43 Movement Disorders
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know lateral ventricle large
Loss of caudate, loss of GABA, no inhibition = breakthrough of movement. Indirect pathway
each generation passes on more repeats to later generation = worse symptoms
anticipation: earlier symptoms with each gen
excitotoxicity mechanism
NMDA binding to glutamate toxicity
usually adopted because most people know about it before have kids
chorea: dance like abnormal movements
No subthalamic nucleus. No inhibitory of thalamus = movement breakthrough
once stroke affects IC = hemiplegia
only half of body
deposit in liver (cirrhosis)
elbows beat like wings of bird
Mood disorders at very young age
dysarthria: difficult to get words out, slow irregular speech
face secondary to medications
antipsychotic/antiemetic blocks D2, increase D2 sensitivity, hyperkinesia via D2 endogenous
hypersensitivity of D2 receptors
D2 preferentially bound = blocked inhibitory pathway = dyskinesia
Dopamine naturally broken down by MAO
MAO sits on outer membrane of mitochondria
result: Parkinson
pt cannot initiate movement
Loss of D1, no disinhibition, less movement
no movement in stopping/ending
initiation is difficult; once initiated, cannot be stopped = festination
Loss of D1, no disinhibition, less movement
parts of brain becomes pale because lose melanin containing dopaminergic neuron
now used to induce parkinson's in lab rats
shuffling: shuffles feet
cogwheel: moving arms stutters as if stopping on stops of cogwheel
simultaneous activation of flexors/extensors
propanolol for central tremor
initially usually tremor symptoms
once develops bradykinesia/rigidity, add more drugs
L dopa last
vit B6 promotes conversion of L-dopa to dopamine in periphery
off so severe akinesia: no movement, frozen
dyskinesia: involuntary
SSRI raises serotonin; selegiline blocks breakdown = very high serotonin
myoclonus: sudden contraction once
dystonia: sustained contraction
writer's cramp: after writing for so long, arms spasm
blepharospasm: twitching of eye muscles (blinking)
