Dissociation of frontal and parietal components of somatosensory evoked potentials in severe head injury

Gütling, Eva; Gonser, Arthur; Regard, Marianne; Glinz, W; Landis, Théodor

doi:10.1016/0168-5597(93)90013-f

Cited by 33 publications

(6 citation statements)

References 24 publications

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“…Electrophysiological evidence for the acute and long-term effects of concussion has been demonstrated using EEG [7][8][9][10][11][12] and various evoked potential techniques: somatosensory evoked potentials (SSEP) [13][14][15][16][17][18][19], brainstem auditory evoked potentials (BSAEP) [18][19][20], visual evoked potentials (VEP) [10,11,19] and motor evoked potentials (MEP) [17,21]. MEPs provide a direct physiological assessment of the integrity of the motor cortex and descending motor pathways [22,23].…”

Section: Introductionmentioning

confidence: 99%

A preliminary investigation of motor evoked potential abnormalities following sport-related concussion

Livingston

Saliba²,

Goodkin³

et al. 2010

Brain Injury

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Section: Introductionmentioning

confidence: 99%

A preliminary investigation of motor evoked potential abnormalities following sport-related concussion

Livingston

Saliba²,

Goodkin³

et al. 2010

Brain Injury

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“…There have been accumulating reports that show the discrepancy in frontal and parietal SEPs (Desmedt and Bourguet, 1985;Furlong et al, 1993;Gütling et al, 1993;Yamada et al, 1984), suggesting that the frontal and parietal SEPs have separate generation mechanisms. In our study, while all the parietal SEP components seemed to recover at 200 milliseconds ISI in all states, the frontal SEP, especially later components, still did not recover in non-REM sleep at 200 milliseconds ISI.…”

Section: Discussionmentioning

confidence: 96%

Changes of Recovery Function in Median Nerve Somatosensory Evoked Potentials From Awake to Sleep

Ichikawa

Yamada²,

Taniguchi³

et al. 2009

Journal of Clinical Neurophysiology

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To investigate how the sleep affects the recovery functions of somatosensory evoked potential, we studied somatosensory evoked potential recovery functions of the median nerve during awake to sleep in eight healthy adults, using the paired conditioning and test stimulus paradigm. The most notable difference between wakefulness and sleep was the much greater enhancement of parietal P26 and frontal P22 in sleep than in awake state at interstimulus intervals of 20 to 100 milliseconds of paired stimulus paradigm. Although the enhanced P26 and P22 were observed in control somatosensory evoked potential during sleep, the augmentation was much greater when conditioned by preceding stimulus. In contrast, the parietal P40-N60 and frontal fP40-fN60 of test response were more depressed in sleep than in wakefulness. As a whole, the recovery curves in sleep appeared to be shifted to the right as compared with those in the awake, suggesting delayed recovery function in sleep. The augmentation of frontal P22 and parietal P26 in sleep, contrasting depressed other components, most notably fP40-fN60 and parietal P40-N60, imply that the former components reflect inhibitory and the latter to the excitatory process. This is the first study that demonstrates the somatosensory evoked potential recovery functions are different from those of awake state.

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“…For instance, clinical studies showed that a complete parietal lesion produced hemianaestesia, without upper motor neurons signs, eliminated the parietal complex N20-P25-P45, while the frontal complex P22-N30 persisted at usual latencies [28], suggesting that the complex N20-P25-P45 involve mainly the parietal region of the scalp. In addition, several studies have also drawn attention to a possible second thalamo-cortical loop that connects the thalamus with the frontal cortex [16,28], suggesting that the frontal complex P22-N30 may have an independent pathway. Since these studies found dissociate alterations of frontal and parietal SEP generators in different physiological condition and neurological diseases, the combined use of the frontal and parietal recording sites referenced to the earlobe in this study were selected to reflect the multiplicity of cortical excitability adaptations provoked by muscle soreness.…”

Section: Accepted Manuscriptmentioning

confidence: 99%

Cortical Somatosensory Excitability Is Modulated in Response to Several Days of Muscle Soreness

Martino

Petrini

Schabrun

et al. 2018

The Journal of Pain

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Changes in excitability of the sensorimotor cortex have been demonstrated in clinical musculoskeletal pain, although the timing is unknown. Eccentric exercise provokes delayed-onset muscle soreness providing a model to study the temporal profile of sensorimotor cortical plasticity during progressively developing muscle soreness. Twelve healthy participants performed eccentric exercise of the wrist extensors. Likert pain scores, pressure pain thresholds at the extensor carpi radialis (ECR) muscle, somatosensory evoked potentials from electrical stimulation of the radial nerve, maximal wrist extension force, and ECR motor evoked potentials to transcranial magnetic stimulation were recorded before (baseline) and at 2 hours (2-h post), 2 days (day 2), and 6 days (day 6) after exercise. Compared with baseline, 1) the Likert pain score was increased at 2-h post and increased further at day 2 (P < .01); 2) the ECR pressure pain thresholds were decreased at day 2 (P < .001); 3) the P45 amplitude of the somatosensory evoked potential from central-parietal recording sites was increased at day 2 (P < .001); 4) maximal wrist extension force was reduced 2-h post and at day 2 (P < .002); and 5) the cortical area from which ECR motor evoked potentials could be elicited was reduced at 2-h post and at day 2 (P < .03). A decrease in the ECR pressure pain thresholds was correlated (P < .027) with an increase in the P45 amplitude at a centroparietal recording site. PERSPECTIVE: These novel data demonstrate that the somatosensory cortical excitability may be affected by muscle soreness developing over days in parallel with a deficit in the motor system. Cortical neuroplasticity may thus develop in the subacute phase and be relevant for understanding neural adaptation in the transition from acute to persistent pain.

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Dissociation of frontal and parietal components of somatosensory evoked potentials in severe head injury

Cited by 33 publications

References 24 publications

A preliminary investigation of motor evoked potential abnormalities following sport-related concussion

A preliminary investigation of motor evoked potential abnormalities following sport-related concussion

Changes of Recovery Function in Median Nerve Somatosensory Evoked Potentials From Awake to Sleep

Cortical Somatosensory Excitability Is Modulated in Response to Several Days of Muscle Soreness

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