.24
There is no evidence to support the use of medicines, exclusion diets or other biological treatment for the core features of autism.32,33 To support comorbidities, psychotropic medicines, antiepileptics and sleep agents may be used short term and under specific circumstances. Off-label use is common and requires careful assessment of risk-benefit balance, adverse effects, formulation choice, monitoring, cumulative treatment burden, and very careful consideration if the medicine is being prescribed as a chemical restraint.4

Autism is subject to persistent myths that pharmacists may encounter. The most damaging is the long-debunked claim that vaccines cause autism.14 The retracted 1998 Lancet study by Andrew Wakefield that claimed a link between the measles, mumps, rubella (MMR) vaccine and autism was a small, flawed study (with only 12 participants) and was exposed for unethical processes, methodological misconduct, and undisclosed conflicts of interest.14 Despite retraction, its claims were (and continue to be) amplified, eroding trust in public health and fuelling vaccine hesitancy. A Cochrane review published in 2021 found no credible evidence of an association between MMR and MMRV vaccines and autism.34
Two medicines made headlines in 2025: paracetamol and leucovorin (folinic acid or calcium folinate) claimed as a cause and treatment of autism respectively. Antenatal paracetamol exposure was alleged to increase autism and ADHD risk; however, major studies have not demonstrated a causal relationship.9 Stronger evidence from a large Swedish population-based cohort of 2,480,797 children born between 1995 and 2019 found no association between paracetamol use during pregnancy and autism, ADHD or IDD in sibling-controlled analysis.16 Cerebral folate deficiency (CFD) has been reported in a subset of autistic individuals, related to impaired folate transport into the brain, and may be associated with symptoms of speech difficulties, seizures and IDD, often within early childhood.35,36 Leucovorin, a folinic acid derivative, has been investigated as a potential treatment for autistic children with CFD. Leucovorin can bypass impaired folate transport, increasing central nervous system folate availability.36 Although some small-scale trials indicate potential minor behavioural improvements, supporting evidence remains limited, inconsistent, and not independently replicated.15,37
As medicines experts, pharmacists are well placed to counter common myths. Responses should prioritise empathetic, respectful communication and the provision of clear, evidence-based information and resources.
Accessibility, strong communication skills, medicines expertise, understanding of health system navigation and ability to synthesise information, position pharmacists to provide continuity of care for autistic individuals. Pharmacists can serve as an integrative link within multidisciplinary teams, supporting autistic individuals and their families across the healthcare continuum.
Effective communication underpins person-centred pharmacy practice. Pharmacists supporting autistic individuals should adapt both verbal and non-verbal communication to meet diverse needs.38 Autism can influence communication and sensory processing in unique ways, with some individuals experiencing sensory sensitivities to sound, light, smell, touch and visual stimuli.3,4,33 Some autistic individuals regulate sensory input through stimming (self-stimulatory behaviour), which may present as repetitive movements or sounds such as fidgeting, rocking or hand-flapping.39 Flexibility, empathy and understanding of sensory needs ensure equitable access to healthcare and fosters the relationship between patient and pharmacist. Verbal communication with autistic individuals should be clear and structured. Pharmacists should use straightforward, unambiguous language and present information in small, logical steps, allowing time for processing and response. Offering a calm, quiet space can both minimise sensory overload and facilitate a more comfortable environment for communication.38,40
Non-verbal communication requires equal attention. Eye contact, facial expressions and gestures can carry unintended meaning for autistic individuals. Some avoid eye contact as a coping mechanism, not as disinterest.38 Pharmacists should avoid assumptions and focus on open, calm body language and a reassuring tone. Visual supports can reinforce verbal explanations to provide ongoing reference, especially for individuals who process visual information more effectively than spoken language.40
A person-centred approach requires pharmacists to recognise, respond and adapt to the communication preferences of each autistic individual. If a caregiver or support worker is present, collaboration should occur while directing communication towards the patient whenever possible.40 Empathy, flexibility and inclusive communication techniques ensure care that is respectful and accessible and upholds an individual’s dignity and autonomy.
By adopting inclusive, neuro-affirming approaches, pharmacists strengthen equity, accessibility and person-centredness within healthcare. In doing so, they uphold the profession’s commitment to compassionate, evidence-based practice and help ensure autistic Australians receive the respect, understanding and tailored support needed to achieve optimal health and wellbeing.
Case scenario continuedEnzo’s mother discloses Enzo’s autism diagnosis and requests a quiet area and slower, step-by-step instructions. You offer a consultation room with dimmed lights, minimal visual clutter and no background noise. Enzo settles, visibly calmer. In this adapted space, you employ person-centred strategies: a soft, steady voice; paced delivery; short, simple sentences; pauses after each point for processing; confirming understanding via yes/no questions or thumbs-up signals; and a clear, written handout with bullet points, icons (e.g. clock for bedtime), and appropriate font. Enzo engages, maintaining partial eye contact and nodding, while his mother clarifies. These modifications demonstrate empathy, flexibility and equitable care, minimising distress, enhancing information access and supporting Enzo’s autonomy. |
Yvette Anderson (she/her) BPharm, MPS, CredPharm (MMR), ANZCAP (MentalHth, Paeds), CPGx, GradCert Autism is an accredited clinical pharmacist with over 20 years’ experience across aged care, consultancy, community pharmacy and hospital pharmacy. In 2020, she launched The Spectrum Pharmacist to increase awareness, promote inclusion, and provide education and support for neurodevelopmental disorders.
Victor Senescall (he/him) BPharm (Hons)
Merck Manual Professional Version. Overview of learning disorders. 2024. Available from: www.merckmanuals.com/professional/pediatrics/learning-and-developmental-disorders/overview-of-learning-disorders?query=neurodevelopment%20disorders
American Psychiatric Association. Diagnostic and statistical manual of mental disorders. 5th ed. Washington (DC): American Psychiatric Publishing; 2022.
Merck Manual Professional Version. Autism spectrum disorder. 2025. Available from: www.merckmanuals.com/professional/pediatrics/learning-and-developmental-disorders/autism-spectrum-disorder
Therapeutic Guidelines. Autism spectrum disorder. Melbourne: Therapeutic Guidelines; 2021.
Australian Bureau of Statistics. Autism in Australia 2022. 2024. Available from: www.abs.gov.au/articles/autism-australia-2022
Bertilsdotter Rosqvist H, Pearson A, Pavlopoulou G, et al. The social model in autism research. Autism. 2025;29(9):2201–2204.
Autism Spectrum Australia. At least 1 in 40 Australians are autistic: new estimate by Aspect on World Autism Understanding Day. 2024. Available from: www.aspect.org.au/news/at-least-1-in-40-australians-are-autistic
Therapeutic Guidelines. Autism spectrum disorder. eTG complete. Melbourne: Therapeutic Guidelines; 2021.
Trollor J, Arnold S, Walker SE. Australian Longitudinal Study of Autism in Adulthood (ALSAA): final report. Brisbane: Autism CRC; 2022.
Rasheed Z. Autism in Australia: understanding, challenges, and support. Int J Health Sci. 2023;17(5):1–4.
Lai M-C, Amestoy A, Bishop S, et al. Improving autism identification and support for individuals assigned female at birth: clinical suggestions and research priorities. Lancet Child Adolesc Health. 2023;7(12):897–908.
National Autistic Society. Masking. 2026. Available from: www.autism.org.uk/advice-and-guidance/topics/behaviour/masking
Ostrowski J, Religioni U, Gellert B, et al. Autism spectrum disorders: etiology, epidemiology, and challenges for public health. Med Sci Monit. 2024;30.
