Multiple sclerosis

Overview

MS causes symptoms from any CNS region; the key pattern is multiple distinct episodes affecting different anatomical locations in a young adult (20-40 years, women 2x more common).

•Optic neuritis - unilateral painful visual loss, reduced colour vision, RAPD; often the first presentation of MS

•Limb weakness - UMN pattern: spastic weakness, brisk reflexes, upgoing plantars

•Sensory disturbance - numbness, tingling, dysaesthesia in dermatomal or cord distribution

•Lhermitte's sign - electric shock down spine into limbs on neck flexion; caused by cervical cord plaque

•Cerebellar features - ataxia, intention tremor, dysarthria, nystagmus

•Bladder dysfunction - urgency, frequency, urge incontinence

•Fatigue and depression - common but fatigue or depression alone without focal neurological symptoms should NOT prompt an MS diagnosis

•Uhthoff's phenomenon - worsening of symptoms with rise in body temperature (exercise, hot bath, fever); demyelinated axons sensitive to even 0.5°C rise; resolves on cooling; not a true relapse

🎯

A prior episode of painful visual loss that resolved spontaneously (optic neuritis) + a new focal neurological deficit in a young woman = MS until proven otherwise. Depression is common in MS and does not mean symptoms are functional.

Investigations

•Diagnosis requires dissemination in space (DIS) and dissemination in time (DIT) - McDonald criteria (2017); only a consultant neurologist should diagnose MS

🥇 First-line

•MRI brain and spine with gadolinium - periventricular, juxtacortical, infratentorial, spinal T2 hyperintense lesions; gadolinium enhancement of active lesions

•Visual evoked potentials (VEPs) - delayed P100 response indicates optic nerve demyelination

•Blood tests to exclude differentials - FBC, ESR, CRP, B12, folate, glucose, TFTs, ANA, anti-dsDNA, AQP4-IgG

🏆 Gold standard

•Lumbar puncture with CSF analysis - oligoclonal bands (OCBs) in >95% of MS, present in CSF but not serum (intrathecal synthesis); mild lymphocytosis; raised IgG index

MS vs neuromyelitis optica (NMO)

Feature	MS	NMO
Antibody	Negative	AQP4-IgG positive
MRI head	Periventricular plaques	Often normal
Spinal lesions	Short (<3 vertebral segments)	Long (>3 vertebral segments)
CSF OCBs	Present in >95%	Usually normal

Management

Three pillars: treat acute relapses, disease-modifying therapies (DMTs) to reduce relapse frequency, and symptom management - all coordinated by specialist neurology.

•Acute relapse: high-dose corticosteroids to shorten duration

•Spasticity - first-line: baclofen or gabapentin

•Spasticity - second-line: diazepam

•Physiotherapy - useful adjunct to pharmacological treatment of spasticity, not first-line alone

•Botulinum toxin - not first-line for spasticity in MS; role still under investigation

🎯

For MS spasticity: first-line = baclofen or gabapentin (not pregabalin); second-line = diazepam. This is a direct exam favourite.

Complications

•Pseudo-relapse - worsening of pre-existing symptoms triggered by infection (especially UTI), fever, or metabolic disturbance; not true inflammatory activity; always exclude infection before treating with steroids

•True relapse - new or distinct neurological symptoms lasting >24 hours without fever

•Depression and anxiety - affect the majority of people with MS; depression may itself be a subtle manifestation of MS

•Cognitive decline - affects up to 50%; memory, attention, and processing speed most affected

⚠️

Always exclude UTI before attributing symptom worsening to a true MS relapse - infection is the most common cause of pseudo-relapse.