Functional Recovery in a Primate Model of Parkinson's Disease following Motor Cortex Stimulation

Drouot, Xavier; Oshino, Satoru; Jarraya, Béchir; Besret, Laurent; Kishima, Haruhiko; Rémy, Philippe; Dauguet, Julien; Lefaucheur, Jean Pascal; Dollé, Frédéric; Condé, Françoise; Bottlaender, Michel; Peschanski, Marc; Kéravel, Y.; Hantraye, Philippe; Palfi, Stéphane

doi:10.1016/j.neuron.2004.11.023

Cited by 159 publications

(117 citation statements)

References 34 publications

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“…More detailed anal- 56 demonstrate a renormalization of both STN and GPi firing rates after motor cortical stimulation in monkeys lesioned with 1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine (MPTP). The stimulation paradigm they used was similar to ours in that they were stimulating with two cathodal leads.…”

Section: Discussionmentioning

confidence: 99%

“…Specifically, Drouot et al 56 mention the possibilities of secondary messengers or longterm potentiation as possible reasons for this time difference. One speculation is that chronic MCS may alter not only the firing patterns in the basal ganglia but also, due to its location, the interactions between the pyramidal and extrapyramidal systems.…”

Section: Discussionmentioning

confidence: 99%

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Motor Cortex Stimulation for Pain and Movement Disorders

Arle

Shils

2008

Neurotherapeutics

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Summary:Since initial reports in the early 1990s, stimulation of the M1 region of the cortex (MCS) has been used to treat chronic refractory pain conditions and a variety of movement disorders. A Medline search of literature between 1991 and 2007 revealed 512 cases using MCS. Although most of these relate to the treatment of pain (422), 84 of them involve movement disorders. More recently, several studies have specifically looked at treating Parkinson's disease (PD) with MCS. We report here several of our own cases using MCS to treat poststroke and non-poststroke pain syndromes and movement disorders (n ϭ 8), PD (n ϭ 4), ET (n ϭ 2), and cortico-basal degeneration (n ϭ 1). We also cover the essential history of this procedure and our current research using computational modeling to understand further the underlying mechanisms of MCS.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Motor Cortex Stimulation for Pain and Movement Disorders

Arle

Shils

2008

Neurotherapeutics

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“…It is worth noting that functional interference with the deranged loop activity of patients by means of high frequency electrical stimulation of these nuclei has major therapeutic value (43). More recently, it has also been demonstrated that motor cortex stimulation alleviates a primate model of the disease (44).…”

Section: Discussionmentioning

confidence: 99%

Resurgent Current and Voltage Sensor Trapping Enhanced Activation by a β-Scorpion Toxin Solely in Nav1.6 Channel

Schiavon

Sacco

Cassulini

et al. 2006

Journal of Biological Chemistry

107

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Resurgent currents are functionally crucial in sustaining the high frequency firing of cerebellar Purkinje neurons expressing Na v 1.6 channels. ␤-Scorpion toxins, such as CssIV, induce a left shift in the voltage-dependent activation of Na v 1.2 channels by "trapping" the IIS4 voltage sensor segment. We found that the dangerous Cn2 ␤-scorpion peptide induces both the left shift voltage-dependent activation and a transient resurgent current only in human Na v 1.6 channels (among 1.1-1.7), whereas CssIV did not induce the resurgent current. Cn2 also produced both actions in mouse Purkinje cells. These findings suggest that only distinct ␤-toxins produce resurgent currents. We suggest that the novel and unique selectivity of Cn2 could make it a model drug to replace deep brain stimulation of the subthalamic nucleus in patients with Parkinson disease.

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“…1) (see also other reviews of DBS elsewhere in this issue [128][129][130][131] ). The primary targets of DBS for PD include the sensorimotor STN and GPi, 132 and recent studies suggest that the PPN, 80 GPe, 47 and motor cortex 133 are also effective targets. For most dystonias, the posteroventral GPi is now the preferred site of stimulation.…”

Section: Why So Many Targets?mentioning

confidence: 99%

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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Functional Recovery in a Primate Model of Parkinson's Disease following Motor Cortex Stimulation

Cited by 159 publications

References 34 publications

Motor Cortex Stimulation for Pain and Movement Disorders

Motor Cortex Stimulation for Pain and Movement Disorders

Resurgent Current and Voltage Sensor Trapping Enhanced Activation by a β-Scorpion Toxin Solely in Nav1.6 Channel

Mechanisms and Targets of Deep Brain Stimulation in Movement Disorders

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