Movement disorders

Abstract

Almost any neurological disorder can produce a disorder of movement but the ‘movement disorders’ include the akinetic rigid syndromes, hyperkinesias, and some tremors. It can sometimes seem, especially with the use of videotape recordings, that diagnosis of movement disorders is mainly a matter of correct visual recognition. Such an approach is not recommended and can lead to mistakes unless, as in other areas of medicine, the history is considered first and the physical signs second. Obvious examples include the family history in Huntington’s disease, developmental history in dystonic cerebral palsy, and neuroleptic drug treatment in patients with tardive dyskinesia. In addition, a single disorder may give rise to several different types of involuntary movement. For example, Huntington’s disease may give rise to an akinetic rigid state, chorea, myoclonus, tics, or dystonia. Patients with Parkinson’s disease taking levodopa may show different types of movement disorder at different times of the day.In akinetic rigid states the diagnostic issue will be whether the patient has idiopathic Parkinson’s disease or one of the other Parkinsonian syndromes. With involuntary movements, the first step in diagnosis is to classify these as dystonia, tics, tremor, chorea, or myoclonus. It must be remembered that involuntary movements are merely physical signs, not diagnostic entities, and that they do not always occur in a pure form; for example, patients with dystonia may have additional choreiform movements or tremor. If more than one form of abnormal movement seems to be present, the diagnosis should be based on the most obvious one. The next step is to decide on the cause of the movements and at this stage the diagnosis must be based upon an accurate and complete history as noted above.The movement disorders are often associated with abnormalities of the basal ganglia and, to some extent, vice versa. This is not entirely correct. Disturbances of basal ganglia function certainly have profound effects on movement with the development of bradykinesia, rigidity, tremor, or the various forms of dyskinesia. However, it is not correct when considering the pathophysiology of movement disorders to regard the basal ganglia as an isolated movement control centre. In fact, they are an important but poorly understood component of a much wider motor system. It is also important to remember that the basal ganglia are involved in the processing of limbic and other cognitive processes which may also be disturbed by basal ganglia dysfunction.