Thalamic post-inhibitory bursting occurs in patients with organic dystonia more often than controls

K. Kobayashi, C. C. Liu, A. L. Jensen, J. L. Vitek, Z. Mari, F. A. Lenz

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4 Scopus citations


We now test the hypothesis that post-inhibitory bursting in the human pallidal receiving nucleus of the thalamus (ventral oral) mediates inhibitory pallido-thalamic transmission during dystonia. We have compared thalamic single neuron activity in nine patients with organic dystonia to that in a patient with psychogenic dystonia (Psyd) and in healthy waking monkeys. In organic dystonia, EMG power is commonly concentrated at the lowest frequency of the smoothed autopower spectrum (0.39 Hz). Therefore, segments of spike trains with a signal-to-noise ratio ≥2 at 0.39 Hz were termed dystonia frequency (DF) segments, which occurred more commonly during dystonia related to movement. Those with a SNR<2 were termed non-dystonia frequency (nDF) segments, which were associated with spontaneous dystonia. We concentrated on nDF activity since neuronal activity in our controls was measured at rest. Neuronal spike trains were categorized into those with post-inhibitory bursts (G, grouped), with single spikes (NG, non-grouped), or with both single spikes and bursts (I, intermediate). nDF spike trains in ventral oral had more G category firing in dystonia than in controls. The burst rate and the pre-burst silent period in nDF firing of organic dystonia were consistently greater than those of both the monkeys and the patient with Psyd. The distribution of the pre-burst silent period was bimodal with a longer mode of approximately GABAb (gamma amino butyric acid receptor-type b) duration. These results demonstrate distinct differences of post-inhibitory bursting in organic dystonia versus controls. The presence of inhibitory events consistent with GABAb duration suggests interventions for treatment of dystonia.

Original languageEnglish (US)
Pages (from-to)81-91
Number of pages11
JournalBrain Research
StatePublished - Dec 6 2013

Bibliographical note

Funding Information:
This work was supported by the National Institutes of Health – National Institute of Neurological Disorders and Stroke ( NS38493 and 40059 to FAL) ( NS058945 to JLV). None of the authors has conflicts of interest related to this work. We thank L.H. Rowland and J. Winberry for excellent technical assistance.


  • Dystonia
  • Low threshold spike burst
  • Single neuron analysis
  • Thalamotomy
  • Thalamus


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