Autoimmune Flashcards
MS causes
mostly environmental?
possible viral infection in childhood
possibly vitamin D deficiency
small genetic risk
Diagnosing MS
clinical diagnosis
clinical evidence of lesions of CNS that are disseminated in time and space (>=2 different regions in central white matter affected at differnet times)
MS imaging
MRI: T1 weighted (fat is bright): hypointense black holes = areas of permanent axonal damage T2 bright areas = demyelinated plaques located in white matter
MS Labs
oligoclonal bands in CSF
synthesis of homogenous Ig by individual plasma cell clones in CSF
sens 80%, spec 92%
Pathophysiology of Relapsing-remitting MS
MS lesions: majority located in white area near cerebellum, spinal cord, brainstem and optic nerve
conduction block, demyelinating
Remyelinating:
- occurs at early stages of disaease
- slow; repeated attacks lead to fewer successful remyelinations
- lesion become irreversible
Inflammation:
- T-cell mediated; infiltrate into brain via BBB
- attack myelin
Course and prognosis of MS
INO
Lhermitte’s symptom
Uhthoff’s phenomenon
Ephatic transmission
Lhermitte’s symptom
electrical sensation that runs down back into limbss when flexing neck
lesion of dorsal columns of cervical cord/caudal medulla
Uhthoff’s phenomenon
increased symptoms due to heat
altering conduction of nerves
Ephatic transmission
tramission of charge between neighbouring axons –> paroxysmal symptoms
Types of MS
Relapsing/remitting
secondary progerssive
primary progressive
progressive/relapsing MS
MS relapse management
corticosteroids
rehab
MS disease-modifying therapies
prevent disability; can help reduce relapse rates
beta-interferons
MS chronic symptom management
spasticity: baclofen/tizanidine
bladder: self-catheterization
pain, erectile impotence, fatigue, depression
Romberg test
positive:
ataxia is sensory in nature; depending on loss of proprioception
affected PCML/peripheral sensory neurons
NOT a test of cerebellar function
