Glossary of Neuro - Basal Ganglia
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- 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
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