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 potential in children

The short latency somatosensory evoked potential was studied in 90 normal children of 1 month to 16 years old and 7 adults. Somatosensory stimuli were delivered through a disc electrode placed over the median nerve at the wrist joint. The uniform recording sites used were the central region of the scalp, and the seventh cervical spine or Erb's point. Reference electrodes were placed on the hand contralateral to the median nerve stimulated. Three positive peaks (P1, P2 and P3) and one negative peak (N1) were consistently recorded, a further positive peak (P4) after N1 was not always observed. The latency of each peak per 1 m body length decreased with age until 2 or 5 years of age. The latency of each peak after 2 years of age was positively correlated with the body length and arm length. The value of P1 peak latency per 1 m body length reaches adult values at an earlier rate than the value of P3 peak latency and P2-P3 latency per 1 m body length. This suggests that central lemmiscal pathways mature at a slower rate than peripheral nerve fibers. The wave form pattern of the short latency somatosensory evoked potential changed to the adult pattern at 10 years of age. The peak latency of P4 during deep sleep was slightly prolonged. In recording on infants during sleep, the EEG should be monitored to determine the stage of sleep.     

Developmental assessment of spinal cord and cortical evoked potentials after tibial nerve stimulation: effects of age and stature on normative data during childhood

Somesthetic information from lower extremities is processed by cerebral cortex after traversing the sensory pathways of peripheral nerve, spinal cord, brain-stem and thalamus. Clinical utility of somatosensory evoked potentials (SSEPs) during human development requires systematic analysis of normative data acquired during various stages of body growth and nervous system maturation. Accordingly, SSEPs after tibial nerve stimulation were studied in 32 normal awake children (1-8 years old) and compared with values obtained in young adults (18-40 years old). Potentials were recorded from the tibial nerve (N5), first lumbar spinous process (N14), seventh cervical spinous process (N20) and from the scalp, 2 cm behind the vertex (P28). In all children studied, the N5, N14 and N20 latencies were positively correlated with age and height yielding a predictive nomogram. An extremely variable electropositive cortical SSEP was recorded from Cz' which did not show a highly predictable linear relationship in association with a relatively poor correlation coefficient for height and age. It may be concluded that between 1 and 8 years of normal postnatal development, latencies reflecting peripheral nerve and lumbar spinal cord vary directly with height and age and can be represented by a simple cable model of a lengthening myelinated pathway. In contrast, the latency of the cortical SSEP reflects asynchronous maturation of elongating polysynaptic pathways and apparently requires a more complex model for prediction in order to enhance its clinical utility.     

Origin of component N16 in short latency somatosensory evoked potentials (SSEP) to median nerve stimulation--correlation between component N16 and thalamus

Short latency somatosensory evoked potentials (SSEP) to median nerve stimulation consists of four main subcortical components, namely P 9, P 11, P 13 and N 16 which appears before cortial N 18. However, the origin of component N 16 is a subject of controversy. In an attempt to learn about the generator source(s) of component N 16, SSEP was recorded from 25 patients with various focal lesions of the brain stem and/or thalamus, and abnormalities of the each potential was correlated to the clinically and radiologically defined site of the lesions. Furthermore, the effects of the different frequency in stimulation were also investigated in 6 normal subjects, because latency changes of each component might contribute to the understanding of the generation. Recordings were obtained from 13 patients with brain stem lesion which included 3 cases with pontine hemorrhage, 3 cases with pontine tumor, 3 cases with cerebello-pontine angle tumor, one case of pontine angioma, one case of chordoma, one case of tentorial tumor and one case of MLF syndrome. SSEP changes in these cases were classified into four types as follows: type 1: no response over the base line was recorded, type 2; some responses over the base line were recorded but N 16 was uncertain, type 3; component N 16 was clearly identified but its latency was significantly prolonged, type 4; component N 16 was divided into two peaks. Bilateral abnormality on SSEP with splitted combination of these four types in various degree was observed. Furthermore, these SSEP abnormalities were seen even in the some cases without sensory disturbance. On the other hand, component N 16 was clearly identified in all 12 patients with thalamic lesion which included 11 cases with thalamic hemorrhage and one case with thalamic tumor on the effected side. Comparison of latency and amplitude between normal side and affected side statistically showed no laterality of components P 9, P 11 and P 13, but a tendency of delay in latency of component N 16 on the affected side. Different stimulus repetition rate revealed some other characteristics of each component. Electrical stimuli to median nerve at the wrist were delivered at rates of 3, 6, 9, 12, 15, 18, 21, 24 and 27 Hz. Latencies of components P 9, P 11, P 13, N 16 in Fro.-Cv 7 lead and component N 18 in Par.-Erb lead were measured and all latency changes were calculated relative to the 3 Hz stimulation.(ABSTRACT TRUNCATED AT 400 WORDS)     

