A study of peripheral cervical and cortical evoked potentials and afferent conduction times in the somatosensory pathway

Somatosensory evoked potentials were recorded from Erb's point (N9), the cervical spine (N14) and the scalp (N20) in 47 volunteer patients to establish the normal impulse conduction time between these recording sites. Either the ulnar or the median nerve or both were stimulated percutaneously, and pure sensory as well as mixed sensorimotor nerve fibres were used. No significant differences in either the N9-N14 or N14-N20 conduction times were found for different sets of peripheral stimuli. The N9-N14 conduction time evidently reflects impulse propagation in the proximal part of the brachial plexus, the cervical roots and the dorsal column. Cross-correlation analysis, however, suggested that the main contribution to this conduction time is a central one, probably the dorsal column. The N14-N20 conduction time represents a pure central conduction time probably between the dorsal column nuclei and the cortex. While the amplitudes, morphologies and latencies of the somatosensory evoked responses N9, N14 and N20 varied significantly, the N9-N14 and N14-N20 conduction times were fairly constant. The results indicate that diagnostic use of the somatosensory evoked potentials based exclusively on the response latencies can be very misleading, both when latencies are normal and when pathologically delayed. In such cases the N9-N14 and N14-N20 conduction times can be conclusive, and we suggest that these times should be included in all SEP tests.     

Short-latency somatosensory evoked potentials following median nerve stimulation in Down's syndrome

Short-latency somatosensory evoked potentials (SEPs) following median nerve stimulation were recorded in 42 patients with Down's syndrome and in 42 age- and sex-matched normal subjects. There were no significant differences between the 2 groups in the absolute peak latencies of N9, N11 and N13 components. However, interpeak latencies, N9-N11, N11-N13 and N9-N13, were prolonged significantly in Down's syndrome. These findings suggest impaired impulse conduction in the proximal part of the brachial plexus, posterior roots and/or posterior column-medial lemniscal pathway. Interpeak latency N13-N20, representing conduction time from cervical cord to sensory cortex, was not significantly different between the 2 groups. Cortical potentials N20 and P25 in the parietal area and P20 and N25 in the frontal area were of significantly larger amplitude in Down's syndrome. P25 had double peaks in 16 of 42 normal subjects, but these were not apparent in any of the patients.     

Peripheral and segmental spinal abnormalities of median and ulnar somatosensory evoked potentials in Hirayama's disease

OBJECTIVES: To investigate the origin of juvenile muscle atrophy of the upper limbs (Hirayama's disease, a type of cervical myelopathy of unknown origin). SUBJECTS: Eight male patients were studied; data from 10 normal men were used as control. METHODS: Median and ulnar nerve somatosensory evoked potentials (SEP) were recorded. Brachial plexus potentials at Erb's point (EP), dorsal horn responses (N13), and subcortical (P14) and cortical potentials (N20) were evaluated. Tibial nerve SEP and motor evoked potentials (MEP) were also recorded from scalp and spinal sites to assess posterior column and pyramidal tract conduction, respectively. RESULTS: The most important SEP findings were: a very substantial attenuation of both the EP potentials and the N13 spinal responses; normal amplitude of the scalp N20; and normal latency of the individual peaks (EP-N9-N13-P14-N20). Although both nerves were involved, abnormalities in response to median nerve stimulation were more significant than those in response to ulnar nerve stimulation. There was little correlation between the degree of alterations observed and the clinical state. Latencies of both spinal and cortical potentials were normal following tibial nerve stimulation. The mean latency of cervical MEP and the central conduction time from the thenar eminence were slightly but significantly longer in patients than in controls. CONCLUSIONS: The findings support the hypothesis that this disease, which is clinically defined as a focal spinal muscle atrophy of the upper limb, may also involve the sensory system; if traumatic injury caused by stretching plays a role in the pathogenesis, the damage cannot be confined to the anterior horn of the spinal cord.     

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.     

Effects of stimulus intensity on latency and conduction time of short-latency somatosensory evoked potentials.

