Multimodality evoked potentials as a prognostic tool in term asphyxiated newborns

Hypoxic-ischemic (HI) events may cause permanent brain damage, and it is difficult to predict the long-term neurological outcome of survivors. Multimodality evoked potentials (MEPs), using flash visual (fVEPs), somatosensory (SEPs), and brain-stem auditory evoked potentials (BAEPs) may assess the cerebral function in term neonates. MEPs were recorded in 40 hypoxic-ischemic term or near-term neonates during the first week of life in order to predict the neurological outcome. A 3 point grading system registered either mild, moderate, or severe abnormalities. At 24 months of corrected age, the infants were assessed with a blind protocol to determine neurological development. Grade 0 fVEPs and SEPs were associated with a normal neurological status with 100% (P<0.001) of the infants. Abnormal SEPs or total grade (VEPs+SEPs)>I were not associated with normal outcomes (P<0.0001). Normal BAEPs did not predict a normal outcome, but severely abnormal BAEPs did predict an abnormal outcome. A significant correlation was found between EP (VEPs+SEPs) grade (r=0.9, P<0.0001), Sarnat stage (r=0.6, P<0.001), and clinical outcome. This study confirmed that both fVEPs and SEPs are more accurate as prognostic indicators for term neonates. EPs (VEPs+SEPs) also are more accurate in predicting the ultimate neurological outcome compared with the Sarnat scoring.     

MEP Latencies Predict the Neuromodulatory Effect of cTBS Delivered to the Ipsilateral and Contralateral Sensorimotor Cortex

Background

Recently, it was shown that the highly variable after-effect of continuous theta-burst stimulation (cTBS) of the primary motor cortex (M1) can be predicted by the latency of motor-evoked potentials (MEPs) recorded before cTBS. This suggests that at least part of this inter-individual variability is driven by differences in the neuronal populations preferentially activated by transcranial magnetic stimulation (TMS).

Methods

Here, we recorded MEPs, TMS-evoked brain potentials (TEPs) and somatosensory-evoked potentials (SEPs) to investigate the effects of cTBS delivered over the primary sensorimotor cortex on both the ipsilateral and contralateral M1, and the ipsilateral and contralateral primary somatosensory cortex (S1).

Results

We confirm that the after-effects of cTBS can be predicted by the latency of MEPs recorded before cTBS. Over the hemisphere onto which cTBS was delivered, short-latency MEPs at baseline were associated with an increase of MEP magnitude (i.e. an excitatory effect of cTBS) whereas late-latency MEPs were associated with reduced MEPs (i.e. an inhibitory effect of cTBS). This relationship was reversed over the contralateral hemisphere, indicating opposite effects of cTBS on the responsiveness of the ipsilateral and contralateral M1. Baseline MEP latencies also predicted changes in the magnitude of the N100 wave of TEPs elicited by stimulation of the ipsilateral and contralateral hemisphere, indicating that this TEP component is specifically dependent on the state of M1. Finally, there was a reverse relationship between MEP latency and the effects of cTBS on the SEP waveforms (50–130 ms), indicating that after-effects of cTBS on S1 are opposite to those on M1.

Conclusion

Taken together, our results confirm that the variable after-effects of cTBS can be explained by differences in the neuronal populations activated by TMS. Furthermore, our results show that this variability also determines remote effects of cTBS in S1 and the contralateral hemisphere, compatible with inter-hemispheric and sensorimotor interactions.     

The role of upper limb somatosensory evoked potentials in the management of cervical spondylotic myelopathy: preliminary data

We studied upper limb somatosensory evoked potentials (SEPs) in 11 patients with MRI and clinical evidence of cervical spondylotic myelopathy (CSM), before and after cervical open-door laminoplasty. SEP studies before surgery revealed two main types of abnormality, the first characterized by the isolated loss of the spinal N13 response, reflecting the dysfunction of dorsal horn cervical cells in 4 patients. The second combined abnormalities of both spinal N13 and scalp far-field P14 potential, suggesting the involvement of both dorsal horn cells and dorsal columns at the cervical level in 7 patients. After surgery, N13 recovered in 9 patients, while P14 abnormalities remained unchanged. Clinical recovery, evaluated by means of the Japanese Orthopaedic Association (JOA) disability scale, was accompanied by SEP improvement. Moreover, this improvement was more pronounced in patients with isolated loss of the N13 than in patients with combined abnormalities of the N13 and scalp P14 response. Our data strongly suggest that upper limb SEPs can be useful in monitoring the effectiveness of surgery, as well as in selecting before surgery patients who are likely to have a better postsurgical outcome.     

