Mapping of early and late human somatosensory evoked brain potentials to phasic galvanic painful stimulation

In the present study, we modeled the spatiotemporal evolution of human somatosensory evoked cortical potentials (SEPs) to brief median-nerve galvanic painful stimulation. SEPs were recorded (-50 to +250 ms) from 12 healthy subjects following nonpainful (reference), slight painful, and moderate painful stimulations (subjective scale). Laplacian transformation of scalp SEPs reduced head volume conduction effects and annulled electric reference influence. Typical SEP components to the galvanic nonpainful stimulation were contralateral frontal P20-N30-N60-N120-P170, central P22-P40, and parietal N20-P30-P60-P120 (N = negativity, P = positivity, number = latency in ms). These components were observed also with the painful stimulations, the N60, N120, P170 having a longer latency with the painful than nonpainful stimulations. Additional SEP components elicited by the painful stimulations were parietomedian P80 as well as central N125, P170 (cP170), and P200. These additional SEP components included the typical vertex negative-positive complex following transient painful stimulations. Latency of the SEP components exclusively elicited by painful stimulation is highly compatible with the involvement of A delta myelinated fibers/spinothalamic pathway. The topography of these components is in line with the response of both nociceptive medial and lateral systems including bilateral primary sensorimotor and anterior cingulate cortical areas. The role of attentive, affective, and motor aspects in the modulation of the reported SEP components merits investigation in future experiments.     

Somatosensory evoked potentials in minor cerebral ischaemia: diagnostic significance and changes in serial records

Frontal, central and parietal short and middle latency somatosensory evoked potentials (SEPs) arising after stimulation of the contralateral median nerve were studied in 10 normal adults. Stable SEPs were recorded: a frontal P21-N30 complex and an N20-P23-P28-N35-P42 complex in the centro-parietal region. The use of a chin reference electrode allowed identification of (the thalamic) P15 and N18. SEP studies of 20 patients with unilateral cerebral ischaemia were also performed, about 4 and 18 days after the stroke. In 13 out of 18 patients with a minor stroke (TIA, RIND and PNS) abnormalities of the frontal and/or parietal SEPs were demonstrated. Improvement in these SEPs occurred in 5 cases. In two patients who suffered from a major ischaemic deficit, the SEPs were highly abnormal and did not show any change in the course of time. SEP studies may be useful for the diagnosis of minor cerebral ischaemia as well as quantification of recovery; an even more important indication for this neurophysiological method might be detection of subclinical lesions in patients who have suffered from transient cerebral ischaemia even weeks before the SEP studies are carried out.     

Neural generators of N18 and P14 far-field somatosensory evoked potentials studied in patients with lesion of thalamus or thalamo-cortical radiations

Somatosensory evoked potentials (SEPs) to electrical stimulation of the right or left median nerve were studied in 4 patients with hemianesthesia and a severe thalamic or suprathalamic vascular lesion on one side. The SEPs were recorded with a non-cephalic reference. The normal side of each patient served as his or her own control. The lesion consistently abolished the parietal N20-P27-P45 and the prerolandic P22-N30 SEP components. It did not significantly affect the P9-P11-P14 positive far fields, nor the widespread bilateral N18 SEP component. This allowed N18 features to be studied without interference from cortical components. It is proposed that N18 reflects several deeply located generators in brain stem and/or thalamus whereas N20 represents the earliest cortical response of the contralateral post-central receiving areas.     

SEPs in two patients with localized lesions of the postcentral gyrus.

Scalp distributions of median nerve SEPs were studied in normal controls and 2 patients with localized lesions of the postcentral gyrus. In controls, parieto-occipital electrodes registered N20-P27 while frontal electrodes registered P20-N27. Other small components, parieto-occipital P22 and frontal N22, were recognized in about half of the control records. The wave forms at a frontal and a parieto-occipital electrode, both distant from the central region, formed exact mirror images of each other concerning N20-(P22)-P27 and P20-(N22)-N27. Electrodes near the central region contralateral to the stimulation registered cP22-cN30 (central P22 and central N30). When the postcentral gyrus was damaged, N20/P20-P27/N27 and cP22-cN30 were eliminated and the only remaining components were a frontal negative wave (frN) and a contralateral parieto-occipital positive wave (poP). Digital nerve stimulation also evoked poP and frN in both cases. In case 2, poP coincided with P22 of the non-affected side. The following generators were proposed; N20/P20-P27/N27: area 3b, cP22-cN30: areas 1 and 2, poP/early frN (= P22/N22): area 4 at the anterior wall of the central sulcus (due to direct thalamic inputs to motor cortex), late frN: uncertain (SMA?, SII?).     