We studied the effect of stimulus intensity on latencies of short-latency somatosensory evoked potentials (SSEP) by measuring both onset and peak latencies individually. The latencies of N9, N13, N20 and N9-N13 peripheral conduction time (PCT) of median nerve (MN) SSEP, and N8, N23, P37 and N8-N23 PCT of tibial nerve (TN) and sural nerve (SN) SSEP significantly shortened with increasing stimulus intensity by onset latency measurement. However, those latencies by peak latency measurement were less significantly shortened or had only a trend of latency shortening without statistical significance. In contrast to PCT, N13-N20 central conduction time (CCT) of MN-SSEP and N23-P37 CCT of TN- or SN-SSEP showed no latency changes with the increased stimulus intensity by both onset and peak latencies measurement. As peak latencies had greater interindividual variability than onset latencies shown by larger standard deviation, shortening of onset latencies were more consistent than that of peak latencies. We think shortening of onset latencies indicates the recruitment of faster conduction fiber along with increased stimulus intensity. As the degree of latency shortening was less if stimulus intensity was above 2.5 times sensory threshold, the stimulus intensity greater than 2.5 times the sensory threshold should be used for clinical application.     

Intersession stability of somatosensory evoked potentials

Upper and lower limb nerve somatosensory evoked potentials (SEPs) were recorded from a group of normal adults in order to assess their intersession stability. Median, peroneal and sural nerve SEPs were recorded from each subject on 3 successive occasions at weekly intervals. For median nerve SEPs, the intrinsic variability was more pronounced for interpeak latencies (N9-N20, N13-N20) than for the latencies of individual components. Their inherent fluctuation was not, however, notably greater for the primary cortical response (N20) than for the more caudally generated components (N9 and N13). These relationships were not so apparent for lower limb SEPs where intersession variability was markedly greater overall than for upper limb SEPs.     

Carbamazepine Does Not Affect Short-Latency Somatosensory Evoked Potentials: A Longitudinal Study in Newly Diagnosed Epilepsy

Somatosensory evoked potentials from median nerve stimulation were recorded in 12 patients with newly diagnosed epilepsy, before and after 1 year of treatment with carbamazepine. The plasma concentrations of the drug were consistently within therapeutic range. We assessed the latencies of the early components at the level of the cervical spine (N9 and N13) and on the parietal scalp (P14, N20, P25) and the interpeak latencies (N9-N13, N13-N20, P14-N20). None of the patients presented anomalies in any of the parameters, and there was no significant difference between the patient and control means or between the patient means before and after 1 year of treatment.     

Origin of the early components of somatosensory evoked potentials by the posterior tibial nerve stimulation--a comparative study of median nerve stimulation in clinical cases

In order to determine the generation sites of short latency somatosensory evoked potentials to the posterior tibial nerve stimulation, scalp topography was performed on 10 normal subjects in the two different band-pass recordings, i.e., wide band-pass filter (5-3000 Hz) and narrow band-pass filter (100-1000 Hz). Furthermore, comparative study of the changes of evoked potentials between posterior tibial nerve stimulation and median nerve stimulation was carried out in 22 cases with well localized lesion of the central nervous system in the same wide band-pass filter setting. The early components of somatosensory evoked potentials elicited by the posterior tibial nerve stimulation were obtained as P 30, N 34, and P 38 in the wide band-pass filter, and P 29, N 32, P 36 in the narrow band-pass filter. Components P 30, N 34 and components P 29, N 32 were widely distributed on the scalp, but were disappeared on the scalp-scalp recording. These results suggested all those components were generated from the deep subcortical structures. In the case with high cervical lesion, component P 30 at the posterior tibial nerve stimulation was remarkably prolonged in latency, and component P 13 at the median nerve stimulation was disappeared. P 30-N 34 interpeak latency at the posterior tibial nerve stimulation was prolonged in the case with pontine lesion, while P 13-N 16 interpeak latency at the median nerve stimulation was also prolonged. In the cases with thalamic and internal capsular lesion, P 30 and N 34 at the posterior tibial nerve stimulation and P 13 and N 16 at the median nerve stimulation were all preserved in normal range. These results revealed that components P 30 and N 34 were almost identical to components P 13 and N 16, respectively. On the other hand, component P 38 at the posterior tibial nerve stimulation was suppressed or disappeared in the cases with well localized lesion at the midcentro parietal region, that includes the primary foot sensory area.(ABSTRACT TRUNCATED AT 400 WORDS)     

