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.     

Frontal SEPs and parietal SEPs following median nerve stimulation--clinical correlation and consideration of their generation sites

In order to know the characteristics of frontal and parietal SEP components following median nerve stimulation, 25 patients with unilateral cerebral lesions above the thalamus were examined, and their SSEPs were carefully compared with the clinical and radiological findings. In 10 normal subjects, there were three cortical components of the frontal SEPs (P 20-N 28-P 44) and four those components of the parietal SEPs (N 18-P 22-N 26-P 42). In patient's group, central conduction times (CCTs) between components P 13 and each cortical component were measured and the latency differences between normal side and affected side were calculated. When the latency differences increased over 3 S.D. from the mean of the control values or the some cortical components disappeared, they were regarded as abnormal. According to the combination of the abnormalities in frontal and parietal SEPs, three groups were classified as follows: group 1; frontal and parietal SEPs were normal (n = 10), group 2; frontal and parietal SEPs were both affected (n = 10), group 3; parietal SEPs were affected but frontal components were preserved in normal range (n = 5). CT scan showed that the region from internal capsule to cortex around the central sulcus remained intact in the patients of group 1, while this region was involved in various degrees in all cases of the group 2. In patients of group 3, frontal or parietal regions were variously affected. Both the motor and sensory functions were mainly intact in group 1, and disturbed in group 2.(ABSTRACT TRUNCATED AT 250 WORDS)     

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.     

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.     

Somatosensory evoked potentials: correlations with height

Somatosensory evoked potentials (SEPs) to median and posterior tibial nerve stimulation were studied in 160 subjects aged 20-90 years. Height was highly correlated with latencies of spinal and cortical SEPs (N13, N20, N22, and P40). Although tibial central conduction (N22-P40) was also highly correlated with height, median conduction (N13-N22) was not correlated with the latter. Multiple correlation and regression analysis showed that except for the median N13-N20 latency, height provided the best prediction of the remaining SEP latencies. Age alone was not correlated with SEP latencies, but its significance was observed when age and height were considered together as the predictors. Effects of age and height on SEP latencies were independent of gender. The present data indicate that except for the N13-N20 conduction, height is the most important parameter for SEP latencies and can be used for construction of normograms.     

Cortical reflex myoclonus. A study of the relationship between giant somatosensory evoked potentials and motor excitability

The excitability cycles of the N1-P1-N2 waveforms of the scalp-recorded somatosensory evoked potential (SEP) and of the long-latency, cortical loop reflex electromyographic (EMG) activity were studied in two patients with cortical reflex myoclonus. Long-latency cortical loop reflex EMG activity in the thenar muscles and giant SEPs occurred following median nerve stimulation. The excitability cycle of the EMG paralleled that of the SEP. There was an initial period of attenuation of SEP and EMG amplitude at interstimulus intervals (ISIs) of less than 40 ms followed by a period of amplitude enhancement at an ISI of up to 200 ms followed by a second period of attenuation. The excitability cycle is abnormal and the SEP and EMG amplitude changes parallel each other. It is therefore likely that a common mechanism determines the abnormal excitability cycle. The substrate for this mechanism is unknown and may be diffuse or restricted. Oral 5-hydroxytryptophan (5-HTP) in therapeutic doses altered the SEP excitability cycle. 5-HTP did not attenuate the giant SEPs but did attenuate the long-latency reflex EMG. Therefore, 5-HTP's site of action may be different from the substrate underlying the mechanism that results in the giant SEPs. Additionally, spinal latency reflex EMG activity occurred following treatment with 5-HTP but was absent when the patient discontinued 5-HTP.     

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.     

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.     

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.     

Evoked potentials and pain. II. Comparative study of subjective sensations, late components of the cortical potentials and afferent volleys

The subjective sensations and late components of the cortical somatosensory evoked potential (SEP) have been correlatively studied when elicited by stimulation parameters which were selected in order to activate selectively, either the largest afferent fibers (train of shocks of 10 mA, with a 0.05-0.2 msec duration for each shock) or the several groups of fibers (A alpha beta; A delta and C) of the cutaneous branches of the median nerve (single shock, 1 msec duration; 20 mA). In both cases, a good correlation was found between the quality and intensity of sensations and the amplitude of the late component N150-P220-N400 of the SEP. However, it was also found that this relationship was not linear and suggested that it is possible to saturate the cortical integrative system responsible for the SEP. A selective blockage of the largest fibers (compression) or of the finest ones (lidocaine) have shown that there is no specific involvement of a particular type of peripheral fiber in the genesis of the N150-P220-N400 components. Moreover, these late components could also be recorded with similar latencies when cutaneous stimulations were applied in any part of the body.     

