Cerebellum, Basal Ganglia, Motor Disorders

mary20's version from 2017-01-09 23:00


Question Answer
purpose of cerebellum modulates movement-aids in coordination and balance 
what is the input to the cerebellum -contralateral cortex via middle cerebellar peduncle -ipsilateral propioceptive information via inferior cerebellar peduncle from spinal cord (the only afferents are MCP and ICP) 
what is the output from the cerebellum sends info to contralateral cortex to modulate movement (superior cerebellar peduncle) 
explain the whole output pathway of the cerebellum purkinje cells-deep nuclei of cerebellum-contralateral cortex via superior cerebellar peduncle 
what are all the deep nuclei lateral to medial (DEG-F=degrees farenheit) -Dentate -Emboliform -Globose -Fastigial 
what happens with lateral lesions of the cerebellum voluntary movement of extremities when injured-propensity to fall toward injured side (ipsilateral)
what happens with medial lesions of the cerebellumlesions involving midline structures (vermis, fastigial nucleus, flocculonodular lobe) -truncal ataxia (wide based cerebellar gait) -nystagmus -head tilting
what usually happens with medial lesions of the cerebellum bilateral motor deficits affecting axial and proximal limb musculature 
purpose of basal ganglia important in voluntary movements and making postural adjustments 
explain how basal ganglia work receives cortical input then provides negative feedback to cortex to modulate that movement 
what is the striatum putamen (motor: if injured=chorea) and caudate (cognitive: if injured=dementia) 
what is the lentiform putamen and globus pallidus
D1 receptor in the basal ganglia is responsible for what excites the direct pathway: D1 is the DIrect pathway (inhibits the inhibitor) 
D2 receptor in the basal ganglia is responsible for what Inhibiting the Indirect pathway (2 I's)
explain the excitatory pathway (direct pathway) cortical inputs stimulate the striatum stimulates the release of GABA GABA inhibits the thalamus via the GPi/SNr (increases motion)
explain the inhibitory pathway (indirect pathway) cortical inputs stimulate the striatum this disinhibits STN via GPe STN stimulates GPi/SNr to inhibit the thalamus (decreases motion)
what happens in dopamine is released from the substantia nigra compacta D1=excitatory=movement D2=inhibits the inhibitory pathway=movement
what are the movement disordersathetosis chorea dystonia essential tremor hemiballismus intention tremor myoclonus resting tremor
presentation of athetosis slow, writhing movements (esp in the fingers!!!!)
what is lesioned in athetosis basal ganglia (ex: Huntingtons Disease)
what is a way to remember athetosis writhing, snake-like movement
presentation of chorea sudden, jerky, purposeless movements
what is lesioned in chorea basal ganglia (ex: Huntingtons Disease)
what is a way to remember chorea dancing
how does dystonia presentsustained, involuntary contractions
what is a way to remember dystoniawriter's cramp, blepharospasm (sustained eyelid twitch)
presentation of an essential tremorhigh frequency tremor with sustained posture (superman) worsened with movement or when anxious
cause of essential tremorfamilial
characteristics of an essential tremorpts often self-medicate with EtOH (this decreases tremor amplitude) 
how do you treat essential tremor beta blockers (esp: propanolol) primidone (type of barbiturate)
presentation of hemiballismus sudden, wild flailing of 1 arm (+/-) ipsilateral leg
what is lesioned in hemiballismus contralateral subthalamic nucleus (ex: lacunar stroke) 
what is a good way to remember what hemiballismus is pronounce it "half-of-body ballistic"
what side is lesioned with hemiballismus contralateral lesion (this is the case with all basal ganglia! whereas cerebellum is ipsilateral) 
presentation of intention tremor slow, zigzag motion when pointing/extending toward a target
what is lesioned with an intention tremor cerebellar dysfunction
presentation of myoclonus sudden, brief, uncontrolled muscle contraction 
what are some different types of myoclonus and in what conditions do they present -jerks -hiccups -common in metabolic abnormalities such as renal and liver failure
presentation of resting tremor uncontrolled movement of distal appendages (mostly in hands) 
what alleviates a resting tremor intentional movement
resting tremore is most common in whatParkinson disease
common phrase of parkinson tremor "pill-rolling tremor" (occurs at rest)
what is parkinson disease degenerative disorder of CNS associated with Lewy bodies and loss of dopaminergic neurons (depigmentation of the substantia nigra compacta) 
what are lewy bodiesalpha-synuclein (intracellular eosinophilic inclusions)
what are the 2 key findings in parkinsons (in the brain) depigmentation of the substantia nigra compacta AND lewy bodies!
s/s of Parkinsons TRAPS your body Tremor (pill-rolling tremor at rest) Rigidity (cogwheel) Akinesia (or bradykinesia) Postural instability Shuffling gait
inheritance of huntingtons disease autosomal dominant
cause of huntingtons disease trinucleotide repeat (CAG with anticipation) disorder on chromosome 4
when do sx of huntingtons disease manifest between ages 20 to 50
s/s of huntingtons disesase choreiform movements aggression depression dementia (sometimes mistaken for substance abuse!)
what are the NT levels in huntingtons diseaseincreased DA (different than Parkinson) decreased GABA decreased ACh in the brain
what is a good way to remember the NT in Huntingtons disease CAG Caudate loses ACh and GABA
neuronal death of HD is caused by what NMDA-R binding and glutamate toxicity
what does the brain look like with HD atrophy of the caudate nuclei! ex vacuo dilatation of frontal horns (on MRI)