Cervical Dystonia

Pathophysiology

No consistent or specific changes in brain tissue or function have been seen in individuals with cervical dystonia. The basic underlying defect or defects in this disorder remain unknown. However, investigators suggest that the primary dystonia, as well as dystonia-plus syndromes, probably result from abnormalities in the activity of certain neurotransmitters, such as an imbalance of dopamine transmission, within the basal ganglia. Neurotransmitters are naturally produced chemicals that transfer nerve impulses across synaptic gaps, thus enabling nerve cells to communicate. The basal ganglia consist of specialized nerve cell clusters deep within the brain that organize motor behavior.

Thus, in some patients, a primary focal dystonia such as CD may be considered neurochemical in origin—i.e., neurochemical disorders that do not appear to result in structural neurodegenerative changes. In contrast, heredodegenerative disorders are usually hereditary disorders in which structural neuronal degeneration may be associated with neurochemical abnormalities. An underlying neurochemical basis for many dystonias may be suggested by multiple factors, including evidence that secondary dystonia may result from treatment with the dopamine precursor L-dopa (such as used for treatment of Parkinson's disease) or therapy with dopamine receptor blockers (antagonists).