Differences between somatosensory-evoked potentials recorded from the ventral posterolateral thalamic nucleus, primary somatosensory cortex and vertex in the rat

Somatosensory-evoked potential (SEP) components recorded over the primary somatosensory cortex (SI) and vertex in the rat within the 10-30 ms latency range were characterised with respect to the anatomy and function of the primary somatosensory pathway. To this aim, these components were compared to SEP components in the similar latency range recorded from the ventral posterolateral thalamic (VPL) nucleus, a nucleus known to be part of the subcortical structure of the primary somatosensory pathway and were described with respect to their stimulus-response characteristics and their response to the mu-opioid agonist fentanyl. The VPL positive (P)11-negative (N)18-P22 and SI P13-N18-P22 differed with respect to peak occurrence (P11 versus P13, respectively) and waveform morphology, but did not differ with respect to stimulus-response characteristics and their response to fentanyl. When compared to the vertex P15-N19-P26, the VPL P11-N18-P22 and SI P13-N18-P22 complex follow a relatively fast acquisition in stimulus intensity-response and were affected significantly less to increasing stimulus frequencies and to fentanyl. These results demonstrated that when compared to the VPL-SEP and SI-SEP, the Vx-SEP was modulated differently by the experimental conditions. It is suggested that this may be related to involvement of neural structures within different functional somatosensory pathways.     

Source generators of the early somatosensory evoked potentials to tibial nerve stimulation: an intracerebral and scalp recording study.

OBJECTIVE: To investigate the location of the cerebral generators of the early scalp somatosensory evoked potentials (SEPs) after tibial nerve stimulation. METHODS: Tibial nerve SEPs were recorded in 15 patients, suffering from Parkinson's disease, who underwent implantation of intracerebral (IC) electrodes in the subthalamic nucleus, in the globus pallidum or in the thalamic ventralis intermediate nucleus. SEPs were recorded both from the scalp surface and from the IC leads. RESULTS: The lemniscal P30 response was recorded by all the electrodes. The IC waveforms included a negative N40IC response, followed by a positive (P50IC) and a negative (N60IC) potential. The N40IC, the P50IC and the N60IC potentials did not differ in latency from the P40, the N50 and the P60 responses recorded by the Cz electrode. In 6 patients, in which SEPs were recorded also during the voluntary movement of the stimulated foot (active gating), an amplitude reduction of the SEP components following the P30 potential was observed during movement at the vertex and in the IC traces. Instead, in the contralateral temporal traces the SEP components (N40temp and P50temp) were not modified by active gating, and in the ipsilateral parietal traces only the positive potentials at about 60ms of latency was decreased. CONCLUSIONS: Two differently oriented generators are active in the contralateral hemisphere at both 40 and 50ms of latency after tibial nerve stimulation. One source is oriented perpendicularly to the mesial hemispheric surface and generates the potentials recorded by the contralateral temporal and the ipsilateral parietal leads; the other dipolar source is radial to the hemispheric convexity, and generates the potentials at the vertex and those recorded by the IC electrodes.     

The effects of focal epileptic activity on the somatosensory evoked potentials in the rat

Summary The cortical somatosensory evoked potential (SEP) of the rat, evoked by contralateral forepaw stimulation, consisted of early (P 1 and N 1) and late components (P 2 and N 2). Microelectrode recording yielded evoked unitary responses of short latencies in the range of the early components and responses of longer latencies in the range of P 2. During the development of focal epilepsy after topical application of penicillin, the late components of SEP were enhanced and the enhanced late negativity corresponded to a surface negative cortical spike. The prominent enlargement of later components was associated with prolonged, often recurrent discharges of longer latency unitary responses and with enlarged local field potentials. Early components of SEP remained relatively unaffected and so did unitary responses with short latencies.Epileptic spike-conditioned SEPs in the cuneate nucleus, thalamic sensory relay nucleus and sensory cortex were depressed from 100 ms (cuneate nucleus) to about 300 ms (thalamus and cortex) subsequent to spike discharge. Transmission in the cuneate nucleus was least affected. Thalamic and cortical early components of SEP had similar time courses of recovery, which differed markedly from that of cortical late components. Our findings suggest that two different neuronal activities generate different components of SEP and are differentially involved in the epileptic activities, which results in the different amplitude recovery following spontaneous epileptic spike discharges.This work was supported by the Deutsche Forschungsgemeinschaft (German Research Council)     

