Sensory, Motor and Intrinsic Mechanisms of Thalamic Activity related to Organic and Psychogenic DystoniaKobayashi K1,2, Chien JH1, Kim JH1,3 and Lenz FA1*
- *Corresponding Author:
- Lenz FA
Department of Neurosurgery
Meyer Building 7-113, Johns Hopkins Hospital
600 North Wolfe Street, Baltimore MD 21287-7713, USA
E-mail: [email protected]
Received date: April 26, 2017; Accepted date: May 08, 2017; Published date: May 15, 2017
Citation: Kobayashi K, Chien JH, Kim JH, Lenz FA (2017) Sensory, Motor and Intrinsic Mechanisms of Thalamic Activity related to Organic and Psychogenic Dystonia. J Alzheimers Dis Parkinsonism 7:324. doi:10.4172/2161-0460.1000324
Copyright: © 2017 Kobayashi K, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
The thalamus is a critical module in the circuit which has been associated with movement disorders including dystonia. This circuit extends from cortex to striatum to pallidum to the thalamic nucleus Ventral Lateral anterior (VLa) to cortex and can be studied by activity recorded during thalamic stereotactic surgery for the treatment of dystonia. Neuronal recordings in the VLa nucleus show low frequency modulation of firing that is correlated with and leads the low frequency modulation of EMG activity; this EMG activity is characteristic of dystonia. Immediately posterior is the Ventral Lateral posterior (VLp) nucleus which, in controls (patients with tremor or chronic pain), is characterized by deep sensory cells which fire at short latency in response to movement of a single joint or to stimulation of deep structures, such as muscles, tendons and joints. In patients with dystonia, neurons with this sensory activity are much more common than in controls and single neurons often respond to movement of multiple joints. In controls operated for the treatment of tremor or chronic pain many neurons in both nuclei are activated during active or involuntary joint movements, such as tremor or dystonia. The active joint movement related to the firing of a cell is usually in the opposite direction to the passive joint movement which causes that cell to fire. This linkage of active or involuntary and passive joint movement is unfocussed in dystonia. The involuntary dystonic joint movement best correlated with firing of a neuron may not activate the neuron when it occurs as a passive movement, while multiple other passive movements will activate the neuron. These linkages may explain the overflow of isolated voluntary activity to multiple other muscles that is seen in dystonia. The activity of either nucleus may have a critical role in dystonia since their disruption by stimulation or lesioning can decrease dystonia.