Pyramidal tract function during onset of brain death

In 51 patients with primary brain lesions, who fulfilled the criteria of brain death, sequential recording of transcranial magnetic evoked potentials (TMEPs) and somatosensory evoked potentials (SEPs) were performed.In all comatose patients with apnoeic cranial nerve areflexia the TMEP could not be elicited, while the response after cervical magnetic stimulation was always preserved. Similarly, no cortical SEPs were preserved in apnoeic cranial nerve areflexia; however, the cervical somatosensory response was preserved in 44%.In deteriorating patients with coma grade III TMEPs were preserved in 3 instances, while cortical SEPs were already absent. Current brain death criteria, however, were not challenged, as TMEPs were absent in all 51 patients, at the latest when apnoea was noted.     

Afferent mechanism of cortical myoclonus studied by proprioception-related SEPs

Proprioception-related somatosensory evoked potentials (SEPs) to passive flexion movement of the middle finger at proximal interphalangeal joint were recorded in 7 patients with myoclonus of cortical origin who demonstrated enlarged electrical SEPs (giant SEPs). In 3 out of the 7 patients, the proprioception-related SEPs were also enlarged. The remaining 4 patients showed giant electrical SEPs without enhancement of proprioception-related SEPs. Long loop electromyographic response was recorded during the resting condition in all of the 3 patients with enlarged proprioception-related SEPs. We have previously reported that proprioception-related SEPs are mainly generated by muscle afferent inputs, though electrical SEPs are thought to reflect mostly cutaneous inputs with some contribution from muscle afferents. Therefore, it is concluded that hyperexcitability of the sensorimotor cortex in cortical myoclonus is modality-specific. Cortical excitability is exaggerated to both cutaneous and deep receptor inputs in some patients, but only to cutaneous input in others.     

Brain-stem somatosensory dysfunction in a case of long-standing left hemispherectomy with removal of the left thalamus: a nasopharyngeal and scalp SEP study

We have studied median nerve somatosensory evoked potentials (SEPs) in a patient who had undergone early surgical removal of the left cerebral hemisphere and left thalamus. Stimulation of the right side evoked normal latency P9, P11 and P13 potentials at scalp as well as at nasopharyngeal (NP) leads, while P14 and N18 potentials were absent. These SEP abnormalities, that have been described previously in cervico-medullary lesions and in comatose patients with upper brain-stem involvement, suggest that in our patient the removal of the left thalamus has caused retrograde degeneration of the cuneate-thalamic projections. Moreover, this study confirms that P13 and P14 potentials have different generators.     

The assessment of severe head injury by short-latency somatosensory and brain-stem auditory evoked potentials

The relative prognostic value of short-latency somatosensory evoked potentials (SEPs) and brain-stem auditory evoked potentials (BAEPs) was assessed in 35 patients with post-traumatic coma. Analysis of the evoked potentials was restricted to those recorded within the first 4 days following head injury. Abnormal SEPs were defined as an increase in central somatosensory conduction time or an absence of the initial cortical potential following stimulation of either median nerve. Abnormal BAEPs were classified as an increase in the wave I–V interval or the loss of any or all of its 3 most stable components (waves I, III and V) following stimulation of either ear. SEPs reliably both good and bad outcomes. All 17 patients in whom SEPs were graded as normal had a favourable outcome and 15 of 18 patients in whom SEPs were abnormal had an unfavourable outcome. Although abnormal BAEPs were associated with an unfavourable outcome in almost all patients (6 of 7), only 19 of 28 patients with normal BAEPs had a favourable outcome. The finding of normal BAEPs was therefore of little prognostic significance. These results confirm the superiority and greater sensitivity of the SEP in detecting abnormalities of brain function shortly after severe head trauma.     

