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28 Cards in this Set
- Front
- Back
What is the overall purpose of the DIRECT PATHWAY of the basal ganglia?
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To EXCITE the motor cortex and promote mvt
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What is the direct pathway of the basal ganglia? (specify NTs)
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Cortex (Glu) -> Striatum (GABA/SP) -| GPi/SNr (GABA) -| VA/VL (Glu) -> cortical motor areas
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What is the overall purpose of the indirect pathway of the basal ganglia?
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To decrease cortical excitation and inhibit mvt
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What is the indirect pathway of the basal ganglia? (specify NTs)
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Cortex (Glu) -> Striatum (GABA/Enk) -| GPe (GABA) -| STN (Glu) -> GPi/SNr (GABA) -| VA/VL (Glu) -> cortical motor areas
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What is the overall purpose of the dopaminergic pathway?
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To promote excitation of cortex and mvt
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How does the dopaminergic pathway affect the direct pathway? (receptor?)
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SNc (DA) -> striatum (D1 receptor)
*excites the excitation* |
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How does the dopaminergic pathway affect the indirect pathway? (receptor?)
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SNc (DA) -| striatum (D2 receptor)
*inhibits the inhibition* |
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What neurostructural deficit is present in PARKINSON DISEASE?
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loss of pigmented dopaminergic neurons from SNc, and depletion of DA
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Histological markers of Parkinson disease?
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Lewy bodies (intracytoplasmic eosinophilic inclusions, contain alpha-synuclein)
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Symptoms of Parkinson disease?
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Bradykinesia, cogwheel rigidity, pill-rolling (resting) tremor, shuffling gait, stooped posture, masked facies, depression, dementia
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Known causes of parkinsonism?
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infections, vascular, and toxic insults (e.g. in MPTP-induced parkinsonism; an analogue of meperidine (Demerol)
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Treatment for Parkinson disease?
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L-DOPA, surgical intervention includes pallidotomy (rigidity) and ventral thalomotomy (tremor)
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What neurostructural deficit is present in HUNTINGTON DISEASE?
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Degeneration of GABAergic neurons in neostriatum, causing atrophy of striatum and frontal/temporal lobes
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Cause of Huntington disease?
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autosomal dominant, unstable nucleotide repeat on chromosome 4
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What is glutamate excitotoxicity (assoc w/Huntington disease)?
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In Huntington's, Glu in striatum is not removed from cytoplasm and binds to NMDA receptor, causing Ca influx and cell death
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Symptoms of Huntington disease?
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CHOREA (multiple, rapid, random mvts), ATHETOSIS (slow writhing mvts), hypotonia, personality changes, dementia, progresses to akinetic and mute
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Onset of Huntington's disease?
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20-40 years
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Treatment for Huntington disease?
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antipsychotics, benzos, anticonvulsants
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Why is Huntington's a hyperkinetic disorder?
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degeneration of striatal GABAergic neurons first occurs in the INDIRECT PATHWAY (which is normally inhibitory)
(as the disease progresses, direct pathway degenerates as well -> pt becomes mute and akinetic |
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What disorder results from a lesion of the subthalamic nucleus?
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Hemiballism
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What is the main pharmacologic goal of Parkinson's treatment?
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Increase DA and/or decrease ACh activity in the striatum (to correct DA/ACh imbalance)
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What is the mechanism of L-dopa as a treatment for Parkinson's disease?
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L-dopa crosses BBB and is taken up by remaining dopaminergic terminals and converted to DA
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What are the downsides and side-effect of L-dopa treatment?
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loses effectiveness due to fewer and fewer DA terminals
side effects: PSYCHOSIS, on/off phenomenon, dyskinesias, postural hypotension, nausea/vomiting |
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What is a surgical treatment for Parkinson's?
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Pallidotomy (ablation of GPi) -> relieves inhibitory drive on thalamus and permits mvt
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When would you prescribe an anticholinergic such as Cogentin?
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In parkinson's patients, or in schizophrenic pts taking antipsychotics w/D2 receptor blocking activity
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What pathway connects GPe to the subthalamic nucleus?
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subthalamic fasiculus (part of indirect pathway)
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What does the ansa lenticularis connect?
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GPi to thalamus - goes around internal capsule
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What does the lenticular fasiculus connect?
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GPi to thalamus - penetrates internal capsule
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