Somatosensory evoked potential (SEP) recordings in patients suffering from cortical myoclonus(CM) are characterised by evidence of abnormally enhanced scalp components. Our aim was to verify whether enhanced activity in giant SEPs arises from the same generators as in healthy subjects. We used the brain electrical source analysis (BESA) to compare scalp SEP generators of healthy subjects to those calculated in 3 patients with CM of varying causes. Firstly, we built a 4-dipole model explaining scalp distribution of early SEPs in normal subjects and then applied it to traces recorded from CM patients. Our model, issued from the right median nerve grand average and applied also to recordings from single individuals, included a dipole at the base of the skull and three other perirolandic dipoles. The first of the latter dipoles was tangentially oriented and was active at the same latencies as the N20/P20 potentials and, with opposite polarity, the P24/N24 responses; the second dipole explained the central P22 distribution and the third had a peak of activity corresponding to the N30 component. When we applied our 4-dipole model to CM recordings, the first perirolandic dipole had a third peak of activity in all patients at the same latency as a parietal negativity and a frontal positivity, both following giant P24/N24 components; on the other hand, in one patient the second perirolandic dipole showed a later activation corresponding to a high central negativity, following a giant P22 response. We suggest that only the initial giant SEPs correspond to physiological potentials evoked in healthy subjects. The occurrence of late giant SEPs could be explained by hyperpolarization, following the postsynaptic excitatory potentials responsible for the early giant components. (C) 1997 Elsevier Science Ireland Ltd.

The pathophysiology of giant SEPs in cortical myoclonus: A scalp topography and dipolar source modelling study

Di Lazzaro V;
1997-01-01

Abstract

Somatosensory evoked potential (SEP) recordings in patients suffering from cortical myoclonus(CM) are characterised by evidence of abnormally enhanced scalp components. Our aim was to verify whether enhanced activity in giant SEPs arises from the same generators as in healthy subjects. We used the brain electrical source analysis (BESA) to compare scalp SEP generators of healthy subjects to those calculated in 3 patients with CM of varying causes. Firstly, we built a 4-dipole model explaining scalp distribution of early SEPs in normal subjects and then applied it to traces recorded from CM patients. Our model, issued from the right median nerve grand average and applied also to recordings from single individuals, included a dipole at the base of the skull and three other perirolandic dipoles. The first of the latter dipoles was tangentially oriented and was active at the same latencies as the N20/P20 potentials and, with opposite polarity, the P24/N24 responses; the second dipole explained the central P22 distribution and the third had a peak of activity corresponding to the N30 component. When we applied our 4-dipole model to CM recordings, the first perirolandic dipole had a third peak of activity in all patients at the same latency as a parietal negativity and a frontal positivity, both following giant P24/N24 components; on the other hand, in one patient the second perirolandic dipole showed a later activation corresponding to a high central negativity, following a giant P22 response. We suggest that only the initial giant SEPs correspond to physiological potentials evoked in healthy subjects. The occurrence of late giant SEPs could be explained by hyperpolarization, following the postsynaptic excitatory potentials responsible for the early giant components. (C) 1997 Elsevier Science Ireland Ltd.
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Utilizza questo identificativo per citare o creare un link a questo documento: https://hdl.handle.net/20.500.12610/6777
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