Australian Academy of Health and Medical Sciences. Autism: an evidence brief. 2025. Available from: https://aahms.org/policy/evidence-brief-on-autism
Love C, Sominsky L, O'Hely M, et al. Prenatal environmental risk factors for autism spectrum disorder and their potential mechanisms. BMC Med. 2024;22.
Ahlqvist VH, Sjöqvist H, Dalman C, et al. Acetaminophen use during pregnancy and children's risk of autism, ADHD, and intellectual disability. JAMA. 2024;331(14):1205–1214.
de Lara I, Wagner P, Matheus G, et al. Association of prenatal exposure to antiseizure medication with risk of autism: a systematic review and meta-analysis. Seizure. 2025;130:41–47.
Government of South Australia Office for Autism. Pathways for assessment and diagnosis. 2023. Available from: www.officeforautism.sa.gov.au/autism/pathways-for-diagnosis
Autism Awareness Australia. Understanding and accessing the NDIS. 2024. Available from: www.autismawareness.com.au/navigating-autism/understanding-and-accessing-the-ndis-for-autism
Estrin GL, Milner V, Spain D, et al. Barriers to autism spectrum disorder diagnosis for young women and girls: a systematic review. Rev J Autism Dev Disord. 2021;8(4):454–470.
Allen-Meares P, Lowry B, Estrella ML, et al. Health literacy barriers in the health care system: barriers and opportunities for the profession. Health Soc Work. 2020;45(1):62–64.
Khalil A, Yatcilla J, Christie N, et al. A systematic review of help-seeking barriers for racial-ethnic minority caregivers accessing autism diagnostic and intervention services. J Racial Ethn Health Disparities. 2025.
Flannery KA, Wisner-Carlson R. Autism and education. Child Adolesc Psychiatr Clin N Am. 2020;29(2).
Autism Awareness Australia. Navigating the health system. 2024. Available from: www.autismawareness.com.au/navigating-autism/navigating-the-health-system-for-autism
Bonti E, Zerva IK, Koundourou C, et al. The high rates of comorbidity among neurodevelopmental disorders: reconsidering the clinical utility of distinct diagnostic categories. J Pers Med. 2024;14(3):300.
Lai M-C, Kassee C, Besney R, et al. Prevalence of co-occurring mental health diagnoses in the autism population: a systematic review and meta-analysis. Lancet Psychiatry. 2019;6(10):819–829.
Mazurek MO, Sadikova E, Cheak-Zamora N, et al. Health care needs, experiences, and perspectives of autistic adults. Autism Adulthood. 2023;5(1):51–62.
Barlattani T, D'Amelio C, Cavatassi A, et al. Autism spectrum disorders and psychiatric comorbidities: a narrative review. J Psychopathol. 2023;29(1):3–24.
Blair J. Diagnostic overshadowing: see beyond the diagnosis. 2017. Available from: www.intellectualdisability.info/changing-values/diagnostic-overshadowing-see-beyond-the-diagnosis
Al-Beltagi M. Autism medical comorbidities. World J Clin Pediatr. 2021;10(3):15–28.
Sung Y-S, Loh SC, Lin L-Y. Physical activity and motor performance: a comparison between young children with and without autism spectrum disorder. Neuropsychiatr Dis Treat. 2021;17:3743–3751.
Turner M. The role of drugs in the treatment of autism. Aust Prescr. 2020;43:185–190.
Mayo Clinic. Autism spectrum disorder. 2025. Available from: www.mayoclinic.org/diseases-conditions/autism-spectrum-disorder/diagnosis-treatment/drc-20352934
Di Pietrantonj C, Rivetti A, Marchione P, et al. Vaccines for measles, mumps, rubella, and varicella in children. Cochrane Database Syst Rev. 2021;(11):CD004407.
Wong A, Frye RE, Ohnemus-Kawamura B, et al. Cerebral folate deficiency. 2019. Available from: https://rarediseases.org/rare-diseases/cerebral-folate-deficiency/
Ramaekers VTH, Quadros EV. Cerebral folate deficiency syndrome: early diagnosis, intervention and treatment strategies. Nutrients. 2022;14(15):3096.
Sheppeard A. What is leucovorin, and can it cure autism? 2025. Available from: www.medicalrepublic.com.au/what-is-leucovorin-and-can-it-cure-autism/120175
Norris JE, Milton D, Heasman B. Adapting communication with autistic service users: a participatory study. Autism. 2024.
National Autistic Society. Repeated movements and behaviour (stimming). 2026. Available from: www.autism.org.uk/advice-and-guidance/topics/about-autism/repeated-movements-and-behaviour-stimming
National Autistic Society. Autism and communication. 2024. Available from: www.autism.org.uk/advice-and-guidance/topics/about-autism/autism-and-communication
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Case scenarioStavros, a 35-year-old male with focal epilepsy, presents to the pharmacy to collect his medicines. He appears tired and mentions he has been having more frequent breakthrough seizures lately. As you chat, he reveals he recently started lorazepam 1 mg twice daily for generalised anxiety disorder (GAD), prescribed by his new GP. Stavros has been missing doses of his anti-seizure medicine, carbamazepine, as he feels it worsens his drowsiness and confusion. |
Dr Ming S Soh PhD, BPharm (Hons)[/caption]
Epilepsy is a chronic neurological condition characterised by a persistent tendency to produce seizures.1,2 According to the International League Against Epilepsy (ILAE), epilepsy is diagnosed when an individual experiences at least two unprovoked seizures more than 24 hours apart, one unprovoked seizure with a high probability (≥60%) of recurrence, or when an epilepsy syndrome is identified.3 Seizures result from abnormal, excessive electrical discharges in the brain, and vary in type, severity and frequency.4 While most seizures are brief, lasting seconds to minutes, they can become prolonged and continuous (i.e. status epilepticus), which requires urgent, intensive medical intervention.4 Globally, epilepsy affects around 50 million people.5,6 It can affect individuals across all age groups, races and ethnicities, and can significantly disrupt quality of life.7,8 Epilepsy is often associated with neurobiological, cognitive, psychological and social sequelae.1,2
Management of epilepsy primarily involves antiseizure medicines (ASM), administered as monotherapy or polytherapy depending on the patient’s response.8,9 In some cases, surgery, dietary therapy or neurostimulation may be considered.9 Treatment complexity, adverse drug reactions and non-adherence to medicines can hinder seizure control and prevent optimal outcomes.8
Learning OutcomesAfter reading this article, pharmacists should be able to:
|
In practice, pharmacists provide therapeutic drug monitoring (hospital setting), Home Medicines Reviews (HMR), MedsChecks and patient counselling, and they support the management of common comorbidities such as depression, anxiety and cognitive impairments, which can complicate treatment.6,8,9

Globally, the pooled incidence rate of epilepsy is estimated at 50–61.4 cases per 100,000 person-years.2,10,11 However, incidence varies by region and income level. In high-income countries, rates typically range from 40–70 per 100,000 person-years, while in low- and middle-income countries, incidence can reach 100–190 per 100,000 person-years, reflecting disparities in healthcare access, diagnostic capacity and exposure to risk factors.2,10 The highest incidence of epilepsy occurs in childhood, reflecting the higher seizure susceptibility of the developing brain.12
In Australia, the lifetime risk of developing epilepsy is estimated to be up to 4%, while approximately 0.6–1% of the population is living with epilepsy at any given time.13,14 Modelled data estimates that prevalence peaks in males aged 60–64 (8.54 per 1,000), and in females aged 50–54 (9.57 per 1,000).15 National surveillance data indicates that prevalence generally remains high into older age groups, largely due to increased rates of stroke, neurodegenerative diseases and brain tumours.2,14,15
Disparities are pronounced among Aboriginal and Torres Strait Islander people, who experience twice the prevalence of epilepsy compared to non-Aboriginal and Torres Strait Islander people.14,16 Aboriginal and Torres Strait Islander people also face higher rates of hospitalisation, reduced access to specialist care and ASM, and significantly elevated epilepsy-related mortality.16 The disability-adjusted life years for Aboriginal and Torres Strait Islander people with epilepsy are double those of non-Aboriginal and Torres Strait Islander people.16
Epilepsy has a multifactorial aetiology. The ILAE classifies epilepsy aetiologies into six main categories: genetic, structural, infectious, metabolic, immune and unknown (see Figure 1).17,18 Genetic mutations generally affect neuronal excitability, especially ion channels, and are linked to specific epilepsy syndromes.18–20 Structural causes include brain malformations, trauma, stroke and tumours. Infections like meningitis or encephalitis can provoke seizures through inflammation. Metabolic causes arise from systemic or inherited metabolic disorders that disrupt brain chemistry or energy production. Autoimmune responses, where the body’s immune system attacks brain tissue, can also lead to seizures. Unknown causes refer to cases where no clear aetiology can be identified despite thorough investigation. Neurodegenerative causes are increasingly recognised as important contributors to epilepsy.18 Despite structured classifications, many overlap. For example, an infection such as encephalitis may lead to structural brain damage.18 Risk factors include family history, perinatal insults, head trauma, brain infections, febrile seizures and socioeconomic disparities, which can influence both the likelihood of developing epilepsy as well as its clinical progression.21

Epilepsy involves several interconnected mechanisms that predominate in different seizure types and epilepsy syndromes and are targeted by specific ASM.
