Karl Ng, Emily Cheung and Tal Koren have an interest in the diagnosis and management of patients with multiple sclerosis and neuroinflammatory disease. Please contact SNNN on 02 82871900 to arrange an appointment with the help of your doctor.
FAQs & information
How common is MS and who is at risk?
Treatment (Disease modifying therapies – DMTs)
Managing relapses and symptoms
Inflammatory diseases other than MS (NMOSD, MOGAD)
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What is Multiple Sclerosis?
Multiple sclerosis (MS) is an immune-mediated disease of the central nervous system (CNS)—that is, the brain and spinal cord. In MS, the immune system attacks myelin, the fatty sheath that normally insulates nerve fibres (axons). Myelin enables rapid conduction of electrical signals. When myelin is damaged (or lost), nerve signal transmission slows or becomes disrupted, leading to neurological symptoms.
Disease Types and Course
Modern understanding of MS emphasises both disease activity (relapses, MRI lesion formation) and progression (gradual accumulation of disability). Key clinical phenotypes include:
- Clinically Isolated Syndrome (CIS): A first clinical episode lasting at least 24 hours, consistent with CNS demyelination, but not yet fulfilling full diagnostic criteria.
- Relapsing-Remitting MS (RRMS): Characterised by distinct attacks (relapses) followed by periods of partial or full recovery, without sustained progression between relapses.
- Secondary Progressive MS (SPMS): Develops in many people with RRMS; over time, there is a gradual worsening of neurologic function, with or without superimposed relapses.
- Primary Progressive MS (PPMS): Progressive worsening of neurological function from onset, without initial relapses (though later superimposed activity may occur).
These definitions align with evolving diagnostic frameworks, including recent updates to the McDonald criteria. MS Australia+1
How Common is MS, and Who is at Risk?
- MS affects tens of thousands of Australians. According to recent consensus estimates, there were over 33,000 people living with MS in Australia by 2021.
- Onset typically occurs between 20–45 years of age, but MS can present earlier or later.
- Women are approximately twice as likely to be affected as men.
- Risk factors are multifactorial and include genetic predisposition, vitamin D levels, smoking, and past infection with Epstein–Barr virus. Geographic factors also play a role: for example, latitude (distance from the equator) has been associated with MS risk.
How does MS progress?
- Many people start with RRMS, experiencing periodic relapses (e.g., vision loss, weakness, sensory changes) that resolve fully or partially.
- Over time, especially without treatment, some individuals enter a secondary progressive phase, gradually accumulating disability even in the absence of relapses.
- A minority have primary progressive MS, marked by gradual decline from the outset.
- Prognosis varies widely: some people remain relatively stable for decades, while others accrue significant impairments. Factors associated with worse long-term outcomes include high relapse frequency in early disease, incomplete recovery from relapses, and higher lesion load on MRI.
Common symptoms of MS
Because MS can affect many parts of the CNS, symptoms vary. Common ones include:
- Fatigue (very common)
- Visual disturbances, such as blurred vision, pain with eye movement, or optic neuritis
- Double vision (diplopia), vertigo, facial numbness or weakness (brainstem involvement)
- Unsteadiness, tremor, ataxia
- Spasticity, muscle stiffness, spasms; problems walking
- Bladder, bowel, or sexual dysfunction
- Mood changes and cognitive issues.
Diagnosis
To diagnose MS, neurologists combine clinical assessment with investigations:
- MRI: Key tool to detect demyelinating lesions in the brain and spinal cord.
- Lumbar puncture (CSF analysis): May show oligoclonal bands or other markers of CNS inflammation.
- Evoked potentials: Tests (visual, somatosensory, auditory) that measure conduction speed and can highlight damage which may not be detected on clinical exam or imaging.
- Blood tests: To exclude other conditions (e.g., infections, vitamin deficiencies, autoimmune disorders). Testing for mimics of MS, such as neuromyelitis Optica spectrum disorder (NMOSD) or MOG (myelin oligodendrocyte glycoprotein) antibody associated disease (MOGAD) may be done if clinically indicated.
Prognosis
- The course of MS is highly variable and difficult to predict in an individual.
- Thanks to advancements in therapy, many people with MS now achieve near-normal life expectancy.
- Risks for more aggressive disease include early disability, frequent relapses, and high lesion burden on MRI.
- Treatment aims to limit relapses, prevent new lesion formation, and slow progression.
Treatment: Disease modifying therapies (DMTs)
The goal of DMTs is to reduce disease activity (relapses, MRI lesions) and delay long term disability. Below is an overview of the major classes of DMTs currently approved (or commonly used) in Australia. The Medical Journal of Australia
| Class | Examples | Mechanism & Notes |
| Injectables | Interferon-β (e.g., interferon β-1a, β-1b), Glatiramer acetate | Traditional immunomodulators; lower efficacy but relatively well-established safety profile. |
| Oral therapies | Teriflunomide, Dimethyl fumarate, Diroximel fumarate, Fingolimod, Siponimod, Ozanimod, Cladribine | Various mechanisms (anti-proliferative, S1P receptor modulation, Cladribine is given in short courses once a year. |
| Monoclonal antibodies | Tysabri (Natalizumab), Ocrevus (Ocrelizumab), Kesimpta (Ofatumumab), Lemtrada (Alemtuzumab) | High-efficacy agents. B-cell depletion (ocrelizumab, ofatumumab), immune cell trafficking blockade (natalizumab), or lymphocyte depletion (alemtuzumab).These medications are first line choice for most newly diagnose patients with MS |
Key points for patients:
- Choice of DMT depends on disease activity, patient preferences, risk profile, and monitoring requirements.
