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Toshiki Yoshimine - One of the best experts on this subject based on the ideXlab platform.

  • motor cortex stimulation in patients with Deafferentation pain activation of the posterior insula and thalamus
    Journal of Neurosurgery, 2007
    Co-Authors: Haruhiko Kishima, Youichi Saitoh, Yasuhiro Osaki, Hiroshi Nishimura, Amami Kato, Jun Hatazawa, Toshiki Yoshimine, Youichi Saitoh, Haruhiko Kishima, Amami Kato, Toshiki Yoshimine
    Abstract:

    Object The mechanisms underlying Deafferentation pain are not well understood. Motor cortex stimulation (MCS) is useful in the treatment of this kind of chronic pain, but the detailed mechanisms underlying its effects are unknown. Methods Six patients with intractable Deafferentation pain in the left hand were included in this study. All were right-handed and had a subdural electrode placed over the right precentral gyrus. The pain was associated with brainstem injury in one patient, cervical spine injury in one patient, thalamic hemorrhage in one patient, and brachial plexus avulsion in three patients. Treatment with MCS reduced pain; visual analog scale (VAS) values for pain were 82 ± 20 before MCS and 39 ± 20 after MCS (mean ± standard error). Regional cerebral blood flow (rCBF) was measured by positron emission tomography with H215O before and after MCS. The obtained images were analyzed with statistical parametric mapping software (SPM99). Results Significant rCBF increases were identified after MCS ...

  • stimulation of primary motor cortex for intractable Deafferentation pain
    Acta Neurochirurgica, 2006
    Co-Authors: Youichi Saitoh, Masayuki Hirata, Azuma Hirayama, Haruhiko Kishima, Satoru Oshino, Amami Kato, Toshiki Yoshimine
    Abstract:

    The stimulation of the primary motor cortex (M1) has proved to be an effective treatment for intractable Deafferentation pain. This treatment started in 1990, and twenty-eight studies involving 271 patients have been reported so far. The patients who have been operated on were suffering from post-stroke pain (59%), trigeminal neuropathic pain, brachial plexus injury, spinal cord injury, peripheral nerve injury and phantom-limb pain. The method of stimulation was: a) epidural, b) subdural, and c) within the central sulcus. Overall, considering the difficulty in treating central neuropathic pain, trigeminal neuropathic pain and certain types of refractory peripheral pain, the electrical stimulation of M1 is a very promising technique; nearly 60% of the treated patients improved with a higher than 50% pain relief after several months of follow-up and sometimes of a few years in most reports. The mechanism of pain relief by the electrical stimulation of M1 has been under investigation. Recently, repetitive transcranial magnetic stimulation (rTMS) of M1 has been reported to be effective on Deafferentation pain. In the future, rTMS may take over from electrical stimulation as a treatment for Deafferentation pain.

  • motor cortex stimulation for central and peripheral Deafferentation pain report of eight cases
    Journal of Neurosurgery, 2000
    Co-Authors: Youichi Saitoh, Masahiko Shibata, S Hirano, Masayuki Hirata, Takashi Mashimo, Toshiki Yoshimine
    Abstract:

    The authors tested a modified motor cortex stimulation protocol for treatment of central and peripheral types of Deafferentation pain. Four patients with thalamic pain and four with peripheral Deafferentation pain were studied. Preoperative pharmacological tests of pain relief were performed using phentolamine, lidocaine, ketamine, thiopental, and placebo. In five patients we placed a 20- or 40-electrode grid in the subdural space to determine the best stimulation point for pain relief for a few weeks before definitive placement of a four-electrode array. In three patients, the four-electrode array was implanted in the interhemispheric fissure as a one-stage procedure to treat lower-extremity pain. In two patients with pain extending from the extremity to the trunk or hip, dual devices were implanted to drive two electrodes. Six of eight patients experienced pain reduction (two each with excellent, good, and fair relief) from motor cortex stimulation. No correlation was apparent between pharmacological test results and the effectiveness of motor cortex stimulation. Patients with peripheral Deafferentation pain, including two with phantom-limb pain and two with brachial plexus injury, attained pain relief from motor cortex stimulation, with excellent results in two cases. Testing performed with a subdural multiple-electrode grid was helpful in locating the best stimulation point for pain relief. Motor cortex stimulation may be effective for treating peripheral as well as central Deafferentation pain.

Youichi Saitoh - One of the best experts on this subject based on the ideXlab platform.

