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