Parkinson's disease pathophysiology: Difference between revisions
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==Pathophysiology== | ==Pathophysiology== | ||
The underlying [[pathophysiology]] of [[Parkinson's disease|Parkinson disease]] is [[dopamine]] depletion.The [[substantia nigra]] ([[Substantia nigra|SN]]), [[striatum]] ([[Caudate nucleus|caudate]] and [[putamen]]), [[globus pallidus]] ([[Globus pallidus|GP]]), [[subthalamic nucleus]] ([[Subthalamic nucleus|STN]]) and [[thalamus]] contribute with each other to make the [[extrapyramidal system]] or [[basal ganglia]]. The impulses from hippocampus, amygdala and prefrontal supplementary motor area to the basal ganglia are excitatory mediated by glutamate. The major dopaminergic neurons are in substantia nigra and are responsible for dopaminergic input of striatum. The striatal output is inhibitpry (GABA) despite the excitatory output of STN to the globus pallidus (medial and lateral). | |||
Revision as of 12:58, 30 March 2018
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Parkinson's disease Microchapters |
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Parkinson's disease pathophysiology On the Web |
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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Overview
Pathophysiology
The underlying pathophysiology of Parkinson disease is dopamine depletion.The substantia nigra (SN), striatum (caudate and putamen), globus pallidus (GP), subthalamic nucleus (STN) and thalamus contribute with each other to make the extrapyramidal system or basal ganglia. The impulses from hippocampus, amygdala and prefrontal supplementary motor area to the basal ganglia are excitatory mediated by glutamate. The major dopaminergic neurons are in substantia nigra and are responsible for dopaminergic input of striatum. The striatal output is inhibitpry (GABA) despite the excitatory output of STN to the globus pallidus (medial and lateral).