Multiple sclerosis: GP shared care, DMTs, and symptom management in Australia

Multiple sclerosis (MS) is a chronic, immune-mediated demyelinating and neurodegenerative disease of the central nervous system. Inflammatory attack on myelin — the insulating sheath around nerve fibres — produces discrete plaques throughout the brain and spinal cord; over years, progressive axonal loss drives accumulating disability that is only partially reversible.

MS Australia estimates around 33,000 Australians live with MS, with roughly 1,000 new diagnoses per year. Women are affected three times as often as men. Peak onset is between 20 and 40 years, though the condition can present in childhood or after 50. The latitude gradient within Australia is pronounced: rates are highest in Tasmania (~210 per 100,000) and lowest in Queensland (~76 per 100,000), reflecting the role of UV exposure and vitamin D status during development.

Epstein-Barr virus (EBV) is now considered a necessary — though not sufficient — contributor to MS risk. Bjornevik et al. (Science 2022) demonstrated a 32-fold increase in MS risk in the years following EBV seroconversion in a large prospective cohort. Smoking, adolescent obesity, and the HLA-DRB1*15:01 genotype are established additional risk factors.

For the GP, MS sits squarely in the shared-care model: neurologists initiate and oversee disease-modifying therapy; GPs manage the daily weight of the condition — relapses, symptoms, comorbidities, vaccinations, pregnancy, NDIS access, and the health of the whole person beyond their diagnosis.

A. Core clinical — the AU general practice framework

Phenotypes

The most common MS phenotype at onset is relapsing-remitting MS (RRMS), affecting around 85% of people at diagnosis. Discrete relapses — episodes of new or worsening neurological function lasting at least 24 hours — are followed by complete or partial recovery with stable intervals between. Without effective treatment, roughly half of RRMS transitions over 20 years to secondary progressive MS (SPMS), where disability accumulates more continuously. This transition rate is falling as more people access high-efficacy disease-modifying therapies earlier in the disease course.

Primary progressive MS (PPMS) affects around 10–15%, more often men with older onset, and involves disability progression from the outset without distinct relapses. Ocrelizumab is the only PBS-listed disease-modifying therapy for PPMS.

Clinically isolated syndrome (CIS) describes a first demyelinating event not yet meeting McDonald criteria for MS. High-risk CIS — with typical MRI lesions — has approximately 80% conversion to RRMS within a decade.

Presentations that reach general practice

Syndrome	Key features
Optic neuritis	Subacute monocular vision loss over hours to days, retro-orbital pain on eye movement, colour desaturation, RAPD, central scotoma; usually recovers partially or fully
Partial transverse myelitis	Sensory level, motor weakness, bladder involvement; partial cord involvement is characteristic of MS; complete transverse myelitis raises NMOSD
Brainstem / cerebellar	Internuclear ophthalmoplegia (bilateral INO in a young person is highly characteristic), atypical trigeminal neuralgia, vertigo, cerebellar ataxia
Lhermitte’s sign	Electric-shock sensation down the spine on neck flexion
Uhthoff phenomenon	Transient neurological worsening with heat — hot showers, exercise, fever
Cognitive	Information-processing slowing, working memory and attention difficulties; often under-recognised

Diagnosis — 2017 McDonald criteria

Diagnosis is the neurologist’s role, but GPs commonly see patients at the point of first presentation or during the diagnostic workup. Thompson et al. (Lancet Neurology 2018) revised the McDonald criteria to require:

• Dissemination in space (DIS) — ≥1 T2 lesion in ≥2 of 4 typical CNS regions (periventricular, juxtacortical/cortical, infratentorial, spinal cord)
• Dissemination in time (DIT) — simultaneous gadolinium-enhancing and non-enhancing lesions on a single MRI; or new T2/gadolinium lesion on follow-up; or CSF oligoclonal bands unique to CSF (substituting for DIT in RRMS)

Excluding alternative diagnoses is mandatory. Key differentials include NMOSD (test aquaporin-4 IgG, MOG-IgG in any optic neuritis or longitudinally extensive transverse myelitis), neurosarcoidosis, CNS vasculitis, vitamin B12 deficiency with subacute combined cord degeneration, and infectious mimics (HIV, syphilis, HTLV-1).

