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28 Cards in this Set

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  • Back
What is the overall purpose of the DIRECT PATHWAY of the basal ganglia?
To EXCITE the motor cortex and promote mvt
What is the direct pathway of the basal ganglia? (specify NTs)
Cortex (Glu) -> Striatum (GABA/SP) -| GPi/SNr (GABA) -| VA/VL (Glu) -> cortical motor areas
What is the overall purpose of the indirect pathway of the basal ganglia?
To decrease cortical excitation and inhibit mvt
What is the indirect pathway of the basal ganglia? (specify NTs)
Cortex (Glu) -> Striatum (GABA/Enk) -| GPe (GABA) -| STN (Glu) -> GPi/SNr (GABA) -| VA/VL (Glu) -> cortical motor areas
What is the overall purpose of the dopaminergic pathway?
To promote excitation of cortex and mvt
How does the dopaminergic pathway affect the direct pathway? (receptor?)
SNc (DA) -> striatum (D1 receptor)

*excites the excitation*
How does the dopaminergic pathway affect the indirect pathway? (receptor?)
SNc (DA) -| striatum (D2 receptor)

*inhibits the inhibition*
What neurostructural deficit is present in PARKINSON DISEASE?
loss of pigmented dopaminergic neurons from SNc, and depletion of DA
Histological markers of Parkinson disease?
Lewy bodies (intracytoplasmic eosinophilic inclusions, contain alpha-synuclein)
Symptoms of Parkinson disease?
Bradykinesia, cogwheel rigidity, pill-rolling (resting) tremor, shuffling gait, stooped posture, masked facies, depression, dementia
Known causes of parkinsonism?
infections, vascular, and toxic insults (e.g. in MPTP-induced parkinsonism; an analogue of meperidine (Demerol)
Treatment for Parkinson disease?
L-DOPA, surgical intervention includes pallidotomy (rigidity) and ventral thalomotomy (tremor)
What neurostructural deficit is present in HUNTINGTON DISEASE?
Degeneration of GABAergic neurons in neostriatum, causing atrophy of striatum and frontal/temporal lobes
Cause of Huntington disease?
autosomal dominant, unstable nucleotide repeat on chromosome 4
What is glutamate excitotoxicity (assoc w/Huntington disease)?
In Huntington's, Glu in striatum is not removed from cytoplasm and binds to NMDA receptor, causing Ca influx and cell death
Symptoms of Huntington disease?
CHOREA (multiple, rapid, random mvts), ATHETOSIS (slow writhing mvts), hypotonia, personality changes, dementia, progresses to akinetic and mute
Onset of Huntington's disease?
20-40 years
Treatment for Huntington disease?
antipsychotics, benzos, anticonvulsants
Why is Huntington's a hyperkinetic disorder?
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
What disorder results from a lesion of the subthalamic nucleus?
What is the main pharmacologic goal of Parkinson's treatment?
Increase DA and/or decrease ACh activity in the striatum (to correct DA/ACh imbalance)
What is the mechanism of L-dopa as a treatment for Parkinson's disease?
L-dopa crosses BBB and is taken up by remaining dopaminergic terminals and converted to DA
What are the downsides and side-effect of L-dopa treatment?
loses effectiveness due to fewer and fewer DA terminals

side effects: PSYCHOSIS, on/off phenomenon, dyskinesias, postural hypotension, nausea/vomiting
What is a surgical treatment for Parkinson's?
Pallidotomy (ablation of GPi) -> relieves inhibitory drive on thalamus and permits mvt
When would you prescribe an anticholinergic such as Cogentin?
In parkinson's patients, or in schizophrenic pts taking antipsychotics w/D2 receptor blocking activity
What pathway connects GPe to the subthalamic nucleus?
subthalamic fasiculus (part of indirect pathway)
What does the ansa lenticularis connect?
GPi to thalamus - goes around internal capsule
What does the lenticular fasiculus connect?
GPi to thalamus - penetrates internal capsule