Origins of short latency somatosensory evoked potentials to median nerve stimulation

Short latency SEPs recorded in hand-scalp, ear-scalp and upper neck-scalp leads with stimulation of the median nerve were examined in 27 normal subjects and in 11 selected patients with unilateral complete loss of position sense in order to provide information concerning the generator sources of these potentials. Evidences obtained from both normal subjects and patients suggest the following origins for these short latency SEPs. In hand reference recording, P1 may arise in the brachial plexus just beneath the clavicle, P2 in the cervical dorsal column, P3 mainly in the caudal brain stem, and P4 primarily in the brain stem lemniscal pathways and partly in the thalamus. The initial negative potential recorded in upper neck-scalp leads may originate largely in the cervical dorsal columns. The early positive potential recorded in ear-scalp leads may reflect activity mainly in the brain stem lemniscal pathways and partly in the thalamus. The initial negative component of the cortical SEPs (N1) may arise in the thalamus, and the subsequent positive component (P1) may reflect activity in the primary somatosensory cortex.     

The effects of sleep on median nerve short latency somatosensory evoked potentials

The effects of sleep on median nerve short latency somatosensory evoked potentials were studied in 7 subjects made up of 6 patients being evaluated for seizure disorders by all-night electroencephalograms and 1 normal healthy volunteer. The median nerve was stimulated at the wrist, and the peripheral (N9), subcortical (P13) and early cortical (N1, P2) evoked potentials were recorded during full wakefulness and natural night-time sleep. Sleep-wake state was monitored by the simultaneously obtained polysomnogram. The latencies of the cortical responses were prolonged during non-rapid eye movement (NREM) sleep. In 3 of the subjects P2 was consistently bifid during NREM sleep only. The second component of the bifid potential, 3-4 msec longer in latency than the first, appeared to be selectively enhanced during NREM sleep whereas the first component tended to become less prominent or even disappear. This suggests that the 2 peaks have different generators that are affected differently by NREM sleep. These are clinically relevant findings for interpretation of routine clinical studies.     

Short latency somatosensory evoked potentials following median nerve stimulation in children

We investigated short latency somatosensory evoked potentials (SSEP) to median nerve stimulation in normal children and children with neurological disorders. The waveform of SSEP in normal children was almost the same as that in adults. The peak latency and interpeak latency in normal children changed during their development. Moreover, after 3 years of age, each peak latency was positively correlated with the body length and arm length. Each peak latency per 1 m of body length decreased with age. We examined SSEP in children with various neurological disorders and found that SSEP was useful for evaluating sensory functions and somatosensory damages in children who were unable to cooperate in clinical examinations. Using SSEP, we could estimate the distal margin of the lesion in the somatosensory pathway, but it was difficult to determine the accurate range of the lesion.     

Short latency somatosensory evoked potentials in patients with neurological lesions

Short latency somatosensory potentials following median nerve stimulation were recorded in patients grouped according to anatomic location of neurological lesion. Patients with cerebral lesions causing severe sensory deficit lacked a major positive wave of cortical origin that in normal subjects peaked at a mean latency of 20.5 ms. Patients with severe cervical spinal cord disease lacked all of the normal somatosensory response except for the earliest component attributed to peripheral nerve activity. Patients with brain-stem lesions showed delayed latencies of later waves and prolonged interwave latencies. However, auditory evoked potentials measured in the group with brain-stem lesions were more helpful in localization. Analysis of short latency somatosensory potentials can discriminate between peripheral nerve, spinal cord, brain-stem, and cerebral lesions. Further experience and refinement of technique of measurement should increase the value of this procedure.     

Topography of somatosensory evoked potentials to median nerve stimulation in patients with cerebral lesions

Scalp distributions and topographies of early cortical somatosensory evoked potentials (SEPs) to median nerve stimulation were studied in 22 patients with 5 different types of cerebral lesion due to cerebrovascular disease or tumor (thalamic, postcentral subcortical, precentral subcortical, diffuse subcortical and parieto-occipital lesions) in order to investigate the origins of frontal (P20, N24) and central-parietal SEPs (N20, P22, P23). In 2 patients with thalamic syndrome, N16 was delayed in latency and N20/P20 were not recorded. No early SEP except for N16 was recorded in 2 patients with pure hemisensory loss due to postcentral subcortical lesion. In all 11 patients with pure hemiparesis or hemiplegia due to precentral subcortical lesion N20/P20 and P22, P23/N24 components were of normal peak latencies. The amplitude of N24 was significantly decreased in all 3 patients with complete hemiplegia. These findings support the hypothesis that N20/P20 are generated as a horizontal dipole in the central sulcus (3b), whereas P23/N24 are a reflection of multiple generators in pre- and post-rolandic fissures. P22 was very localized in the central area contralateral to the stimulation.     