The initial investigation panel includes MRI brain and whole spine with gadolinium, CSF oligoclonal bands and IgG index, and bloods excluding mimics: FBC, B12, TSH, ANA, ENA, dsDNA, ANCA, complement, HIV, syphilis serology, aquaporin-4 IgG, MOG-IgG, and serum ACE.

Relapse recognition — the GP’s front line

The GP is often the first contact when an established MS patient’s symptoms change. Distinguishing true relapse from pseudo-relapse completely changes management.

True relapse: new or worsening symptoms ≥24 hours, ≥30 days from the last event, without fever or active infection. Significant new disability — worsening gait, visual loss, loss of hand function — warrants neurologist review and consideration of methylprednisolone 1 g IV daily for 3–5 days (or oral bioequivalent). Mild sensory relapse without functional impairment is often managed with watchful waiting and close review.

Pseudo-relapse: symptoms triggered by infection — most often a UTI — fever, heat exposure, or severe sleep deprivation. In MS, a UTI can produce a convincing picture of a spinal cord relapse. A midstream urine is the first investigation in any apparent exacerbation. Treating the infection resolves the pseudo-relapse within days; steroids are not indicated and can mask the infection.

B. Disease-modifying therapy — the evidence landscape

All disease-modifying therapies slow relapse rate and MRI activity; the evidence increasingly supports earlier use of high-efficacy agents in active RRMS. eTG Neurology and RACGP resources recommend neurologist-led initiation with shared monitoring in general practice.

Efficacy tier	Agents	Route	Key risks and monitoring
Moderate	Interferon-β 1a/1b, glatiramer acetate, teriflunomide, dimethyl fumarate	Injection or oral	Hepatotoxicity (teriflunomide), lymphopenia (DMF), flu-like effects (IFN-β)
High	Natalizumab, ocrelizumab, ofatumumab, cladribine, fingolimod, ozanimod	IV, SC monthly self-injected, oral short courses, oral daily	PML risk on natalizumab (JCV serology 6-monthly); infections, hypogammaglobulinaemia on anti-CD20; cardiac monitoring for first dose of fingolimod
Very high / rescue	Alemtuzumab, autologous haematopoietic stem cell transplantation (AHSCT)	IV courses / inpatient	Secondary autoimmunity (alemtuzumab); AHSCT at accredited AU centres for highly active disease only

The OPERA I/II trials (Hauser et al. NEJM 2017) established that ocrelizumab reduces annualised relapse rate by 46–47% versus interferon-beta. AFFIRM (Polman et al. NEJM 2006) showed natalizumab reduced relapse rate by 68% and disability progression by 42%. ASCLEPIOS I/II (Kappos et al. NEJM 2020) showed ofatumumab was superior to teriflunomide on relapse and MRI endpoints. These high-efficacy agents are increasingly used first-line in active RRMS, moving away from the traditional escalation model.

The GP’s monitoring role during DMT includes reviewing results communicated from the neurologist (FBC, LFTs, JCV serology for natalizumab every 6 months), recognising early warning signs of serious complications — progressive cognitive or motor deterioration on natalizumab raises PML until proven otherwise — and ensuring vaccinations are current before and during therapy. Live vaccines are contraindicated on most high-efficacy agents; non-live vaccines should be given before DMT initiation where possible.

C. Symptom management in general practice

The day-to-day clinical work of MS in general practice is symptom management. Neurologists lead DMT decisions; GPs lead symptom control, comorbidities, and quality of life.

Fatigue affects 75–90% of people with MS and is the most common cause of employment change. Screen for obstructive sleep apnoea — it is prevalent in MS and significantly worsens fatigue when untreated; the Sleep Health Foundation has GP-facing screening resources. Treat depression, which coexists frequently. Aerobic and resistance exercise reduce MS fatigue per Cochrane review and are central to management; exercise physiologist referral under MBS 10987 (CDM) is appropriate. Pacing strategies and OT referral support energy conservation. Pharmacologically, modafinil has modest trial evidence but is off-label and not PBS-funded for MS fatigue.