Neuronal hyperexcitability is increased neuronal responsiveness due to ion-channel dysfunction, resulting in spontaneous, excessive neuronal firing. This is a key mechanism underlying all seizure types, but is not the sole pathophysiological mechanism.4,22,23
Hypersynchrony is the abnormal synchronisation of neuronal activity which facilitates seizure propagation across brain regions, particularly in generalised epilepsies such as absence and tonic-clonic seizures.1,4,12,18
Excitatory/inhibitory neurotransmitter imbalance refers to the disruption of glutamate and gamma-aminobutyric acid (GABA) neurotransmission, shifting networks toward hyperexcitability and is central to both focal and generalised epilepsy.4,17
Neuroinflammation refers to the immune activation and cytokine release (e.g. IL-1 beta, TNF-alpha) that can enhance excitability, and are implicated in structural focal epilepsies, post-stroke epilepsy and autoimmune epilepsies. Anti-inflammatory and immunomodulatory therapies may be used in selected cases.4,24
mTOR pathway dysregulation is the abnormal mTOR signalling that alters synaptic plasticity, contributing to epileptogenesis, most notably in tuberous sclerosis complex–associated epilepsy, where mTOR inhibitors such as everolimus are used as targeted therapy.18
Oxidative stress is the excess reactive oxygen species that can damage neurons and lower seizure thresholds, contributing to seizures in metabolic and neurodegenerative epilepsies.24
Mitochondrial dysfunction refers to impaired energy metabolism, which reduces neuronal resilience and is characteristic of mitochondrial epilepsies and some childhood epileptic encephalopathies.24
Synaptic reorganisation refers to structural changes, including aberrant axon sprouting and new excitatory circuit formation, and are commonly seen in temporal lobe epilepsy following brain injury or prolonged seizures.4
Recognising underlying epileptogenic mechanisms aids interpretation of seizure type/classification and guides appropriate ASM selection.
Focal seizures (formerly known as partial)
Focal seizures originate in a specific area of one cerebral hemisphere. Depending on the brain area affected, they may present with localised motor activity like rhythmic jerking or muscle stiffening, sensory changes such as tingling or visual distortions, or autonomic signs, including flushing and gastrointestinal discomfort.12 Awareness may or may not be impaired during these seizures.25 Some focal seizures begin with an aura, such as déjà vu or intense emotions, during which a person remains alert. First-line treatment includes carbamazepine, lamotrigine or levetiracetam, where selection is guided by contraindications and other patient-specific factors.26
Generalised seizures
Generalised seizures involve widespread electrical activity across both cerebral hemispheres and typically include tonic-clonic, absence, myoclonic and atonic seizures.12,25
Tonic-clonic seizures (formerly known as grand mal)
Tonic-clonic seizures are characterised by a sudden loss of consciousness, muscle stiffening followed by rhythmic jerking, and a post-seizure phase with confusion, agitation or fatigue. They can sometimes be fatal due to associated complications. Some tonic-clonic seizures begin as focal seizures with preserved awareness, but progress to loss of consciousness as they generalise across both hemispheres of the brain.12 First-line treatment is sodium valproate, unless contraindicated or otherwise inappropriate for the patient (e.g. individuals of childbearing potential).26
Absence seizures (formerly known as petit mal)
Absence seizures are typically characterised by brief episodes of staring or unresponsiveness, and are often unnoticed or mistaken for daydreaming.12,25 First-line treatment includes ethosuximide or sodium valproate where selection is guided by contraindications and other patient-specific factors.26
Myoclonic seizures
Myoclonic seizures present as sudden and brief muscle jerks.12,25 First-line treatment is sodium valproate unless contraindicated or otherwise inappropriate (e.g. individuals of childbearing potential).26
Atonic seizures
Atonic seizures result in a sudden loss of muscle tone, leading to falls.12,25
For further information, see Australian Medicines Handbook: Epilepsy.26
Diagnosis of epilepsy involves detailed clinical history, neurological examination and supportive investigations.12,17 Electroencephalogram (EEG) is central for detecting epileptiform discharges, while neuroimaging techniques such as computed tomography (CT) and magnetic resonance imaging (MRI) can help identify structural causes.12 In complex cases, additional tools including positron emission tomography (PET)/single photon emission computed tomography (SPECT), magnetoencephalography (MEG) and genetic testing can support diagnosis and guide treatment. The advanced neuroimaging modalities are especially useful for presurgical evaluations in specialised centres.12 Neuropsychological assessments can also provide insight into cognitive impacts.1 ILAE classification recommends a structured, three-level diagnostic approach, identifying seizure type, epilepsy type and specific epilepsy syndrome, while integrating aetiology at each stage to inform treatment decisions.3 Syncope, psychogenic non-epileptic seizures, transient ischaemic attacks, migraine auras and sleep disorders can mimic epileptic seizures but differ in aetiology and treatment.12,27
Prognosis varies widely, depending on seizure type, aetiology, age of onset and treatment response.12 Many patients can achieve seizure control with ASM, and some enter long-term remission. However, around one-third of patients develop drug-resistant epilepsy, unresponsive to two or more ASM.12 Early age of onset, especially in infancy, and epilepsy with structural lesions such as hippocampal sclerosis, are often linked to poorer outcomes.28,29 Sudden unexpected death in epilepsy remains a serious risk,30 particularly in patients with uncontrolled generalised tonic-clonic seizures and early-onset syndromes such as Dravet syndrome (severe infantile-onset developmental epileptic encephalopathy), which has a 3–5-fold higher mortality risk than the general epilepsy population.31 Early diagnosis and individualised treatment strategies improve outcomes.