  • mirror visual feedback alleviates Deafferentation pain depending on qualitative aspects of the pain a preliminary report
    Rheumatology, 2008
    Co-Authors: Masahiko Sumitani, Youichi Saitoh, Satoru Miyauchi, Candy Mccabe, M Shibata, L Maeda, T Tashiro, Takashi Mashimo
    Abstract:

    Objectives. Following lesions in somatosensory pathways, Deafferentation pain often occurs. Patients report that the pain is qualitatively complex, and its treatment can be difficult. Mirror visual feedback (MVF) treatment can improve Deafferentation pain. We sought to classify the qualities of the pain in order to examine whether the potential analgesic effect of MVF depends on these qualities. Methods. Twenty-two patients with phantom limb pain, or pain related to spinal cord or nerve injury, performed a single MVF procedure. Before and after the MVF procedure, we evaluated phantom limb awareness, movement representation of the phantom or affected/paralysed limb, pain intensity on an 11-point numerical rating scale (0–10) and the qualities of the pain [skin surface-mediated (superficial pain) vs deep tissue-mediated (deep pain)] using lists of pain descriptors for each of the two categories. Results. Fifteen of the patients perceived the willed visuomotor imagery of the phantom or affected/paralysed limb after the MVF procedure. In most of the patients, a reduction in pain intensity and a decrease in the reporting of deep-pain descriptors were linked to the emergence of willed visuomotor imagery. Conclusions. In this pilot study, we roughly classified the pain descriptor items into two types for evaluating the qualities of Deafferentation pain. We found that visually induced motor imagery by MVF was more effective for reducing deep pain than superficial pain. This suggests that the analgesic effect of MVF treatment does depend on the qualities of the pain. Further research will be required to confirm that this effect is a specific consequence of MVF.

  • motor cortex stimulation in patients with Deafferentation pain activation of the posterior insula and thalamus
    Journal of Neurosurgery, 2007
    Co-Authors: Haruhiko Kishima, Youichi Saitoh, Yasuhiro Osaki, Hiroshi Nishimura, Amami Kato, Jun Hatazawa, Toshiki Yoshimine, Youichi Saitoh, Haruhiko Kishima, Amami Kato, Toshiki Yoshimine
    Abstract:

    Object The mechanisms underlying Deafferentation pain are not well understood. Motor cortex stimulation (MCS) is useful in the treatment of this kind of chronic pain, but the detailed mechanisms underlying its effects are unknown. Methods Six patients with intractable Deafferentation pain in the left hand were included in this study. All were right-handed and had a subdural electrode placed over the right precentral gyrus. The pain was associated with brainstem injury in one patient, cervical spine injury in one patient, thalamic hemorrhage in one patient, and brachial plexus avulsion in three patients. Treatment with MCS reduced pain; visual analog scale (VAS) values for pain were 82 ± 20 before MCS and 39 ± 20 after MCS (mean ± standard error). Regional cerebral blood flow (rCBF) was measured by positron emission tomography with H215O before and after MCS. The obtained images were analyzed with statistical parametric mapping software (SPM99). Results Significant rCBF increases were identified after MCS ...

  • stimulation of primary motor cortex for intractable Deafferentation pain
    Acta Neurochirurgica, 2006
    Co-Authors: Youichi Saitoh, Masayuki Hirata, Azuma Hirayama, Haruhiko Kishima, Satoru Oshino, Amami Kato, Toshiki Yoshimine
    Abstract:

    The stimulation of the primary motor cortex (M1) has proved to be an effective treatment for intractable Deafferentation pain. This treatment started in 1990, and twenty-eight studies involving 271 patients have been reported so far. The patients who have been operated on were suffering from post-stroke pain (59%), trigeminal neuropathic pain, brachial plexus injury, spinal cord injury, peripheral nerve injury and phantom-limb pain. The method of stimulation was: a) epidural, b) subdural, and c) within the central sulcus. Overall, considering the difficulty in treating central neuropathic pain, trigeminal neuropathic pain and certain types of refractory peripheral pain, the electrical stimulation of M1 is a very promising technique; nearly 60% of the treated patients improved with a higher than 50% pain relief after several months of follow-up and sometimes of a few years in most reports. The mechanism of pain relief by the electrical stimulation of M1 has been under investigation. Recently, repetitive transcranial magnetic stimulation (rTMS) of M1 has been reported to be effective on Deafferentation pain. In the future, rTMS may take over from electrical stimulation as a treatment for Deafferentation pain.