Short latency somatosensory evoked potentials to peroneal nerve stimulation in normal Japanese children

Short latency somatosensory evoked potentials (SSEP) were elicited by stimulation of the peroneal nerve in 68 normal children of 39 weeks to 15 years old. In all subjects, three positive potentials (P1, P2 and P3) and one negative potential (N1) were consistently recorded. A further positive potential (P4) after N1 was not always observed. There was no change of wave form with development. P1, P2, P3 and N1 might be generated in subcortical structures; caudal cervical spine, brainstem, thalamus and thalamocortical pathway, respectively. The latency of each peak per one meter body length decreased with age until 5 or 6 years of age. Moreover, the latency between peaks per one meter body length also decreased with age until 5 to 6 years of age. These findings are consistent with the development of SSEP on median nerve stimulation and with the developmental phenomenon of spinal conduction velocity, and might be related to the increase in the diameter and the progressive myelination of nerve fibers.     

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.     

Analysis of somatosensory evoked potentials in peroneal nerve palsy

The peroneal nerve SEPs over the CZ' of the scalp were studied in patients with peroneal nerve palsy. The initial positive peak latencies of P27 (to popliteal fossa stimulation), P30 (to fibular neck stimulation) and P37 (to dorsum of the foot stimulation) were measured. The latency difference P30-P27 was prolonged in all patients with the fibular head lesions. In patients with the superficial peroneal nerve lesions at the foreleg, P37-P27 was prolonged whereas P30-P27 was normal. Clinical application of peroneal nerve SEPs was useful in deciding the site of the lesion causing the peroneal nerve palsy.     

Hypothermia-induced changes in rat short latency somatosensory evoked potentials

Under general anesthesia, rats were gradually cooled from 37°C to 24°C. Slowly cooling avoided large temperature gradients between central and peripheral nervous systems. Short latency somatosensory potentials were evoked by forepaw stimulation and recorded from skull and depth structures. Cooling progressively increased onset and peak latencies and duration of all potentials. Amplitude of surface and depth recorded potentials decreased with decreasing temperatures except amplitude of surface component I increased. The response of surface and depth components to different rates of stimulation and cooling clearly indicates that cooling slows synaptic transmission much more than fiber conduction. The response of surface and depth recorded potentials to hypothermia suggests that evoked activity in cervical dorsal column and cuneate nucleus contributes to surface component I, that activity in cuneate nucleus, medial lemniscus, and inferior cerebellar peduncle contributes to surface component II, and that activity in thalamocortical fibers and probably cerebellum contributes to surface component III. These conclusions agree with our previous thoughts about the origin of short latency, surface recorded somatosensory evoked potentials.     

Short latency somatosensory evoked potentials from radial, median and ulnar nerve stimulation in man

Short latency somatosensory evoked potentials (SEPs) were elicited by stimulation at the wrist of median, radial, and ulnar nerves, singly or in combination, using normal subjects. Amplitude of P10 was strikingly lower with radial stimulation than with median stimulation, while ulnar-derived P10 was intermediate in amplitude. This difference probably reflects the antidromic firing of motor fibers contained in median nerves as compared with the superficial branch of radial nerve, which is entirely sensory. Beyond P10, there appear to be no significant differences between median, radial and ulnar-derived SEPs. With simultaneous stimulation of several nerves within one arm, larger potentials were sometimes achieved but with poorer definition of P12 and P14. The clinical utility of radial, ulnar, and median stimulation for localizing peripheral lesions derives from the distinct anatomical pathways of the stimulated fibers through the brachial plexus and from the separable motor and sensory components of P10. SEP is less invasive than EMG; this fact, plus its freedom from sampling error, make it potentially more suitable than conventional EMG for sequentially following a patient's clinical course.     

Study of early somatosensory evoked potentials by stimulation of the median nerve at the wrist in 6 patients with unilateral thalamic lesions

Somatosensory evoked potentials were recorded at Erb's point, over the cervical spine (C7) and over the cortex: parietal and frontal electrodes were contralateral and ipsilateral to the stimulus which was applied on the median nerve at the wrist. The stimulation was performed on 2 control groups, the first consisting of 10 subjects (average age: 33.6 years), the second of 16 subjects (average age: 66.2 years) and on 6 patients presenting unilateral thalamic lesions. These lesions were circumscribed, ischaemic or haemorrhagic and were visualized by a scanner. In 5 of our patients, a diffusion of the P14 wave with normal latency and a delay in the N20 cortical wave was obtained at the parietal electrode contralateral to the stimulus and homolateral to the lesion. Normal latencies were observed for the diffusion of the N18 wave recorded at the frontal electrode contralateral to the stimulus. In the 6th patient, the evoked potentials were normal. The results of the somatosensory evoked potentials observed in our patients are discussed in the context of the anatomical lesions.     