Estimation of cervical cord dysfunction by somatosensory evoked potentials

The purpose of this study was to examine the relationship of abnormal short-latency somatosensory evoked potentials (SSEPs) recorded by a noncephalic reference montage with clinical variables in cervical myelopathy patients and to reexamine the diagnostic utility of SSEPs in such patients. We studied cervical SSEPs elicited by stimulating the median and ulnar nerves in 87 patients. Our grade classification of spinal N13, which is based on the normal limits of latencies or amplitudes, corresponded well with the clinical variables and is of value when trying to localize the cervical lesion segmentally. The N9-P14 interpeak latency in response to ulnar nerve stimulation correlated well with lower extremity function (r = -0.440, P <0.0001). We suggest a combined assessment of N13 amplitude, and N9-N13 and N9-P14 interpeak latencies to estimate dorsal column and dorsal horn function separately in patients with cervical myelopathy.     

Peripheral and central conduction abnormalities in diabetes mellitus

OBJECTIVES: To investigate peripheral and central somatosensory conduction in patients with diabetes. METHODS: The authors recorded sensory nerve action potentials and 5-channel somatosensory evoked potentials (SEPs) with noncephalic reference after median nerve stimulation in 55 patients with diabetes and 41 age- and height-matched normal subjects. The authors determined onset or peak latencies of the Erb's potential (N9) and the spinal N13-P13 and the cortical N20-P20 components, and obtained the central conduction time (CCT) by onset-to-onset and peak-to-peak measurements. RESULTS: Both onset and peak latencies of all SEP components were prolonged in patients with diabetes. The mean onset CCT in the diabetic group was 6.3 +/- 0.5 msec (mean +/- SD)-significantly longer than that in the control group (6.1 +/- 0.2 msec)-whereas no significant difference was found in the peak CCT. The amplitudes of N9 and N13-P13 components (but not N20-P20) were significantly smaller in the diabetic group. The peripheral sensory conduction velocity was also decreased in the diabetic group, but there was no significant correlation between peripheral conduction slowing and the onset of CCT prolongation. CONCLUSIONS: Diabetes affects conductive function in the central as well as peripheral somatosensory pathways. The CCT abnormality does not coincide with lowering of the peripheral sensory conduction. The current results do not favor a hypothesis that a central-peripheral distal axonopathy plays an important role in development of diabetic polyneuropathy.     

Short-latency somatosensory evoked potentials in infantile autism: evidence of hyperactivity in the right primary somatosensory area

Children with infantile autism sometimes show hyperesthesia or hypoesthesia to touch, pain, and/or temperature. To clarify the pathophysiology, we examined short-latency somatosensory evoked potentials (S-SEPs), elicited by median nerve stimulation, in 24 children with infantile autism (17 males, seven females; age range 2y 2mo-9y; mean age 4y 2mo [SD 1y 7mo]). We also evaluated relationships between S-SEP findings and clinical manifestations. Of the 24 children, 10 showed abnormal S-SEPs as follows: prolonged peak latency of N20 (n=2), extended interpeak latency of P13/14-N20 (n=7), appearance of a giant SEP (n=1), and a more than twofold right hemispheric peak-to-peak amplitude predominance of N20-P25 (n=5). In addition, a peak-to-peak amplitude of N20-P25 elicited by left median nerve stimuli was significantly higher than that obtained with right median nerve stimuli, which indicated right hemispheric hyperactivity relative to the left (p=0.008). Infantile autism is frequently associated with somatosensory abnormalities and right hemispheric hyperactivity relative to the left, especially in the primary somatosensory area. This is believed to contribute to the pathophysiology of infantile autism, especially the idiopathic form.     

Somatosensory pathway dysfunction in uremic children

Neurophysiological studies have shown defects in peripheral conduction in up to 75% of adults with end-stage renal disease (ESRD), though abnormalities of central conduction seem more variable. There are no comparable pediatric data. We therefore measured median nerve somatosensory evoked potentials (SEPs) in 10 children with ESRD, maintained by hemodialysis, who had no neurological signs or symptoms, and compared the results with those for age-matched controls. The latencies of N9, P14, N20 and P22, and interpeak latencies, N9-N20, N9-P14 and P14-N20, were not significantly different between the two groups (Student's t test). However, the children with ESRD were significantly retarded in growth and when arm length was taken into account, a significant difference in peripheral conduction was revealed. There was no correlation with other indexes of disease severity (parathormone, aluminium, Hb, Na, K, Cl, BUN and creatinine). SEPs appear to reflect subclinical changes in peripheral conduction in sensory pathways in children with ESRD which are not correlated with other measures of disease severity.     