Somatosensory evoked potentials of the dog: recording techniques and normal values

Median and tibial nerve somatosensory evoked potentials (SSEPs) of 5 sedated dogs were studied to determine their normal features and optimal stimulation and recording techniques. Cortical potentials were mapped from an extensive array of skull electrodes as each limb was independently stimulated with subdermal needles. The effects of bandpass and stimulus intensity and rate were also assessed. Three cortical components (P1, N1, P2) were evoked by median or tibial nerve stimulation and were localized along the coronal suture at lateral and medial electrodes, respectively. SSEP voltage varied much more than morphology, topography, or latency. The inion was a stable, indifferent reference site. Cortical SSEP frequency content was mostly below 250 Hz. Maximal SSEP voltage was achieved only at stimulus intensities 2-3 times motor threshold. Appropriate methods minimize technical difficulties and consistently yield legible SSEPs.     

Multimodal evoked potentials in the early period after cranio-cerebral trauma]

In 83 patients aged 17-68 years somatosensory evoked potentials by median nerve stimulation, and visual and auditory evoked potentials were studied 5-28 days after craniocerebral trauma. Brain concussion was diagnoses in 43 cases on the basis of neurological examination, CT and duration of unconsciousness. In the remaining 40 cases brain contusion was diagnosed. In SSEP the latency was calculated of waves N9, N13, P16, N20, P22, N35 and P40: in the visual evoked potentials the latency of the P100 component, and in auditory evoked potential the latency of waves I, III and V, and interpeak latency I-III, III-V and I-V SSEP changes were found in 39% of cases of brain concussion and 52.9% of brain contusion cases. The abnormalities in both groups involved mainly the component of latency and deviation P100 of visual evoked potential P40 and N35. Prolongation of the latency of P100 of the visual evoked potential was recorded in 20% of patients with brain concussion and 16.7% with brain contusion. Auditory evoked potentials were abnormal in 10.3% of brain concussion and 26.5% of brain contusion cases. In 64 cases all three types of evoked potentials were studied and pathological changes in at least one of these types were found in 56.4% of brain concussion and 72% of brain contusion cases. The results show that as least in a part of cases diagnosed as brain concussion according to generally accepted criteria, central nervous system injury is present.     

Electrophysiological studies on hydranencephaly

Electrophysiological studies were performed on two children with hydranencephaly that was diagnosed by CT and/or magnetic resonance imaging (MRI). Case 1 was a 4-months-old boy who had no rostral tissue above the midbrain. Case 2 was a 5-years-old boy in whom CT showed the presence of the thalamus. Short latency somatosensory evoked potentials (SSEP) in both cases exhibited the absence of cortical activity (N1 and P4) with the preservation of waves of brainstem origin. However, in case 1, the wave component N0 was not observed, while N0 was seen in case 2. Thus, the N0 was component of SSEP on median nerve stimulation in children, which corresponds to N16 in adults, may originate in the thalamus.     

Median nerve somatosensory evoked potentials recorded with cephalic and noncephalic references in central and peripheral nervous system lesions.

