Scalp attached tangential magnetoencephalography using tunnel magneto-resistive sensors

Non-invasive human brain functional imaging with millisecond resolution can be achieved only with magnetoencephalography (MEG) and electroencephalography (EEG). MEG has better spatial resolution than EEG because signal distortion due to inhomogeneous head conductivity is negligible in MEG but serious in EEG. However, this advantage has been practically limited by the necessary setback distances between the sensors and scalp, because the Dewar vessel containing liquid helium for superconducting sensors requires a thick vacuum wall. Latest developments of high critical temperature (high-Tc) superconducting or optically pumped magnetometers have not allowed scalp-attached MEG due to cold or hot temperatures at the sensing point, respectively. Here we applied tunnel magneto-resistive (TMR) sensors that operate at room temperature. Improvement of TMR sensitivity with magnetic flux concentrators enabled scalp-attached and scalp-tangential MEG to target the largest signal component produced by the neural current below. In a healthy subject, our single-channel TMR-MEG system clearly demonstrated the N20m, the initial cortical component of the somatosensory evoked response after median nerve stimulation. Multisite measurement confirmed a spatially and temporally steep peak of N20m, immediately above the source at a latency around 20 ms, indicating a new approach to non-invasive functional brain imaging with millimeter and millisecond resolutions.

Awake state-specific suppression of primary somatosensory evoked response correlated with duration of temporal lobe epilepsy

Epilepsy is a network disease. The primary somatosensory cortex (S1) is usually considered to be intact, but could be subclinically disturbed based on abnormal functional connectivity in patients with temporal lobe epilepsy (TLE). We aimed to investigate if the S1 of TLE is abnormally modulated. Somatosensory evoked magnetic fields (SEFs) evoked by median nerve stimulation were recorded in each hemisphere of 15 TLE patients and 28 normal subjects. All responses were separately averaged in the awake state and light sleep using background magnetoencephalography. Latency and strength of the equivalent current dipole (ECD) was compared between the groups for the first (M1) and second peaks. Latencies showed no significant differences between the groups in either wakefulness or light sleep. ECD strengths were significantly lower in TLE patients than in controls only during wakefulness. The reduction of M1 ECD strength in the awake state is significantly correlated with duration of epilepsy. SEFs of TLE patients showed pure ECD strength reduction without latency delay. The phenomenon occurred exclusively during wakefulness, suggesting that a wakefulness-specific modulator of S1 is abnormal in TLE. Repetitive seizures may gradually insult the modulator of S1 distant from the epileptogenic network.

The Neurophysiological Basis of Myoclonus

There are several types of myoclonus, with a variety of classification schemes, and the clinician must determine what type of myoclonus a patient has and what type of neurophysiological assessment can facilitate diagnosis. The electromyographic (EMG) correlate of the myoclonus should be examined, including the response to sensory stimuli (C-reflex). The electroencephalographic (EEG) correlate of the myoclonus should then be examined, possibly including back-averaging from the myoclonus or looking at corticomuscular (EEG–EMG) coherence. The somatosensory evoked response (SEP) should be obtained. Such studies will help determine the myoclonus origin, most commonly cortical or brainstem. One form of cortical myoclonus has the clinical appearance of a tremor (cortical tremor). Brainstem myoclonus includes exaggerated startle (hyperekplexia). Other forms of myoclonus include spinal myoclonus and functional myoclonus, which have their own distinct physiological signature. Several causes of myoclonus are reviewed, including rare types such as Creutzfeldt-Jakob disease and subacute sclerosing panencephalitis.