Somatosensory evoked potential recovery in kii amyotrophic lateral sclerosis/parkinsonism-dementia complex (kii AlS/PDC).

OBJECTIVE: To evaluate the recovery function of the sensory cortex in patients with Kii amyotrophic lateral sclerosis/parkinsonism-dementia complex (Kii ALS/PDC) using somatosensory evoked potentials (SEPs) elicited by paired stimuli of the median nerve at the wrist. METHODS: Five patients with Kii ALS/PDC were compared with 5 patients with classical ALS, 5 with Parkinson's disease (PD), and 7 healthy normal volunteers. SEPs were recorded from the hand sensory area contralateral to the side of stimulation. Recovery functions of N20-P25 and P25-N33 components were evaluated by comparing the second SEPs elicited by paired pulse stimuli at various interstimulus intervals (ISIs, 20-300 ms) with the SEPs elicited by single stimuli. RESULTS: Conventional SEPs to a single stimulus had a normal latency and size in all patients. The recovery function of the N20-P25 and P25-N33 components showed significantly less suppression at short ISIs without any facilitation at long ISIs in Kii ALS/PDC patients than in normal subjects, classical ALS or PD patients. CONCLUSIONS: In Kii ALS/PDC, the sensory cortex is disinhibited or hyperexcitable. These abnormalities may reflect cortical pathology in the sensory cortex and may be partly due to a secondary effect on the sensory cortex from the primary parkinsonian pathological changes.     

Monitoring of subcortical and cortical somatosensory evoked potentials during carotid endarterectomy: comparison with stump pressure levels

Monitoring of multichannel somatosensory evoked potentials (SEPs) has been performed in 40 cases of carotid endarterectomy (CEA). SEPs were obtained after median nerve stimulation at wrist, recording from 2nd cervical and from the scalp parietal (ipsi- and contralateral) and central (contralateral) positions. The reduction of CBF due to clamping of the carotid artery provoked SEP abnormalities in 10 of the 40 cases. None of the 30 patients with unmodified SEPs developed post-surgical neurological sequelae. SEP alterations were characterized exclusively by amplitude decrements and latency increases of the cortical components, the subcortical ones being unaffected. In 5 of these patients, SEPs returned to normal values before the end of the intervention and no neurological deficit was observed on awakening. In the remaining 5 cases SEPs retained their abnormalities and patients developed post-surgery neurological sequelae (4 immediately, 1 the day after). SEP alterations affected parietal and central components to a similar extent; however, in a few cases cerebral blood flow deficits provoked by carotid clamping modified differently the central P22 and the parietal N20-P25 waves. Comparisons with stump (back) pressure in the carotid artery revealed a higher sensitivity of the SEP technique in detecting vascularization problems due to carotid clamping. The time course of the appearance of SEP abnormalities seems to discriminate alterations secondary to collateral revascularization from those determined by embolization.     

Origin of frontal N15 component of somatosensory evoked potential in man

Origin of the frontal somatosensory evoked potential (SEP) by median nerve stimulation was investigated in normal volunteers and in patients with localized cerebrovascular diseases, and the following results were obtained. (1) In normal subjects, SEPs recorded at F3 (or F4) contralateral to the stimulating median nerve were composed of P12, N15, P18.5 and N26. Similar components were recognized in SEP recorded at Fz. (2) In patients in whom putaminal or thalamic hemorrhages had destroyed the posterior limbs of the internal capsules, frontal N15 and parietal N18 (N20) disappeared. These components were also absent in patients with cortical (parietal) infarctions. Among these patients, the thalamus was not affected in cases with putaminal hemorrhages and cortical infarctions. These facts indicate that the generator of the frontal N15 does not exist in the thalamus but that it originates from the neural structure central to the internal capsule, which suggests a similarity to the generator of the parietal N18. Because N15 was recorded in the midline of the frontal region with shorter latency than parietal N18, the frontal N15 might represent a response to the sensory input of the frontal lobe via the non-specific sensory system.     

Somatosensory evoked potential recovery in myotonic dystrophy.

