Circadian modulation of GABA-mediated cortical inhibition

Circadian rhythms exert powerful influence on various aspects of human physiology and behavior. Here, we tested changes of human cerebral cortex excitability over the course of the day with transcranial magnetic stimulation (TMS). At different times of the day, intracortical and corticospinal excitability of the primary motor cortex (M1) was evaluated in 15 healthy subjects by TMS of left M1. While motor thresholds, short-interval intracortical inhibition and facilitation and input/output curves remained unchanged, we found that a specific form of γ-aminobutyric acid (GABA)-mediated intracortical inhibition, revealed by long-interval intracortical inhibition and cortical silent periods, progressively decreased during the course of the day. Additional experiments demonstrated that morning inhibition persisted irrespective of previous sleep or sleep deprivation. Corticotropin-releasing hormone (CRH) infusions in the evening lead to morning cortisol levels but did not restore levels of morning inhibition, whereas suppression of endogenous CRH release by repeated oral dexamethasone intake over 24 h prevented morning inhibition. The findings suggest a specific modulation of GABAergic motor cortex inhibition within the circadian cycle, possibly linked to the CRH system, and may indicate a neurobiological basis for variable neuroplasticity over the course of the day.     

Alteration of cortical but not spinal inhibitory circuits in idiopathic scoliosis

Background: The pathogenesis of adolescent idiopathic scoliosis (AIS), including the role of brain and spinal inhibitory circuits, is still poorly elucidated. The aim of this study was to identify which central inhibitory mechanisms are involved in the pathogenesis of AIS.Design: A prospective neurophysiological study, using a battery of neurophysiological tests, such as cutaneous (CuSP) and cortical (CoSP) silent periods, motor evoked potentials (MEP) and paired-pulse transcranial magnetic stimulation (ppTMS).Settings: Neurophysiological laboratory.Participants: Sixteen patients with AIS (14 females, median age 14.4) and healthy controls.Outcome measures: MEPs were obtained after transcranial magnetic stimulation (TMS) and recorded from the abductor pollicis muscle (APB). ppTMS was obtained at interval ratios (ISI) of 1, 2, 3, 6, 10, 15 and 20 ms. The cortical silent period (CoSP) was recorded from the APB. The cutaneous silent period (CuSP) was measured after painful stimuli delivered to the thumb while the subjects maintained voluntary contraction of the intrinsic hand muscles. The data were analyzed and compared with those from healthy subjects.Results: The CoSP duration was significantly prolonged in AIS patients. A significantly higher amplitude of ppTMS for ISI was found in all AIS patients, without remarkable left-right side differences. No significant difference in MEP latency or amplitude nor in the CuSP duration was obtained.Conclusion: Our observation demonstrates evidence of central nervous system involvement in adolescent idiopathic scoliosis (AIS). Lower intracortical inhibition, higher motor cortex excitability, and preserved spinal inhibitory circuits are the main findings of this study. A possible explanation of these changes could be attributed to impaired sensorimotor integration predominantly at the cortical level.     

Altered bidirectional plasticity and reduced implicit motor learning in concussed athletes

Persistent motor/cognitive alterations and increased prevalence of Alzheimer's disease are known consequences of recurrent sports concussions, the most prevalent cause of mild traumatic brain injury (TBI) among youth. Animal models of TBI demonstrated that impaired learning was related to persistent synaptic plasticity suppression in the form of long-term potentiation (LTP) and depression (LTD). In humans, single and repeated concussive injuries lead to lifelong and cumulative enhancements of gamma-aminobutyric acid (GABA)-mediated inhibition, which is known to suppress LTP/LTD plasticity. To test the hypothesis that increased GABAergic inhibition after repeated concussions suppresses LTP/LTD and contributes to learning impairments, we used a paired associative stimulation (PAS) protocol to induce LTP/LTD-like effects in primary motor cortex (M1) jointly with an implicit motor learning task (serial reaction time task, SRTT). Our results indicate that repeated concussions induced persistent elevations of GABA(B)-mediated intracortical inhibition in M1, which was associated with suppressed PAS-induced LTP/LTD-like synaptic plasticity. This synaptic plasticity suppression was related to reduced implicit motor learning on the SRTT task relative to normal LTP/LTD-like synaptic plasticity in unconcussed teammates. These findings identify GABA neurotransmission alterations after repeated concussions and suggest that impaired learning after multiple concussions could at least partly be related to compromised GABA-dependent LTP/LTD synaptic plasticity.     

Cortical motor activation patterns following hand transplantation and replantation

We studied cortical activation patterns by functional MRI in a patient who received bilateral hand transplantation after amputation 6 years ago and in a patient who had received unilateral hand replantation within 2 hours after amputation. In the early postoperative period, the patient who had had the hand transplantation revealed strong activation of a higher motor area, only weak activation of the primary sensorimotor motor cortex and no activation of the primary somatosensory cortex. At 1-year follow-up, a small increase in primary sensorimotor motor cortex activation was observed. Activation of the primary somatosensory cortex was only seen at the 2 year follow-up. By contrast, after hand replantation, the activation pattern was similar to that of the uninjured hand within 6 weeks. This included activation of the primary sensorimotor motor cortex, higher motor areas and primary somatosensory cortex. Transplantation after long-standing amputation results in cortical reorganization occurring over a 2-year period. In contrast, hand replantation within a few hours preserves a normal activation pattern.     

