Brain : a journal of neurology
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Changes in the cerebral metabolism and the excitability of brain areas remote from an ischaemic brain lesion have been reported in animals and humans and implicated as a mechanism relevant to functional recovery. The aim of the present study was to determine whether changes in the inhibitory and excitatory activity in motor cortex of the non-affected hemisphere are present in stroke patients, and whether these changes are related to the extent of the patients' recovery of function. Transcranial magnetic stimulation (TMS) was used to study the first dorsal interosseus muscle (FDI) of the non-affected hand in 13 patients with good recovery of hand function after stroke, and was compared with left hemispheric stimulation in 13 healthy age-matched volunteers. ⋯ The similarity of the inhibitory effect at low CS intensities in the patients with good recovery and healthy subjects, and the steeper increase of conditioned MEP amplitude at higher CS intensities in the recovering patients suggest that in the patients' contralesional motor cortex the balance of excitatory and inhibitory activity was shifted towards an increase of excitatory activity in the neuronal circuits tested at ISIs of 2 and 3 ms. This shares similarities to mechanisms implicated as relevant for reorganizational processes after experimental brain injury and may be relevant for functional recovery after stroke. The absence of changes in cortical excitability in patients with poor recovery supports the relevance of our findings for recovery.
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We report the response properties of the suprasylvian opercular and insular cortices to a painful stimulation delivered by a CO(2) laser recorded by depth intracerebral electrodes in epileptic patients. We defined two cortical areas of activation in the operculo-insular cortex in response to a painful laser stimulation: a suprasylvian opercular area, where we recorded responses peaking 140-170 ms after a painful stimulation (N140-P170), and a deeper insular area, where responses with a similar pattern peaked 180-230 ms after the stimulus (N180-P230). The average delay of 50 ms measured between the opercular and insular responses may reflect either sequential activation of the suprasylvian cortex then of the insula via corticocortical connections, or direct activation of the insula by inputs conveyed via thalamocortical projections through distinct fibres with different conduction times. ⋯ We were able to distinguish the suprasylvian opercular and insular cortices in terms of response latencies evoked by a painful stimulus and in terms of stereotactic coordinates of the sources of these responses. The sequential timing of activation of the suprasylvian and insular cortices shown in this study thus complements in the time domain the spatial information provided by neuroimaging studies of the cortical processing of pain. It strongly suggests that these cortical areas are those responding with the shortest latency to peripheral pain inputs in the human brain.
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Spinal cord injury (SCI) frequently results in neuropathic pain. However, the pathophysiology underlying this pain is unclear. In this study, we compared clinical examination, quantitative sensory testing (QST) and somatosensory evoked potentials (SEPs) in SCI patients with and without pain below spinal lesion level, with a control group of 20 subjects without injury. ⋯ There was no difference in intensity of pain evoked by repetitive pinprick at lesion level between patient groups. There was a significant correlation between intensity of brush-evoked dysaesthesia at lesion level and spontaneous pain below lesion level of SCI. These data suggest that lesion of the spinothalamic pathway alone cannot account for central pain in SCI patients, and that neuronal hyperexcitability at injury or higher level may be an important mechanism for pain below injury level.
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Review Multicenter Study
Demyelinating and axonal features of Charcot-Marie-Tooth disease with mutations of myelin-related proteins (PMP22, MPZ and Cx32): a clinicopathological study of 205 Japanese patients.
Three genes commonly causing Charcot-Marie-Tooth disease (CMT) encode myelin-related proteins: peripheral myelin protein 22 (PMP22), myelin protein zero (MPZ) and connexin 32 (Cx32). Demyelinating versus axonal phenotypes are major issues in CMT associated with mutations of these genes. We electrophysiologically, pathologically and genetically evaluated demyelinating and axonal features of 205 Japanese patients with PMP22 duplication, MPZ mutations or Cx32 mutations. ⋯ Median nerve MCVs were well maintained independently of age, disease duration and the severity of clinical and pathological abnormalities, confirming that median nerve MCV is an excellent marker for the genetically determined neuropathic phenotypes. Amplitude of CMAPs was correlated significantly with distal muscle strength in PMP22 duplication, MPZ mutations and Cx32 mutations, while MCV slowing was not, indicating that clinical weakness results from reduced numbers of functional large axons, not from demyelination. Thus, the three major myelin-related protein mutations induced varied degrees of axonal and demyelinating phenotypic features according to the specific gene mutation as well as the stage of disease advancement, while clinically evident muscle wasting was attributable to loss of functioning large axons.
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Randomized Controlled Trial Clinical Trial
Migraine can be induced by sildenafil without changes in middle cerebral artery diameter.
Migraine is considered a neurovascular disease involving dilatation of cerebral arteries. Nitric oxide (NO) donors induce dilatation of cerebral and extracranial arteries and migraine, but NO has several mechanisms of action in addition to its cyclic guanosine monophosphate (cGMP)-mediated vasodilatation. We examined whether sildenafil (Viagra), a selective inhibitor of cGMP-hydrolysing phosphodiesterase 5 (PDE5), which acts exclusively by increasing cGMP, can induce migraine and dilatation of cerebral arteries. ⋯ We propose that triggering mechanisms may reside within the perivascular sensory nerve terminals or the brainstem. However, other sites of action may also be possible and future studies are needed to elucidate this. In the clinical use of sildenafil, patients who have migraine should be informed about the risk of migraine attacks.