  • motor cortex stimulation for central and peripheral Deafferentation pain report of eight cases
    Journal of Neurosurgery, 2000
    Co-Authors: Youichi Saitoh, Masahiko Shibata, S Hirano, Masayuki Hirata, Takashi Mashimo, Toshiki Yoshimine
    Abstract:

    The authors tested a modified motor cortex stimulation protocol for treatment of central and peripheral types of Deafferentation pain. Four patients with thalamic pain and four with peripheral Deafferentation pain were studied. Preoperative pharmacological tests of pain relief were performed using phentolamine, lidocaine, ketamine, thiopental, and placebo. In five patients we placed a 20- or 40-electrode grid in the subdural space to determine the best stimulation point for pain relief for a few weeks before definitive placement of a four-electrode array. In three patients, the four-electrode array was implanted in the interhemispheric fissure as a one-stage procedure to treat lower-extremity pain. In two patients with pain extending from the extremity to the trunk or hip, dual devices were implanted to drive two electrodes. Six of eight patients experienced pain reduction (two each with excellent, good, and fair relief) from motor cortex stimulation. No correlation was apparent between pharmacological test results and the effectiveness of motor cortex stimulation. Patients with peripheral Deafferentation pain, including two with phantom-limb pain and two with brachial plexus injury, attained pain relief from motor cortex stimulation, with excellent results in two cases. Testing performed with a subdural multiple-electrode grid was helpful in locating the best stimulation point for pain relief. Motor cortex stimulation may be effective for treating peripheral as well as central Deafferentation pain.

Terrence J. Sejnowski - One of the best experts on this subject based on the ideXlab platform.

  • pathological effect of homeostatic synaptic scaling on network dynamics in diseases of the cortex
    The Journal of Neuroscience, 2008
    Co-Authors: Maxim Bazhenov, Flavio Fröhlich, Terrence J. Sejnowski
    Abstract:

    Slow periodic EEG discharges are common in CNS disorders. The pathophysiology of this aberrant rhythmic activity is poorly understood. We used a computational model of a neocortical network with a dynamic homeostatic scaling rule to show that loss of input (partial Deafferentation) can trigger network reorganization that results in pathological periodic discharges. The decrease in average firing rate in the network by Deafferentation was compensated by homeostatic synaptic scaling of recurrent excitation among pyramidal cells. Synaptic scaling succeeded in recovering the network target firing rate for all degrees of Deafferentation (fraction of deafferented cells), but there was a critical degree of Deafferentation for pathological network reorganization. For Deafferentation degrees below this value, homeostatic upregulation of recurrent excitation had minimal effect on the macroscopic network dynamics. For Deafferentation above this threshold, however, a slow periodic oscillation appeared, patterns of activity were less sparse, and bursting occurred in individual neurons. Also, comparison of spike-triggered afferent and recurrent excitatory conductances revealed that information transmission was strongly impaired. These results suggest that homeostatic plasticity can lead to secondary functional impairment in case of cortical disorders associated with cell loss.

  • pathological effect of homeostatic synaptic scaling on network dynamics in diseases of the cortex
    The Journal of Neuroscience, 2008
    Co-Authors: Maxim Bazhenov, Flavio Fröhlich, Terrence J. Sejnowski
    Abstract:

    Slow periodic EEG discharges are common in CNS disorders. The pathophysiology of this aberrant rhythmic activity is poorly understood. We used a computational model of a neocortical network with a dynamic homeostatic scaling rule to show that loss of input (partial Deafferentation) can trigger network reorganization that results in pathological periodic discharges. The decrease in average firing rate in the network by Deafferentation was compensated by homeostatic synaptic scaling of recurrent excitation among pyramidal cells. Synaptic scaling succeeded in recovering the network target firing rate for all degrees of Deafferentation (fraction of deafferented cells), but there was a critical degree of Deafferentation for pathological network reorganization. For Deafferentation degrees below this value, homeostatic upregulation of recurrent excitation had minimal effect on the macroscopic network dynamics. For Deafferentation above this threshold, however, a slow periodic oscillation appeared, patterns of activity were less sparse, and bursting occurred in individual neurons. Also, comparison of spike-triggered afferent and recurrent excitatory conductances revealed that information transmission was strongly impaired. These results suggest that homeostatic plasticity can lead to secondary functional impairment in case of cortical disorders associated with cell loss.

Flavio Fröhlich - One of the best experts on this subject based on the ideXlab platform.

