Movement, disordering

Guttman M, Leger G, Reches A, et al (1993) Administration of the new COMT inhibitor OR-611 increases striatal uptake of fluorodopa. Movement Disord 8 298-304... 

VMATs are irreversibly inhibited by the potent antihypertensive drug reserpine. The depressive effects of reserpine helped to formulate the original monoamine hypothesis of affective disorders. Reseipine also appears to interact with the transporters near the site of substrate recognition. Tetrabenazine, which is used in treatment of movement disorders, inhibits VMAT2 much more potently than VMAT1, consistent with the less hypotensive action of this agent. 

King GR, Ellinwood EH Amphetamines and other stimulants, in Substance Abuse A Comprehensive Textbook, 3rd Edition. Edited by Lowinson JH, Ruiz P, Mill-man RB, et al. Baltimore, MD, Williams Wilkins, 1997, pp 207—233 Klawans HE, Margolin Dl Amphetamine-induced dopaminergic hypersensitivity in guinea pigs implications in psychosis and human movement disorders. Arch Gen Psychiatry 32 725—732, 1975... 

Chesselet, M-F and Delfs, JM (1996) Basal ganglia and movement disorders. Trends Neurosci. 19 417-422. 

Hemiballismus A rare movement disorder that can be life-threatening. Patients with hemiballismus have a dismal prognosis, with physical exhaustion, injuries, and medical complications often leading to... 

Gray, G. E. Pi, E. H. (1998). Ethnicity and medication-induced movement disorders. /. Pract. 

Jellinger KA. Movement disorders with tau protein cytoskeletal pathology. Parkinson s disease. In Stern GM, ed. Advances in Neurology. Vol. 80. Philadelphia Lippincott, Williams Wilkins, 1999 393-311. 

Goetz, Christopher G., Joanne Wuu, Michael P. McDermott, Charles H. Adler, Stanley Fahn, Curt R. Freed, Robert A. Hauser, Warren C. Olanow, Ira Shoulson, P. K. Tandon, Parkinson Study Group and Sue Leurgans, Placebo Response in Parkinson s Disease Comparisons among 11 Trials Covering Medical and Surgical Interventions , Movement Disorders 5 (2008) 690-99... 

Alexander G. (1997). Anatomy of the basal ganglia and related motor structures. In Watts R., Roller W., editors. Movement Disorders Neurologic Principles and Practice. New York, NY McGraw-Hill. pp. 73-86. 

DeLong M. R. (1990). Primate models of movement disorders of basal ganglia origin. Trends Neurosci. 13, 281-5. 

Rye D., Daley J., Freeman A., Bliwise D. (2003). Daytime sleepiness and sleep attacks in idiopathic parkinson s disease. In Bedard M-A., Agid Y., Chouinard S. et al. editors. Mental and Behavioral Dysfunction in Movement Disorders. Totawa, NJ Humana Press pp. 527-38. 

Rye D. (2003). Modulation of normal and pathologic motoneuron activity during sleep. In Chokroverty S., Hening W., Walters A., editors. Sleep and Movement Disorders. Philadelphia, PA Butterworth-Heinemann pp. 94-119. 

Gabapentin Movement disorders, behavioral aberrations in children... 

Kato, S. etal. Amyotrophic lateral sclerosis, in D. Dickson (ed.), Neurodegeneration - The Molecular Pathology of Dementia and Movement Disorders. Basel ISN Neuropathology Press, 2003, pp. 350-368. 

Goldstein, L. S. Do disorders of movement cause movement disorders and dementia Neuron 40 415-425, 2003. 

Giasson, B.I. et al. Neuronal a-synucleinopathy with severe movement disorder in mice expressing A53T human a-synuclein. Neuron 34 521-533, 2002. 

Parkinson s disease (PD) is a hypokinetic movement disorder 766 Huntington s disease is a hyperkinetic movement disorder 771 Wilson s disease is a disease of copper accumulation 773 Dystonia is characterized by sustained muscle contractions 775 Many drugs and toxins induce movement disorders 776... 

The basal ganglia are a group of subcortical nuclei which are components of modular circuits involved in many cortical functions. They have received considerable attention from basic scientists and clinicians alike because of their prominent involvement in movement disorders, a spectrum of diseases including disorders which are characterized by poverty of movement (hypokinetic disorders), as well as disorders characterized by excess movement (hyperkinetic disorders). It has become clear in recent years that most basal ganglia disorders are not restricted to motor disturbances, but involve cognitive and emotional features as well. 

Due to its relevance to an understanding of movement disorders, the motor circuit has received the most attention. This circuit is centered on somatosensory, motor and premotor cortices, which send projections to the motor portions of striatum. The connections between the striatum and the basal ganglia output nuclei (GPi/SNr) are organized into direct and indirect pathways [1]. The direct pathway is a monosynaptic projection between striatum and GPi/ SNr, while the indirect pathway is a polysynaptic connection that involves intercalated neurons in GPe and STN. Some striatofugal neurons may also collateralize more extensively, reaching GPe, GPi/SNr and STN. Other motor -related inputs to striatum and STN arise from the intralaminar thalamic nuclei, i.e. the centromedian and parafascicular nuclei (CM/Pf). 

The motor circuit of the basal ganglia has received the greatest attention from researchers, because of its perceived involvement in movement disorders. Due to the modular organization of the basal ganglia, many of the findings discussed below for the motor circuit may be applicable to the other circuits as well. 

Wilson s disease is an autosomal recessive disorder characterized by the accumulation of copper in liver and brain [21]. Hepatic involvement may result in liver cirrhosis and hepatic cancer. The deposition of copper in the basal ganglia results in a variety of movement disorders, including... 

Many drugs and toxins induce movement disorders. 

Almasy, L., Bressman, S., de Leon, D. and Risch, N. Ethnic variation in the clinical expression of idiopathic torsion dystonia. Movement Disorders 12 715-721,1997. 

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