Recovery of sensation and somatosensory evoked potentials following toe-to-digit transplantation in man

Recovery of digital nerve function in 21 patients with toe-to-digit transplantation was evaluated by clinical sensory tests and somatosensory evoked potentials (SEPs) to median and digital nerve stimulation. The mean interval between injury and surgery was 7 months, and that between surgery and study was 31 months. The transplanted toes achieved a satisfactory but incomplete recovery in temperature (warm and cold), pinprick, touch, vibration, and two-point discrimination in that order. The overall sensory status of the transplanted toes appeared to be closer to normal toes than to normal fingers. In SEPs from the transplanted side, median N9, N13, and N20 components had normal latency but reduced amplitude, whereas digital N9 component was usually absent, but N13 and N20 components had prolonged latency and reduced amplitude. Transplantation performed within 1 month after injury prevented amplitude reduction in median SEPs and latency prolongation in digital SEPs. The SEP data suggest that timing of surgery was critical in preventing retrograde effect on the median nerve, and that recovery of digital nerve function was incomplete correlating with clinical sensory findings. © 1995 John Wiley & Sons, Inc.     

Brain volume analyses and somatosensory evoked potentials in multiple system atrophy

We investigated a progression of brain atrophy and somatosensory system dysfunction in multiple system atrophy (MSA). Subjects were 21 MSA patients [12 MSA-C (cerebellar type) and 9 MSA-P (parkinsonism type)]. The relative volumes of cerebrum, brainstem and cerebellum to the intracranial volume were obtained from three-dimensional computed tomography (3D-CT) of the brain. The median nerve somatosensory evoked potentials (SEPs) were recorded, and the latencies and amplitudes of N9, N11, P13/14, N20 and P25 components were measured. We studied correlations between brain volumes, SEP and clinical features. The brainstem and cerebellar atrophies were aggravated with progression of the disease. The central sensory conduction time (CSCT) was progressively prolonged in parallel with the disease duration irrespective of the actual age of the patients. In MSA patients, the volume reductions of cerebellum and brainstem could be one of structural markers of disease progression, and the sensory pathway is progressively involved with the progression of disease processes.     

Abnormalities of parietal and prerolandic somatosensory evoked potentials in Huntington's disease.

Cervical, parietal and prerolandic somatosensory evoked potentials (SEPs) to median nerve stimulation at the wrist were recorded with an earlobe reference in 24 patients with Huntington's disease (HD) and in 24 age-matched normal controls. Cortical responses of abnormal wave form and reduced amplitude were constantly observed in HD patients. SEP changes affected more severely the prerolandic (P22/N30) pattern, which could not be recognized in two-thirds of patients, than the parietal (N20/P27) pattern, which could be identified in all cases. The N20 latency and the central conduction time (N13-N20 interval) were significantly increased. The occurrence of abnormalities of central conduction and of a predominant involvement of the prerolandic SEP pattern suggests an impairment of impulse transmission along the somatosensory lemniscal pathway at subcortical, possibly thalamic, level in HD.     

肌萎缩性侧索硬化症患者体感诱发电位研究

目的 研究肌萎缩性侧索硬化症(ALS)患者体感诱发电位(SEP)变化。方法 采用正中神经及肠后神经体感诱发电位(mSEP、tSEP)对30例患者进行检测，并与27例健康人作对比。结果 mSEP和tSEP的异常率分别为43．3％(13／30)及28％(7/5)，除N9、PF(腘点)、LP(T12点)峰潜伏期和对照组相比无显著差异外，其余各峰潜伏期及峰间期和对照组相比均有显著性差异。结论 ALS患者存在感觉通路损害，且中枢的改变较周围更明显，SEP检查对患者感觉损害的定位有一定价值。     

