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Publisher Summary This chapter discusses information that is available on the clinical manifestations of myoclonus and the diseases that cause the syndrome. Myoclonus must be distinguished from other dyskinesias. The history of myoclonus is intertwined with that of epilepsy and most movement disorders, and it is necessary to review a great deal of the history of neurology to understand how the various terms arose. The term myoclonus was first used in a case report by Friedreich in 1881, when he described the syndrome of paramyoclonus multiplex. Despite considerable experimental and clinical neurophysiological study, understanding of the pathophysiology of the many varieties of myoclonus encountered in clinical practice is not complete.

Publisher Summary This chapter focuses on problems in dyskinesias. One of the more difficult decisions facing the physician looking after patients with dyskinesias is when to consider the various surgical approaches used to treat these conditions. Much has been written about the beneficial effects of haloperidol in the treatment of tics. Misdiagnosis of dystonia as other movement disorders commonly occurs because too much attention is paid to the accompanying features of the illness than to the underlying dystonia itself. In general, chair- or bed-bound children with dystonia do not gain useful benefit from antipsychotic drugs or tetrabenazine. Antipsychotic drugs such as phenothiazine, haloperidol, or pimozide are also sometimes used to treat dystonia. The treatment of dystonia is not an easy task. At least 50% of patients do not gain useful benefit from drug therapy, and even in those who do respond, it may be difficult to discover the most effective agent.

Publisher Summary This chapter discusses various surgical approaches to the dyskinesias. Although the editors rarely advise surgical treatment for their patients with Parkinson's disease today, an occasional patient is seen for whom the technique of stereotaxic thalamotomy seems ideal. Stereotaxic surgery has been used to treat torsion dystonia. The editors have less reluctance in advising a unilateral stereotaxic thalamotomy for hemiplegie dystonia or focal dystonia affecting the opposite arm or leg. The problem of spasmodic torticollis requires further consideration. Meige's syndrome, another focal dystonia, also deserves separate consideration. Brain stimulation as a treatment of abnormal involuntary movements remains entirely experimental and not suitable for routine recommendation to any patient at present.

Experimental studies on acute dystonic reactions in baboons and chronic neuroleptic administration to rats in relation to chronic tardive dyskinesias are described.

Publisher Summary This chapter discusses problems in Parkinson's disease. The management of Parkinson's disease today is a complex and demanding affair. Although peripherally acting dopa decarboxylase inhibitors have markedly reduced the incidence of anorexia, nausea, and vomiting provoked by levodopa, this still remains a major problem in a minority of patients. The sudden cessation of levodopa in a patient who has taken the drug for many years may cause a confusing akinetic coma-vigil state, which can easily be reversed by reintroducing levodopa, if necessary, by a nasogastric tube. Commonly, those developing mental changes already have early or obvious dementia. Most patients with Parkinson's disease or postencephalitic Parkinsonism show some response to levodopa.

Attention is drawn to the dose-dependent and biphasic locomotor effects of bromocriptine in animals, and to their dependence upon intact pre-synaptic action. Clinical observation does not suggest that very low or very high doses of bromocriptine frequently have adverse effects in Parkinson's disease. It is unlikely that the doses given to man are high enough to provoke deterioration. Further animal experiments suggest that bromocriptine-, but not apomorphineinduced circling behaviour is due to metabolism in liver and catecholamine neurones to active metabolites.

Unilateral 6-hydroxydopamine (60HDA) lesions of the nigrostriatal pathway resulted in contraversive rotation to apomorphine and ipsiversive rotation to amphetamine. Electrolytic lesioning of the nucleus reticularis gigantocellularis or kainic acid lesions of the nucleus tegmenti pedunculopontis on the same side as the 60HDA lesion did not reduce apomorphine- or amphetamine-induced circling. Unilateral or bilateral electrolytic lesions of the rostral and caudal medial superior colliculus or a unilateral lesion of the deep lateral superior colliculus did not reduce apomorphine- or amphetamine-induced rotation in 60HDA lesioned animals. An electrolesion of the angular complex (periaqueductal grey and adjacent reticular formation) on the same side as the 60KDA lesion reduced apomorphine-induced circling and increased amphetamine-induced circling. Bilateral electrolesions of the angular complex reduced both apormophine- and amphetamine-induced rotation. The decrease in rotation was due to a loss of postural asymmetry while locomotor hyperactivity was maintained. A unilateral kainic acid lesion of the angular complex alone caused weak ipsiversive rotation which was enhanced by apomorphine and amphetamine. When a unilateral kainic acid lesion of the angular complex was made on the same side as a prior 60HDA lesion, both apomorphine and amphetamine induced ipsiversive rotation. Unilateral injection of muscimol into the angular complex caused ipsiversive rotation which reversed the contraversive rotation elicited either by unilateral injection of muscimol into substantia nigra or by apomorphine administration to rats with a prior 60HDA lesion, on the same side. The area of the angular complex is critically involved in the mediation of drug-induced circling in unilaterally 60HDA lesioned rats and in particular the postural component.