The primary aim is to achieve seizure freedom with minimal side effects, improving quality of life. Treatment recommendations follow a stepwise approach, guided by seizure classification, epilepsy type, underlying aetiology, side effect profile, cost, potential for measuring serum drug concentration, pharmacokinetics and patient-specific factors such as age, pregnancy, medicine interactions and comorbidities.17,26,32,33
Initial management involves monotherapy with an appropriate ASM. Dose is generally started low and titrated slowly to achieve seizure control. If control is not achieved with maximally tolerated doses of a single agent, a second agent may be added. The second agent may be considered for monotherapy if the patient and prescriber are willing to gradually withdraw the first agent. If two agents do not promote seizure control, the second agent may be withdrawn gradually and replaced with a third.34
Treatment with an ASM should never be ceased abruptly.34
Key treatment considerations
For further information, see Therapeutic Guidelines: Neurology.34
Evidence is limited for cannabis-derived products. Cannabidiol is approved for specific syndromes but requires specialist oversight.33,34
Non-pharmacological management includes surgery following EEG/MRI evaluation, vagus nerve and deep brain stimulation, ketogenic diet and gene therapy. Yoga, meditation and acupuncture have limited evidence for use.17,31–35
One of the most common challenges during epilepsy treatment is adherence. Missed doses or abrupt discontinuation can trigger recurrent seizures which significantly increase mortality risk.33 Medicine interactions are another significant concern, particularly with older ASM such as phenytoin and carbamazepine, which are enzyme inducers and can alter the efficacy of other medicines.33 Patients should be informed that some medicines can lower their seizure threshold. These include theophylline, pethidine, certain antidepressants (uncommon), and some antipsychotics. Some important medicine interactions are shown in Table 1.

Treatment complications range from mild to severe. Common side effects include fatigue, dizziness, cognitive issues such as memory or attention difficulties, and abdominal upset including pain, nausea and vomiting.33
More serious but less frequent reactions include liver and renal toxicity, bone marrow suppression and skin reactions.26 Long-term use of certain ASM including carbamazepine and phenytoin may also reduce bone density, increasing fracture risk.12,33 Additionally, some ASM including levetiracetam and topiramate can worsen mood disorders, contributing to anxiety and depression.26,33
Age also influences management.32,33 Children often require weight-based dosing and closer monitoring due to variable metabolism, while older adults are more susceptible to adverse effects and medicine interactions due to comorbidities and declining organ function.34
To manage these risks, routine monitoring, including liver and renal function tests, therapeutic drug monitoring, bone health assessments and mental health screening, is essential.
Epilepsy treatment requires regular follow-up to assess seizure control, treatment efficacy and adverse effects. Monitoring for drugs with narrow therapeutic index should also be considered. Treatment plans should be reviewed annually, or sooner, to discuss any changes in seizure occurrence.
Patients in Australia can access further advice and support through multiple channels, including:
Epilepsy Action Australia – education, telehealth and resources
Epilepsy Foundation – seizure management and support services
National Epilepsy Support Service/Epilepsy Smart Australia – 1300 761 487 Monday to Friday, from 9 am to 5 pm (AEST).
Pharmacists support epilepsy management across both community and hospital settings. Hospital pharmacists contribute by implementing therapeutic drug monitoring, especially for ASM with narrow therapeutic windows, collaborating with multidisciplinary teams to optimise treatment plans, monitoring for adverse drug reactions, and managing complex cases involving polytherapy or comorbidities. Community pharmacists can provide ongoing support and medicines counselling, and conduct MedsChecks, detect side effects early, and address mental health concerns. Together, pharmacists provide personalised care that can help improve seizure control, enhance treatment safety and reduce mortality.
With appropriate treatment, many people with epilepsy can achieve good seizure control and lead full, active lives. However, outcomes depend on early intervention, consistent follow-up, monitoring and personalised care. Pharmacist involvement helps reduce complications, improves medicine adherence and supports overall wellbeing.
Case scenario continuedYou recognise that emotional stress, non-adherence and adverse effects are likely precipitating Stavros’ seizures. Concomitant use of lorazepam and carbamazepine contributes to additive CNS depression, causing sedation. As Stavros prefers pharmacological treatment for GAD, you call his GP and suggest sertraline 50 mg daily, noting that carbamazepine may reduce sertraline concentrations via enzyme induction, and clinical response should be monitored. You recommend ceasing lorazepam and encourage cognitive behavioural therapy. The GP reviews Stavros and he returns with a cessation plan for lorazepam and a prescription for sertraline. You counsel on treatment expectations and the importance of adherence. A month later, Stavros returns, feeling alert with no recent seizures. |
DR Ming S Soh PhD, BPharm (Hons) is a Research Fellow at the Florey Institute of Neuroscience and Mental Health, University of Melbourne, with expertise in preclinical models of genetic epilepsy and therapeutic development.
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Stafstrom CE, Carmant L. Seizures and epilepsy: an overview for neuroscientists. Cold Spring Harb Perspect Med. 2015;5(6):a022426.
Mohanannair Geethadevi G, Chen Z, et al. Impact of epilepsy on productivity and quality of life: the Australian epilepsy project. Neurology. 2025;105(5):e214011.
Australian Institute of Health and Welfare. Epilepsy in Australia. Canberra: AIHW; 2022. Available from: www.aihw.gov.au/reports/chronic-disease/epilepsy-in-australia/contents/about
Foster E, Chen Z, Zomer E, et al. The costs of epilepsy in Australia: a productivity-based analysis. Neurology. 2020;95(24):e3221–e3231.
Keenan NF, Aitchison SG, Jetté N, et al. Epilepsy in the Indigenous peoples in Canada, Australia, New Zealand, and the USA: a systematic scoping review. Lancet Glob Health. 2025;13(4):e656–e668.
Vera-González A. Pathophysiological mechanisms underlying the etiologies of seizures and epilepsy. In: Czuczwar SJ, editor. Epilepsy. Brisbane: Exon Publications; 2022. p. 1–13.
Balestrini S, Arzimanoglou A, Blümcke I, et al. The aetiologies of epilepsy. Epileptic Disord. 2021;23(1):1–16.
Perucca P, Bahlo M, Berkovic SF. The genetics of epilepsy. Annu Rev Genomics Hum Genet. 2020;21(1):205–230.
Scheffer IE, Berkovic SF. The genetics of human epilepsy. Trends Pharmacol Sci. 2003;24(8):428–433.
Bhalla D, Godet B, Druet-Cabanac M, Preux P-M. Etiologies of epilepsy: a comprehensive review. Expert Rev Neurother. 2011;11(6):861–876.
Reid CA. Preface: ion channels and genetic epilepsy. J Neurochem. 2024;168(12):3829–3830.
Oyrer J, Maljevic S, Scheffer IE, et al. Ion channels in genetic epilepsy: from genes and mechanisms to disease-targeted therapies. Pharmacol Rev. 2018;70(1):142–173.
Fabisiak T, Patel M. Crosstalk between neuroinflammation and oxidative stress in epilepsy. Front Cell Dev Biol. 2022;10:976953.
Fisher RS, Cross JH, French JA, et al. Operational classification of seizure types by the International League Against Epilepsy: position paper of the ILAE commission for classification and terminology. Epilepsia. 2017;58(4):522–530.
Buckley N, editor. Australian medicines handbook. Adelaide: Australian Medicines Handbook Pty Ltd; 2025. Available from: https://amhonline.amh.net.au/
Cook M. Differential diagnosis of epilepsy. In: Shorvon S, Perucca E, Engel J Jr, editors. The treatment of epilepsy. 4th ed. Hoboken (NJ): John Wiley & Sons; 2015. p. 24–37.
Semah F, Picot M-C, Adam C, et al. Is the underlying cause of epilepsy a major prognostic factor for recurrence? Neurology. 1998;51(5):1256–1262.
Nickels K. Earlier is not always better: outcomes when epilepsy occurs in early life versus adolescence. Epilepsy Curr. 2020;20(1):27–29.
Devinsky O, Hesdorffer DC, Thurman DJ, et al. Sudden unexpected death in epilepsy: epidemiology, mechanisms, and prevention. Lancet Neurol. 2016;15(10):1075–1088.
