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Neuronal globus pallidus activity in patients with generalised dystonia

Authors

  • Marcelo Merello MD, PhD,

    Corresponding author
    1. Movement Disorders Section, Raul Carrea Institute for Neurological Research, FLENI, Buenos Aires, Argentina
    2. Neurology Department, Raul Carrea Institute for Neurological Research, FLENI, Buenos Aires, Argentina
    • Movement Disorders Department, FLENI, Montañeses 2325, C1428AQK Buenos Aires, Argentina
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  • Daniel Cerquetti PhD,

    1. Movement Disorders Section, Raul Carrea Institute for Neurological Research, FLENI, Buenos Aires, Argentina
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  • Angel Cammarota MD,

    1. Movement Disorders Section, Raul Carrea Institute for Neurological Research, FLENI, Buenos Aires, Argentina
    2. Neurology Department, Raul Carrea Institute for Neurological Research, FLENI, Buenos Aires, Argentina
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  • Eduardo Tenca MD,

    1. Functional Neurosurgery Department, Raul Carrea Institute for Neurological Research, FLENI, Buenos Aires, Argentina
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  • Carlos Artes PhD,

    1. Functional Neurosurgery Department, Raul Carrea Institute for Neurological Research, FLENI, Buenos Aires, Argentina
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  • Julio Antico MD,

    1. Functional Neurosurgery Department, Raul Carrea Institute for Neurological Research, FLENI, Buenos Aires, Argentina
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  • Ramon Leiguarda MD

    1. Neurology Department, Raul Carrea Institute for Neurological Research, FLENI, Buenos Aires, Argentina
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Abstract

We studied 516 globus pallidus neurons in dystonic patients. The firing rate was analysed. We classified the burst activity into tonic, burst, and pause patterns. Mean ± SD firing rates and tonicity score for internal globus pallidus (GPi) and external globus pallidus (GPe) were 54.6 ± 28.6; 58.01 ± 39.1 and 1.18 ± 0.55; 0.95 ± 0.43, respectively. Differences in percentage appearance of tonic, burst, or paused neurons were not statistically significant for GPi versus GPe. GPi firing features in dystonic patients were closely similar to those of GPe. This could suggest that the abnormally patterned output from GPi would not result from increased differential inhibitory/excitatory input arising from the direct/indirect pathway but rather be transmitted from GPe, striatum, or either centromedian nucleus. © 2003 Movement Disorder Society

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