Neurophysiologie clinique = Clinical neurophysiology
-
Review
Stroke recovery can be enhanced by using repetitive transcranial magnetic stimulation (rTMS).
Post-stroke recovery is based on plastic changes in the central nervous system that can compensate the loss of activity in affected brain regions. In particular, monohemispheric stroke is thought to result in disinhibition of the contralesional unaffected hemisphere. Neurorehabilitation programs improve function partly by enhancing cortical reorganization. ⋯ Cortical stimulation is an exciting perspective for improving functional recovery from stroke. Transient application of non-invasive transcranial stimulation during the time of the rehabilitation process will be preferable to the temporary implantation of epidural cortical electrodes, as recently proposed. Therefore, in the future, acute or recent stroke might be a major indication of rTMS in neurological practice.
-
Chronic motor cortex stimulation using implanted epidural stimulation was proposed to treat chronic, drug-resistant neuropathic pain. Various studies showed that repetitive transcranial magnetic stimulation (rTMS) applied over the motor cortex could also relieve neuropathic pain, at least partially and transiently. Controlled rTMS studies with other cortical targets, such as the dorsolateral prefrontal cortex, are in waiting. ⋯ The efficacious rTMS parameters could differ from those used in chronic epidural stimulation. Differences in the pattern of the current fields respectively induced in the brain by these two techniques might explain this finding. Actually, stimulation parameters remain to be optimised and clinical efficacy to be confirmed by multicentre randomised trials, before considering rTMS as therapeutic tool for patients with chronic pain in neurological practice.
-
Lesch-Nyhan syndrome is a rare and debilitating condition characterized by dystonia and self-mutilating behavior. In order to shed light on the pathophysiology of dystonia, we report the pallidal electrophysiological activity recorded in two patients during deep brain stimulation surgery (DBS). ⋯ This observation may confirm the Albin and Delong's model of the basal nuclei in hypokinetic and hyperkinetic disorders.
-
Clinical Trial
Impaired corticolingual pathways in patients with or without dysarthria after acute monohemispheric stroke.
The occurrence of dysarthria is not infrequent in stroke but little is known about its pathophysiology. The aims of the present study were to assess the central motor innervation of the tongue in normal adults using transcranial magnetic stimulation (TMS) and to compare this with that seen in stroke patients with or without dysarthria. The study included 46 patients with acute monohemispheric stroke due to occlusion of the territory of the middle cerebral artery as documented by CT brain scan (26 patients with dysarthria and 20 patients without dysarthria). ⋯ There were no significant associations between neurophysiological parameters and side of infarction. We conclude that interruption of the corticolingual pathways is frequent in stroke patients with or without dysarthria. The ability of unaffected hemisphere to evoke responses in the side contralateral to the lesion may relate to the absence or presence of dysarthria.
-
Little is known on effects taking place in the CNS during rapid opioid detoxification (ROD) while the patient is under anesthesia. We therefore measured EEG-power spectra in the beta, alpha, Theta, and delta-band in 36 patients undergoing ROD. Measurements were taken before, during steady-state anesthesia and following administration of the antagonist naltrexone. ⋯ Subsequent administration of S+-ketamine induced a reversal of acute abstinence-related EEG power changes: compared to anesthesia with naltrexone on board, power in the EEG increased by 65% in the delta- and decreased by 723% in the beta-band. While sympathetically induced hemodynamic alterations in anesthesia-assisted opioid detoxification can be attenuated by the alpha2-agonist clonidine and sedation, central nervous sensory activation can be attenuated by the administration of S+-ketamine (1.5 mg/kg). Since EEG alterations during acute withdrawal with naltrexone can be controlled by the non-specific NMDA-antagonist S+-ketamine, this latter presents a useful adjunct during ROD management.