Somatosensory evoked potentials (SSEP) to electrical stimulation of the median nerve by using cephalic and noncephalic references were studied to detect the generator sources of short latency evoked potentials in 29 patients with cerebral, brainstem, spinal and peripheral nerve lesions. Patients were divided into six groups according to the localization of their lesions: group 1: cortical and subcortical lesions, group 2: basal ganglion lesions, group 3: pons and mesencephalon lesions, group 4: diffuse cerebral lesions, group 5: cervical cord lesions, group 6: brachial plexus lesions. Potentials were recorded using cephalic and noncephalic references after median nerve stimulation. Evidence obtained from patients suggested the following origins for these short latency SSEPs: P9 may arise in brachial plexus, P11 in dorsal basal ganglions or dorsal column, P13 and P14 in the nucleus cuneatus and lemniscal pathways, N16 in subthalamic structures and most likely mid and lower pons, N18 from the thalamus and thalamocortical tract, and N20 from primary somatosensory cortex.     

Neuroanatomic substrates of lower extremity somatosensory evoked potentials.

After stimulation of the lower extremity nerve (tibial nerve), N21 and N23 are recorded from L4 and T12 spine respectively. The far-field potentials of P31 and N35 are registered from Fpz-C5s (fifth cervical spine) or CPi (ipsilateral with respect to the side of stimulation)-ear derivation. Additional far-field potentials of P17 and P24 may be recorded from the scalp when a noncephalic (knee) reference is used. The major positive peak, P40, is registered at the vertex and the CPi. Preceding P40, there is a small negative peak, N37, recorded at the contralateral (CPc) hemisphere. Neuroanatomic substrates of these somatosensory evoked potential (SSEP) components are less well clarified compared with those of upper extremity (median nerve) SSEPs, primarily because clinical application of lower extremity SSEPs is more difficult, and all of the aforementioned potentials but one (P40) are not obligatory components. The concept of "paradoxical lateralization" complicates the issue further. Accumulating evidence, however, suggests that the far-field potentials of P17 and P31 arise from the distal portion of the sacral plexus and brainstem respectively. These correspond to P9 and P14 of the median nerve SSEPs respectively. The spinal potential of N23 is equivalent to the N13 cervical potential of the median nerve SSEP. N35 recorded from the ipsilateral hemisphere is analogous to N18 of the median nerve. Paradoxically lateralized P40 has been thought to represent the positive end of a dipole field, reflected by the negativity at the mesial surface of the contralateral hemisphere, and has commonly been considered to be equivalent to the first cortical potentials (N20) of the median nerve SSEP. However, more recent evidence suggests that the primary positivity is at the mesial cortical surface, and it more likely corresponds to P26 of the median nerve SSEP. Thus the first cortical potential corresponding to N20 is probably a small and inconsistent N37 recorded on the contralateral hemisphere. These assumptions need to be verified further by more extensive clinical studies applied to various neurologic disorders.     

Electrophysiological study on hydranencephaly.

An electrophysiological study was performed on 2 children with hydranencephaly diagnosed by CT and/or MRI. Case 1 was a 4-month-old boy who had no rostral tissues above the midbrain. Case 2 was a 5-year-old boy in whom CT showed retention of the thalamus. Short latency somatosensory evoked potentials (SSEP) in both cases exhibited the absence of cortical activity (N1 and P4) with the preservation of waves of brain stem origin. However, in case 1, wave component No was not observed, while No was seen in case 2. It was postulated, thus, that the No component of SSEP on median nerve stimulation in children, which corresponds to N16 in adults, may originate in the thalamus.     

Influence of GAA expansion size and disease duration on central nervous system impairment in Friedreich's ataxia: contribution to the understanding of the pathophysiology of the disease.