Bladder dysfunction affects approximately 75% of people with MS over the disease course. Detrusor overactivity — frequency, urgency, and urgency incontinence — is most common; check post-void residual before prescribing any bladder agent. Mirabegron (PBS Authority for overactive bladder) is preferred over oxybutynin given its more favourable cognitive safety profile. Intermittent self-catheterisation is often the most effective long-term strategy for incomplete bladder emptying; continence nurse referral is valuable. Treat UTIs promptly and aggressively — they drive pseudo-relapses and accelerate bladder deterioration.

Spasticity — stretching and physiotherapy are foundational. Baclofen (oral, PBS-listed) is first-line pharmacologically; tizanidine is an alternative. Botulinum toxin injections for focal spasticity are effective and accessible via specialist physiotherapy or rehabilitation medicine referral.

Neuropathic pain — gabapentin and pregabalin (PBS Authority for neuropathic pain) and amitriptyline are the most used agents per eTG and AMH. Trigeminal neuralgia in MS often presents atypically — bilateral, or in younger people — and carbamazepine or oxcarbazepine are first-line.

Depression and anxiety affect approximately 50% of people with MS over their lifetime, and suicide risk is elevated compared with the general population. Active assessment at every review is warranted. SSRIs are first-line; CBT is effective and can be accessed via a Mental Health Treatment Plan (MBS 2715/2717).

Walking and mobility — fampridine (PBS Authority Required, response must be demonstrated) improves walking speed in selected patients. Physiotherapy, exercise programmes, and occupational therapy assessment of walking aids are standard management. An OT driving assessment is important for people with gait, visual, or cognitive involvement.

D. Australian operations

MBS items relevant to GP shared care

MBS Online provides the billing framework for MS management in general practice:

• Standard, long, and prolonged consultation items: 23, 36, 44
• Chronic Disease Management plan and review: 721 / 723 — allows up to 5 allied health sessions per year (physiotherapy, OT, exercise physiology, dietitian, psychologist, continence nursing)
• Mental Health Treatment Plan: 2715 / 2717 — up to 10 psychology sessions per year; particularly relevant given high depression prevalence
• Home Medicines Review: 900 — valuable when polypharmacy is complex
• Telehealth consultations — appropriate for rural and remote patients with limited specialist access
• Health assessment (Aboriginal and Torres Strait Islander): 715 — relevant for ATSI patients with MS

PBS — DMTs and symptomatic medications

All DMTs are PBS Authority Required with neurologist initiation. Section 100 Highly Specialised Drugs covers monoclonal antibodies (natalizumab, ocrelizumab, ofatumumab) — administered in hospital or accredited day-stay centres. Cladribine is oral self-administered. Symptomatic agents on PBS: baclofen (general), tizanidine (general), gabapentin (general), pregabalin (Authority, neuropathic pain), mirabegron (Authority, OAB), fampridine (Authority, demonstrated response), solifenacin and oxybutynin (general).

NDIS and disability support

Australians under 65 with MS-related functional impairment may qualify for NDIS. Neurologist documentation of the diagnosis and a functional capacity assessment are required. NDIS funds support workers, home modifications, mobility equipment, and allied health not otherwise covered. Over 65, My Aged Care and Home Care Packages apply. The state MS organisations — MS Plus, MS WA, MS Queensland, MS South Australia — have dedicated NDIS navigators and can assist with applications. GPs are often the key navigator for initial access and ongoing support coordination.

MS clinics and shared-care pathways

ANZAN (Australia and New Zealand Association of Neurologists) and the RACP have published DMT shared-care position statements. Tertiary MS clinics operate in all capital cities and many regional centres. MS nurse specialists are a critical link between the clinic and general practice — involving them early in newly diagnosed patients significantly improves care continuity.

E. Special populations

Women of reproductive age. Proactive discussion about contraception and pregnancy planning at every review is standard. Many DMTs require washout before conception: teriflunomide (cholestyramine washout, then 1.5-year interval); fingolimod (2-month washout); cladribine (approximately 6 months). Natalizumab can generally continue until approximately 34 weeks gestation, then restart promptly postpartum to prevent rebound disease. Ocrelizumab and ofatumumab — last infusion timed with conception planned afterward. The PRIMS study established the third-trimester reduction in relapse rate and the postpartum relapse risk spike; the Australian PRiMUS registry provides local pregnancy outcomes data. Interferon-beta and glatiramer have the most safety data during pregnancy. Folic acid 5 mg is standard pre-conception and in the first trimester when any DMT is present. Breastfeeding is generally compatible with interferon-beta and glatiramer; discuss other agents with the neurologist.

