Basal ganglia Flashcards
4 components of basal ganglia
1) striatum = caudate + putamen
2) globus pallidus
3) substantia nigra
4) STN
general function of basal ganglia
modulation of motor performance with cerebellum and serves as feedback loop to ipsil motor and assoc cortex
NT synthesis
NOT SENSATION OR STRENGTH
major input source to basal ganglia
cerebral cortex (frontal and sensorimotor areas for planning movement) –> caudate and putamen –> globus pallidus
major output from basal ganglia
basal ganglia –> globus pallidus
basal ganglia –> thalamus –> cerebral cortex
NO CONNECTIONS DIRECT WITH SENSORY OR SPINAL MOTOR
internal feedback loops
3
caudate and putamen –> Subst nigra PC –> ganglia via DA neurons
caudate and putamen –> Subst nigra PR –> thalamus
GPE –> STN –> GPi and GPe
character of parkinson’s
1) resting tremor (3-6 Hz) lost with intentional movement
2) incr muscle tone
3) difficult with movement intiation
4) bradykinesia
5) shaking head, tremulous speec, littel facial expression
probable etiology of parkinson’s
loss of DA neurons in subst nigra
normally, DA released diffusely into striatum for excitation which disinhib (excites) motor cortex
therefore, parkinson’s have decr disinhibition or decr excitation so hard to initate movement
is output of basal ganglia excitatory or inhib
why
inhib
GPi –> (GABA inhib) thalamus –> (Glut excite) cortex
output of GPi via pallidothalamic fibers have GABAergic
basal ganglia always inhib thalamus until signal from cortex causes disinhib of thalamus (direct path)
excitation of caudate or putamen by cerebral cortex causes
removal of disnhib of basal ganglia on thalamus
genetics of huntingon’s
what areas of basal ganglia affected
AD mutation of 4p
XS CAG repeat (40+)
affects striatum esp caudate –>
lose cholinergic and GABAergic neurons so lose effect of striatum on globus pallidus –>
athetososis (writhing slow movement) or chorea (contin rapid movement of face, tongue, distal limb)
Describe direct pathway from cortex to basal ganglia and back
motor cortex path
1) sensorimotor cortex (layer V)
2) excites through striatum (caudate/putamen) with glutamate
3) inhib GPi with GABA
4) decr inhib VA some VL thalamus using GABA
5) excites cortex with glutamate (supplementary motor area)
path from association cortex through basal ganglia and back
frontal assoc cortex –> caudate –> GPi –> dorsomedial thal –> assoc cortex
without cortical input, Globus pallidus fire spontaneously, effect?
With cortical exictation of caudate and putamen what happens
GP normally inhib thalamus
if excite caudate and putamen, inhibition is inhibited and cortex allows movement
why does stroke in STN cause hemiballismus
where is stroke
STN normally excites GPi
lose excitation –> decr inhib outflow from GP –> inappropriate excitation of motor cortex thru thalamus –> contralateral flailing
stroke in small ganglionic branch of PCA
what type of stim (depol or hyperpol) would be used in DBS of parkinson’s patient
in STN?
in globus pallidus
hyperpolarizing
both STN and GPI inhib thalamus
so have to remove inhib
DBS of STN/GPi= hyperpolarizing
inhib STN, decr excitation of GP, decr inhibition of cortex
