neuro8 Flashcards
(28 cards)
vermal lesions
prominent truncal and gait ataxia
cerebellar hemispheric lesions
ipsilateral limb ataxia
cerebellar hemorrhage or infarction presentation
abrupt onset of vertigo, vomiting, and inability to walk
alcoholic cerebellar degeneration
consequence of longstanding alcohol abuse; vermis bears the brunt of damage; progressive gait and truncal ataxia that evolves over a period of weeks or months
postinfectious cerebellitis
kids between ages 2 and 7; usually follows varicella or other viral infx; acute onset of limb and gait ataxia and dysarthria; lasts a few weeks and full recovery
paraneoplastic cerebellar degeneration
pancerebellar; usually evolves over a period of weeks and thenstabilizes, leaving the patient with profound disability; typically assoc with gyn or SCLC and may manifest prior to dx of tumor
MRI in paraneoplastic cerebellar degeneration
normal
CSF in paraneoplastic cerebellar degeneration
may have an elevated protein or a lymphocytic pleocytosis, but is frequently normal; sometimes there are autoantibodies anti-Yo and anti-Hu
freidrich ataxia
aut recessive; progressive ataxia that usually affects the arms more than the legs; severe dysarthria; onset usuallyin childhood; classicly loss of reflexes, spasticity, and extensor plantar responses
inherited episodic ataxia
brief episodes of ataxia, vertigo, and n/v
EA1
cuased by mutations in a voltage gated potassium channel; episodes are brief and an interattack skeletal muscle myokymia is associated
EA2
mutations in the pore-forming alpha 1 subunit of the P/Qtype voltage gated calcium channel; attacks are longer, lasting a few mins; interictal nystagmus; progressive irrev ataxia may develop late in the disease
aut dom spinocerebellar degenerations
cerebellar ataxia with ot without additions neuro signs and a fam hx consisten with aut dom inheritance; mild cognitive decline is often a late feature
many spinocerebelar ataxias for which the genetic defect has been identified are caused by what
CAG trinucleotide repeats
Miller Fisher syndrome
triad of ataxia (due to proprioceptive loss), areflexia, and ophthalmoplegia; variant of guillan barre; IgG anti-GQ1b antibodies in the serum; full recovery
hemiparetic gait
affected leg is stuff and does not flex at the hip, knee, or ankle; leg is circumducted; arm is flexed and adducted and does not swing freely
spastic (paraparetic) gait
essentially a bilateral hemiparesis; adductor tone is increased and the legs tend to cross during walking (scissoring gait)
akinetic-rigid gait
posture is stooped, with flex of the shoulders, neck and trunk; gait is narrow based, slow, and shuffling with small steps and reduced arm movement
gait initiation difficulty
seen in akinetic rigid gait
festination
rapid small steps
frontal gait
posture is flexed, and the feet may be slighly apart; gait initiation is impaired; advances with small, shuffling, and hesistant steps; abortive stepping movements without being able to move forward
waddling gait
hip-gurdle weakness; pelvis and trunk tilt toward the opposite side during walking
psychogenic gait
range of presentations;
hemiparetic gait
suggests hemispheric dysfunction, most often stroke
