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To elucidate whether the selective electrical stimulation of muscle as well as cutaneous afferents evokes modality-specific responses in somatosensory evoked potentials (SEPs) recorded on the scalp of humans, we compared scalp SEPs to electrical stimuli applied to the median nerve and to the abductor pollicis brevis (APB) motor point. In three subjects, we also recorded SEPs after stimulation of the distal phalanx of the thumb, which selectively involved cutaneous afferents. Motor point and median nerve SEPs showed the same scalp distribution; moreover, very similar dipole models, showing the same dipolar time courses, explained well the SEPs after both types of stimulation. Since the non-natural stimulation of muscle afferents evokes responses also in areas specifically devoted to cutaneous input processing, it is conceivable that, in physiological conditions, muscle afferents are differentially gated in somatosensory cortex. The frontocentral N30 response was absent after purely cutaneous stimulation; by contrast, it was relatively more represented in motor point rather than in mixed nerve SEPs. These data suggest that the N30 response is specifically evoked by proprioceptive inputs. © 2002 Wiley Periodicals, Inc. Muscle Nerve 26: 44–55, 2002

Dipolar source modeling might help in clarifying whether somatosensory evoked potentials (SEPs) after electrical stimulation at painful intensity contain any information related to the nociceptive processing. SEPs were recorded after left median nerve stimulation at three different intensities: intense but nonpainful (intensity 2); slightly painful (pain threshold; intensity 4); and moderately painful (intensity 6). Scalp SEPs at intensities 2, 4, and 6 were fitted by a five-dipole model. When the strength modifications of the source activities up to 40 ms were examined across the different stimulus intensities, no significant difference was found. In the later epoch (40–200 ms), a posterior parietal dipole and two bilateral sources probably located in the second somatosensory (SII) areas increased significantly their dipole moments when the stimulus was increased from 2 to 4 and became painful. Since no difference was found when the stimulus intensity was increased from 4 to 6, the observed increase of the dipolar strengths is probably related to a variation of the stimulus quality (nonpainful vs. painful), rather than of the stimulus intensity per se. Our findings lead us to conclude that a large convergence of nociceptive and non-nociceptive afferents probably occurs bilaterally in the SII areas. © 2000 John Wiley & Sons, Inc. Muscle Nerve 23: 1194–1203, 2000

To elucidate whether the frontal components of scalp somatosensory evoked potentials (SEPs) depend on the type of peripheral input, we compared scalp SEPs in response to electrical stimuli applied to: (i) the proximal phalanx of the thumb, involving both deep and cutaneous afferents; and (ii) the distal phalanx of the thumb, involving cutaneous afferents, but excluding joint inputs coming from the interphalangeal articulation. We applied the same dipolar model that we built to explain the scalp SEP distribution to median nerve stimulation in previous investigations. Cortical SEPs after proximal stimulation were generated by three dipolar sources, one of which was likely to account for the frontal scalp N30. When we analyzed SEPs for distal (purely cutaneous) stimulation, the frontal and central recordings showed a clear reduction in amplitude of the negative responses having a latency of about 30 ms. Moreover, when applying the dipole model derived from analysis of responses to proximal stimulation to SEPs to distal stimulation, the source corresponding to the N30 distribution showed no activity, suggesting a strong relationship between joint and tendinous inputs and the activity of the N30 generator. © 1999 John Wiley & Sons, Inc. Muscle Nerve 22: 910–919, 1999

The early scalp somatosensory evoked potentials (SEPs) to median and tibial nerve stimulation were recorded at rest and during voluntary movement of the stimulated hand and foot, respectively. Both tibial and median nerve SEP distributions at rest could be explained by four-dipole models, in which one dipole was activated at the same latency as the subcortical far field and the three remaining dipolar sources were located in the perirolandic region contralateral to the stimulated side. Voluntary movement reduced all cortical dipoles in strength, while the subcortical one remained unchanged, suggesting that the effect of movement occurs above the cervicomedullary junction. In animals, cutaneous inputs are suppressed during movement and we therefore interpreted the depression of activity in the primary somatosensory cortex induced by movement as due to selective “gating” of cutaneous afferents. Because the reduction in strength of the cortical dipoles was generally lower during passive than active movement, both centrifugal and centripetal mechanisms probably contribute to the phenomenon of “gating.” © 1999 John Wiley & Sons, Inc. Muscle Nerve 22: 1510–1519, 1999

We studied 6 patients with adrenomyeloneuropathy (AMN) showing mild signs of central nervous system involvement. All patients underwent brain and spinal magnetic resonance imaging (MRI) and somatosensory (SEP) and motor (MEP) evoked potential study. Whereas SEPs and MEPs were abnormal in all patients, only 1 patient showed brain MRI abnormalities; spinal MRI showed hypotrophy without focal abnormalities in 4 of 6 patients. Median nerve SEPs, which were recorded with noncephalic reference montage, revealed delayed or absent scalp P14 far-field potential in all patients and abnormal spinal N13 in 2. Moreover, tibial nerve SEPs revealed abnormalities of the subcortical P30 response in all 4 patients in whom scalp-to-ear recording was employed. These findings strongly suggest that in the early stages of disease neurological dysfunction is localized in the spinal cord, where it is difficult to assess using MRI. However, SEPs and MEPs, which show a typical pattern of abnormality in these patients, could be useful in disclosing signs of long tract involvement and in monitoring treatment. © 1997 John Wiley & Sons, Inc. Muscle Nerve 20: 1249–1257, 1997