Brain Advance Access originally published online on November 7, 2003
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Brain, Vol. 127, No. 1, 4-20, 2004
© 2004 Guarantors of Brain
doi: 10.1093/brain/awh029
Review Article |
The subthalamic nucleus in the context of movement disorders
1 Division of Neurosurgery, Toronto Western Hospital, Toronto Western Research Institute, Ontario, Canada and 2 Department of Neurological Surgery, Weill Medical College of Cornell University and Division of Neurosurgery, Memorial-Sloan Kettering Cancer Center, New York, NY, USA
Correspondence to: Andres M. Lozano Division of Neurosurgery, Toronto Western Hospital, West Wing 4-447, 399 Bathurst Street, Toronto, Canada ON M5T 2S8E-mail: lozano{at}uhnres.utoronto.ca or c.hamani{at}sympatico.ca
The subthalamic nucleus (STN) has been regarded as an important modulator of basal ganglia output. It receives its major afferents from the cerebral cortex, thalamus, globus pallidus externus and brainstem, and projects mainly to both segments of the globus pallidus, substantia nigra, striatum and brainstem. The STN is essentially composed of projection glutamatergic neurons. Lesions of the STN induce choreiform abnormal movements and ballism on the contralateral side of the body. In animal models of Parkinsons disease this nucleus may be dysfunctional and neurons may fire in oscillatory patterns that can be closely related to tremor. Both STN lesions and high frequency stimulation ameliorate the major motor symptoms of parkinsonism in humans and animal models of Parkinsons disease and reverse certain electrophysiological and metabolic consequences of dopamine depletion. These new findings have led to a renewed interest in the STN. The aim of the present article is to review briefly the major anatomical, pharmacological and physiological aspects of the STN, as well as its involvement in the pathophysiology and treatment of Parkinsons disease.
Key Words: subthalamic nucleus; Parkinsons disease; basal ganglia; deep brain stimulation; movement disorders
Abbreviations: AMPA = 2-aminomethyl-phenylacetic acid; BG = basal ganglia; CM = centromedian; EPSP = excitatory post-synaptic potential; GPe = globus pallidus externus; GPi = globus pallidus internus; HFS = high frequency stimulation; IPSP = inhibitory post-synaptic potential; mGluR = multiple glutamate receptors; MPTP = 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine; NMDA = N-methyl-D-aspartate; Pf = parafascicular; PPN = pedunculopontine nucleus; SNc = substantia nigra compacta; SNr = substantia nigra reticulata; STN = subthalamic nucleus
Received June 18, 2003. Revised September 3, 2003. Accepted September 8, 2003.
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