The diagnostic value of sensory evoked potentials in pediatric Wilson disease

We studied the sensory evoked potentials in pediatric Wilson disease to verify their subclinical neurologic involvement and to elucidate the role of cirrhosis in abnormal evoked potentials in non-neurologic Wilson disease. Thirty children (17 male, 13 female), diagnosed with Wilson disease before 18 years, were enrolled. The mean age during studies was 15.8 +/- 6.3 years, and disease duration since diagnosis was 3.0 +/- 3.3 years. In 12 neurologic Wilson disease cases, there were prolonged interpeak latencies of brainstem auditory evoked potentials III-V, I-V, somatosensory evoked potentials N13-N20 (P < 0.01 vs controls and non-neurologic cases), and P100 latency (P < 0.01 vs controls). All 12 patients had at least one abnormal evoked potential, including 91.7% brainstem auditory, 58.3% somatosensory, and 25% visual evoked potentials. In 18 non-neurologic Wilson disease cases, there were still prolonged interpeak latencies for brainstem auditory evoked potentials I-V and somatosensory evoked potentials N13-N20 (P < 0.05 vs controls), with 27.8% of them having at least one abnormal evoked potential, including 16.6% brainstem auditory, 5.6% somatosensory, and 11.1% visual evoked potentials. In those with non-neurologic Wilson disease, there were no significant differences in all the evoked potential parameters between the cirrhotic and non-cirrhotic patients.     

Influences of transcutaneous electrical stimulation of cutaneous and mixed nerves on subcortical and cortical somatosensory evoked potentials

Aim of this study was to assess whether transcutaneous electrical nerve stimulation (TENS) 'gates' somatosensory evoked potentials (EPs) peripherally or centrally, and which afferent fibres and sensory nuclei mediate this effect. The following waves were recorded after stimulation of the median nerve at the wrist or of the digital nerves of the index finger: N9, the cervical N11 and N13, the parietal P9, P11, P14, N18, N20, P22, P27, P40. When both median or digital nerve EPs were conditioned by TENS delivered to the median nerve, reduction in amplitude of N9, P14, N18 and later generated cortical waves was observed. To measure the central contribution to this decrease, unconditioned 'reference' EPs were evoked by stimulating with a current strength yielding an N9 potential of an amplitude equal to that obtained during TENS. In this case, the amplitude of P14, N18 and later cortical waves was significantly greater than during TENS. When both median or digital nerve EPs were conditioned by TENS delivered to the digital nerves, waves were only slightly affected. No effects were seen on the EPs elicited from the median or index finger digital nerves when TENS was administered to the contralateral median or digital nerves or to the ipsilateral middle finger. It is concluded that TENS gates the somatosensory volley, both at a peripheral level through a 'busy line-effect' on large afferent fibres, and centrally at the level of the cuneatus nucleus.     

Effects of age and body height on somatosensory evoked potentials]

The influence of age and height on somatosensory evoked potentials (SEP) following median and tibial nerve stimulation was studied. Age correlated with increase of latencies and decrease of amplitudes; exceptionally the amplitude of cortical N20 component increased with age. The central conduction time P31-P40 (tibial nerve stimulation) was longer in elderly subjects, whereas the time N13-N20 (median nerve stimulation) was independent of age. Height showed a positive correlation with latencies and peripheral conduction times; central conduction times (N13-N20 and P31-P40) were independent on height. The correlations of SEP parameters with age and height were expressed quantitatively by regression equations. The presented equations should be treated as a valuable complement to normative data in interpretation of SEP testing results.     

Somatosensory evoked potentials reflect the upper limb motor performance in multiple sclerosis

OBJECTIVE: The aim of this multicentric study was to multidimensionally evaluate the relationship among somatosensory evoked potentials (SEPs) parameters, patient's perspective and clinical measures of the upper limb impairment in patients with multiple sclerosis (MS). METHODS: We consecutively enrolled 39 MS patients. For median nerve SEPs we acquired the N9, P14, N20 responses and the N9-P14 and P14-N20 interpeak latencies on the dominant side. We also used a validated patient-oriented questionnaire (Disabilities of the Arm, Shoulder and Hand - DASH) and a test of dexterity quantification as the 9-Hole Peg Test (9-HPT). RESULTS: A significant longer time to complete the 9-HPT (p<0.00006) was observed in patients with abnormal SEPs. Patients with undetectable N20 or P14 responses performed the 9-HPT in a significant longer time than patients with detectable responses (p<0.0006 and p<0.001 respectively). Concerning the perspective of patient (evaluated with the DASH questionnaire) significant differences in patients with undetectable P14 response (p<0.01) were observed. CONCLUSIONS: Our data provide further information useful for interpretation of SEPs results, being the median nerve SEPs related to the upper limb performance in MS patients. SIGNIFICANCE: These data increase the significance of SEPs both in clinical practice and in experimental studies in MS.