Temporal organization of cerebral events: neuromagnetic studies of the sensorimotor system.

Somatosensory and motor processes are closely linked to each other; smooth voluntary movements require continuous interaction of sensory and motor cortices. Sensorimotor cortical processes are readily studied with magnetoencephalography (MEG) by recording evoked responses to external stimuli or spontaneous brain oscillations. With whole-scalp coverage activation of several cortical source areas can be detected even when they are temporally overlapping. For example, electric median nerve stimuli has been shown to activate at least five different widely distributed cortical areas. With MEG recordings, temporal order of activation of different areas can be monitored to reveal functional organization of the somatosensory cortical network. Temporal resolution in millisecond scale is needed also in studies of spontaneous brain rhythms. Somatomotor mu-rhythm, with its characteristic 10 and 20Hz peaks, is typically observed over bilateral sensorimotor cortex. Mu rhythm is dampened during tactile stimulation, movement or even during action observation. Reactivity of the cortical rhythm can be quantified by temporal spectral evolution (TSE) analyses; changes in reactivity of rhythm may reveal modifications in exitatory/inhibitory balance of the sensorimotor cortex. Many neurological diseases, such as stroke and cortical myoclonus, distort activation of sensorimotor cortical network. Identification of modified activation sequences and their comparison with patients' clinical signs and symptoms may reveal pathophysiological mechanisms underlying the diseases.

Lack of activation of human secondary somatosensory cortex in Unverricht-Lundborg type of progressive myoclonus epilepsy.

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.

Abnormal reactivity of the approximately 20-Hz motor cortex rhythm in Unverricht Lundborg type progressive myoclonus epilepsy.

The approximately 20-Hz component of the human mu rhythm originates predominantly in the primary motor cortex. We monitored with a whole-scalp neuromagnetometer the reactivity of the approximately 20-Hz rhythm as an index of the functional state of the primary motor cortex in seven patients suffering from Unverricht-Lundborg type (ULD) progressive myoclonus epilepsy (PME) and in seven healthy control subjects. In patients, the motor cortex rhythm was on average 5 Hz lower in frequency and its strength was double compared with controls. To study reactivity of the approximately 20-Hz rhythm, left and right median nerves were stimulated alternately at wrists. In controls, these stimuli elicited a small transient decrease, followed by a strong increase ("rebound") of the approximately 20-Hz level. In contrast, the patients showed no significant rebounds of the rhythm. As the approximately 20-Hz rebounds apparently reflect increased cortical inhibition, our results indicate that peripheral stimuli excite motor cortex for prolonged periods in patients with ULD.