Alterations in tactile sensitivity are common in patients with chronic pain. Recent brain imaging studies have indicated that brain areas activated by acute experimental pain partly overlap with areas processing innocuous tactile stimuli. However, the possible effect of chronic pain on central tactile processing has remained unclear. We have examined, both clinically and with whole-head magnetoencephalography, six patients suffering from complex regional pain syndrome (CRPS) of the upper limb. The cortical somatosensory responses were elicited by tactile stimuli applied to the fingertips and the reactivity of spontaneous brain oscillations was monitored as well. Tactile stimulation of the index finger elicited an initial activation at 65 ms in the contralateral SI cortex, followed by activation of the ipsi- and contralateral SII cortices at about 130 ms. The SI responses were 25-55% stronger to stimulation of the painful than the healthy side. The distance between SI representations of thumb and little finger was significantly shorter in the hemisphere contralateral than ipsilateral to the painful upper limb. In addition, reactivity of the 20-Hz motor cortex rhythm to tactile stimuli was altered in the CRPS patients, suggesting modified inhibition of the motor cortex. These results imply that chronic pain may alter central tactile and motor processing.

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Previous electroencephalographic and magnetoencephalographic studies have demonstrated giant early somatosensory cortical responses in patients with cortical myoclonus. We applied whole-scalp magnetoencephalography to study activation sequences of the somatosensory cortical network in 7 patients with Unverricht-Lundborg-type progressive myoclonus epilepsy diagnostically verified by DNA analysis. Responses to electric median nerve stimuli displayed 30-msec peaks at the contralateral primary somatosensory cortex that were four times stronger in patients than in control subjects. The amplitudes of 20-msec responses did not significantly differ between the groups. In contrast to control subjects, 5 patients displayed ipsilateral primary somatosensory cortex activity at 48 to 61 msec in response to both left- and right-sided median nerve stimuli. Furthermore, their secondary somatosensory cortex was not significantly activated. These abnormalities indicate altered responsiveness of the entire somatosensory cortical network outside the contralateral primary somatosensory cortex in patients with Unverricht-Lundborg-type progressive myoclonus epilepsy. The deficient activation of the secondary somatosensory cortex in Unverricht-Lundborg patients may reflect disturbed sensorimotor integration, probably related to impaired movement coordination.

Previous electroencephalographic and magnetoencephalographic studies have demonstrated giant early somatosensory cortical responses in patients with cortical myoclonus. We applied whole‐scalp magnetoencephalography to study activation sequences of the somatosensory cortical network in 7 patients with Unverricht‐Lundborg–type progressive myoclonus epilepsy diagnostically verified by DNA analysis. Responses to electric median nerve stimuli displayed 30‐msec peaks at the contralateral primary somatosensory cortex that were four times stronger in patients than in control subjects. The amplitudes of 20‐msec responses did not significantly differ between the groups. In contrast to control subjects, 5 patients displayed ipsilateral primary somatosensory cortex activity at 48 to 61 msec in response to both left‐ and right‐sided median nerve stimuli. Furthermore, their secondary somatosensory cortex was not significantly activated. These abnormalities indicate altered responsiveness of the entire somatosensory cortical network outside the contralateral primary somatosensory cortex in patients with Unverricht‐Lundborg–type progressive myoclonus epilepsy. The deficient activation of the secondary somatosensory cortex in Unverricht‐Lundborg patients may reflect disturbed sensorimotor integration, probably related to impaired movement coordination. Ann Neurol 2001;49:90–97