Effect of deep brain stimulation of GPI on neuronal activity of the thalamic nucleus ventralis oralis in a dystonic patient

Pralong, Étienne; Debatisse, D.; Maeder, Malin; Vingerhoets, François; Ghika, J.; Villemure, Jean‐Guy

doi:10.1016/j.neucli.2003.07.001

Cited by 43 publications

(33 citation statements)

References 21 publications

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“…44 The 'output activation' hypothesis appears to hold for other target nuclei as well. 36,[45][46][47] A study examining motor scores in parkinsonian monkeys during GPe HFS 48 found that therapeutic stimulation parameters led to a pronounced reduction in firing rate and bursting in 67% of the recorded STN neurons, whereas only 31% of STN neurons were significantly inhibited for nontherapeutic stimulation. In untreated monkeys, Anderson et al 36 reported that GPi HFS inhibited 77% of thalamic neurons, which is consistent with orthodromic activation of GABAergic projections.…”

Section: Axonal Output Of the Stimulated Nucleusmentioning

confidence: 99%

“…Montgomery 45 described a similar reduction in thalamic neuronal activity in humans during GPi HFS with time-locked responses involving an overall suppression in the firing probability, except for a brief excitatory phase at 3.5 ms to 5 ms. In a dystonic patient, Pralong et al 46 observed that GPi HFS induced thalamic inhibition only in a subpopulation of ventralis oralis anterior (Voa) thalamic neurons that exhibited intrinsically high firing rates and a low burst index. Voa neurons expressing lower firing rates and a higher burst index were unaffected by GPi HFS.…”

Section: Axonal Output Of the Stimulated Nucleusmentioning

confidence: 99%

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Mechanisms and Targets of Deep Brain Stimulation in Movement Disorders

et al. 2008

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Summary:Chronic electrical stimulation of the brain, known as deep brain stimulation (DBS), has become a preferred surgical treatment for medication-refractory movement disorders. Despite its remarkable clinical success, the therapeutic mechanisms of DBS are still not completely understood, limiting opportunities to improve treatment efficacy and simplify selection of stimulation parameters. This review addresses three questions essential to understanding the mechanisms of DBS. 1) How does DBS affect neuronal tissue in the vicinity of the active electrode or electrodes? 2) How do these changes translate into therapeutic benefit on motor symptoms? 3) How do these effects depend on the particular site of stimulation? Early hypotheses proposed that stimulation inhibited neuronal activity at the site of stimulation, mimicking the outcome of ablative surgeries. Recent studies have challenged that view, suggesting that although somatic activity near the DBS electrode may exhibit substantial inhibition or complex modulation patterns, the output from the stimulated nucleus follows the DBS pulse train by direct axonal excitation. The intrinsic activity is thus replaced by high-frequency activity that is time-locked to the stimulus and more regular in pattern. These changes in firing pattern are thought to prevent transmission of pathologic bursting and oscillatory activity, resulting in the reduction of disease symptoms through compensatory processing of sensorimotor information. Although promising, this theory does not entirely explain why DBS improves motor symptoms at different latencies. Understanding these processes on a physiological level will be critically important if we are to reach the full potential of this powerful tool.

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Section: Axonal Output Of the Stimulated Nucleusmentioning

confidence: 99%

Section: Axonal Output Of the Stimulated Nucleusmentioning

confidence: 99%

Mechanisms and Targets of Deep Brain Stimulation in Movement Disorders

et al. 2008

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“…And finally, the two groups showed similar improvement in movement score despite greater improvement of the contralateral upper extremity in group II. Pralong et al [27] reported that Voa could be classified in two cell subpopulations. GPi electrical stimulation reduced the frequency and increased the burst index of high firing rate cells, while leaving other cell types unchanged.…”

Section: Discussionmentioning

confidence: 99%

The Effect of Bilateral Globus Pallidus Internus Deep Brain Stimulation plus Ventralis Oralis Thalamotomy on Patients with Cerebral Palsy

Kim

Chang

Cho

et al. 2012

Stereotact Funct Neurosurg

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Objective: We compared bilateral globus pallidus internus (GPi) deep brain stimulation (DBS) with bilateral GPi DBS plus ventralis oralis (Vo) thalamotomy to analyze the effect of the combined Vo thalamotomy. Methods: Between March 2003 and December 2008, 10 patients underwent DBS and/or Vo thalamotomy for treatment of cerebral palsy in our institute of neurosurgery and rehabilitation medicine. Four patients received bilateral posteroventral GPi DBS as group I and 6 patients received GPi DBS plus unilateral thalamotomy as group II. Results: The movement and disability scores of group I improved by 32 and 14.3%, respectively, at the last follow-up compared with baseline. The movement and disability scores of group II improved by 31.5 and 0.18%. The BFMDRS-movement subscores of group II demonstrated statistically significant improvement in the contralateral arm compared to group I (p = 0.042). Body pain, vitality and mental health seemed to improve in group II, in terms of health-related quality of life. Conclusions: Contrary to our expectations, we were unable to demonstrate clear improvements in overall BFMDRS scores between group I and group II. However, movements of the contralateral upper extremities improved and health-related quality of life in group II showed satisfactory results.

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“…It is now more than 14 years that we first published observations of the effect of motor internal pallidum (mGPi) stimulation on the neuronal activity in the thalamic nucleus ventralis oralis anterior (VOA) [1]. One of the main conclusions of this study was that DBS of mGPi decreased firing activity of a subpopulation of VOA neurones.…”

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confidence: 83%