The basal ganglia and disorders of movement: pathophysiological mechanisms.

The basal ganglia are part of a neuronal network organized in parallel circuits. The "motor circuit" is most relevant to the pathophysiology of movement. Abnormal increment or reduction in the inhibitory output activity of basal ganglia give rise, respectively, to poverty and slowness of movement (i.e., Parkinson's disease) or dyskinesias.

[1]  L. Tremblay,et al.  Effects of dopamine agonists on the spontaneous activity of globus pallidus neurons in monkeys with MPTP-induced parkinsonism , 1991, Brain Research.

[2]  J. Penney,et al.  The functional anatomy of basal ganglia disorders , 1989, Trends in Neurosciences.

[3]  G. E. Alexander,et al.  Parallel organization of functionally segregated circuits linking basal ganglia and cortex. , 1986, Annual review of neuroscience.

[4]  J A Obeso,et al.  Basal ganglia pathophysiology. A critical review. , 1997, Advances in neurology.

[5]  A. Rosell,et al.  Considerations upon the anatomical model of reward-based learning in the basal ganglia. , 2000, Medical hypotheses.

[6]  K. Doya,et al.  Parallel neural networks for learning sequential procedures , 1999, Trends in Neurosciences.

[7]  E. Oldfield,et al.  Convection-enhanced selective excitotoxic ablation of the neurons of the globus pallidus internus for treatment of parkinsonism in nonhuman primates. , 1999, Journal of neurosurgery.

[8]  J. Lanciego,et al.  Considerations on the thalamostriatal system with some functional implications. , 2000, Histology and histopathology.

[9]  J. Obeso,et al.  Pathophysiology of the basal ganglia in Parkinson's disease , 2000, Trends in Neurosciences.

[10]  M R DeLong,et al.  The primate subthalamic nucleus. III. Changes in motor behavior and neuronal activity in the internal pallidum induced by subthalamic inactivation in the MPTP model of parkinsonism. , 1994, Journal of neurophysiology.

[11]  A. Graybiel,et al.  Role of [corrected] nigrostriatal dopamine system in learning to perform sequential motor tasks in a predictive manner. , 1999, Journal of neurophysiology.

[12]  E. Hirsch,et al.  Subthalamotomy in parkinsonian monkeys. Behavioural and biochemical analysis. , 1996, Brain : a journal of neurology.

[13]  A. Crossman,et al.  Primate models of dyskinesia: The experimental approach to the study of basal ganglia-related involuntary movement disorders , 1987, Neuroscience.

[14]  D. Inzitari.  Age‐related white matter changes and cognitive impairment , 2000, Annals of neurology.

[15]  J. Dostrovsky,et al.  Neuronal recordings in Parkinson's disease patients with dyskinesias induced by apomorphine. , 2000, Annals of neurology.

[16]  C. Gerfen.  The neostriatal mosaic: multiple levels of compartmental organization , 1992, Trends in Neurosciences.

[17]  A. Crossman,et al.  A hypothesis on the pathophysiological mechanisms that underlie levodopa‐ or dopamine agonist‐induced dyskinesia in Parkinson's disease: Implications for future strategies in treatment , 1990, Movement disorders : official journal of the Movement Disorder Society.

[18]  A Jackson,et al.  Chorea and myoclonus in the monkey induced by gamma-aminobutyric acid antagonism in the lentiform complex. The site of drug action and a hypothesis for the neural mechanisms of chorea. , 1988, Brain : a journal of neurology.

[19]  J A Obeso,et al.  Pathophysiology of levodopa-induced dyskinesias in Parkinson's disease: problems with the current model. , 2000, Annals of neurology.