Non-Drug-Induced Movement Disorders
Huntington’s Disease
Huntington’s disease is a genetically transmitted degenerative disease of the CNS.In addition to choreiform movements and a variety of disturbances of the neuromuscular system, patients with Huntington’s disease may have psychiatric complaints including irritability, obstinance , moodiness, and lack of initiative. These patients may at times be destructive or assaultive and may have great difficulties in interpersonal relationships. As the condition progresses these patients often become severely depressed. Dopamine levels in the corpus striatum are normal in patients with Huntington’s whereas they are low in patients with Parkinson’s disease. Levodopa exacerbates, while dopamine antagonists alleviate, the choreic movements of Huntington’s disease. In the caudate nucleus of the brain in a choreic patient there is a decrease in synthesizing enzymes for GABA as well as acetylcholine-synthesizing enzymes. Likewise, there is a decrease in muscarinic cholinergic as well as serotonin receptor binding in the caudate nucleus. Sodium valproate, which increases brain GABA levels, has not been effective in controlling involuntary movements in patients with Huntington’s disease. The potent cholinergic agonist, arecoline, has also failed to improve chorea, and has produced an exacerbation in patients with Huntington’s disease. With increasing availability of substances that affect neurotransmitter function in the brain, it is hoped that more effective therapeutic agents will be found for controlling the abnormal movements of Huntington’s disease. At this point however, neuroleptics such as haloperidol do have some beneficial effect and may likewise be of value in managing psychotic symptoms in these patients. Because of the previously noted disturbance in acetylcholine synthesis, it seems prudent to treat depressed patients with this condition with those antidepressants having lower anticholinergic potential.