OBJECTIVE: To verify if GAA expansion size could account for the severity of the central nervous system involvement in Friedreich's ataxia (FA). METHODS: Retrospective study of 52 FA patients (mean age 26.9+/-12.1 years; mean disease duration 10.6+/-7.6 years) homozygous for GAA expansion. Median nerve somatosensory evoked potentials (SSEPs) were available in 36 FA patients, upper limb motor evoked potentials (MEPs) to transcranial magnetic stimulation in 32, brainstem auditory evoked potentials (BAEPs) in 24, and visual evoked potentials (VEPs) in 34. N20, P100, MEP amplitude, SSEP and MEP central conduction time (CCT and CMCT), P100 latency and I-III and I-V interpeak latency, and a BAEP abnormality score were correlated with disease duration and GAA expansion size on the shorter (GAA1) and larger (GAA2) allele in each pair. RESULTS: The GAA1 size inversely correlated with the N20 amplitude (r = -0.49; P<0. 01). Disease duration directly correlated with CMCT (r = 0.57; P<0.01) and BAEP score (r = 0.61; P<0.01) and inversely with MEP (r = -0.40; P<0.05) and P100 amplitude (r = -0.39; P<0.05). CONCLUSIONS: Our data suggest that central somatosensory pathway involvement in FA is mainly determined by GAA1 expansion size. Vice versa, degeneration of pyramidal tracts, auditory and visual pathways seems to be a continuing process during the life of FA patients.     

Electrophysiological studies in siblings of De Sanctis-Cacchione syndrome

Multi-modality evoked potentials in two cases, who were siblings, of De Sanctis-Cacchione syndrome were reported. The case 1, who was elder sister of the case 2, was a 25-year-old female. And the case 2 was a 23-year-old female. They have the history of consanguinity. They were first noted to have skin erythema on exposure to sunlight, and a diagnosis of xeroderma pigmentosum was made. At the childhood neurological manifestation, such as mental retardation, deafness and muscular weakness developed gradually. The case 2, who was a elder sister, was operated on for squamous cell carcinoma of the eyelid at the age of 20 and 21 years old. Motor conduction velocity obtained from lower limbs were severely reduced and that from upper limbs were moderately delayed. Sensory conduction velocity of median nerve were severely diminished. Auditory brainstem responses (ABR) of the case 1 showed the prolongation in interpeak latency of I-V. ABR of the case 2 could not be obtained. N19 and N13 of short-latency somatosensory evoked potentials (SSEP) to median nerve stimulation with case 2 could not be obtained too. N13-N19 latency of case 1 was remarkably prolonged compared to the normal subjects. Central motor conduction time (CMCT) was studied in case 2 by using the magnetic stimulator. CMCT of case 2 was within the upper limit of normal control. Interpeak latency of I-V in ABR represents the brainstem dysfunction in auditory pathway, and interpeak latency of N13-N19 in SSEP was recognized as central conduction time from medial lemniscus to primary sensory area of cortex. So the prolongation of these interpeak latency in this cases may mean the dysfunction in the central nervous system.(ABSTRACT TRUNCATED AT 250 WORDS)     

Effects of hypothermia on short latency somatosensory evoked potentials in humans.

Short latency somatosensory evoked potentials (SSEPs) elicited by median nerve stimulation were monitored in 14 adult patients undergoing cardiac surgery under cardiopulmonary bypass and induced hypothermia. SSEPs were recorded at 1-2 degrees C steps as the body temperature was lowered from 37 degrees C to 20 degrees C to determine temperature-dependent changes. Hypothermia produced increased latencies of the peaks of N10, P14 and N19 components, the prolongation was more severe for the later components so that N10-P14 and P14-N19 interpeak latencies were also prolonged. The temperature-latency relationship had a linear correlation. The magnitude of latency prolongation (msec) with 1 degree C decline in temperature was 0.61, 1.15, 1.56 for N10, P14 and N19 components, respectively, and 0.39 and 0.68 for interpeak latencies N10-P14 and P14-N19, respectively. The rise time and duration of the 3 SSEP components increased progressively with cooling. Cortically generated component, N19, was consistently recordable at a temperature above 26 degrees C, usually disappearing between 20 degrees C and 25 degrees C. On the other hand, more peripherally generated components, N10 and P14, were more resistant to the effect of hypothermia; P14 was always elicitable at 21 degrees C or above, whereas N10 persisted even below 20 degrees C. The amplitude of SSEP components had a poor correlation with temperature; there was a slight tendency for N10 and P14 to increase and for N19 to decrease with declining temperature. Because incidental hypothermia is common in comatose and anesthetized patients, temperature-related changes must be taken into consideration during SSEP monitoring under these circumstances.     

