Computational study of subdural and epidural cortical stimulation of the motor cortex

1. Stimulation of the sensorimotor cortex was found to excite and/or inhibit nociceptive spinothalamic tract cells. Thirteen wide dynamic range cells were inhibited by cortical stimulation, 6 were excited and 14 were both excited and inhibited. Four of six high-threshold cells were excited and one was inhibited. 2. Intermediate (200 ms) or long (2 s) duration conditioning trains were effective in reducing responses of spinothalamic cells evoked by noxious mechanical or thermal stimuli and by A- and C-fiber volleys in the sural nerve. Preferential inhibition of low-threshold responses with little or no effect on high-threshold discharges was observed in some cases. 3. Inhibitory actions were obtained primarily from stimulation of the SI sensory cortex and area 5, while excitation or excitation followed by inhibition was the dominant effect from motor cortex (area 4). Spinothalamic cells were also excited by stimulation of the medullary pyramid. 4. In eight animals extensive mapping of the sensorimotor cortex showed that for a given cell, stimulation of the sensory cortex produced inhibition while stimulation of motor cortex resulted in excitation. 5. The average latency of inhibition from sensory cortex was 29.8 +/- 10 ms, while the average latency of excitation from motor cortex was significantly shorter, 13.5 +/- 9 ms. The shortest latencies for excitation from pyramidal stimulation in the cases evaluated ranged from 2 to 9 ms. 6. Spinal cord lesions were made in five animals to determine the descending pathway(s) mediating corticofugal effects. Cortical and pyramidal effects were eliminated or considerably reduced by lesions involving the dorsal part of the lateral funiculus. This observation combined with latency data suggest that the corticospinal tract may be involved in the mediation of cortical excitation, while both pyramidal and extrapyramidal pathways are likely to be involved in cortical inhibition.

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Epidural Cortical Stimulation of the Left Dorsolateral Prefrontal Cortex for Refractory Major Depressive Disorder

Neurosurgery ◽

10.1227/neu.0b013e318229cfcd ◽

2011 ◽

Vol 69 (5) ◽

pp. 1015-1029 ◽

Cited By ~ 42

Author(s):

Brian Harris Kopell ◽

Jerry Halverson ◽

Christopher R. Butson ◽

Mercedes Dickinson ◽

Julie Bobholz ◽

...

Keyword(s):

Major Depressive Disorder ◽

Prefrontal Cortex ◽

Depressive Disorder ◽

Dorsolateral Prefrontal Cortex ◽

Rating Scale ◽

Cortical Stimulation ◽

Major Depressive ◽

Dorsolateral Prefrontal ◽

Epidural Cortical Stimulation ◽

Stimulation Of

Abstract BACKGROUND: A significant number of patients with major depressive disorder are unresponsive to conventional therapies. For these patients, neuromodulation approaches are being investigated. OBJECTIVE To determine whether epidural cortical stimulation at the left dorsolateral prefrontal cortex is safe and efficacious for major depressive disorder through a safety and feasibility study. METHODS Twelve patients were recruited in this randomized, single-blind, sham-controlled study with a 104-week follow-up period. The main outcome measures were Hamilton Depression Rating Scale-28 (HDRS), Montgomery-Asberg Depression Rating Scale (MADRS), Global Assessment of Function (GAF), and Quality of Life Enjoyment and Satisfaction (QLES) questionnaire. An electrode was implanted over Brodmann area 9/46 in the left hemisphere. The electrode provided long-term stimulation to this target via its connections to an implanted neurostimulator in the chest. RESULTS During the sham-controlled phase, there was no statistical difference between sham and active stimulation, although a trend toward efficacy was seen with the active stimulation group. In the open-label phase, we observed a significant improvement in outcome scores for the HDRS, MADRS, and GAF but not the QLES (HDRS: df = 7, F = 7.72, P < .001; MADRS: df = 7, F = 8.2, P < .001; GAF: df = 5, F = 16.87, P < .001; QLES: df = 5, F = 1.32, P > .2; repeated measures ANOVA). With regard to the HDRS, 6 patients had ≥ 40% improvement, 5 patients had ≥ 50% improvement, and 4 subjects achieved remission (HDRS < 10) at some point during the study. CONCLUSION Epidural cortical stimulation of the left dorsolateral prefrontal cortex appears to be a safe and potentially efficacious neuromodulation approach for treatment-refractory major depressive disorder.

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Effects of epidural cortical stimulation on motor recovery after a primary motor cortex ischemic stroke: preliminary results in a non-human primate model

Brain Stimulation ◽

10.1016/j.brs.2015.01.371 ◽

2015 ◽

Vol 8 (2) ◽

pp. 430 ◽

Cited By ~ 1

Author(s):

A. Balossier ◽

C. Orset ◽

O. Etard ◽

C. Gakuba ◽

E. Emery ◽

...

