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Query: UMLS:C0027066 (myoclonus)
4,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of myoclonus from overnight exposure to methyl bromide. Myoclonus was either spontaneous or induced by somatosensory stimulation or voluntary movements, multifocal and sometimes generalized. Median SEP showed normal size P14-N20, but giant parietal P25, N33 and frontal P22-N30 waves. Back-averaging showed a biphasic EEG spike of maximal amplitude at the central region contralateral to the corresponding myoclonic jerk recorded from abductor pollicis brevis and preceding it by a short interval consistent with conduction in corticospinal pathways. Long latency reflexes from cutaneous and mixed nerve stimulation were enhanced. The above electrophysiological findings suggest that myoclonus following methyl bromide poisoning belongs to the cortical reflex myoclonus category.
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PMID:Methyl bromide myoclonus: an electrophysiological study. 232 37

Pathologically enhanced somatosensory evoked potentials (giant SEPs) were recorded in 10 patients with cortical myoclonus of various origins. With non-cephalic reference electrodes a giant frontal negativity corresponding to normal N30 was found over the contra- and ipsilateral hemispheres which was not simply a phase reversal of the well-known enhanced parietal P25. The preceding far-field P14, parietal N20 and frontal P22 were of normal size. A similar result was found when SEPs were studied during the action of etomidate, an ultrashort-acting non-barbiturate hypnotic which produced a marked increase of the parietal P25 and frontal N30 after intravenous administration. These increased components, on the other hand, were abolished when recording was repeated immediately after application of electroconvulsive shock whereas P14, N20, and P22 remained more or less unchanged in both conditions. Our results indicate that there are neuronal elements in the sensorimotor cortex which are more resistant to influences such as narcotic drugs and seizure activity than others, being highly modifiable by these alterations. It is speculated whether these highly modifiable cortical systems are those in which giant SEPs, as well as pharmacologically increased SEP components, arise.
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PMID:Frontal and parietal components of enhanced somatosensory evoked potentials: a comparison between pathological and pharmacologically induced conditions. 245 99

Giant and asymmetric SEPs were recorded in a patient with predominantly unilateral, spontaneous and intention myoclonus due to voluntary intoxication with methyl bromide as soon as day 3 after intoxication. The N10 Erb's point potential, cervical N13 and scalp recorded P15 potentials were found to be normal in latency, morphology and amplitude. The somesthetic informations could be considered as normally processed up to the subcortical levels of the somatosensory pathways. The parietal cortical potentials N20 and P25 and the frontal cortical potentials P22 and N30, contralateral to myoclonus, were abnormally large. This suggests that myoclonus could be related with an abnormal reactivity of somatomotor and somatosensory cortices to the afferent volleys triggered by voluntary movements. The prerolandic components P22 and N30 were found to be relatively more enhanced than the parietal N20 and P15.
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PMID:[Rare cause of myoclonus with giant SEP's: methyl bromide poisoning. Apropos of a case with unilateral predominance]. 404 10

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.
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PMID:The pathophysiology of giant SEPs in cortical myoclonus: a scalp topography and dipolar source modelling study. 914 78

We report a 66-year-old woman clinically diagnosed as having a corticobasal degeneration (CBD), who showed electrophysiologically cortical reflex myoclonus. She developed a clumsiness and action myoclonus on the right extremities, and aphasia. The extrapyramidal signs such as dystonia and rigidity were also noted on the right side. Sequential MR images showed a progressive brain atrophy in the left frontoparietal area, where a blood perfusion was reduced on single photon emission computed tomography (SPECT). The median nerve stimulation on the affected right side, but not left side, elicited an enhanced long-loop reflex. The onset latency of the long-loop reflex (43.8msec) was similar to that of the reported cases of CBD (Thompson et al, 1994); but, significantly shorter than that reported in the patients with typical cortical reflex myoclonus. The right median nerve stimulation also elicited so-called giant somatosensory evoked potentials (SEPs). On the basis of the scalp topography of the giant SEPs, we found the high amplitude central P22-N30 components to reflect a radial dipole. We also recorded the myoclonus-related cortical spike by jerk-locked back averaging. Both the giant SEP and myoclonus-related cortical spike were recorded only on the left scalp. We therefore suggest that these two cortical activities are similar in terms of wave form, scalp topography and time relationship to either the long-loop reflex or myoclonus and may be located in the precentral area. This is the first report of a patient with CBD presenting both the giant SEP and myoclonus-related cortical spike.
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PMID:[A case of clinically diagnosed corticobasal degeneration with unilateral cortical reflex myoclonus showing so-called giant SEP]. 1054 7