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Physiology of Basal Ganglia Disorders: an Overview

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Physiology of Basal Ganglia Disorders: an Overview LE JOURNAL CANADIEN DES SCIENCES NEUROLOGIQUES SILVERSIDES LECTURE Physiology of Basal Ganglia Disorders: An Overview Mark Hallett ABSTRACT: The pathophysiology of the movement disorders arising from basal ganglia disorders has been uncer­ tain, in part because of a lack of a good theory of how the basal ganglia contribute to normal voluntary movement. An hypothesis for basal ganglia function is proposed here based on recent advances in anatomy and physiology. Briefly, the model proposes that the purpose of the basal ganglia circuits is to select and inhibit specific motor synergies to carry out a desired action. The direct pathway is to select and the indirect pathway is to inhibit these synergies. The clinical and physiological features of Parkinson's disease, L-DOPA dyskinesias, Huntington's disease, dystonia and tic are reviewed. An explanation of these features is put forward based upon the model. RESUME: La physiologie des affections du noyau lenticulaire, du noyau caude, de I'avant-mur et du noyau amygdalien. La pathophysiologie des desordres du mouvement resultant d'affections du noyau lenticulaire, du noyau caude, de l'avant-mur et du noyau amygdalien est demeuree incertaine, en partie parce qu'il n'existe pas de bonne theorie expliquant le role de ces structures anatomiques dans le controle du mouvement volontaire normal. Nous proposons ici une hypothese sur leur fonction basee sur des progres recents en anatomie et en physiologie. En resume, le modele pro­ pose que leurs circuits ont pour fonction de selectionner et d'inhiber des synergies motrices specifiques pour ex£cuter Taction desiree. La voie directe est de selectionner et la voie indirecte est d'inhiber ces synergies. Nous revoyons les mani­ festations cliniques et physiologiques de la maladie de Parkinson, des dyskinesies dues a la L-DOPA, de la maladie de Huntington, de la dystonie et des tics. Nous proposons une explication de ces manifestations basee sur le modele expos6. Can. J. Neurol. Sci. 1993; 20:177-183 Movement disorder is becoming more popular these days as voluntary movement or is a conscious perception produced by a subspeciality interest in Neurology. The clinical problems are the brain during the normal course of movement production. In common, often visually dramatic, and a number of good therapies the latter view, a movement that is "voluntarily" produced is the are available. On the other hand, much remains unknown, and product of various forces, both intrinsic and extrinsic, acting on there are fertile fields for research in anatomy, physiology and the motor system. pharmacology. Many movement disorders have their origin in I will first review some pertinent features of the principal basal ganglia dysfunction, which focuses interest on this primi­ movement disorders. Then I will review what is known about tive structure, deep within the brain. Understanding the genesis the anatomy and physiology of the basal ganglia. Lastly, I will of these movement disorders requires understanding of the role propose a scheme to explain how the movement disorders are of the basal ganglia in movement, but this has been produced. "mysterious."1 The basal ganglia disorders have been divided into the hyperkinetic movement disorders and the akinetic-rigid Parkinson's Disease syndromes. The first, including chorea, dyskinesias and dystonia, Parkinson's disease is the prototypical akinetic-rigid syndrome, are characterized by the prominent feature of involuntary, unde- characterized by slowness of movement and increased tone. The sired movements. The second, including Parkinson's disease, slowness of movement can be divided into failure to move or are characterized by the prominent feature of difficulty in gener­ slowness to initiate movement, which might be called akinesia, ating voluntary movement. Voluntary and involuntary move­ and slowness of movement itself, which might be called bradykinesia. ments may share similar pathways, and the major difference In the experimental setting, akinesia is measured by reaction between the two may just be the presence of volition. Volition, at time and bradykinesia is measured by movement time. Patients the present time, is a philosophical rather than a neurophysio- are also characterized by loss of associated movements. logical concept and is not understood. In particular, it has not Increased tone in Parkinson's disease is called rigidity. Its physiol­ been settled whether volition is a process that actually initiates ogy has been studied extensively, and one highly characteristic From the Human Motor Control Section, Medical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, Maryland Received