OBJECTIVE: To evaluate recovery functions of the sensory cortex using somatosensory evoked potentials (SEPs) elicited by paired stimuli of the median nerve in patients with myotonic dystrophy (MD). SUBJECTS/METHODS: Twelve MD patients were enrolled in the present investigation. Five patients with facioscapulohumeral muscular dystrophy (FSH) and 12 healthy volunteers were studied as control groups. SEP was recorded from the hand sensory area contralateral to the median nerve stimulated at the wrist. Single pulse or paired-pulse stimuli at various interstimulus intervals (ISIs) (10, 20, 40, 60, 80, 100, 150, 200 and 300 ms) were given. Recovery functions of N9, N20onset-N20peak, N20-P25 and P25-N33 components were studied. RESULTS: Conventional SEPs to a single stimulus were normal in the latency and amplitude in all the patients. Recovery functions of both N9 and N20o-N20p components were normal in the patients. In contrast, in MD patients, disinhibited or hyperexcitable recovery pattern was observed in recovery curves of the N20-P25 or P25-N33 components, whereas those were normal in FSH patients. CONCLUSIONS: Disinhibited cortical excitability (or hyperexcitability) is present in the sensory cortex in patients with myotonic dystrophy. This may reflect cortical pathology or functional alteration of the sensory cortex in MD.     

Changes of middle latency somatosensory evoked potentials (SEPs) and alpha rythmicity associated with oculomotor processes

OBJECTIVES: To evaluate median nerve somatosensory evoked potentials (SEPs) and alpha waves during different eye conditions. METHODS: Median SEPs and occipital electroencephalographs (EEG) were recorded in 6 eye conditions: eye-closed (EC), goggle (G), goggle+saccade (GS), saccade (S), eye-opened (EO) and pursuit (P), in 8 normal adults. Subjects saccaded their eyes reacting to auditory cues to watch a diode on the right or left side alternatively during the S condition, or imitated the same saccadic eye-movement as that in the S condition during the GS condition. In the P condition, subjects traced a small circle moving on a computer screen. RESULTS: Compared with the EC and G conditions, N30 (P25-N30 or P14-N30) amplitudes in C4' were significantly larger and the mean amplitude and power of the alpha band was significantly attenuated in the other 4 conditions. The amplitude and power of the alpha band differed significantly between the GS and S conditions, whereas N30 amplitudes were similar between the two conditions. N30-P45 or P45-N60 amplitudes in C4' were significantly larger in the P condition than in other conditions. CONCLUSIONS: Present findings suggest that different neural mechanisms cause alpha blocking and the modification of middle latency SEPs associated with oculomotor control.     

Short latency SEPs in infants and children: developmental changes and maturational index of SEPs

Short latency SEPs were studied in 56 normal subjects, aged 1 month to 34 years. To identify wave components definitely, simultaneous recordings not only with bipolar leads but also with superimposing methods (comparing the recordings with postcentral- and frontal-non-cephalic references (NC), contralateral to the stimulation side) were obtained in addition to routine recordings with postcentral-NC leads. Four positive (P1, P2, P3 and P4) and 2 negative (N' and N1) peak components were usually identified in all age groups, which represented the developmental changes in their features. By the method of serial representation of SEPs at each age, P1, P2, P3, P4, N' and N1 in children were found to correspond to P9, P11, P13, P14, N18 and N20 in adults, respectively. The features of SEPs in children showed great maturational changes until adolescence when they showed adult patterns. The values of the latencies of P1 and P2 divided by body height, which may be regarded as a maturational index mainly in the peripheral part of the sensory pathway, decreased with age, reaching the adult range at 3-4 years of age. The value of the N1-P3 interpeak latency divided by head circumference, which may be regarded as a maturational index mainly in the central part of the sensory pathway, also decreased with age, reaching the adult range at school age. These indices may be useful in practice for developmental evaluation of the nervous system in children.     

Abnormality of N30 somatosensory evoked potentials in Parkinson's disease: a multidisciplinary approach.

PURPOSE OF THE STUDY: Assess the N30 component of median nerve somatosensory evoked potentials (SEPs) in patients with Parkinson's disease (PD) and correlate its parameters with the severity of the disease, general cognitive ability and regional cerebral blood flow (rCBF). PATIENTS AND METHODS: Twenty-three non-demented, non-depressed PD patients (at stage II and III of the disease) and 23 age- and education-matched normal controls were enrolled in the study. SEPs were elicited by median nerve stimulation. PD patients' cognitive ability was assessed by means of: 1) Raven's Colored Progressive Matrices (RCPM); 2) the Test of Non-Verbal Intelligence (TONI-2); and 3) the Wisconsin Card Sorting Test (WCST). The patients' rCBF was evaluated by HMPAO SPECT. RESULTS: There was no difference between SEP N30 latency in PD patients and controls (P > 0.05). The P20-N30 peak-to-peak amplitude was lower in PD patients bilaterally (P < 0.05), and the amplitude of N30-P40 was lower on the right side only (P < 0.05). A significant increase in the amplitude ratio P14-N20/P20-N30 was observed in PD patients (P < 0.05). The correlation of these findings with the clinical parameters of the disease, and notably motor signs, was not significant. Of the three neuropsychological tests only the RCPM showed a positive relation to right P20-N30 amplitude. Regression analysis between SEP parameters and rCBF showed a correlation of N30 amplitude with blood flow in parietal cortical areas, but not in frontal regions.     

