| pubmed-article:18467168 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18467168 | lifeskim:mentions | umls-concept:C0242422 | lld:lifeskim |
| pubmed-article:18467168 | lifeskim:mentions | umls-concept:C0277785 | lld:lifeskim |
| pubmed-article:18467168 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:18467168 | pubmed:dateCreated | 2008-6-16 | lld:pubmed |
| pubmed-article:18467168 | pubmed:abstractText | The motor signs of Parkinson's disease are thought to result in large part from a reduction of the level of dopamine in the basal ganglia. Over the last few years, many of the functional and anatomical consequences of dopamine loss in these structures have been identified, both in the basal ganglia and in related areas in thalamus and cortex. This knowledge has contributed significantly to our understanding of the link between the degeneration of dopamine neurons in the midbrain and the development of parkinsonism. This review discusses the evidence that implicates electrophysiologic changes (including altered discharge rates, increased incidence of burst firing, interneuronal synchrony, oscillatory activity, and altered sensorimotor processing) in basal ganglia, thalamus, and cortex, in parkinsonism. From these studies, parkinsonism emerges as a complex network disorder, in which abnormal activity in groups of neurons in the basal ganglia strongly affects the excitability, oscillatory activity, synchrony and sensory responses of areas of the cerebral cortex that are involved in the planning and execution of movement, as well as in executive, limbic or sensory functions. Detailed knowledge of these changes will help us to develop more effective and specific symptomatic treatments for patients with Parkinson's disease. | lld:pubmed |
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