Somatosensory evoked potentials in Huntington's disease

Scalp recorded somatosensory evoked potentials (SEPs) elicited by left and right median nerve stimulation were obtained in 21 patients with Huntington's disease (HD), 14 individuals at risk (AR) for HD, and 21 non-patient controls matched for age and sex. Although SEP abnormalities were not uniform in the HD group, no HD patient had SEPs that conformed fully to the normal configuration with respect to peak latencies, presence of all components and spatial distribution. The most common abnormality was non-specific in nature, consisting of amplitude reduction or virtual abscence of components after 100 msec. More specific deviations were noted in the early SEP events. In half of the HD patients, peak P30 seemed to occur at approximately 45 msec poststimulus; this peak could have been taken as the normal P45 had it not reversed in phase between the central and frontal leads. In these cases peak P45 prepared to be missing. Peak N20 latency values were longer in the HD group than in the non-patient controls, whereas the P15 latencies did not differ significantly. The conduction time between P15 and N20 was significantly longer in HD patients than the non-patient controls. SEPs of the majority of the ARs were similar to those of the non-patients controls in terms of overall configuration, although mean amplitudes were generally lower for ARs than non-patient controls and 4 ARs exhibited prolonged P15-N20 latency differences.     

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.     

Reduction in amplitude of the subcortical low- and high-frequency somatosensory evoked potentials during voluntary movement: an intracerebral recording study.

OBJECTIVE: To investigate whether the reduction of amplitude of the scalp somatosensory evoked potentials (SEPs) during movement (gating) is due to an attenuation of the afferent volley at subcortical level. METHODS: Median nerve SEPs were recorded from 9 patients suffering from Parkinson's disease, who underwent implant of intracerebral (IC) electrodes in the subthalamic nucleus or in the globus pallidum. SEPs were recorded from Erb's point ipsilateral to stimulation, from the scalp surface and from the IC leads, at rest and during a voluntary flexo-extension movement of the stimulated wrist. The recorded IC traces were submitted to an off-line filtering by a 300-1500 bandpass to obtain the high-frequency SEP bursts. RESULTS: IC leads recorded a triphasic component (P1-N1-P2) from 14 to 22 ms of latency. The amplitudes of the scalp N20, P20 and N30 potentials and of the IC triphasic component were significantly decreased during movement, while the peripheral N9 amplitude remained unchanged. Also the IC bursts, whose frequency was around 1000 Hz, were reduced in amplitude by the voluntary movement. CONCLUSIONS: Since the IC triphasic component is probably generated by neurons of the thalamic ventro-postero-lateral nucleus, which receive the somatosensory afferent volley, the P1-N1 amplitude reduction during movement suggests that the gating phenomenon involves also the subcortical structures.     

Operant conditioning of somatosensory evoked potential (SEP) amplitude in rats. I. Specific changes in SEP amplitude and a naloxone-reversible somatotopically specific change in facial nociception

The aim of this experiment was to investigate possible endogenous opioid modulation of innocuous somatosensory activity. Somatosensory activity was measured by recording cortical somatosensory evoked potential (SEP) and reflex movement amplitude evoked by innocuous electrical stimulation of the spinal trigeminal tract in awake rats. Putative endogenous opioid activity was blocked using the opiate antagonist naloxone (1 mg/kg). The amplitude of midlatency SEP components (14-50 ms latency) increased following administration of naloxone and repeated stimulus presentations. The amplitude of these components decreased following administration of the opiate agonist morphine (3 mg/kg). An early cortical component (10 ms latency) habituated following the administration of saline but did not habituate following naloxone. Naloxone also enhanced habituation of the late SEP components (60-120 ms latency) and reflex movement evoked at higher stimulus intensities. Morphine decreased the amplitude of the early cortical component but had no consistent effect on the amplitude of the late SEP components.     