Older adults. Immunosenescence raises infection risk with anti-CD20 therapies in older patients. Polypharmacy management becomes more complex. Fatigue must be distinguished from depression, hypothyroidism, sleep-disordered breathing, and cardiac disease. Bone health deserves active attention: reduced mobility and cumulative steroid use create falls and fracture risk; DEXA, vitamin D, and calcium are warranted. Standard cancer screening programmes apply and should not be neglected — BreastScreen, cervical screening, bowel cancer screening, and skin checks all remain relevant, with some DMTs modulating immunosurveillance.

People with progressive MS. PPMS and SPMS patients carry greater disability burden and have fewer DMT options. GP involvement expands into: falls prevention, pressure area care for those with reduced mobility, advance care planning conversations, NDIS and Home Care navigation, carer wellbeing support, and palliative symptom management in advanced disease.

Aboriginal and Torres Strait Islander peoples. MS prevalence is lower in Indigenous Australians, but access to neurological expertise in remote and regional communities is a significant barrier. Telehealth and the ATSI Health Assessment (MBS 715) support continuity of care. Consider that NMOSD — which may be more prevalent in some non-European populations — is an important differential.

When to escalate

Refer immediately or contact neurology urgently when:

• First presentation with a demyelinating syndrome — optic neuritis, transverse myelitis, brainstem event — urgent neurologist assessment and MRI
• Significant new disability from a relapse — worsening gait, vision, or hand function not responding to initial management
• Suspected PML — progressive, subacute cognitive or motor deterioration in a person on natalizumab; urgent MRI and JCV PCR; do not delay
• Serious suspected DMT adverse event — anaphylaxis, severe lymphopenia, unexpected infection, significant LFT rise
• Suicidal ideation

Escalate non-urgently to neurology when:

• Relapse pattern suggests DMT failure — switch requires re-Authority application and specialist review
• Bladder dysfunction not responding to mirabegron or self-catheterisation — urodynamics warranted
• Spasticity causing falls or significant loss of function — intrathecal baclofen assessment or botulinum toxin programme
• Significant cognitive impairment affecting work or safety — neuropsychological assessment and OT input

What this article is and is not

This is general health information drawn from current Australian guidelines — eTG Neurology, NICE NG220, RACGP clinical resources, and ANZAN/RACP shared-care positions — alongside major MS clinical trials. It is not personal medical advice, does not create a doctor–patient relationship, and does not substitute for neurologist- and GP-led care tailored to an individual’s MS phenotype, DMT, and circumstances.

For reliable patient information grounded in AU guidelines: MS Australia, HealthDirect — Multiple sclerosis, Better Health Channel.

For a first neurological presentation or sudden worsening of established MS symptoms, contact your GP urgently or go to an emergency department.

For acute mental-health crisis: Lifeline 13 11 14, Beyond Blue 1300 22 4636, 13YARN 13 92 76 (Aboriginal and Torres Strait Islander peoples).

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Sources cited

1. Therapeutic Guidelines (eTG) — Neurology: Multiple sclerosis
2. NICE NG220 — Multiple sclerosis in adults: management (2022)
3. MS Australia — clinical and patient resources
4. PBS — MS disease-modifying therapies
5. RACP / ANZAN — DMT shared-care position statements
6. Bjornevik et al. — EBV and MS risk (Science 2022)
7. Hauser et al. — OPERA I/II — ocrelizumab vs interferon-beta (NEJM 2017)
8. Kappos et al. — ASCLEPIOS — ofatumumab vs teriflunomide (NEJM 2020)
9. Polman et al. — AFFIRM — natalizumab (NEJM 2006)
10. Thompson et al. — 2017 McDonald criteria revisions (Lancet Neurol 2018)
11. HealthDirect — Multiple sclerosis
12. Better Health Channel — Multiple sclerosis