- There’s no “one size fits all” — neurologists often use a shared decision-making approach to balance risks and benefits.
- Regular monitoring is required (blood tests, imaging, safety reviews)
- Switching between DMTs may be considered if efficacy or tolerability is suboptimal.
Managing relapses and symptoms
- Relapses are typically treated with high-dose corticosteroids (e.g., methylprednisolone), often given intravenously.
- Symptomatic management is tailored to the individual and may include:
- Spasticity: baclofen, benzodiazepines, physiotherapy, botulinum toxin
- Bladder issues: anticholinergic agents (e.g., oxybutynin), intermittent catheterisation, bladder botulinum toxin (Botox) therapy
- Mobility issues: Some medications may be helpful (e.g. Fampridine) but focus is on regular exercise, physiotherapy and occupational therapy
- Fatigue: behavioural modifications and some medications, such as B12 injections and modafinil.
- Pain: can be managed with neuropathic agents, such as gabapentin and tricyclic antidepressants, as well as cannabis-based therapies.
Lifestyle and self-management
Beyond medications, other important elements include:
- Regular exercise, physiotherapy, occupational therapy
- Healthy nutrition and vitamin D management
- Smoking cessation
- Mood and mental health support
Other – Neuromyelitis Optica spetrum disorder (NMOSD) and MOGAD
The past 10 years increased our understanding of conditions that are similar, but not the same as multiple sclerosis. NMOSD (neuromyelitis optica spectrum disorder) and MOGAD (myelin oligodendrocyte glycoprotein antibody–associated disease) are two conditions that are often mistaken with MS, but present and diagnosed differently, and require different disease modifying therapies.
- What they are:
- NMOSD is an autoimmune disease in which antibodies (often against aquaporin-4, AQP4) attack astrocytes, especially in the optic nerve and spinal cord.
- MOGAD involves antibodies against MOG, a myelin-associated protein, leading to demyelination.
- How they differ from MS:
- Clinical presentation can overlap with MS (e.g., optic neuritis, transverse myelitis), but treatment is different.
- Some MS therapies can be ineffective or even harmful in NMOSD, so accurate diagnosis is critical.
- Diagnosis:
- Blood tests for AQP4-IgG (NMOSD) and MOG-IgG (MOGAD) are standard.
- MRI features and clinical history (e.g., severe optic neuritis, longitudinally extensive spinal cord lesions) help distinguish them.
- Treatment:
- In Australia, ravulizumab (Ultomiris®) is now PBS-subsidised for NMOSD.
- Other approved treatments include eculizumab and rituximab and traditional oral immunosuppressants (e.g., methotrexate, mycophenolate).
- For MOGAD, therapy often includes steroids and long-term immunosuppression with similar medications, tailored by a neurologist with experience in neuroimmunology.
When to see a neurologist/MS specialist
You should have regular follow-up with a neurologist experienced in MS to:
- Monitor disease activity (clinical review, MRI)
- Review and adjust DMTs if needed
- Manage symptoms and complications
- Address family planning, pregnancy, vaccinations, and other special situations.
Summary
- MS is a chronic, immune-mediated disease of the CNS characterized by demyelination.
- There are different clinical types (relapsing, progressive), and disease courses vary widely among individuals.
- Diagnosis relies on history, examination, MRI, and, sometimes, lumbar puncture or antibody testing.
- A wide range of disease-modifying therapies is now available, and treatment is highly individualized.
- NMOSD and MOGAD are different but related disorders that require separate diagnosis and treatment.
- With modern therapy and care, many people with MS live long, active lives.
References
- Shipley J, Beharry J, Yeh W, et al. Consensus recommendations on multiple sclerosis management in Australia and New Zealand: Part 1. Med J Aust. 2025;222(7). The Medical Journal of Australia+1
- Thompson AJ, Banwell BL, Barkhof F, et al. Diagnosis of multiple sclerosis: 2017 revisions of the McDonald criteria. Lancet Neurol. 2018;17(2):162–173. PubMed
- Travers BS, Wong SH, Dayan CM. Multiple-sclerosis diagnosis, therapy and prognosis. Aust J Gen Pract. 2022;51(4):170–177. RACGP
- Brownlee WJ, Jauhiainen A, Chopra R, et al. Towards a Unified Set of Diagnostic Criteria for Multiple Sclerosis. Ann Neurol. 2025. Wiley Online Library
- MS Australia. Types of MS. MS Australia website. MS Australia
- Ford H, Chiaravalloti N, Bruce JM. Clinical presentation and diagnosis of multiple sclerosis. Handbook of Clinical Neurology. 2020;Volume 174:3–16. ScienceDirect
- Sechi C, Cacciaguerra L, Chen JJ, et al. Clinical features and management of MOG-IgG associated disease. J Neurol Neurosurg Psychiatry. 2022;93(8):800–810. PubMed
- Alzarooni H, Whittam DH, Merheb V, et al. NMOSD and MOGAD: insights on patients’ radiological and clinical features. Front Neurol. 2024;15:1480723. Frontiers
Section editor – Dr Tal Koren
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