January 18, 1992. Accepted March 31, 1993 Based on the 12th J.L. Silversides Lecture, University of Toronto, May 21, 1992 Reprint requests to: Mark Hallett, M.D., Clinical Director, NINDS, National Institutes of Health, Building 10, Room 5N226, Bethesda, Maryland 20892, USA 177 Downloaded from https://www.cambridge.org/core. IP address: 170.106.40.139, on 28 Sep 2021 at 10:50:50, subject to the Cambridge Core terms of use, available at https://www.cambridge.org/core/terms. https://doi.org/10.1017/S0317167100047909 THE CANADIAN JOURNAL OF NEUROLOGICAL SCIENCES feature is enhancement of long-latency reflexes, such as the grip" and fluctuation in tongue protrusion is called "darting long-latency stretch reflex. The experimental way to assess for tongue". an increased response to stretch is to give controlled stretches to Another abnormality in chorea is that tendon reflexes can be a muscle and measure the response in terms of force or EMG. "hung-up". This has the appearance of a prolonged contraction Although there is some controversy about it, several studies of the muscle whose tendon is stretched. Both in Sydenham's show that the magnitude of the increase correlates with the chorea and in Huntington's disease, this abnormality has been clinical impression of increased tone.2 Other studies of reflexes demonstrated to be due to a late sensory-provoked choreic in Parkinson's disease have shown a reduction in inhibition of movement.7 On the other hand, there is a dramatic loss of standard interneuronal circuits; for example, there is enhanced recovery long-latency reflexes in Huntington's disease, including the in the blink reflex recovery cycle. long-latency stretch reflex. Another reflex abnormality is that Patients with Parkinson's disease may also have prominent blink reflex recovery is delayed, suggesting enhanced inhibition tremors. The most classic is a tremor-at-rest. The presence and in interneuronal circuits. degree of severity of tremor seem to be independent of the Symptomatic treatment is with dopamine-blocking agents, movement slowness, which clearly is the most significant func­ such as haloperidol, or dopamine-depleting agents, such as tional problem for these patients. reserpine. Later in the course of Huntington's disease, brady- Studies with positron emission tomography show a reduced kinesia and akinesia develop. Thompson et al.8 have highlighted activation of the supplementary motor area (SMA) with voluntary the apparent paradox of the coexistence of chorea and bradykinesia. movement and normalization of the activation with apomor- phine, a dopaminergic agent that improves the patients clinically.3-4 Hemiballismus Additionally, Rossini et al.5 showed that the N30 of the median Hemiballismus is characterized by wild, large-amplitude, nerve somatosensory evoked potential (SEP) was diminished in irregular limb movements. The responsible lesion is typically in Parkinson's disease. Other peaks of the SEP were normal, and the contralateral subthalamic nucleus, although lesions of the the N30 had normal latency and topography, but its amplitude putamen can be responsible.9 Hemiballismus in animal models was diminished. The origin of the N30 (as most of the waves of can be produced with subthalamic lesions. The most common the SEP) is debated, but its topography is anterior and medial to clinical circumstance in which hemiballismus can be observed is the N20 that is thought to arise from the hand area of the a stroke where the involuntary movements begin suddenly but somatosensory cortex. While far from proven, the N30 could only remain violent for a few days before fading into what looks come at least in part from the SMA, which should anatomically like typical chorea. Hemiballismus is clearly related to chorea, lie beneath the topographic peak of the wave. The N30 abnor­ and, like chorea, can be improved with dopamine antagonists. mality may also be reversible with apomorphine.6 Dystonia L-DOPA Dyskinesias Dystonia is a disorder characterized by involuntary move­ Patients who receive too much L-DOPA treatment may ments of sustained muscle contractions, causing prolonged develop involuntary movements. The movements may affect all movements or abnormal postures. Movements are often twisting parts of the body, and their appearance is similar to chorea. The in nature, meaning rotatory about the long axis of a body part. process is assumed to be an excessive reversal of the dopamine Some patients may also have quick movements, myoclonic dys­ deficiency of Parkinson's disease with excessive facilitation of tonia, or tremor, but ordinarily there will have to be some sus­ movement. One curiosity, which has never been satisfactorily tained movements for the dystonia to be recognized. Dystonia explained, is that in late Parkinson's disease treated patients
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