Cooper MS, McIntosh A, Crompton DE, et al. Mortality in Dravet syndrome. Epilepsy Res. 2016;128:43–47.
Perucca E. General principles of medical management. In: Shorvon S, Perucca E, Engel J Jr, editors. The treatment of epilepsy. 4th ed. Hoboken (NJ): John Wiley & Sons; 2015. p. 110–123.
Perucca P, Scheffer IE, Kiley M. The management of epilepsy in children and adults. Med J Aust. 2018;208(5):226–233.
Therapeutic Guidelines Limited. eTG complete. Melbourne: Therapeutic Guidelines; 2025. Available from: www.tg.org.au
Baxendale S. Complementary and alternative treatments for epilepsy. In: Shorvon S, Perucca E, Engel J Jr, editors. The treatment of epilepsy. Hoboken (NJ): John Wiley & Sons; 2015. p. 298–310.
Johannessen SI, Johannessen Landmark C. Antiepileptic drug interactions: principles and clinical implications. Curr Neuropharmacol. 2010;8(3):254–267.
Buchanan N. Medications which may lower seizure threshold. Aust Prescr. 2001;24(1):8–9.
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[post_content] => New avenues for nurse prescribing have the potential to reshape frontline care. For pharmacists, it’s a live example of how scope expansion translates into real impact.
Nurse prescribing is entering a new phase in Australia, and pharmacists should be paying close attention.
While nurse practitioners and endorsed midwives have been able to prescribe Pharmaceutical Benefits Schedule (PBS) subsidised medicines since 2010, a new pathway will soon expand prescribing to a broader group of experienced nurses.
‘A lot of people wouldn't even know that nurses are already prescribing medications that are funded on the PBS,’ said Denise Lyons, President of the Australian Primary Health Care Nurses Association. ‘But there are more than 3,000 nurse practitioners and endorsed midwives in Australia now who are already prescribing.’
Under a new registration standard which came into effect in September last year, suitably qualified registered nurses will be able to prescribe medicines in Schedules 2, 3, 4 and 8 in partnership with an authorised prescriber.
‘It took until this year for universities to start the course that enables registered nurses to meet [the new standard],’ Ms Lyons said. ‘Most are 6-month postgraduate courses … So it will probably be around July 2026 that we will see the first [wave] of nurses completing the educational requirement.’
For pharmacists, this shift offers a live view of how prescribing reform is built – through legislation, governance, defined scope and, crucially, access to the PBS.
What’s changing?
The new framework is deliberately cautious. To become a designated RN prescriber, a nurse must:
‘Pharmacists and nurses are often people's first point of contact with the healthcare system, and it's really good if we can work to the top of our scope and do what we know we can do, with the right guardrails in place.' denise lyons
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[post_date] => 2026-04-07 14:50:18
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[post_content] => Case scenario
Sarah, a 42-year-old woman, presents to the pharmacy reporting a small lump near the anus, occasional bright red bleeding on toilet paper after bowel movements, anal itching and discomfort. She mentions feeling embarrassed to seek advice and has been self-managing with sitz baths. She reports a history of chronic constipation with frequent training during defecation. She is not taking any regular medicines and requests an over-the-counter product to relieve her symptoms. You take the time to explore Sarah’s symptoms in more detail, to help identify any red flags that would require immediate referral. You ask about the duration, severity and other symptoms such as fatigue, unintentional weight loss and changes in bowel habits, all of which she denies.
Learning objectivesAfter reading this article, pharmacists should be able to:
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Anal fissures and haemorrhoids are commonly encountered, but their epidemiology is not well documented. Haemorrhoids represent the most frequent reason for proctology consultations, followed by anal fissures.1 Haemorrhoids are estimated to affect up to 40% of adults in the general population, although many individuals are asymptomatic.2 Anal fissures occur in approximately 10–15% of the population.3

An anal fissure is a longitudinal tear in the anal canal, most often occurring in the posterior midline, just below the dentate line.4 Anal fissures are typically classified as primary or secondary, depending on the cause. Primary fissures are usually benign and caused by local trauma, such as the passage of hard stools, prolonged diarrhoea, vaginal delivery, repeated injury or anal penetration.4 Secondary fissures, which are often multiple and located off the midline, are uncommon, accounting for less than 1% of cases.5 They result from underlying conditions like previous anal surgery, inflammatory bowel disease (e.g. Crohn’s disease), colorectal malignancy, infections (e.g. HIV/AIDS), or dermatological conditions (e.g. psoriasis).6 Anal fissures are further described as acute or chronic, with chronic fissures lasting more than 6 weeks.7
[caption id="attachment_31774" align="alignright" width="200"]
DR Amy Page (she/her) PhD, MClinPharm, GradDipBiostat, GCertHProfEd, GAICD, GStat, FSHPA, FPS is a consultant pharmacist, biostatistician, and the director of the Centre for Optimisation of Medicines at UWA’s School of Allied Health.[/caption]
Anal fissures are often mistaken for haemorrhoids because of their overlapping symptoms. Haemorrhoids differ in that they are normal vascular cushions within the anal canal that maintain continence. Although part of normal anatomy, the term ‘haemorrhoid’ is commonly used when these vascular anal cushions, containing a rich arteriovenous network, become enlarged or displaced.8 Haemorrhoids may be classified as internal (located above the dentate line) or external (located below the dentate line). Factors such as constipation, straining during bowel movements and a low-fibre diet are commonly considered to increase the risk of haemorrhoids.9,10 However, the causal relationship between these factors and the development of haemorrhoids remains unclear. A possible genetic component that predisposes to smooth muscle, epithelial and connective tissue dysfunction, may contribute to haemorrhoids.11
It is important to note that certain medicines can contribute to or worsen constipation as an adverse effect, thereby aggravating haemorrhoids and anal fissures.9,10 Common examples include opioids, anticholinergics, and iron and calcium supplements.12 Regular medication review should be incorporated into comprehensive care to identify opportunities for deprescribing and prevent inappropriate prescribing cascades, with further guidance available in the new deprescribing guidelines.13
The symptoms of haemorrhoids may include rectal bleeding, anal pruritus, prolapse, faecal seepage and mucus discharge.7
Internal haemorrhoids are usually painless because the columnar epithelium is insensitive to touch and temperature.8 In contrast, external haemorrhoids are pain sensitive and may become thrombosed, often following straining during defecation.8
Anal fissures, by comparison, typically cause severe tearing pain that is provoked by defecation.4 A key distinguishing feature is that the pain of an anal fissure typically occurs during or immediately after defecation.