  • pathological effect of homeostatic synaptic scaling on network dynamics in diseases of the cortex
    The Journal of Neuroscience, 2008
    Co-Authors: Maxim Bazhenov, Flavio Fröhlich, Terrence J. Sejnowski
    Abstract:

    Slow periodic EEG discharges are common in CNS disorders. The pathophysiology of this aberrant rhythmic activity is poorly understood. We used a computational model of a neocortical network with a dynamic homeostatic scaling rule to show that loss of input (partial Deafferentation) can trigger network reorganization that results in pathological periodic discharges. The decrease in average firing rate in the network by Deafferentation was compensated by homeostatic synaptic scaling of recurrent excitation among pyramidal cells. Synaptic scaling succeeded in recovering the network target firing rate for all degrees of Deafferentation (fraction of deafferented cells), but there was a critical degree of Deafferentation for pathological network reorganization. For Deafferentation degrees below this value, homeostatic upregulation of recurrent excitation had minimal effect on the macroscopic network dynamics. For Deafferentation above this threshold, however, a slow periodic oscillation appeared, patterns of activity were less sparse, and bursting occurred in individual neurons. Also, comparison of spike-triggered afferent and recurrent excitatory conductances revealed that information transmission was strongly impaired. These results suggest that homeostatic plasticity can lead to secondary functional impairment in case of cortical disorders associated with cell loss.

  • pathological effect of homeostatic synaptic scaling on network dynamics in diseases of the cortex
    The Journal of Neuroscience, 2008
    Co-Authors: Maxim Bazhenov, Flavio Fröhlich, Terrence J. Sejnowski
    Abstract:

    Slow periodic EEG discharges are common in CNS disorders. The pathophysiology of this aberrant rhythmic activity is poorly understood. We used a computational model of a neocortical network with a dynamic homeostatic scaling rule to show that loss of input (partial Deafferentation) can trigger network reorganization that results in pathological periodic discharges. The decrease in average firing rate in the network by Deafferentation was compensated by homeostatic synaptic scaling of recurrent excitation among pyramidal cells. Synaptic scaling succeeded in recovering the network target firing rate for all degrees of Deafferentation (fraction of deafferented cells), but there was a critical degree of Deafferentation for pathological network reorganization. For Deafferentation degrees below this value, homeostatic upregulation of recurrent excitation had minimal effect on the macroscopic network dynamics. For Deafferentation above this threshold, however, a slow periodic oscillation appeared, patterns of activity were less sparse, and bursting occurred in individual neurons. Also, comparison of spike-triggered afferent and recurrent excitatory conductances revealed that information transmission was strongly impaired. These results suggest that homeostatic plasticity can lead to secondary functional impairment in case of cortical disorders associated with cell loss.

Leonardo G Cohen - One of the best experts on this subject based on the ideXlab platform.

  • improving hand function in chronic stroke
    JAMA Neurology, 2002
    Co-Authors: Wolf Muellbacher, Ulf Ziemann, Leonardo G Cohen, Coletta Richards, George F Wittenberg, Deborah Weltz, Babak Boroojerdi, Mark Hallett, Babak Boroojerdi, Mark Hallett
    Abstract:

    Background Recovery of function following stroke plateaus in about 1 year, typically leaving upper arm function better than that in the hand. Since there is competition among body parts for territory in the sensorimotor cortex, even limited activity of the upper arm might prevent the hand from gaining more control, particularly when the territory is reduced in size because of the stroke. Deafferentation of a body part in a healthy brain enhances cortical representations of adjacent body parts, and this effect is markedly increased by voluntary activity of the adjacent part. Objective To explore whether Deafferentation of the upper arm, produced by a new technique of regional anesthesia during hand motor practice, helps recovery of hand function in patients with long-term stable weakness of their hand following stroke. Methods and Results Deafferentation, produced by a new technique of regional anesthesia of the upper arm during hand motor practice, dramatically improved hand motor function including some activities of daily living. The improvement was associated with an increase in transcranial magnetic stimulation–evoked motor output to the practice hand muscles. Conclusion This is a novel therapeutic strategy that may help improve hand function in patients with long-term weakness after stroke.

  • cortical excitability changes induced by Deafferentation of the contralateral hemisphere
    Brain, 2002
    Co-Authors: Konrad J Werhahn, Jennifer Mortensen, Alain Kaelinlang, Babak Boroojerdi, Leonardo G Cohen
    Abstract:

    Summary Short-term deprivation of sensory input by ischaemic nerve block (INB) leads to functional reorganization in the deafferented motor cortex. Here, we show that INB also elicits functional changes in homotopic regions of the cortex contralateral to the deafferented one. We measured motor evoked potential (MEP) amplitudes elicited by transcranial magnetic stimulation (TMS) in small hand and biceps brachii muscles before, during and after INB of the right hand. INB increased excitability of the cortical representation of (i) the intact hand and (ii) body parts proximal to the deafferented hand (upper arm), in the absence of excitability changes in other body part representations such as thorax or leg muscles. This effect persisted throughout the entire period of Deafferentation and returned to baseline values afterward. Motor responses to brainstem electrical stimulation remained unchanged during INB, indicating that the effect is probably of cortical origin. Lorazepam, a GABAA receptor agonist, blocked this increased excitability. Interhemispheric inhibition between hand muscles decreased during INB. After chronic Deafferentation in amputees, MEP amplitudes and motor output curves in small hand muscles were depressed and motor thresholds were elevated compared with aged-matched controls. These results indicate that acute hand Deafferentation can elicit a focal increase in excitability in the hand motor representation contralateral to the deafferented cortex that is influenced by transcallosal interactions and GABAergic transmission, and is balanced in the setting of chronic Deafferentation.