Parkinson's disease and lower limb somatosensory evoked potentials: apomorphine-induced relief of the akinetic-rigid syndrome and vertex P37-N50 potentials.

We evaluated brainstem P30, vertex-central P37-N50 and contralateral frontal N37 somatosensory evoked potentials (SEPs) from the tibial nerve in 14 patients affected by Parkinson's disease (PD) with akinetic-rigid syndrome. In seven patients SEPs were recorded after administration of apomorphine. The cortical P37-N50 complex was either absent (five patients, eight tested sides) or significantly smaller in patients as compared to the control group (n = 18). There was a relationship between abnormalities of early vertex potentials and degree of motor impairment. Administration of apomorphine was followed by an increase in amplitude of P37-N50 response, which was maximal after 15-30 min and then progressively returned to basal values in parallel with clinical improvement. Amplitude of brainstem P30 and frontal N37 responses was within normal values and did not vary following drug administration. These results suggest that the P37-N50 complex arises from independent cortical generators, probably located in the pre-rolandic cortex, which may be selectively affected by basal ganglia dysfunction. Amplitude decrease of the P37-50 complex may reflect an abnormal processing of somatosensory inputs within the pre-central cortex due to defective modulation exerted by basal ganglia circuitry on cortical excitability. SEP potentiation following apomorphine, besides indicating that this dysfunction is partly reversible, might suggest objective method to measure therapeutic efficacy.     

Assessing brain function in post-traumatic coma by means of bit-mapped SEPs, BAEPs, CT, SPET and clinical scores. Prognostic implications.

Sixty-eight severely head injured comatose patients were studied. Bit-colour-mapped SEPs to median nerve stimulation, BAEPs, CT and SPET regional values and ICP were assessed in relation to clinical information in evaluating cerebral function. All these variables were related to a 1-year outcome. Statistical tests confirmed the higher predictive reliability of both neurophysiological and perfusive (SPET) functional parameters compared to CT structural findings. Generally, SEPs appeared to be more reliable in predicting outcome than BAEPs. Modifications of frontal components could occur independently of post-central ones, being closely related to underlying cerebral lesions. The parameter showing the greatest correlation with outcome in the first recording session was the P25 latency, whereas this prognostic role was mainly assumed by the amplitude value of the frontal N30-P45 complex in a second recording session carried out during the third week following head trauma.     

Time course of frontal somatosensory evoked potentials. Relation to L-dopa plasma levels and motor performance in PD.

OBJECTIVE: To verify whether the change in L-dopa plasma levels after a single dose of carbidopa/L-dopa 50/200 (controlled-release) transiently modifies frontal components of somatosensory evoked potentials (SEPs) in patients with PD in parallel with improvement of motor performance. BACKGROUND: Apomorphine, a potent dopamine-agonist drug, transiently increases frontal SEP components, which may be depressed in PD; however, relationships between clinical status, frontal SEPs, and therapy are still unclear. METHODS: Nineteen PD patients (mean age 65.9 years, range 52 to 77, responders to L-dopa therapy, were studied in the same day at times T0 (baseline predose level), T1 (presumed L-dopa peak time), and T2 (end of dose-induced motor response). The following were monitored: L-dopa plasma concentration, tapping test, reaction times, peak latency (with central conduction times), and amplitude of cervical, subcortical, as well as cortical parietal and frontal SEP components elicited by median nerve stimulation of the more clinically affected arm. RESULTS: The average amplitude of frontal components of PD patients was significantly reduced at T0 with respect to control subjects. A significant and transient amplitude increase of frontal SEPs was found at T1, in parallel with the L-dopa peak concentration and improvement in motor performance (tapping and reaction times), without significant changes in amplitude of parietal SEP waves. No latency shifts were observed in brain and spinal waves. CONCLUSIONS: L-Dopa may influence the responsiveness of the parkinsonian brain as assessed by frontal somatosensory evoked potentials. The time course of these modifications coincides with that of the clinical response in the motor performance.     

Frontal and parietal components of enhanced somatosensory evoked potentials: a comparison between pathological and pharmacologically induced conditions

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.     

