The early negative potential evoked by stimulation of the tibial nerve in man

Berić, Aleksandar; Prevec, Tine S.

doi:10.1016/0022-510x(81)90175-1

Cited by 44 publications

(8 citation statements)

References 15 publications

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“…The dissociated involvement of the vertex-ipsilateral central P37 and of the contralateral N37 in patients with dystonia supports the concept that these potentials arise from multiple and partially independent cortical generators [16][17][18][19][20]28,29 rather than from a unique generator located in the primary somatosensory cortex [30][31][32][33][34] contralateral to the stimulated side. The question that now needs to be resolved is what the vertex-ipsilateral central P37-N50 represents and why it should be affected in dystonia.…”

Section: Discussionsupporting

confidence: 68%

“…[12][13][14] Our findings of an enhanced vertex-ipsilateral central P37-N50 response (but not of the contralateral N37) following tibial nerve stimulation validate these results, because the P22-N30 complex is thought to originate in the precentral cortex (more precisely in the supplementary motor area) 44,45 and is probably the analogue of the P37-N50 response, 21,22 whereas the parietal N20 is thought, like the tibial N37, to arise in area 3b of S1. 16,21,22 All these findings suggest that tibial nerve P37-N50 and median nerve P22-N30 might have a similar meaning in dystonia: both might be indicative of enhanced excitato-ry effects on the cortex resulting from disorders of the basal ganglia.…”

Section: Discussionmentioning

confidence: 94%

“…An increasing number of observations suggests that the generators of the N37 and P37-N50 are respectively related to the activation of the postcentral and precentral cortex. [16][17][18][19][20][21][22] To assess possible abnormalities of scalp SEPs from the lower limb in dystonia, we studied subcortical and cortical SEPs from tibial nerve stimulation in a group of patients who had dystonia involving at least one leg. The data were compared with those found in a group of normal age-matched subjects.…”

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confidence: 99%

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Evidence for an abnormal cortical sensory processing in dystonia: Selective enhancement of lower limb P37-N50 somatosensory evoked potential

et al. 1999

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We evaluated brain stem P30, contralateral frontal N37, and the vertex‐ipsilateral central P37, N50 somatosensory evoked potentials (SEPs) obtained in response to stimulation of the tibial nerve in 10 patients with idiopathic dystonia. Results were compared with those obtained in 10 healthy subjects matched for age and sex. The amplitude of the brain stem P30 potential and of the contralateral frontal N37 response in dystonic patients was not significantly different from that recorded in normal subjects. The vertex‐ipsilateral central P37‐N50 complex, which is thought to originate in the pre‐rolandic cortex, was significantly enhanced in patients compared with the control group. These results suggest the enhancement of the vertex‐ipsilateral central P37‐N50 complex might reflect an abnormal response to somatosensory inputs of a precentral cortex which is excessively activated because of a disorder of the basal ganglia. Such inefficient sensory processing in motor areas might contribute to motor impairment in dystonia.

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Section: Discussionsupporting

confidence: 68%

Section: Discussionmentioning

confidence: 94%

mentioning

confidence: 99%

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Evidence for an abnormal cortical sensory processing in dystonia: Selective enhancement of lower limb P37-N50 somatosensory evoked potential

et al. 1999

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“…Cerebral potentials evoked through stimulation of the leg have the advan-tage of monitoring conduction through the whole neuraxis. Their use is gaining popularity (Tsumoto et al, 1972;Dorfman, 1977;Kimura et al, 1978;Jones and Small, 1978;Eisen and Nudleman, 1979;Eisen and Odusote, 1980;Vas et al, 1981;Beric and Prevec, 1981). With tibial nerve stimulation at the ankle a prominent positive wave occurs at about 40 msec (P40).…”

Section: Lower Limb and Lumbar-spinal Sepsmentioning

confidence: 99%

“…This is the equivalent of N20 evoked by median nerve stimulation (figure 4, table 2). It and earlier subcortically generated peaks (gracile nucleus amongst others) have been recently recorded using both non-cephalic references (Vas et al, 1981) and bipolar cephalic montages (Beric and Prevec, 1981;Leandri et al, 1981;Lueders et al, 1981). Figure 4 schematically shows the early latency SEP components and their presumed neural generators evoked by lower extremity stimulation.…”

Section: Lower Limb and Lumbar-spinal Sepsmentioning

confidence: 99%

The Somatosensory Evoked Potential

Eisen

1982

Can. j. neurol. sci.

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Three decades have elapsed since Dawson (1947) recorded the first somatosensory evoked potential (SEP). Simple superimposition of individual responses was possible because the patient had progressive myoclonic epilepsy. In this disease the SEP amplitude is much enhanced (Shibasaki et al, 1978; Kelly et al, 1981). Subsequently Dawson (1951, 1954) presented his averager to the Physiological Society, thereby initiating the present-day explosive growth of evoked potentials.SEPs are made up of components with varying latencies. The components are best identified by latency and polarity as recorded at the scalp (P = positive and N = negative). Nevertheless, the nomenclature of somatosensory evoked potentials can be extremely confusing, mainly because the same component can have a different polarity depending on the electrode montage used. Generally speaking (but this is not a firm rule), far-field (subcortical) potentials are positive in polarity when a non-cephalic reference is used, whereas these same components have a negative polarity when the reference is on the scalp. It is therefore useful to always indicate the recording montage being employed. In addition, use of absolute latencies in the terminology can cause confusion because they are dependent upon length and body height. For example, the brachial plexus component usually occurs at about 9 msec, but may extend to as long as 11 or more msec in a very tall individual. Subsequent components then become difficult to identify in relation to normal means.

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Characterizing somatosensory evoked potential sources with dipole models: Advantages and limitations

2001

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Several methods have been developed to investigate the cerebral generators of scalp somatosensory evoked potentials (SEPs), because simple visual inspection of the electroencephalographic signal does not allow for immediate identification of the active brain regions. When the neurons fired by the afferent inputs are closely grouped, as usually occurs in SEP generation, they can be represented as a dipole, that is, as a linear source with two opposite poles. Several techniques for dipolar source modeling, which use different algorithms, have been employed to build source models of early, middle‐latency, and late cognitive SEPs. Modifications of SEP dipolar activities after experimental maneuvers or in pathological conditions have also been observed. Although the effectiveness of dipolar source analysis should not be overestimated due to the intrinsic limitations of the approach, dipole modeling provides a means to assess SEPs in terms of cerebral sources and voltage fields that they produce over the head. © 2001 John Wiley & Sons, Inc. Muscle Nerve 24: 325–339, 2001

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The early negative potential evoked by stimulation of the tibial nerve in man

Cited by 44 publications

References 15 publications

Evidence for an abnormal cortical sensory processing in dystonia: Selective enhancement of lower limb P37-N50 somatosensory evoked potential

Evidence for an abnormal cortical sensory processing in dystonia: Selective enhancement of lower limb P37-N50 somatosensory evoked potential

The Somatosensory Evoked Potential

Characterizing somatosensory evoked potential sources with dipole models: Advantages and limitations

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