Motor potentials evoked by paired cortical stimuli

We recorded the motor evoked potentials (MEPs) from the abductor pollicis brevis muscle, after supramaximal electrical transcranial stimulation, and studied the effect of paired transcranial shocks with varying interstimulus time intervals, in 10 normal subjects, 4 patients with median nerve neuropathy and 2 patients with motoneurone disease.In relaxed muscles the amplitude of the MEP evoked by a single shock averaged 30% of the M wave. With intervals from 1 to 2.5 msec 2 shocks evoked one MEP far larger in size than the control MEP (70% of the M wave). With intervals of 10 msec and longer, the 2 shocks evoked 2 independent MEPs; the size of the MEP following the second shock (test) was inversely correlated with the size of the control MEP: the more the control MEP approached the size of the M wave, the smaller the test MEP. Single motor unit records showed that, in the normal subjects and patients with peripheral neuropathy, the same motor unit was activated either by the first or the second shock, whereas in the patients with motoneurone disease it fired twice. In active muscles, the control MEP averaged 70% of the M wave. With intervals of 10 msec and longer the test MEP was markedly suppressed; with 100 msec intervals it fully recovered. In relaxed muscles, by delivering a double shock at a 1.5 msec interval, thus evoking a large MEP, followed by a second double-shock, the test MEP was completely suppressed for a period of 20 msec; it began to recover at 50 msec intervals and fully recovered after 150 msec.These results indicate that: (1) high-threshold spinal motoneurones can profit from temporal summation if double-shocks are delivered at short time intervals; (2) the synchronous excitation of the motoneuronal pool produced by transcranial stimulation is followed by a 20 msec period of absolute inhibition, possibly through a massive activation of the Renshaw system; (3) during voluntary contraction, only a portion of the motoneuronal pool remains refractory, possibly because of the enhanced spinal excitability.     

SEP testing in deeply comatose and brain dead patients: the role of nasopharyngeal,scalp and earlobe derivations in recording the P14 potential

Median nerve somatosensory evoked potentials (SEPs) were tested in 50 patients (20 brain dead, 18 comatose and in 12 progessing from coma to brain death, i.e., 32 cases with brain death and 30 cases with coma were recorded).Derivations were taken from nasopharynx, earlobes, scalp, and neck using cephalic and non-cephalic references. Cortical and subcortical SEP components were evaluated, focussing on the P14 potential. There is evidence that rostral and caudal parts of the P14 generator (lemniscus medialis) are differently affected in brain death, resulting in an abolition of the rostral part, while occassionally leaving intact for some time the caudal part. Non-cephalic referenced scalp records pick up the whole P14 dipole, whereas nasopharyngeal and earlobe derivations pick up different parts of P14, depending on the reference used. Scalp-to-nasopharynx records derive the most rostral part of P14; this “rostral P14” was bilaterally lost in all brain dead patients, but preserved in all deeply comatose patients with diffuse brain-sttem injuries. Scalp-to-earlobe records in contrast, picked up a P14 dipole segment reaching more caudally, resulting in a P14 potential also in brain dead patients. It is concluded that midfrontal scalp-to-nasopharynx derivations give the moset valuable contribution to the electrophysiological assessment of brain death versus deep coma.     

New Insight into the Time-Course of Motor and Sensory System Changes in Pain

Background

Pain-related interactions between primary motor (M1) and primary sensory (S1) cortex are poorly understood. In particular, the time-course over which S1 processing and corticomotor output are altered in association with muscle pain is unclear. We aimed to examine the temporal profile of altered processing in S1 and altered corticomotor output with finer temporal resolution than has been used previously.

Methods

In 10 healthy individuals we recorded somatosensory evoked potentials (SEPs) and motor evoked potentials (MEPs) in separate sessions at multiple time-points before, during and immediately after pain induced by hypertonic saline infusion in a hand muscle, and at 15 and 25 minutes follow-up.

Results

Participants reported an average pain intensity that was less in the session where SEPs were recorded (SEPs: 4.0±1.6; MEPs: 4.9±2.3). In addition, the time taken for pain to return to zero once infusion of hypertonic saline ceased was less for participants in the SEP session (SEPs: 4.7±3.8 mins; MEPs 9.4±7.4 mins). Both SEPs and MEPs began to reduce almost immediately after pain reached 5/10 following hypertonic saline injection and were significantly reduced from baseline by the second (SEPs) and third (MEPs) recording blocks during pain. Both parameters remained suppressed immediately after pain had resolved and at 15 and 25 minutes after the resolution of pain.

