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42 Cards in this Set

  • Front
  • Back
Basal ganglia
components of feedback loops that regulation initiation and maintenance of planned movement, suppression of unwanted movement.
Striatum
input region of basal ganglia; caudate + putamen
Pallidum
output region of basal ganglia; globus pallidus (i and e) regulate limbs, SNr regulates eyes
SNc
domapinergic projections to striatum
subthalamic nucleus
projects to GP **only excitatory input to GPi (glutamic)
Types of input to basal nuclei
Cortical projections (excitatory, glutamic) and projections from SNc (dopaminergic, excitatory)
Direct Pathway
circuit goes directly from striatum to output region (GPi or SNr) promotes movement. key = inhibition of GPi allows activation of thalamus.
Direct pathway - limbs
excitatory dopamine (D1R) from SNc activates Striatum, which inhibits GPi, which disinhibits VA/VL of thalamus, activating frontal cortex and facilitating movement
Direct pathway - eyes
Striatum inhibits SNr, which inhibits Superior Colliculus
thalamus
gateway to cortical activation
Indirect pathway
Dop (D2R) from SnC inhibits striatum, which inhibits GPe, inhibits STN, activates GPi; inhibits thalamocortical neurons, inhibits movement. activation of GPi inhibits movement
Medium spiny neurons
Key neuron in striatum. Modulated by dopaminergic neurons from SNc; GABAergic and inhibits neurons in GP and SNr
GPi role
GPi is tonically active, suppressing VA/VL (gabaergic). When striatum activates, it inhibits GPi w/ GABA, so VA/VL can become active.
GABA
released by medium spiny neurons and output neurons of GPi
Dopamine
released by neurons in SNc, pro-movement. direct path - activates D1 receptors that increase camp; indirect path - activates D2 receptors that decrease camp. Dop is always excitatory
Huntington's
selective atrophy of medium spiny neurons in striatum; indirect path most effected early on (unwanted movement). personality change, movement disorder, progressive demensia. Autosomal Dom, trinucleotide repeat
Parkinson's
progressive loss of dopaminergic neurons in SNc leads to bradykinesia, low-freq resting tremor, sometimes cognitive decline.
hemiballism
unwanted flailing on one side of body due to lesion in STN. Removes excitation of GPi, which inhibits VA/VL. So VA/VL is less inhibited, leading to unwanted movement.
Cerebellum
error detection/correction system for movement. 50% of all neurons in CNS.
Cerebrocerebellum
lateral hemispheres that receive info from cerebral cortex and deal with complex skilled movement. Motor planning.
spinocerebellum
central hemispheres receives input from spinal cord, deal with movement of distal muscles. vermis deals w/ posture
vestibulocerebellum
Flocculus gets input from vestibular system; deals w/ eye movement
4 key cerebellar functions
motor planning, motor execution, gait and posture, eye movement
deep cerebellar nuclei
provide all output from cerebellum
cerebellar peduncles
tracts that contain all incoming and outgoing axons
input via Middle cerebellar peduncle
Info from contralateral cerebral hemisphere via pontine nuclei and middle cerebellar peduncle; crosses at midline. This is the largest source of input.
input via Inferior cerebellar peduncle
sensory from ipsilateral spinal cord, brainstem and vestibular nuclei. info from contralateral inferior olive.
Ascending output from Cerebellum
superior cerebellar peduncle to contralateral motor cortex via VA/VL of thalamus (motor planning). via dendate nucleus.
Descending output from Cerebellum
Cerebellar cortex >> deep cerebellar nuclei >> inferior peduncle >>( SC, Reticular formation) >> anterior white matter in SC >> LMN in ventral horn.
output to reticular formation
via inferior peduncle; postural responses
output to Superior Colliculus
via inferior peduncle. eye movement.
output to vestibular nuclei
via inferior cerebellar peduncle; balance; ** doesn't go through deep nuclei.
Intention tremor
Damage to cerebrocerebellum causes uncoordinated movements of the extremities.
ataxia
Damage to vermis causes gait ataxia with a characteristic wide-based, unsteady gait.
dysarthria
Patients may have obvious difficulty with cadence and smoothness of speech.
nystagmus
Damage to the vestibulo-cerebellum causes difficulty maintaining fixation, eyes drift form the target and then jump back with a corrective saccade.
spinocerebellar ataxias
most due to tri-nucleotide repeats; usually AD inheritance
Friedrich's ataxia
protein frataxin is abundant in mitochondria. degeneration of nerve tissue in SC that go to cerebellum, help direct arm/leg movement. unsteady gait, muscle weakness, speech difficulty, loss of coordination.
MS and cerebellum
inflow/outflow frequently damaged. intention tremor, gait ataxia, nystagmus are common.
alcohol and cerebellum - acute effects
DUI assesses cerebellar functions;
alcohol and cerebellum - chronic effects
marked atrophy of anterior lobule; gait disorder
Blood flow and cerebellum
blood flow (signalling activity) increases in cerebrocerebellum 1-2 seconds before movement and in vermis during movement.