For diagnostic purposes, medical practitioners perform a physical examination with the individual lying on their side, gently parting the buttocks to inspect the posterior midline.4 Several other anorectal disorders may present with similar symptoms to anal fissures and haemorrhoids. Differential diagnoses include anal fistula and solitary rectal ulcer syndrome, which can often be distinguished based on their clinical appearance through careful physical examination. An anal fistula typically presents as a draining skin punctum.14 It is an abnormal hollow tract, most often arising from infection of an anal gland.15 Solitary rectal ulcer syndrome may present with anal pain, rectal bleeding, constipation, mucus discharge, excessive straining and a sensation of incomplete evacuation. Despite its name, the condition does not always involve an ulcer. Diagnosis requires a combination of endoscopic and histopathological findings, together with the individual’s reported symptoms.16
Haemorrhoids
[caption id="attachment_31775" align="alignright" width="200"]
Hui Wen Quek (she/her) BPharm(Hons), GradCertAppPharmPrac is a pharmacist and PhD candidate at the University of Western Australia (UWA).[/caption]
Non-pharmacological treatment options
First-line management for haemorrhoids usually involves lifestyle measures, which include ensuring adequate fluid and fibre intake, reducing prolonged time on the toilet and avoiding excessive straining, the use of sitz baths, and maintaining anal hygiene.10 In practice, dietary and lifestyle modifications are usually recommended as a conservative and preventive measure for haemorrhoids.17
Pharmacological treatment options
Over-the-counter therapies for internal haemorrhoids include ointments and suppositories that contain emollients, mild astringents, local anaesthetics and/or corticosteroids.8 These preparations temporarily relieve itching and discomfort. Prolonged use of topical corticosteroids is not recommended, as it increases the risk of local infections such as candidiasis.8 Similarly, prolonged use of anaesthetic-containing products should be avoided due to potential adverse effects, including skin sensitisation and dermatitis.8
Outpatient procedures and surgery
For individuals who do not respond to conservative measures, other treatment options for haemorrhoids include outpatient procedures and surgery.10 Outpatient procedures include rubber band ligation, infrared coagulation, bipolar probe, heater probe, sclerotherapy and cryotherapy.10 These are generally reserved for people with grade I or grade II haemorrhoids.10 Surgery can be considered for people who do not respond to or cannot tolerate outpatient procedures, as well as those with large external haemorrhoids, or combined internal and external haemorrhoids with prolapse.10
A recent meta-analysis found that surgical treatments, compared with conservative treatments, offer greater symptom relief, quicker recovery and lower recurrence rates.18 However, they do carry risks of procedure-related complications. In contrast, conservative treatments are safer and less invasive, but tend to provide slower symptom improvement and have higher recurrence rates.18 Therefore, treatment decisions should be individualised, taking into account symptom severity, individual preferences and risk tolerance.
Anal fissures
The primary aim of treatment for anal fissures is to reduce anal sphincter spasm, improve blood flow and promote healing.6 First-line management is usually non-operative and includes increasing dietary fibre, use of sitz baths and applying glyceryl trinitrate 0.2% ointment, three times daily for up to 4 weeks to relieve pain.19 Headache is a common adverse effect of glyceryl trinitrate due to systemic absorption, which could limit its use.20 Other topical agents used in clinical practice include lidocaine and hydrocortisone, although these are less effective than a combination of fibre intake and warm sitz baths.4
Botulinum toxin injections may also be considered and can achieve good healing rates.6,19 However, botulinum toxin may cause temporary reduced control of wind or bowel motions, which usually resolves as the effect of the injection wears off.4 Due to these adverse effects and the invasive nature of the procedure, botulinum toxin is generally reserved as a second-line therapy.4 If these treatment options are unsuccessful, surgical treatment may be required.6
Secondary or chronic anal fissures warrant additional investigation and multidisciplinary management is advised, especially when malignancy is suspected or confirmed.4
Pharmacists play a key role in recognising the symptoms of haemorrhoids and anal fissures, providing timely advice and suggesting a suitable course of action. Pharmacists can also educate individuals on first-line management strategies and provide lifestyle advice where appropriate to prevent recurrence. In addition, pharmacists can advocate for the safe use of over-the-counter treatments, advise on appropriate duration of use and counsel individuals on potential adverse effects.
Referral to a medical practitioner is advisable for individuals who21:
Anal fissures and haemorrhoids are common conditions encountered in primary care and can greatly impact quality of life. Pharmacists play a critical role in early management and referral, helping prevent complications and improve outcomes.
Case scenario continuedYou identify that Sarah has haemorrhoids and provide lifestyle advice, including increasing fluid and dietary fibre intake, avoiding prolonged straining during bowel movements and practising good anal hygiene. For symptomatic relief, you suggest a topical ointment containing cinchocaine 0.5% and zinc oxide 20%, to be applied as needed. You also advise her to consult her general practitioner if she experiences persistent bleeding, ongoing pain or worsening prolapse. With your support and advice, Sarah feels more confident in managing her condition effectively while reducing the risk of recurrence. |
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Hui Wen Quek (she/her) BPharm(Hons), GradCertAppPharmPrac is a pharmacist and PhD candidate at the University of Western Australia (UWA).
DR Amy Page (she/her) PhD, MClinPharm, GradDipBiostat, GCertHProfEd, GAICD, GStat, FSHPA, FPS is a consultant pharmacist, biostatistician, and the director of the Centre for Optimisation of Medicines at UWA’s School of Allied Health.
Manisha Pillai (she/her) BPharm
Higuero T. Update on the management of anal fissure. J Visc Surg. 2015;152(2 Suppl):S37–S43.
Riss S, Weiser FA, Schwameis K, Riss T, Mittlböck M, Steiner G, et al. The prevalence of hemorrhoids in adults. Int J Colorectal Dis. 2012;27(2):215–220.
Vitton V, Bouchard D, Guingand M, Higuero T. Treatment of anal fissures: results from a national survey on French practice. Clin Res Hepatol Gastroenterol. 2022;46(4):101821.
Schlichtemeier S, Engel A. Anal fissure. Aust Prescr. 2016;39(1):14–17.
Zaghiyan KN, Fleshner P. Anal fissure. Clin Colon Rectal Surg. 2011;24(1):22–30.
Newman M, Collie M. Anal fissure: diagnosis, management, and referral in primary care. Br J Gen Pract. 2019;69(685):409–410.
Lyle V, Young C. Anal fissures: an update on treatment options. Aust J Gen Pract. 2024;53:33–35.
Therapeutic Guidelines Limited. Haemorrhoids. Melbourne: Therapeutic Guidelines Limited; 2022. Available from: https://www.tg.org.au
Lohsiriwat V. Hemorrhoids: from basic pathophysiology to clinical management. World J Gastroenterol. 2012;18(17):2009–2017.
Sandler RS, Peery AF. Rethinking what we know about hemorrhoids. Clin Gastroenterol Hepatol. 2019;17(1):8–15.
Zheng T, Ellinghaus D, Juzenas S, Cossais F, Burmeister G, Mayr G, et al. Genome-wide analysis of 944 133 individuals provides insights into the etiology of haemorrhoidal disease. Gut. 2021;70(8):1538–1549.
Therapeutic Guidelines Limited. Functional constipation in adults. Melbourne: Therapeutic Guidelines Limited; 2022. Available from: https://www.tg.org.au
Quek HW, Reus X, Lee K, Etherton-Beer C, Page A; Guideline Development Group. Deprescribing in older people: a clinical practice guideline. Perth (WA): The University of Western Australia; 2025.
Stewart D. Anal fissure: clinical manifestations, diagnosis, prevention. UpToDate. 2025. Available from: https://www.uptodate.com/contents/anal-fissure-clinical-manifestations-diagnosis-prevention
Therapeutic Guidelines Limited. Anorectal abscess and fistula. Melbourne: Therapeutic Guidelines Limited; 2022. Available from: https://www.tg.org.au
Sadeghi A, Biglari M, Forootan M, Adibi P. Solitary rectal ulcer syndrome: a narrative review. Middle East J Dig Dis. 2019;11(3):129–134.
Lohsiriwat V. Treatment of hemorrhoids: a coloproctologist's view. World J Gastroenterol. 2015;21(31):9245–9252.
Quan L, Bai X, Cheng F, Chen J, Ma H, Wang P, et al. Comparison of efficacy and safety between surgical and conservative treatments for hemorrhoids: a meta-analysis. BMC Gastroenterol. 2025;25(1):492.
Therapeutic Guidelines Limited. Anal fissure. Melbourne: Therapeutic Guidelines Limited; 2022. Available from: https://www.tg.org.au
Australian Medicines Handbook Pty Ltd. Glyceryl trinitrate (rectal). Adelaide: Australian Medicines Handbook Pty Ltd; 2025. Available from: https://amhonline.amh.net.au/
Allen S. Haemorrhoids and anal fissures. S Afr Pharm J. 2008;75(5):36.