Keyword(s):

Ischemic Stroke ◽

Motor Cortex ◽

Primary Motor Cortex ◽

Motor Recovery ◽

Cortical Stimulation ◽

Primate Model ◽

Preliminary Results ◽

Epidural Cortical Stimulation ◽

Human Primate

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Magnetic stimulation of the human motor cortex evokes skin sympathetic nerve activity

Journal of Applied Physiology ◽

10.1152/jappl.2000.88.1.126 ◽

2000 ◽

Vol 88 (1) ◽

pp. 126-134 ◽

Cited By ~ 31

Author(s):

David H. Silber ◽

Lawrence I. Sinoway ◽

Urs A. Leuenberger ◽

Vahe E. Amassian

Keyword(s):

Motor Cortex ◽

Sympathetic Nerve ◽

Sympathetic Nerve Activity ◽

Cortical Stimulation ◽

Motor Cortex Stimulation ◽

Nerve Activity ◽

Human Motor Cortex ◽

Skin Sympathetic Nerve Activity ◽

Motor Cortical ◽

Stimulation Of

Single-pulse magnetic coil stimulation (Cadwell MES 10) over the cranium induces without pain an electric pulse in the underlying cerebral cortex. Stimulation over the motor cortex can elicit a muscle twitch. In 10 subjects, we tested whether motor cortical stimulation could also elicit skin sympathetic nerve activity (SSNA; n = 8) and muscle sympathetic nerve activity (MSNA; n = 5) in the peroneal nerve. Focal motor cortical stimulation predictably elicited bursts of SSNA but not MSNA; with successive stimuli, the SSNA responses did not readily extinguish (94% of discharges to the motor cortex evoked SSNA responses) and had predictable latencies [739 ± 33 (SE) to 895 ± 13 ms]. The SSNA responses were similar after stimulation of dominant and nondominant sides. Focal stimulation posterior to the motor cortex elicited extinguishable SSNA responses. In three of six subjects, anterior cortical stimulation evoked SSNA responses similar to those seen with motor cortex stimulation but without detectable movement; in the other subjects, anterior stimulation evoked less SSNA discharge than that seen with motor cortex stimulation. Contrasting with motor cortical stimulation, evoked SSNA responses were more readily extinguished with 1) peripheral stimulation that directly elicited forearm muscle activation accompanied by electromyograms similar to those with motor cortical stimulation; 2) auditory stimulation by the click of the energized coil when off the head; and 3) in preliminary experiments, finger afferent stimulation sufficient to cause tingling. Our findings are consistent with the hypothesis that motor cortex stimulation can cause activation of both α-motoneurons and SSNA.

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Noninvasive Stimulation of Human Corticospinal Axons Innervating Leg Muscles

Journal of Neurophysiology ◽

10.1152/jn.90380.2008 ◽

2008 ◽

Vol 100 (2) ◽

pp. 1080-1086 ◽

Cited By ~ 34

Author(s):

P. G. Martin ◽

J. E. Butler ◽

S. C. Gandevia ◽

J. L. Taylor

Keyword(s):

Motor Cortex ◽

Thoracic Spine ◽

Rectus Femoris ◽

Electrical Stimulus ◽

Cortical Stimulation ◽

Leg Muscles ◽

Descending Volleys ◽

Interstimulus Intervals ◽

The Moment ◽

Stimulation Of

These studies investigated whether a single electrical stimulus over the thoracic spine activates corticospinal axons projecting to human leg muscles. Transcranial magnetic stimulation of the motor cortex and electrical stimulation over the thoracic spine were paired at seven interstimulus intervals, and surface electromyographic responses were recorded from rectus femoris, tibialis anterior, and soleus. The interstimulus intervals (ISIs) were set so that the first descending volley evoked by cortical stimulation had not arrived at (positive ISIs), was at the same level as (0 ISI) or had passed (negative ISIs) the site of activation of descending axons by the thoracic stimulation at the moment of its delivery. Compared with the responses to motor cortical stimulation alone, responses to paired stimuli were larger at negative ISIs but reduced at positive ISIs in all three leg muscles. This depression of responses at positive ISIs is consistent with an occlusive interaction in which an antidromic volley evoked by the thoracic stimulation collides with descending volleys evoked by cortical stimulation. The cortical and spinal stimuli activate some of the same corticospinal axons. Thus it is possible to examine the excitability of lower limb motoneuron pools to corticospinal inputs without the confounding effects of changes occurring within the motor cortex.

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