  • modulation of practice dependent plasticity in human motor cortex
    Brain, 2001
    Co-Authors: Ulf Ziemann, Wolf Muellbacher, Mark Hallett, Leonardo G Cohen
    Abstract:

    Motor practice may lead to expansion of trained representations in the motor cortex, but it is unknown whether this practice-dependent plasticity can be purposefully enhanced or depressed. Evidence, mainly based on animal experiments, indicates that the activity of GABA-related cortical inhibition is important in controlling the extent to which plasticity may occur. We tested the role of GABA in modulating practice-dependent plasticity in the human motor cortex. A decrease in GABA-related cortical inhibition was achieved by ischaemic nerve block (INB) in the hand by Deafferentation/deefferentation and an increase was achieved by administration of the GABAA receptor agonist lorazepam. In Experiment 1, healthy subjects performed motor practice (MP), consisting of repeated ballistic contractions of the biceps muscle in the absence (MP alone) or presence of INB (MP+INB). Changes in the biceps motor cortex representation were assessed by transcranial magnetic stimulation (TMS). MP+INB resulted in a dramatic increase in the size of the motor evoked potential (MEP) and in paired-pulse excitability compared with mild or no changes in the MP-alone and INB-alone conditions. In Experiment 2, this dramatic increase in biceps representation induced by MP+INB was replicated when subjects were pretreated with placebo, but this increase was prevented or even switched to a decrease when subjects were pretreated with lorazepam. These findings indicate that a decrease in GABA-related inhibition facilitates practice-dependent plasticity in the human motor cortex, whereas an increase depresses it. In Experiment 3, practice-dependent plasticity (assessed by TMS, as in the first two experiments) was also tested at the behavioural level. The dramatic increase in biceps MEP size induced by MP+INB was paralleled by an increase in peak acceleration of the fastest elbow flexion movements. Similarly, the lack of change in MEP size in the MP-alone condition was paralleled by a lack of change in peak acceleration. We propose that changes in GABA activity may be instrumented to modulate plasticity purposefully; for instance, to enhance plastic change and recovery of function after a lesion in neurological patients.

  • modulation of plasticity in human motor cortex after forearm ischemic nerve block
    The Journal of Neuroscience, 1998
    Co-Authors: Ulf Ziemann, Brian Corwell, Leonardo G Cohen
    Abstract:

    Deafferentation leads to cortical reorganization that may be functionally beneficial or maladaptive. Therefore, we were interested in learning whether it is possible to purposely modulate Deafferentation-induced reorganization. Transient forearm Deafferentation was induced by ischemic nerve block (INB) in healthy volunteers. The following five interventions were tested: INB alone; INB plus low-frequency (0.1 Hz) repetitive transcranial magnetic stimulation of the motor cortex ipsilateral to INB (INB+rTMSi); rTMSi alone; INB plus rTMS of the motor cortex contralateral to INB (INB+rTMSc); and rTMSc alone. Plastic changes in the motor cortex contralateral to Deafferentation were probed with TMS, measuring motor threshold (MT), motor evoked-potential (MEP) size, and intracortical inhibition (ICI) and facilitation (ICF) to the biceps brachii muscle proximal to the level of Deafferentation. INB alone induced a moderate increase in MEP size, which was significantly enhanced by INB+rTMSc but blocked by INB+rTMSi. INB alone had no effect on ICI or ICF, whereas INB+rTMSc reduced ICI and increased ICF, and conversely, INB+rTMSi deepened ICI and suppressed ICF. rTMSi and rTMSc alone were ineffective in changing any of these parameters. These findings indicate that the deafferented motor cortex becomes modifiable by inputs that are normally subthreshold for inducing changes in excitability. The Deafferentation-induced plastic changes can be up-regulated by direct stimulation of the “plastic” cortex and likely via inhibitory projections down-regulated by stimulation of the opposite cortex. This modulation of cortical plasticity by noninvasive means might be used to facilitate plasticity when it is primarily beneficial or to suppress it when it is predominately maladaptive.