Maturation of cerebral somatosensory evoked potentials

Cerebral somatosensory evoked potentials (SEPs) were elicited by stimulation of the median nerve and/or posterior tibial nerve in 117 children of 1 day to 16 years old. A major negative wave (N) was consistently recorded from the parietal region of the scalp when the arm was stimulated. The peak latency, the onset latency, the rising time and the duration of H wave are closely correlated with age and body length. The latencies are shortest in the subjects of 1-3 years old. SEPs to lower extremity stimulation were inconstant in the infants before the age of one. The major positive wave (P) has a variable topographic distribution along the middle line, over the scalp. The latencies are also very variable in the different subjects of the same age as well as in the same subject with different locations of active electrode. Among the parameters studied as for N wave, only the rising time of P wave is significantly correlated with age. The latencies of P wave have the shortest value in the subjects of 1-3 years old. The comparison of SEPs to upper and to lower limb stimulations shows that there is no relationship between them in respect to their morphology and amplitude. The minimum value of the latencies of N and P waves was observed at the same age but the difference between the peak latencies of P and N waves in the same subject increases considerably after 2 years of age and reaches the adult value after 5 years of age. These resultats indicate that the maturation of the peripheral somatosensory pathways proceeds at a higher rate than that of the central somatosensory pathways, that the maturation of the somatosensory pathways of the upper limb precedes that of the lower limb, and that the rising time of N or P waves is a good index of cortical maturation. The clinical utility of these SEPs in pediatrics is discussed.     

Origin of short latency somatosensory evoked potential in cats: especially potentials derived from thalamus and cortex

Short latency somatosensory evoked potential (SSEP) was recorded in cats to identify the potentials originating from the cortex and the thalamus, and the following results were obtained. When SSEP was elicited on the bregma by stimulation of the contralateral superficial radial nerve, P2, P4, P4.5, P5.5, P7, P8, N8.5, P11, P9.5, N11.5, N12.5 and N14 were recognized. Of these components N11.5, N12.5 and N14 consisted of large negative potential (LNP). When KCl was applied to the sensorimotor cortex to induce spreading depression, the positive component of the primary evoked potential was markedly decreased and the negative component disappeared. In SSEP, components preceding N8.5 were unchanged. N8.5-P11 and P11-N12.5, however, markedly diminished or disappeared. The latency of the first component of the field potential recorded in the VPL nucleus of the thalamus was about 5 ms. When a small amount of Nembutal was injected into VPL nucleus, components between P2 and P4.5 remained unchanged, but P5.5 disappeared. P7, P8 and N8.5 were preserved. The amplitude of N8.5-P11 was markedly decreased and LNP disappeared. From these results, among various components of SSEP, P5.5 should originate from the thalamus, and P7, P8 and N8.5 from the extralemniscal system. N8.5-P11 should mainly represent post-synaptic potential (PSP) in the deep somatic layer, and P11-N12.5 represent PSP in the apical dentrites of the sensorimotor cortex. N14 probably represents PSP via the diffuse projection system. Thus, LNP should consist of complex potentials of specific and non-specific sensory systems.     

Correlation between morphological abnormalities of Chiari malformation and evoked potentials]

We studied correlation between morphological abnormalities of Chiari malformation and evoked potentials (short-latency somatosensory evoked potential [SSEP] and auditory brainstem response [ABR]). On SSEP the inter-peak latency prolongation of P3-N1 was revealed in 6 out of 8 cases with Chiari malformations. The feature of positive wave between P3 and N1 was divided into 2 groups. The tendency of the positivity between P3 and N1 was more marked in cases of prolonged P3-N1 latency and correlated with the medullary kink. On ABR the prolongation of III-V inter-peak latency was revealed in one side in 3 patients Chiari malformations with malformed pons and tegmentum.     