Serial recording of median nerve stimulated subcortical somatosensory evoked potentials (SEPs) in developing brain death

Subcortical somatosensory evoked potentials (SEPs) to median nerve stimulation were recorded serially in 35 patients during the evolution towards brain death and in brain death. Neuropathological alterations of the central nervous system down to the C1/C2 spinal cord segment in brain death are well known. SEP components supposed to be generated above this level should be lost in brain death, while components generated below should not be altered. Erb's point, scalp and neck potentials were recorded at C3/4, or over the spinous process C7, using an Fz reference. In 10 patients additional montages, including spinous process C2-Fz, a non-cephalic reference (Fz-contralateral shoulder) and a posterior to anterior neck montage (spinous process C7-jugulum) were used. The cephalic referenced N9 and N11 peaks remained unchanged until brain death. N9 and N11 decreased in parallel in amplitude and increased in latency after systemic effects like hypoxia or hypothermia occurred. The cephalic referenced 'N14' decreased in amplitude and increased in latency after the clinical brain death syndrome was observed, while N13 in the posterior to anterior neck montage remained unchanged. The alteration of 'N14' went parallel to the decrease of the P14 amplitude. The subcortical SEPs in the cephalic referenced lead are supposed to be a peak composed by a horizontally orientated dorsal horn generated N13 and a rostrally orientated P14 arising at the level of the foramen magnum. The deterioration of the non-cephalic referenced P14 and of its cephalic referenced reflection 'N14' seems to provide an additional objective criterion for the diagnosis of brain death.     

Short latency somatosensory evoked potentials in patients with syringomyelia

Short latency somatosensory evoked potentials (SSEPs) following median nerve and posterior tibial nerve stimulation were studied in six patients with syringomyelia. Three patients had Chiari malformations, two patients experienced fracture of the spine and one patient had a cauda equina ependymoma. SSEPs following median nerve stimulation were abnormal in all patients, of which five patients showed abnormal SSEPs only in the unilateral stimulation on the side of sensory deficits. SSEPs obtained from three out of eight upper extremities which showed no disturbance of deep sensation, were abnormal, so SSEPs were able to detect subclinical abnormality indicating dorsal column dysfunction. Abnormal patterns of SSEPs were classified in three types as follows; Type 1: disappearance of P13, N16 and N18 (3 cases), Type 2: the prolonged interpeak latency P11-P13 (2 cases), and Type 3: abnormal N16 and N18 with preserving P13 (1 case with Chiari malformation). P9 and P11 were present without prolonged latencies in all cases. SSEPs following posterior tibial nerve stimulation were abnormal in two of the three tested patients. Those two patients had disturbance of deep sensations in the lower extremities. All patients underwent surgical treatment, syringo-peritoneal shunt in four patients, foramen magnum decompression with syringo-subarachnoid shunt in one patient, and total removal of an ependymoma of the cauda equina with syringotomy in one patient. Postoperative neurological improvement were found in three patients, of which two cases also showed improvement in SSEPs. On the contrary SSEPs were unchanged in two patients with posttraumatic syringomyelia, whose postoperative neurological condition was also unchanged.(ABSTRACT TRUNCATED AT 250 WORDS)     

Short-latency somatosensory evoked potentials to median nerve stimulation in patients with diffuse neurologic disease

Short-latency somatosensory evoked potentials were found to be abnormal in 15 of 28 patients with diffuse neurologic disease of varying etiology and severity. These abnormalities often did not directly correlate with the presence or degree of clinical sensory impairment. They were similar to findings in patients with demyelinating and focal lesions of the nervous system. This suggests that the interpretation of these potentials can be done only in the context of the patient's clinical assessment.     

Changes in short latency SEPs (S-SEPs) to median nerve stimulation in brain dead patients

Short latency SEPs (S-SEPs) to median nerve stimulation consist of positive waves of P1, P2, P3 and P4, followed by negative waves of N 16 and N 19. These potential reflect activities of peripheral nerve, dorsal column of the cervical cord and medial lemniscus. The origins of these waves are considered as follows, P1--peripheral part of the brachial plexus, P2--the entry into the spinal cord or the dorsal column, P3--dorsal column nucleus or upper cervical cord, P4--the medial lemniscus, N 16--rostral brain stem or the thalamus, and N 19--thalamocortical projection or the cortex. The purpose of the present study is to elucidate changes of S-SEPs in brain dead patients. Fifteen brain dead patients were examined with S-SEPs. In addition to that, thirteen cases with lesions of subcortical or the brain stem but not in the state of brain death were studied for the controls. S-SEPs with non-cephalic references, conventional SEPs with earlobe reference and the evoked potentials at the Erb's point were recorded in all these cases. Serial recordings were performed in six brain dead cases during the process of rostro-caudal deterioration of the brain stem functions due to cerebral herniation. In the state of brain death, only P1 and P2 were recorded in eleven cases, and in three cases, only P1 was recorded. The other case with anoxic brain damage showed flat S-SEPs and the evoked potentials at the Erb's point could merely be obtained by the supramaximal stimulation.(ABSTRACT TRUNCATED AT 250 WORDS)