Multiple Sclerosis Flashcards
Is MS more common in males or females?
Females
MS is a disease of
the white matter of the CNS which causes demyelination and relapsing, remitting disease
Factors of pathogenesis of MS
Complex genetic inheritance
Association with autoimmune disease
More common in temperate climates
Possible relationship to viruses and vitamin D exposure
Initial presentation of MS
80% present with a relapse - attack of demyelination or inflammation
Gradual onset over days
Stabilises over days/weeks
Gradual resolution to complete or partial recovery
Symptoms of relapse of MS
Optic neuritis Sensory symptoms Limb weakness Diplopia/vertigo/ataxia Bilateral symptoms and signs of spinal cord pathology Bladder and bowel symptoms
Presentation of optic/retrobulbar neuritis
Subacute vision loss in one eye
Pain on moving eye
Colour vision disturbed/desaturated
Process of optic neuritis
Initial swelling of optic disc followed by optic atrophy
Affect of optic neuritis on pupillary reflex
Relative afferent pupillary defect - dilation rather than constriction when light shone on pupil
Possible differential diagnoses for optic neuritis
Neuromyelitis optica Sarcoidosis Ischaemic optic neuropathy Toxin/drugs/B12 deficiency Wegners granulomatosis Local compression Leber's hereditary optic neuropathy
Presentation of brainstem relapse
Cranial nerve invovlement Internuclear opthalmoplegia Diplopia Vertigo Nystagmus Ataxia Upper motor neurone changes in limbs
Presentation of myelitis
Numbness/pins and needles in legs
Weakness/upper motor neurone changes below the level of numbness/pins and needle
Bladder and bowel invovlement
Increased reflexes
Presentation of further relapses of MS
May occur within months or years of first relapse Variable site and severity Optic nerve involvement Sensory involvement Limb weakness Diplopia Vertigo Ataxia Sphincter disturbance
Describe process of demyelination
Autoimmune process
Activated T cells cross blood-brain barrier and cause demyelination
Demyelination can repair, full recovery if normal repair, or scarring and gliosis if not completely repaired
How does demyelination appear on MRI?
As lesions or plaques
Describe the progression of demyelination in MS
Axonal loss - may be important in progression and development of disability
Black holes appear on MRI, later seen as cerebral atrophy
Presentation of progressive phase of MS
Accumulation of symptoms and signs Fatigue, temperature sensitivity Sensory involvement Stiffness/spasms Poor balance Slurred speech Difficulty swallowing Diplopia, oscillopsia, visual loss Cognitive - dementia, emotional liability
Most patients who present with relapsing remitting MS will go on to develop
secondary progressive disease
Possible examination findings in MS (depends on location of demyelination and stage of disease)
Afferent pupillary defect Nystagmus/abnormal eye movements Cerebellar signs Sensory signs Weakness Spasticity Hyperreflexia Plantar extensor reflex
How is MS diagnosed?
Based on clinical presentation, MRI and evidence of demyelination separated in time and space
Investigations that should be done in suspected MS with an atypical clinical picture or MRI
Lumbar puncture
Visual/somatosensory evoked response
Bloods to exclude other inflammatory conditions
CXR
Differential diagnoses for suspected MS with atypical presentation
Acute disseminated encephalomyelitis Other autoimmune conditions e.g. SLE Sarcoidosis Vasculitis Infection e.g. Lyme disease Adrenoleukodystrophy
Type of MS
Relapsing remitting Secondary progressive Primary progressive Sensory Malignant
First line agents for disease-modifying treatment of MS
Beta-interferons/glatiramer acetate daily/weekly IM/SC injection
Oral treatments - teriflunomide, dimethyl fumarate
Possible side effects of first line agents for disease modifying treatment of MS
Flu-like symptoms
Injection site reaction
Abnormalities of blood count and liver function
Second line agents for disease-modifying treatment of MS
Natalizumab
Fingolimod
Alemtuzumab
Treatment of Progressive Multifocal Leukencephalopathy
Natalizumab, dimethyl fumarate or fingolimod
Annual MRI
JC virus antibody blood and urine 6-monthly
Treatment of acute relapse of MS
Look for underlying infection Exclude worsening of usual symptoms with intercurrent illness Oral prednisolone Rehabilitation Symptomatic treatment
Treatments for spasticity in MS
Muscle relaxants
Antispasmodics
Physiotherapy
Treatments for dysaesthesia in MS
Amitriptyline
Gabapentin
Treatments for urinary problems in MS
Anticholinergics
Bladder stimulation
Catheterisation
Treatment for constipation in MS
Laxatives
Treatment for vision problems/oscillopsia in MS
Carbamazepine
Features of upper motor neurone lesion
Muscle weakness (pyramidal) Decreased control of active movement Spasticity Clasp-knife response Babinski sign Increased deep tendon reflex Pronator drift
Features of lower motor neurone lesion
Muscle paresis/paralysis Fibrillation Fasciculations Hypotonia/atonia Hyporeflexia Strength not affected Muscle wasting (end stage)