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[post_content] => Community pharmacies are often the first place people turn when something feels ‘off’. But as pharmacists know, many requests for over-the-counter medicines are more complex than they may initially seem.
AP took a look at some presentations which might signal hidden red flags.
‘I just want a multivitamin’
When people present to community pharmacies, they often arrive with a solution already in mind. For example, ‘I need a strong painkiller,’ ‘I just want a multivitamin,’ or ‘What do you have for nerve pain?’
Nearly always, consistent with professional standards, these invite an open ended question to uncover the rationale for the request
Gauri Godbole FPS[/caption]
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[post_content] => Case scenario
During peak hour, 19-year-old Enzo and his mother arrive to collect a new prescription for melatonin MR 2 mg. The pharmacy is highly stimulating: background music blares, customers converse loudly nearby, staff assist others in a cramped space, and general noise amplifies the chaos. While processing Enzo’s prescription and attempting to deliver verbal instructions, you observe Enzo avoiding eye contact, fidgeting intensely, and appearing overwhelmed, with reduced capacity to process verbal or non-verbal cues due to sensory overload.
Learning objectivesAfter reading this article, pharmacists should be able to:
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Yvette Anderson (she/her) BPharm, MPS, CredPharm (MMR), ANZCAP (MentalHth, Paeds), CPGx, GradCert Autism[/caption]
Neurodevelopmental disorders (NDDs) arise from differences in brain development and typically affect cognition, communication, behaviour and occupational functioning. Common NDDs include attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), referred to as autism in this article, and intellectual developmental disorder (IDD).1 Autism is characterised by persistent social interaction and communication difficulties and restricted behavioural patterns.2 Symptoms begin in early childhood; however, diagnosis can occur at any age.3 Autism affects how the brain processes information, shaping how autistic people see, understand and respond to the world around them, with marked variability in presentation, day-to-day functioning and support needs.3,4
In Australia, autism prevalence has increased due to evolving diagnostic practices and awareness,5 meaning pharmacists now routinely engage with autistic individuals as part of everyday practice.
The challenge and opportunity for pharmacy is to shift from a medical model of crisis response, treatments and cures to a neuro-affirming social model that helps autistic individuals thrive, not just survive.
A neuro-affirming social model conceptualises neurodevelopmental differences as natural variations within human diversity and rejects deficit-based assumptions that frame these differences as disorders.6 Rather than ‘correcting’ individual traits, this approach provides reasonable adjustments while supporting autonomy, community participation and wellbeing, alongside awareness of diagnostic criteria, comorbidities, communication styles, lived realities and the impact of misinformation.6 The shift to a neuro-affirming social model calls for reducing systemic and environmental barriers, while still addressing health needs.6,7
For pharmacists, it means making practice adjustments in the way that the profession engages with and provides support for autistic individuals.
According to the Australian Bureau of Statistics, approximately 290,900 Australians (1.1%) are reported to have had an autism diagnosis in 2022.5 A recent estimate by Autism Spectrum Australia (Aspect) suggested at least 1 in 40 Australians are autistic.7
Rising prevalence reflects improved awareness and diagnostic practices rather than a true increase in incidence, including better recognition in historically underdiagnosed groups such as females and older adults.7 Autism prevalence peaks in children and adolescents, particularly those aged 10–14 years, and is markedly lower in adults, acknowledging limited adult data.5,8,9
Autism prevalence rates may appear to vary among ethnic and cultural groups, reflecting inequities such as access to healthcare, effective communication, diagnostic practices and cultural perceptions.10
Prevalence remains higher in males than females, with 1.6% of males identified compared with 0.7% of females, and the greatest disparity is seen in children aged 5–9 years.5 Autism in females is frequently underdiagnosed, as characteristics may manifest differently, be masked (e.g. forced eye contact, rehearsed social scripts, suppressing stimming or copying peers), or fail to align with historically male-centred diagnostic criteria, leading to misdiagnosis as mood or personality disorders.11,12 Masking may occur due to a desire to fit in, fear of stigma or bullying, previous negative reactions to autistic behaviours, and expectations of how females are ‘supposed’ to behave.12 Increasing awareness of the under-recognition of autism in females and gender-diverse individuals, and the social drivers of masking, is anticipated to influence future prevalence estimates.4,5,11
There is no single cause of autism, and despite extensive research, aetiology remains incompletely understood. Current evidence indicates autism arises from a complex interaction between genetic susceptibility and environmental influences on neurodevelopment.13
Family history is one of the strongest predictors of autism.13,14 Researchers have identified hundreds of genes, with approximately 10–20% of cases associated with rare genetic variants arising from mutations in sperm or egg cells.14 Autism is considered polygenic, meaning overall risk typically reflects the cumulative effect of multiple inherited variants, each contributing a small effect.14
The expression of genetic susceptibility is known to be influenced by prenatal, perinatal and postnatal environmental factors.13 Environmental factors appear most relevant during the prenatal period.14 Modest associations have been reported between autism likelihood and maternal factors such as hypertension, gestational diabetes, obesity, alcohol and substance use, poor antenatal care, and infection or fever during pregnancy.15
Imprecise and inconsistent associations have been reported for folate status, exposure to some air pollutants, and the use of some medicines.15–17 Importantly, these findings are largely derived from observational studies and are subject to confounding. While some prenatal medicine exposures show more consistent associations with autism, there is no clear evidence that associations between autism and other environmental and medicine exposures represent a causal relationship, and any contribution to autism risk remains limited and uncertain.14,17

Autism is diagnosed according to Diagnostic and Statistical Manual of Mental Disorders (DSM-5-TR) criteria: ‘persistent deficits in social communication and social interaction across multiple contexts’, with the presence of ‘restricted, repetitive patterns of behaviour, interests or activities’.2
‘Symptoms must be present in the early development period’, although they may only become fully apparent later in life.
‘Symptoms cause clinically significant impairment in social, occupational or other important areas of functioning’ and ‘these disturbances are not better explained by IDD’ although both can co-occur.2 The DSM-5-TR also specifies severity levels (1–3) to indicate the degree of support required.2
In Australia, individuals may pursue an autism diagnosis through public or private pathways.18 Both are typically lengthy and necessitate a degree of health literacy and English proficiency. Diagnostic assessments may be conducted by a multidisciplinary team, including paediatricians, psychiatrists, psychologists, speech pathologists and occupational therapists.4 Multiple appointments may be needed, drawing on input from family, carers or teachers.18,19
Barriers to diagnosis include limited awareness of early signs among caregivers and clinicians, long wait times and out-of-pocket costs for specialist assessment, socioeconomic and geographic disparities, and bias in recognising diverse presentations.11,20,21 Limited health literacy and the complexity of navigating multidisciplinary assessments and National Disability Insurance Scheme requirements further impede access.21 In some communities, stigma, fear of labelling, and differing cultural interpretations of behaviour may delay help-seeking.22
A best-practice diagnostic approach should promote cultural safety and sensitivity, acknowledge variations in health literacy, address socioeconomic barriers, and be grounded in person-centred care.
Autism is a spectrum, with each individual having a unique mix of strengths, challenges, interests, needs and way of interacting with the world. Autism advocate Dr Stephen Shore states, ‘If you have met one autistic person, you have met one autistic person’.23
Beyond the core featuresComorbid NDDs, and psychiatric and medical conditions can create significant challenges for autistic individuals in relation to diagnosis, selection of appropriate interventions, medicines and support services.1,24
Comorbid NDDs among autistic individuals include ADHD, developmental coordination disorder (dyspraxia), IDD, and specific learning disorders such as dyslexia, dysgraphia and dyscalculia.25 Psychiatric comorbidities are also prevalent, including anxiety, depression, obsessive-compulsive disorder, and post-traumatic stress disorder.26 These conditions can intensify social and sensory challenges, increase vulnerability to stress, and impair emotional regulation and executive functioning.