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.     

Decrement of N20 amplitude of the median nerve somatosensory evoked potential in Creutzfeldt-Jakob disease patients.

We studied somatosensory evoked potentials (SSEPs) in eight Creutzfeldt-Jakob disease (CJD) patients presenting with subacute progressive dementia, generalized myoclonus, and characteristic periodic sharp wave complexes in EEG. Somatosensory evoked potentials were elicited by median nerve stimulation at the wrist. We compared SSEP findings with EEG and the clinical stage proposed by the Japanese Slow Virus Infection Research Committee (stage 1: early stage to stage 5: terminal stage). Until clinical stage 3, short-latency SSEPs showed normal findings despite the severely abnormal EEG. With the progression to clinical stages 4 and 5, however, the amplitude of N20 began to decrease and finally disappeared without prolongation of the latency of N20, whereas other short-latency components were preserved. We recorded giant SSEPs in two of three patients in stage 4, when the periodic sharp wave complex in EEG began to decrease in amplitude. The giant SSEPs decreased in amplitude with the progression of the illness. These findings suggest that the short-latency SSEP is relatively preserved until the middle phase of the disease but that it is eventually affected in the terminal phase. We conclude that our results are compatible with the CJD pathologic findings and that the amplitude of N20 reflects the extent of cortical damage in CJD patients.     

Cortical somatosensory evoked potentials to posterior tibial nerve stimulation in newborn infants

Successful cortical recordings of somatosensory-evoked potentials (SEPs) to posterior tibial nerve (PTN) stimulation were obtained in 21 (87.5%) for P1 and 22 (91.7%) for N1 of 24 infants who were followed up for at least 3 years and had a normal outcome. There were linear decreases with increasing post menstrual age in both P1 and N1 peak latency. Of the four cases with diplegia later, three showed definite abnormalities, no responses and delayed latency in PTN SEPs respectively, however, the other case showed normal responses. Of the three cases with mental retardation, two showed relatively long latency and borderline responses respectively, and the other case showed normal responses. As the pathway of PTN SEPs traverses the periventricular area of the brain likely to be affected by ischemic lesions in premature infants, abnormalities in the responses might indicate a later motor disorder.     

Accuracy of somatosensory evoked potentials in diagnosis of mild idiopathic carpal tunnel syndrome

OBJECTIVE: Concerning prevalence of carpal tunnel syndrome (CTS) and the difficulties with electromyography (EMG) and nerve conduction studies (NCS), this study was designed to evaluate the power of somatosensory evoked potential (SSEP) in CTS diagnosis among Iranian patients. PATIENTS AND METHODS: SSEP was performed on 100 asymptomatic hands of 50 healthy participants (40 female, age range 38-59 years) and on 61 hands of 46 patients (39 female, age range 34-58 years). Mean difference between N(20) latency of the middle finger and the wrist (median nerve innervation) as well as N(20) latency of the third finger and the fifth finger (ulnar nerve innervation) were measured. Using receiver operating characteristic (ROC) curve analysis, the upper limits of these variables were defined as 6.0 and 1.5 ms, respectively. Higher amounts in either of these variables were considered as positive SSEP for diagnosis of CTS. Measures of accuracy for SSEP were measured getting clinical diagnosis by two separate neurologists as the reference standard. In the patients' group who underwent both techniques of SSEP and EMG-NCS, kappa statistic as the agreement coefficient between two procedures was calculated. RESULTS: Sensitivity, specificity, and likelihood ratios for positive and negative results of SSEP in diagnosis of CTS were 70.4%, 91.0%, 7.83 and 0.32, respectively. Sensitivity of EMG-NCS in diagnosis of CTS was measured as 81.9%. Measure of agreement between two procedures (kappa) was calculated as 0.42. CONCLUSION: This study showed that positive results of SSEP might have a role in diagnosis of CTS. However, larger studies to demonstrate diagnostic power of SSEP in comparison with EMG-NCS seem necessary.