MS Flashcards
investigations required after presentation of optic neuritis
b12 - deficiency can cause optic neuropathy which can mimic optic neuritis
CPR/ESR - signs of systemic inflammation
antibodies - SLE, GPA, EGPA
serology for possible
infectious triggers - HIV, syphilis, Hep B and C - rarely the cause but don’t miss as treatable
LFTs U&Es calcium glucose TFTs
aqua porin 4 AB - neuromyelitis or devics = antibody mediated attack on specific parts of the CNS - optic nerves and SC
MRI - brain and SC
LP - oligoclonal bands in CSF but not serum
questions to ask someone with ataxia
nausea and vertigo - vestibular or cerebellar
voice change - cerebellar lesion
both or one side of body - lesion in half or whole of cerebellum
sensory disturbance - numbness, pain, tingling = sensory ataxia, SC, peripheral nerves or roots
bladder involvement - SC
balance worse in shower/washing face - sensory ataxia
cerebellar ataxia
lesion in cerebellar
vertigo and nausea, change in patients voice (staccato dysarthria)
poor coordination in arms, unsteadiness walking
sensory ataxia
lesion in SC, peripheral nerves, or nerve roots
numbness, pain, pins and needles
fall over when eyes are closed - shower, washing face
L’hermittes phenomenon (tingling sensations upon flexion and extension of neck) - SC
bladder frequency or urgency - SC
vestibular pathology causing ataxia
location in vestibular
vertigo made worse by head movements
nausea
sometimes hearing loss or tinnitus
what is MS
UMN - CNS, brain and SC
autoimmune
multifactorial - genes and environment
white women 20-40
presentation of MS
optic neuritis - pain on movement, blurring of vision, red colour saturation, Uhtoffs phenomenon (visual fatigue with excessive use of vision)
fatigue weakness sensory disturbance dysarthria vertigo slurred speech ataxia incoordination facial numbness double vision sensory disturbance autonomic dysfunction urinary urgency, frequency, retention - common.
types of MS
- relapsing and remitting (85-90%)
attacks with partial or complete recovery
no progression between attacks - secondary progressive MS
after about 15 years of relapsing and remitting MS patient slowly deteriorates, with or without attacks - primary progressive (10-15%)
progression from onset, no attacks, patient usually >40 - progressive-relapsing MS (5%)
begin with progression then have attacks
types of plaques in MS
active acute plaques: clinical relapses
chronic active plaques: axonal damage, active microbial still destroy plaque
chronic inactive plaque: old scar, completely demyelinated
demyelinating disease, neuronal loss can be seen, re-myelination is variable
MS diagnosis
2 or more attacks with 2 or more clinical lesions
dissemination in time and space - lesions can be clinically diagnosed or MRI
McDonald criteria
MS differentials
sjorgens
anticardiolipin antibody syndrome
neurosarcoidosis
neurolyelitis optica - causes longitudinally extensive transverse myelitis, and optic neuritis
long term management in MS
all drugs reduce relapse by 1/3
effects on immune system
highly effet
long term management in MS
all drugs reduce relapse by 1/3
effects on immune system
disease modifying treatment
interferon beta-1a, interferon beta-1b, teriflunomide, ocrelizumab, alemtuzumab, natalizumab
symptomatic treatment of MS
neuropathic pain: TCAs, gabapentin
incontientce: intermittent self-catheterisation, anticholinergics, pelvic floor exercises, even fluid intake
spasticity: physio, baclofen, gabapentin
oscillopsia (visual disturbance, things appear to oscillate): gabapentin
fatigue: exercise, diet, rule out other causes, screen and treat for depression - SSRI
if suspecting spinal cord disease
MRI relevant area - priority
B12
MRI brain - dependent on history, wide spread neurological disease e.g. MS
MRI lumbar no good! - SC ends L1
no nerve conduction studies - peripheral nerves
LP - if MS considered