Autistic individuals experience higher rates and severity of mental and physical health comorbidities than neurotypical individuals. Neurodivergent mental health outcomes are influenced by the interaction between individual differences and environmental and societal factors.25–28 Diagnostic overshadowing, whereby mental health symptoms are erroneously attributed to autism, should be avoided.29 Comorbid conditions warrant assessment and treatment according to the same clinical standards applied to neurotypical individuals, with adaptations made to accommodate the communication, sensory and support needs of autistic people. Neurodivergent individuals experience the full range of medical comorbidities seen in the general population; however, research indicates higher prevalence of certain conditions, including gastrointestinal disorders (e.g. irritable bowel syndrome, chronic constipation), sleep disturbances, epilepsy, and immune or metabolic disorders.30 These conditions may worsen fatigue, concentration and mood regulation, while motor difficulties may contribute to musculoskeletal pain, reduced physical activity and secondary health issues.31
Physical health conditions may be underdiagnosed when the clinical focus is limited to behavioural or psychological symptoms.29
Recognising the complex interconnections between physical, psychiatric and NDD health is paramount. Pharmacists can play a vital role in this process. Effective care relies on health professionals working collaboratively to identify how comorbid conditions, treatment burden and medicines may influence behaviour, cognition and developmental outcomes.
Autism is a lifelong NDD for which there is no curative treatment.4 Clinical care focuses on supporting health, functioning and community participation, addressing comorbidities, and optimising quality of life, while recognising and respecting the individual strengths, capabilities and perspectives of autistic individuals.3
Supports and interventions are individualised and typically involve a multidisciplinary team to address evolving needs.10 Allied health professionals may include speech pathologists to support communication, occupational therapists to address sensory processing and daily living skills, and psychologists to support emotional regulation and mental health. Physiotherapists may support gross motor skills, while dietitians support feeding and nutritional adequacy, alongside specialist educational support and therapy (e.g. play therapy, art therapy).3 Effective management relies on coordinated care, regular goal review and clear communication between the autistic individual, families and carers, and the multidisciplinary team.24
There is no evidence to support the use of medicines, exclusion diets or other biological treatment for the core features of autism.32,33 To support comorbidities, psychotropic medicines, antiepileptics and sleep agents may be used short term and under specific circumstances. Off-label use is common and requires careful assessment of risk-benefit balance, adverse effects, formulation choice, monitoring, cumulative treatment burden, and very careful consideration if the medicine is being prescribed as a chemical restraint.4

Autism is subject to persistent myths that pharmacists may encounter. The most damaging is the long-debunked claim that vaccines cause autism.14 The retracted 1998 Lancet study by Andrew Wakefield that claimed a link between the measles, mumps, rubella (MMR) vaccine and autism was a small, flawed study (with only 12 participants) and was exposed for unethical processes, methodological misconduct, and undisclosed conflicts of interest.14 Despite retraction, its claims were (and continue to be) amplified, eroding trust in public health and fuelling vaccine hesitancy. A Cochrane review published in 2021 found no credible evidence of an association between MMR and MMRV vaccines and autism.34
Two medicines made headlines in 2025: paracetamol and leucovorin (folinic acid or calcium folinate) claimed as a cause and treatment of autism respectively. Antenatal paracetamol exposure was alleged to increase autism and ADHD risk; however, major studies have not demonstrated a causal relationship.9 Stronger evidence from a large Swedish population-based cohort of 2,480,797 children born between 1995 and 2019 found no association between paracetamol use during pregnancy and autism, ADHD or IDD in sibling-controlled analysis.16 Cerebral folate deficiency (CFD) has been reported in a subset of autistic individuals, related to impaired folate transport into the brain, and may be associated with symptoms of speech difficulties, seizures and IDD, often within early childhood.35,36 Leucovorin, a folinic acid derivative, has been investigated as a potential treatment for autistic children with CFD. Leucovorin can bypass impaired folate transport, increasing central nervous system folate availability.36 Although some small-scale trials indicate potential minor behavioural improvements, supporting evidence remains limited, inconsistent, and not independently replicated.15,37
As medicines experts, pharmacists are well placed to counter common myths. Responses should prioritise empathetic, respectful communication and the provision of clear, evidence-based information and resources.
Accessibility, strong communication skills, medicines expertise, understanding of health system navigation and ability to synthesise information, position pharmacists to provide continuity of care for autistic individuals. Pharmacists can serve as an integrative link within multidisciplinary teams, supporting autistic individuals and their families across the healthcare continuum.
Effective communication underpins person-centred pharmacy practice. Pharmacists supporting autistic individuals should adapt both verbal and non-verbal communication to meet diverse needs.38 Autism can influence communication and sensory processing in unique ways, with some individuals experiencing sensory sensitivities to sound, light, smell, touch and visual stimuli.3,4,33 Some autistic individuals regulate sensory input through stimming (self-stimulatory behaviour), which may present as repetitive movements or sounds such as fidgeting, rocking or hand-flapping.39 Flexibility, empathy and understanding of sensory needs ensure equitable access to healthcare and fosters the relationship between patient and pharmacist. Verbal communication with autistic individuals should be clear and structured. Pharmacists should use straightforward, unambiguous language and present information in small, logical steps, allowing time for processing and response. Offering a calm, quiet space can both minimise sensory overload and facilitate a more comfortable environment for communication.38,40
Non-verbal communication requires equal attention. Eye contact, facial expressions and gestures can carry unintended meaning for autistic individuals. Some avoid eye contact as a coping mechanism, not as disinterest.38 Pharmacists should avoid assumptions and focus on open, calm body language and a reassuring tone. Visual supports can reinforce verbal explanations to provide ongoing reference, especially for individuals who process visual information more effectively than spoken language.40
A person-centred approach requires pharmacists to recognise, respond and adapt to the communication preferences of each autistic individual. If a caregiver or support worker is present, collaboration should occur while directing communication towards the patient whenever possible.40 Empathy, flexibility and inclusive communication techniques ensure care that is respectful and accessible and upholds an individual’s dignity and autonomy.
By adopting inclusive, neuro-affirming approaches, pharmacists strengthen equity, accessibility and person-centredness within healthcare. In doing so, they uphold the profession’s commitment to compassionate, evidence-based practice and help ensure autistic Australians receive the respect, understanding and tailored support needed to achieve optimal health and wellbeing.
Case scenario continuedEnzo’s mother discloses Enzo’s autism diagnosis and requests a quiet area and slower, step-by-step instructions. You offer a consultation room with dimmed lights, minimal visual clutter and no background noise. Enzo settles, visibly calmer. In this adapted space, you employ person-centred strategies: a soft, steady voice; paced delivery; short, simple sentences; pauses after each point for processing; confirming understanding via yes/no questions or thumbs-up signals; and a clear, written handout with bullet points, icons (e.g. clock for bedtime), and appropriate font. Enzo engages, maintaining partial eye contact and nodding, while his mother clarifies. These modifications demonstrate empathy, flexibility and equitable care, minimising distress, enhancing information access and supporting Enzo’s autonomy. |
Yvette Anderson (she/her) BPharm, MPS, CredPharm (MMR), ANZCAP (MentalHth, Paeds), CPGx, GradCert Autism is an accredited clinical pharmacist with over 20 years’ experience across aged care, consultancy, community pharmacy and hospital pharmacy. In 2020, she launched The Spectrum Pharmacist to increase awareness, promote inclusion, and provide education and support for neurodevelopmental disorders.
Victor Senescall (he/him) BPharm (Hons)
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