Define multiple sclerosis?
CNS demyelination causing neurological impairment that is disseminated in time and space.
Explain MS in layman’s terms.
In simple terms, Multiple Sclerosis (MS) is a condition where the body’s immune system mistakenly attacks the protective covering of nerve cells in the brain and spinal cord, called the myelin sheath. This damage can disrupt the signals traveling through the nervous system, leading to a variety of symptoms like vision problems, muscle weakness, and balance issues.
What are the different types of MS?
Relapsing-remitting
Primary progressive
Secondary progressive
Clinically isolated syndrome
Clinical signs present in MS?
Mobility aids, catheter if spinal plaque
Cranial nerves: bilateral INO, optic atrophy, reduced visual acuity, cranial nerve palsies
UL/LL exam: UMN spasticity, weakness, brisk reflexes, altered sensation
Cerebellar dysfunction
Other clinical features include: depression, autonomic (urinary retention + bowel problems), Uthoff’s phenomenon (worsening of sx after hot bath or exercise), L’hermitte’s sign: lightening pain down spine on flexion of neck
Differential diagnosis for MS?
If acute onset, consider vascular cause.
Disc prolapse.
Demyelination (MS) is more likely if there are other features such as RAPD, pale optic disc (optic neuritis), and INO.
Transverse myelitis
SACD
Investigations to perform in suspected MS?
CSF: oligoclonal IgG bands
MRI brain/spinal cord: periventricular white matter plaques
Visual evoked potentials (VEPs): delayed velocity but normal amplitude (evidence of previous optic neuritis)
Management of MS?
MDT approach: nursing, PT, OT, social worker, doctor.
Disease-modifying treatments:
RRMS: interferon beta (1/3 reduction in relapse) and glatiramer, fingolimod (1/2 reduction). MAB therapy (natalizumab) - 80-90% reduction. Also graded effects on delaying conversion to SPMS but with greater efficacy = greater toxicity.
Early PPMS: ocrelizumab (anti-CD20) modestly effective if active on MRI
Symptomatic treatments:
IV/PO methylprednisolone for acute attacks (does not alter prognosis).
Antispasmodics (baclofen).
Carbamazepine, amitriptyline, pregabalin, gabapentin (neuropathic pain).
Laxatives / intermittent catheterisation for bladder and bowel symptoms.
What is internuclear ophthalmoplegia?
Indicates a lesion in the heavily myelinated medial longitudinal fasciculus, which connects the paramedian pontine reticular formation and VIth nerve nucleus on one side to the third nerve nucleus on the other, enabling conjugate eye movements.
Unilateral: stroke
Left INO: on left gaze, left eye adducts normally with nystagmus, right eye either unable to abduct or abducts sluggishly. Both eyes converge normally.
Right INO: on right gaze, right eye adducts normally with nystagmus, left eye either unable to abduct or abducts sluggishly. Both eyes converge normally.
Bilateral INO: MS - each eye abducts normally on ipsilateral gaze, with nystagmus. Contralateral eye to gaze adducts sluggishly. Both eyes converge normally.
What are the key features to cover in MS extended consultation?
HPC, PMH, FH
If looking like MS - ruling out differentials
- disc prolapse (back pain, trauma, infective sx, red flag malignancy symptoms, bladder/bowel dysfunction - could still be MS)
- transverse myelitis (may be part of MS)
- B12 deficiency - diet in SHx, functional B12 - use of N2O
- acute ascending neuropathy (recent viral illness, progression of symptoms)
- stroke (acuity of onset, smoking, htn, diabetes)
Will guide advice to give to patient for their safety and guide treatment options for relapse.
Hx of previous MS type symptoms i.e. double vision, weakness,
Associated features:
- mood disturbance
- cognitive impairment
- bladder/bowel dysfunction, if man impotence
- Uthoff’s phenomenon (worse with hot bath)
- Lhermitte’s (shock pain on neck flexion)
Examine eyes (pupils, RAPD, acuity, INO, offer fundoscopy), arms and legs - focus on presenting complaint locality
Discussion with patient:
- what have they been telling themself about it?
- layman explanation of most likely differential being MS, possible other causes and why they might be less likely
- investigations: bloods FBC/U&E/CRP/bone profile/B12/HC/MMA/Igs & electrophoresis, may consider autoimmune screen
- MRI brain and spine with contrast
- lumbar puncture: oligoclonal bands
- treatment options if patient asks or if time
- summarise and agree next steps
How would you localise the lesion of MS from the history in your exam?
Optic neuritis: (painful, unilateral vison loss with reduced colour vision) - retrobulbar optic nerve most commonly
- start with examining eyes, RAPD
- fundoscopy
- move on to limbs, (start with where the history has guided), good idea to start with gait, asking them to rise with arms folded and march on the spot - quick way of establishing equal 4/5 power
INO: (diplopia) - heavily myelinated medial longitudinal fasciculus (brainstem)
- start with eyes: movements, acuity, RAPD, fields
- fundoscopy looking for previous optic neuritis changes (optic atrophy)
- limbs based on assessment, good idea to start with gait
Poor balance: cerebellum
- begin with gait. asking them to rise from the chair with arms crossed and then march on the spot (gives clues about power in legs) - may not be able to if ataxic
- history will guide what to examine
Limb weakness: spinal cord, typically bilateral but can be asymmetrical dependent on which specific part of cord is effected (typically 2-3 level of cord, only really relevant to imaging). Lateral and dorsal columns usually affected more commonly but could be transverse myelitis causing whole cord sensory level cut off
Paraesthesia: spinal cord, affecting sensory tracts
- start with affected limbs - if legs start with gait
- inspection
- tone/power/reflexes
- pain, vibration
- coordination
Next would be what has been eluded to in history as per previous attacks (if relapsing remitting)
- eyes at a minimum if time (state you would examine all cranial nerves)
How is a relapse of MS defined?
Sub-acute onset (hours-days)
New neurological symptoms or sub-acute sustained worsening of symptoms without trigger
Pseduo-relapse: temporary worsening of MS symptoms due to a trigger such as infection, heat, stress