Giant SEPs and SEP-recovery function in Unverricht–Lundborg disease

ObjectiveTo evaluate the relationship between sensory hyperexcitability as revealed by giant SEPs and the SEP recovery function (SEP-R) in a series of patient with progressive myoclonic epilepsy of Unverricht–Lundborg type, identified as epilepsy, progressive myoclonic 1A (EPM1A), MIM #254800.MethodsWe evaluated SEPs by applying median nerve stimuli and SEP-R using paired stimuli at inter-stimulus intervals (ISIs) of between 20 and 600 ms in 25 patients and 20 controls. The SEPs were considered “giant” if the N20P25 and P25N33 amplitudes exceeded normal mean values by +3SD.ResultsDuring the paired-stimulus protocol, the SEPs elicited by the second stimulus (S2) were detectable at all ISIs but consistently suppressed in the 13 patients with giant SEPs reflecting a significantly delayed SEP-R. Maximal suppression roughly corresponded to the plateau of a broad middle latency (>100 ms) wave pertaining to the S1 response.ConclusionsThe cortical processing dysfunction generating giant SEPs in EPM1A patients consistently combines with a long-lasting suppression of hyperexcitability that leads to a delayed giant SEP-R without obstructing the response to incoming stimuli.SignificanceThe delayed SEP-R is not due to true inhibition but the suppression of aberrant hyper-synchronisation sustaining giant SEPs. A broad middle latency SEP component adds a significantly suppressive effect. This suggests that cortico-subcortical circuitries contribute to both the gigantism and the delayed SEP-R.     

Topography and intracranial sources of somatosensory evoked potentials in the monkey. II. Cortical components

Averaged somatosensory evoked potentials (SEPs) and associated multiple unit activity (MUA) were recorded from a series of epidural and intracortical locations following stimulation of the contralateral median nerve in the monkey. Cortical components were differentiated from the earlier subcortical activity and the intracerebral distribution and sources of each cortical potential were determined. Under barbiturate anesthesia the SEP wave form is simplified and can be wholly attributed to two sources. The earliest cortical activity consists of a biphasic P10-N20 wave which is generated in the posterior bank of the central sulcus. A second wave form, P12-N25, originates in the crown of the postcentral gyrus. No other cortical areas are active. In the alert state the morphology of the surface SEP is complex and reflects the interaction of volume conducted activity from several adjacent cortical sources. The wave form overlying the hand area of the postcentral gyrus consists of P12, P20, P40, N45 and P110. Precentral recordings exhibit P10, P13, N13, N20, P24, N45 and P110. Six anatomical sources have been identified. P10 and N20 originate in the posterior bank of the central sulcus including areas 3a and 3b and are volume conducted in an anteroposterior direction. P12 originates in area 1 as well as the anterior portion of area 2. P20 is generated in the medial portion of the postcentral gyrus including area 5. The source of P40 lies within the lateral portion of the parietal lobe including area 7b. Two components were generated in precentral cortex: P13/N13 originates principally in area 4 within the anterior bank of the central sulcus and P24 reflects activity in the anteromedial portion of the precentral gyrus including area 6. The long latency SEP components, N45 and P110, are generated widely within the somesthetic areas of postcentral cortex. The early cortical SEP components recorded in the monkey closely resemble in configuration and topography those recorded from man although the latter are longer in latency, reflecting interspecies differences in the length of conduction pathways as well as in cortical processing time.     

Median and tibial somatosensory evoked potentials. Changes in short- and long-latency components in patients with lesions of the thalamus and thalamo-cortical radiations

Alterations in short- and long-latency components of median and tibial somatosensory evoked potentials (SEPs) were studied in patients with lesions in the thalamus and thalamo-cortical radiations. When the lesions were located primarily in the ventro-posterior thalamus, the SEP changes consisted of the following combination: absence of response; decrease in response amplitude; delay in peak latency; and attenuation of median N20-P25 and tibial P40. The laterally situated ventro-posterior lesions tended to preferentially affect tibial SEPs whereas the medially situated lesions tended to preferentially affect median SEPs. The lateral thalamic lesions affected primarily the long-latency SEP components, whereas the medial thalamic lesions affected primarily the mid-latency or the mid- and long-latency SEP components. Corona radiata infarcts produced SEP changes similar to those with the ventro-posterior thalamic lesions except that absence of evoked responses was not observed. Subcortical infarcts tended to affect the mid- and long-latency SEP components with relative preservation of the short-latency components. The present data indicate that only the lesions involving the primary thalamic relay area affected all SEP components, particularly the short-latency components, and that the lesions in other thalamic areas can also influence the SEPs, particularly the mid- and long-latency components. The present study further demonstrates that a combined use of median and tibial SEPs is useful in delineating the topographic organization of the somatosensory system in the thalamus.