Conclusions

These data suggest S1 processing and corticomotor output may be co-modulated in association with muscle pain. Interestingly, this is in contrast to previous observations. This discrepancy may best be explained by an effect of the SEP test stimulus on the corticomotor pathway. This novel finding is critical to consider in experimental design and may be potentially useful to consider as an intervention for the management of pain.     

Transpinal and Transcortical Stimulation Alter Corticospinal Excitability and Increase Spinal Output

The objective of this study was to assess changes in corticospinal excitability and spinal output following noninvasive transpinal and transcortical stimulation in humans. The size of the motor evoked potentials (MEPs), induced by transcranial magnetic stimulation (TMS) and recorded from the right plantar flexor and extensor muscles, was assessed following transcutaneous electric stimulation of the spine (tsESS) over the thoracolumbar region at conditioning-test (C-T) intervals that ranged from negative 50 to positive 50 ms. The size of the transpinal evoked potentials (TEPs), induced by tsESS and recorded from the right and left plantar flexor and extensor muscles, was assessed following TMS over the left primary motor cortex at 0.7 and at 1.1× MEP resting threshold at C-T intervals that ranged from negative 50 to positive 50 ms. The recruitment curves of MEPs and TEPs had a similar shape, and statistically significant differences between the sigmoid function parameters of MEPs and TEPs were not found. Anodal tsESS resulted in early MEP depression followed by long-latency MEP facilitation of both ankle plantar flexors and extensors. TEPs of ankle plantar flexors and extensors were increased regardless TMS intensity level. Subthreshold and suprathreshold TMS induced short-latency TEP facilitation that was larger in the TEPs ipsilateral to TMS. Noninvasive transpinal stimulation affected ipsilateral and contralateral actions of corticospinal neurons, while corticocortical and corticospinal descending volleys increased TEPs in both limbs. Transpinal and transcortical stimulation is a noninvasive neuromodulation method that alters corticospinal excitability and increases motor output of multiple spinal segments in humans.     

Recovery function of somatosensory evoked potentials in juvenile myoclonic epilepsy*

Abstract

Objective: We analysed the recovery function of somatosensory evoked potentials (SEPs) in juvenile myoclonic epilepsy (JME) patients. We hypothesized that there may be disinhibition in the recovery of SEPs at 20–100?ms intervals in JME patients.

Methods: We recorded SEPs and SEP recovery in 19 consecutive patients with JME admitted for a routine follow-up examination, and in a control group composed of 13 healthy subjects who were similar to the patient group regarding age and sex. The recovery function of SEPs was examined using paired stimuli at 30, 40, 60, and 100?ms intervals.

Results: The amplitudes of N20-P25 and P25-N33 components were higher in patients with JME. Ten patients had high-amplitude SEPs. By paired stimulation, there was inhibition of SEPs in both groups. The mean recovery percentages of N20-P25 and P25-N33 components at 30, 40, 60, and 100?ms were not different between healthy subjects and patients with JME.

Conclusions: The recovery function of SEP is normal in JME even in the presence of high-amplitude SEPs.     

Central excitability does not limit postfatigue voluntary activation of quadriceps femoris.

After fatigue, motor evoked potentials (MEP) elicited by transcranial magnetic stimulation and cervicomedullary evoked potentials elicited by stimulation of the corticospinal tract are depressed. These reductions in corticomotor excitability and corticospinal transmission are accompanied by voluntary activation failure, but this may not reflect a causal relationship. Our purpose was to determine whether a decline in central excitability contributes to central fatigue. We hypothesized that, if central excitability limits voluntary activation, then a caffeine-induced increase in central excitability should offset voluntary activation failure. In this repeated-measures study, eight men each attended two sessions. Baseline measures of knee extension torque, maximal voluntary activation, peripheral transmission, contractile properties, and central excitability were made before administration of caffeine (6 mg/kg) or placebo. The amplitude of vastus lateralis MEPs elicited during minimal muscle activation provided a measure of central excitability. After a 1-h rest, baseline measures were repeated before, during, and after a fatigue protocol that ended when maximal voluntary torque declined by 35% (Tlim). Increased prefatigue MEP amplitude (P=0.055) and cortically evoked twitch (P<0.05) in the caffeine trial indicate that the drug increased central excitability. In the caffeine trial, increased MEP amplitude was correlated with time to task failure (r=0.74, P<0.05). Caffeine potentiated the MEP early in the fatigue protocol (P<0.05) and offset the 40% decline in placebo MEP (P<0.05) at Tlim. However, this was not associated with enhanced maximal voluntary activation during fatigue or recovery, demonstrating that voluntary activation is not limited by central excitability.     

