| Literature DB >> 20817092 |
Abstract
The pathophysiology of dystonia has been best studied in patients with focal hand dystonia. A loss of inhibitory function has been demonstrated at spinal, brainstem and cortical levels. Many cortical circuits seem to be involved. One consequence of the loss of inhibition is a failure of surround inhibition, and this appears to directly lead to overflow and unwanted muscle spasms. There are mild sensory abnormalities and deficits in sensorimotor integration; these also might be explained by a loss of inhibition. Increasing inhibition may be therapeutic. A possible hypothesis is that there is a genetic loss of inhibitory interneurons in dystonia and that this deficit is a substrate on which other factors can act to produce dystonia. This article is part of a Special Issue entitled "Advances in dystonia". Published by Elsevier Inc.Entities:
Mesh:
Year: 2010 PMID: 20817092 PMCID: PMC3016461 DOI: 10.1016/j.nbd.2010.08.025
Source DB: PubMed Journal: Neurobiol Dis ISSN: 0969-9961 Impact factor: 5.996