Scalp-recorded short and middle latency peroneal somatosensory evoked potentials in normals: comparison with peroneal and median nerve SEPs in patients with unilateral hemispheric lesions

Peroneal somatosensory evoked potentials (SEPs) were performed on 23 normal subjects and 9 selected patients with unilateral hemispheric lesions involving somatosensory pathways. Recording obtained from right and left peroneal nerve (PN) stimulations were compared in all subjects, using open and restricted frequency bandpass filters. Restricted filter (100-3000 Hz) and linked ear reference (A1-A2) enhanced the detection of short latency potentials (P1, P2, N1 with mean peak latency of 17.72, 21.07, 24.09) recorded from scalp electrodes over primary sensory cortex regions. Patients with lesions in the parietal cortex and adjacent subcortical areas demonstrated low amplitude and poorly formed short latency peroneal potentials, and absence of components beyond P3 peak with mean latency of 28.06 msec. In these patients, recordings to right and left median nerve (MN) stimulation showed absence or distorted components subsequent to N1 (N18) potential. These observations suggest that components subsequent to P3 potential in response to PN stimulation, and subsequent to N18 potential in response to MN stimulation, are generated in the parietal cortical regions.     

Effects of alcohol on myoclonus and somatosensory evoked potentials in dyssynergia cerebellaris myoclonica.

Three brothers with dyssynergia cerebellaris myoclonica received alcohol to study the correlation between improvement of myoclonus and alteration in somatosensory evoked potentials (SEPs). Alcohol considerably improved myoclonus for about six hours in two patients (cases 1 and 2) but had only a mild effect in one (case 3). All three patients had giant cortical SEPs. The amplitudes of median N20-P25 and P25-N35 components and tibial N30-P40 and P40-N50 components were considerably decreased after alcohol ingestion in two patients (cases 1 and 2) but unchanged or slightly decreased in one (case 3). The peak latencies of those components were not affected by alcohol. There was thus a good correlation between the suppression of myoclonus and the decrease in giant SEP amplitude.     

Rare cause of myoclonus with giant SEP's: methyl bromide poisoning. Apropos of a case with unilateral predominance

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.     

The prognostic value of evoked responses from primary somatosensory and auditory cortex in comatose patients.

OBJECTIVE: To evaluate somatosensory and auditory primary cortices using somatosensory evoked potentials (SEPs) and middle latency auditory evoked potentials (MLAEPs) in the prognosis of return to consciousness in comatose patients. METHODS: SEPs and MLAEPs were recorded in 131 severe comatose patients. Latencies and amplitudes were measured. Coma had been caused by transient cardiac arrest (n=49), traumatic brain injury (n=22), stroke (n=45), complications of neurosurgery (n=12) and encephalitis (n=3). One month after the onset of coma patients were classified as awake, still comatose or dead. Three months after (M3), they were classified into one of the 5 categories of the Glasgow outcome scale (GOS). RESULTS: At M3, 41.2% were dead, 47.3% were conscious (GOS 3-5) and 11.5% had not recovered consciousness. None of the patients in whom somatosensory N20 and auditory Pa were absent did return to consciousness and in the post-anoxic group, reduced cortical amplitude too was always associated with bad outcome. Conversely, N20 and Pa were present, respectively, in 33/69 and 34/69 patients who did not recover. CONCLUSIONS: The prognostic value of SEPs and MLAEPs in comatose patients depends on the cause of coma. Measurement of response amplitudes is informative. Abolition of cortical SEPs and/or cortical MLAEPs precludes post-anoxic comatose patients from returning to consciousness (100% specificity). In any case, the presence of short latency cortical somatosensory or auditory components is not a guarantee for return to consciousness. Late components should then be recorded.     

正中神经短潜伏期躯体感觉诱发电位头部分布研究及其临床意义

对46例健康成人,30例缺血性脑血管疾病、10例局灶性皮质病变病人进行4或5道记录,研究正中神经短潜伏期躯体感觉诱发电位(SEP)头部分布。顶 N20波、前额 P20波与中央前 P22波的时间-空间特征明显不同;在缺血性脑血管疾病中,中央前成分异常率(80%)明显比顶成分(30%)高,X~2=9.3,P<0.01;局灶性皮质病变,顶 N20-前额 P20与中央前 P22出现分离性异常现象。多道记录可以明确区分中央前 P22与前额 P20,顶 N20-前额 P20与中央前 P22有不同的神经起源,中央前 P22对缺血性脑血管疾病是一种敏感的诊断指标,同时记录这几个成分将提高 SEP 的诊断敏感性。