The value of ulnar somatosensory evoked potentials (SEPs) in cervical myelopathy

In 57 patients with clinical signs and surgical documentation of compressive myelopathy, ulnar nerve somatosensory evoked potentials (SEPs) were more sensitive (with 74% abnormal) than either median or tibial nerve SEPs. The most frequent abnormalities were reduced or absent neck evoked responses and prolonged central conduction time. All subjects who had an SEP abnormality were identified by combined tibial and ulnar SEPs. Median nerve SEP added no additional information. Normal ulnar and tibial nerve SEPs were also able to exclude major cord damage in patients with cervical radiculopathy but little evidence of myelopathy.     

Clinical effects of intrathecal administration of expanded Wharton jelly mesenchymal stromal cells in patients with chronic complete spinal cord injury: a randomized controlled study

Background aimsSpinal cord injury (SCI) represents a devastating condition leading to severe disability related to motor, sensory and autonomic dysfunction. Stem cell transplantation is considered a potential emerging therapy to stimulate neuroplastic and neuroregenerative processes after SCI. In this clinical trial, the authors investigated the safety and clinical recovery effects of intrathecal infusion of expanded Wharton jelly mesenchymal stromal cells (WJ-MSCs) in chronic complete SCI patients.MethodsThe authors designed a randomized, double-blind, crossover, placebo-controlled, phase 1/2a clinical trial (NCT03003364). Participants were 10 patients (7 males, 3 females, age range, 25–47 years) with chronic complete SCI (American Spinal Injury Association A) at dorsal level (T3-11). Patients were randomly assigned to receive a single dose of intrathecal ex vivo-expanded WJ-MSCs (10 × 10⁶ cells) from human umbilical cord or placebo and were then switched to the other arm at 6 months. Clinical evaluation (American Spinal Injury Association impairment scale motor and sensory score, spasticity, neuropathic pain, electrical perception and pain thresholds), lower limb motor evoked potentials (MEPs) and sensory evoked potentials (SEPs), Spinal Cord Independence Measure and World Health Organization Quality of Life Brief Version were assessed at baseline, 1 month, 3 months and 6 months after each intervention. Urodynamic studies and urinary-specific quality of life (Qualiveen questionnaire) as well as anorectal manometry, functional assessment of bowel dysfunction (Rome III diagnostic questionnaire) and severity of fecal incontinence (Wexner score) were conducted at baseline and at 6 months after each intervention.ResultsIntrathecal transplantation of WJ-MSCs was considered safe, with no significant side effects. Following MSC infusion, the authors found significant improvement in pinprick sensation in the dermatomes below the level of injury compared with placebo. Other clinically relevant effects, such as an increase in bladder maximum capacity and compliance and a decrease in bladder neurogenic hyperactivity and external sphincter dyssynergy, were observed only at the individual level. No changes in motor function, spasticity, MEPs, SEPs, bowel function, quality of life or independence measures were observed.ConclusionsIntrathecal transplantation of human umbilical cord-derived WJ-MSCs is a safe intervention. A single intrathecal infusion of WJ-MSCs in patients with chronic complete SCI induced sensory improvement in the segments adjacent to the injury site.     

Giant central N20-P22 with normal area 3b N20-P20: an argument in favour of an area 3a generator of early median nerve cortical SEPs?

Generators of early cortical somatosensory evoked potentials (SEPs) still remain to be precisely localised. This gap in knowledge has often resulted in unclear and contrasting SEPs localisation in patients with focal hemispheric lesions. We recorded SEPs to median nerve stimulation in a patient with right frontal astrocytoma, using a 19-channel recording technique. After stimulation of the left median nerve, N20 amplitude was normal when recorded by the parietal electrode contralateral to the stimulation, while it was abnormally enhanced in traces obtained by the contralateral central electrode. The amplitude of the frontal P20 response was within normal limits. This finding suggests that two dipolar sources, tangential and radial to the scalp surface, respectively, contribute concomitantly to N20 generation. The possible location of the N20 radial source in area 3a is discussed. The P22 potential was also recorded with increased amplitude by the central electrode contralateral to the stimulation, while N30 amplitude was normal in frontal and central traces. We propose that the radial dipolar source of P22 response is independent from both N20 and N30 generators and can be located either in 3a or in area 4. This report illustrates the usefulness of multichannel recordings in diagnosing dysfunction of the sensorimotor cortex in focal cortical lesions.     

