Neuro Dz 1 Flashcards
most freq. cause of acute flaccid paralysis
GBS
GBS
immune mediated disorder directed against myelin or Schwann cells
variants of GBS
AIDP
MFS
AMAN
AMSAN
common antecedent illnesses of GBS
campylobacter infection
preceded by URI or GI infection
other potential causes of GBS
HIV, Zika, influenza, EBV, CMV etc
vaccinations
PCN, OCs, TNFs
epitropic mimicry
found in GBS
following illness, immune system goes into overdrive and begins attacking the myelin sheath and/or Schwann cells on peripheral n.
Pathophys of GBS
following epitropic mimicry,
demyelination of the nerve and axon degeneration
unable to pass on nerve impulses
all myelinated nerves are affected + protein movement to CSF = edema
GBS epidemiology
Bimodal presentation (50-79 y/o, 15-35 y/o)
Men > Women (pregnant women have increased incidence)
GBS presentation
symmetric paresthesias
early loss of DTRs
affecting lower extremities first
ascending weakness (can get to muscles of respiration)
severe pain
sensory changes
what is a significant source of mortality in GBS pts
autonomic changes + decreased Lung expansion/respiratory failure
autonomic changes in GBS
tachycardia –> bradycardia
paroxysmal HTN/HoTN
Urinary retention, ileum, loss sweating, flushing
cranial nerves affected by GBS
facial weakness (VII)
impaired EOMs, dysphagia and dysarthria (VI, III, XII, V, IX, X)
natural progression of GBS
rapidly progressive weakness and others peak 14-30 days
plateau phase 2-4 weeks (persistent, non progressive)
recovery time is 7 months
steps in diagnosis of GBS
- CBC/Chem panel
- Imaging
- LP
- Conduction studies
- NIP/FEV (staging)
LP of GBS
albuminocytologic findings
high protein levels, normal WBCs
tx of GBS
hospitalized +/- intubation, supportive care
plasmapheresis OR IVIG (no steroids)
plasmapheresis
HD catheter to filter out and remove Ags attacking the myelin
replace plasma with donor plasma so they don’t attack myelin
6-10 tx
IVIG
gives pts donor IVIG to decrease body’s production of bad IG cells
“tames immune system”
caution for renal failure, thrombosis
which tx for unstable GBS pt?
`IVIG
CIDP
chronic (over 8weeks) demyelination and demyelination of nerves + axon degeneration
CIDP s/s
fairly symmetric motor and sensory loss
motor > sensory
large and small muscles affected
diminished DTRs globally
CIDP work up
Lab work up
LP
imaging
EMG
CIDP tx
glucocorticoids
plasmapheresis
IVIG
distinguishing features of CIPD
Chronic onset motor > sensory old men not as commonly cranial nerves Tx with steroids
distinguishing features of GBS
acute onset all nerves equally affected bimodal presentation EOM issues steroids don't work
myasthenia Gravis
autoimmune destruction of nicotinic acetylcholine post synaptic receptors of skeletal muscle
abnormality of T cells and thymic function
pathophys of MG
- autoAbs block and destroy Ach Receptors
- deep folds of motor endplate are flattened = widened gap
THEREFORE: normal Ach release but insufficient number of receptors on muscle is triggered so contraction is weak or non existent
muscles affected by MG
skeletal muscles ONLY
no smooth/cardiac muscles