Changes of somatosensory evoked potentials with increase of intracranial pressure in the rat's brain

Somatosensory evoked potentials (SEPs) to various combinations of two independent brain compression modalities (localized epidural pressure and intracerebral pressure evoked by an inserted balloon) were investigated in 24 rats. The SEP pattern in response to gradually expanding volume wihtout additional epidural pressure remained unchanged for a certain period. SEP changes occurred only shortly prior to death. On the other hand, remarkable SEP changes were observed in a gradually expanding intracerebral mass, when combined with epidural pressure application at about 50% of the lethal volume. SEP changes in response to intermittent and continuous epidural pressure, in addition to a small intracerebral mass, were investigated too. Intermittent application of minor epidural pressure led to specific P1 changes, which recovered after each pressure step. The same pressure, administered continuously, evoked SEP changes with only partial recovery in some instances. Severe epidural pressure, administered intermittently, gave rise to severe SEP changes with only partial recovery after each step. The same epidural pressure delivered continuously led to SEP changes with very small recovery. SEPs have proved to be a reliable method for signalling brain dysfunction corresponding to various modalities and degrees of intracranial pressure.     

Evoked potential findings in Behçet's disease. Brain-stem auditory,visual, and somatosensory evoked potentials in 44 patients

We studied 54 patients with Behçet's disease, 41 males and 13 females, mean age 28 years. Forty-four patients had auditory brain-stem evoked potential (BAEP) recordings, 39 had pattern reversal visual evoked potentials (VEP), 27 had median nerve somatosensory evoked potential (SEP) recordings, and 25 tibial nerve SEPs. BAEPs were abnormal in 16 patients (52%) with neurological manifestations and in 4 (31%) without, because of decreased amplitude of wave V, prolonged I–III or III–V interpeak latencies, or uncertain/absent waves III and/or V. Eleven patients (40%) with neurological symptoms and 3 patients (25%) without, had abnormal VEPs. Absent potentials, decreased amplitude, with or without prolonged P100 latency, were found in 75% of the cases, the rest had prolonged P100 latency only. Median SEPs were abnormal in 8 patients (38%) with neurological manifestations. Four patients (21%) had abnormal tibial SEPs. Decreased amplitude with or without mild slowing in central conduction was the predominant SEP abnormality. SEPs were normal in all patients without neurological symptoms. In total, 84% of patients with, and 38% of patients without, neurological symptoms had abnormalities of one or more EP modality.When used cautiously, EP studies in Behçet's disease might be helpful to separate neuro-Behçet from other disorders with similar symptomatology, to disclose subclinical CNS involvement, to evaluate and monitor CNS disease activity, and to provide objective measures of treatment response.     

Dermatomal and mixed nerve somatosensory evoked potentials in the diagnosis of neurogenic thoracic outlet syndrome

To evaluate the diagnostic utility of dermatomal and mixed nerve somatosensory evoked potentials (SEPs) in patients with thoracic outlet syndrome (TOS) and to compare their value with routine electrodiagnostic methods, we studied a group of 44 patients with neurogenic TOS and 30 healthy controls. In addition to bilateral median and ulnar SEPs, evoked potentials were recorded after stimulation of C6 and C8 dermatomes from the first and fifth digits, respectively. The patients were classified into 3 groups according to the nature of their clinical condition. The abnormality rate for both ulnar and C8 dermatomal SEPs was 100% in a small group of patients with severe neurological signs like atrophy. In groups of patients with lesser degrees of neurogenic damage, abnormality rates for ulnar and C8 dermatomal SEPs on affected limb(s) were 67 and 50%, respectively. Same abnormality rates were 25 and 18% in patients with only subjective symptoms. In patients with objective neurological signs, the major increase in sensitivity was with electromyography (EMG). Abnormalities of routine nerve conduction studies and F-wave latency were observed in patients with severe neurogenic damage. We concluded that the most useful tests in the diagnosis of neurogenic TOS are needle EMG and ulnar SEPs.