Pitfalls in cortical localization by intraoperative recording of cortical somatosensory evoked potentials]

Cortical somatosensory evoked potential (SEP) recordings were made in 11 patients who had lesions located in or near the somatosensory or motor gyri to localize the central sulcus and sensorimotor cortex during neurosurgical operations. Cortical localization was successful in 7 of the 11 patients by recording phase reversal waveforms of N20 and P20 at electrode sites in the hand area on opposite sides of the central sulcus. There were 4 cases in which the cortical localization failed. Locations of craniotomy were far distant from the central sulcus retrospectively in 2 of the 4 patients. Cortical SEPs couldn't be recorded despite probable exposure of the hand area and apparently adequate stimulation and recording conditions in 2 patients who had showed no or low amplitude scalp SEP preoperatively. In one of these 2 patients only low amplitude negative waves were recorded at the cortex which was thought far field potentials originated from subcortical structures. In 2 patients cortical SEP was monitored during the removal of the tumors and was useful to estimate the effects of the operative procedures on the sensorimotor cortex. It is concluded that the localization of cortical functions using cortical SEP is useful for reducing risk associated with intracranial surgery. However, we must be aware that there are some pitfalls in this method.     

No difference observed in short-interval intracortical inhibition in older burn-injury survivors compared to non-injured older adults: A pilot study

ObjectiveThe study aimed to investigate short-interval intracortical inhibition (SICI) in burns survivors and non-injured controls, and establish whether paired-pulse transcranial magnetic stimulation (TMS) is a sensitive tool to investigate SICI after burn-injury.MethodsBurn survivors underwent experimental assessments at 6- and 12-weeks after injury, and control participants underwent two equivalent sessions 6 weeks apart. Single-pulse transcranial magnetic stimulation (TMS) was used to record motor-evoked potentials (MEPs) from a hand muscle and paired-pulse TMS was used to measure SICI. Functional measures were obtained for comparison at 12-weeks after injury.ResultsThere was no significant difference in SICI between burns survivors and non-injured controls at either 6- or 12-weeks after burn injury. There was no evidence of correlations between SICI and functional outcome measures in burns survivors.ConclusionsThese results show that paired-pulse TMS is a useful method for investigating cortical inhibition following burn injury, and that SICI circuits in the primary motor cortex are not affected by minor burn injury. This study presents details for definitive future studies of primary motor cortex function after minor burn injury.     

Cortical excitability changes in patients with sleep-wake disturbances after traumatic brain injury

Although chronic sleepiness is common after head trauma, the cause remains unclear. Transcranial magnetic stimulation (TMS) represents a useful complementary approach in the study of sleep pathophysiology. We aimed to determine in this study whether post-traumatic sleep-wake disturbances (SWD) are associated with changes in excitability of the cerebral cortex. TMS was performed 3 months after mild to moderate traumatic brain injury (TBI) in 11 patients with subjective excessive daytime sleepiness (EDS; defined by the Epworth Sleepiness Scale ≥10), 12 patients with objective EDS (as defined by mean sleep latency <5 on multiple sleep latency tests), 11 patients with fatigue (defined by daytime tiredness without signs of subjective or objective EDS), 10 patients with post-traumatic hypersomnia "sensu strictu," and 14 control subjects. Measures of cortical excitability included central motor conduction time, resting motor threshold (RMT), short-latency intracortical inhibition (SICI), and intracortical facilitation to paired-TMS. RMT was higher and SICI was more pronounced in the patients with objective EDS than in the control subjects. In the other patients all TMS parameters did not differ significantly from the controls. Similarly to that reported in patients with narcolepsy, the cortical hypoexcitability may reflect the deficiency of the excitatory hypocretin/orexin-neurotransmitter system. These observations may provide new insights into the causes of chronic sleepiness in patients with TBI. A better understanding of the pathophysiology of post-traumatic SWD may also lead to better therapeutic strategies in these patients.     

The functional organization and cortical connections of motor cortex in squirrels

Despite extraordinary diversity in the rodent order, studies of motor cortex have been limited to only 2 species, rats and mice. Here, we examine the topographic organization of motor cortex in the Eastern gray squirrel (Sciurus carolinensis) and cortical connections of motor cortex in the California ground squirrel (Spermophilus beecheyi). We distinguish a primary motor area, M1, based on intracortical microstimulation (ICMS), myeloarchitecture, and patterns of connectivity. A sensorimotor area between M1 and the primary somatosensory area, S1, was also distinguished based on connections, functional organization, and myeloarchitecture. We term this field 3a based on similarities with area 3a in nonrodent mammals. Movements are evoked with ICMS in both M1 and 3a in a roughly somatotopic pattern. Connections of 3a and M1 are distinct and suggest the presence of a third far rostral field, termed "F," possibly involved in motor processing based on its connections. We hypothesize that 3a is homologous to the dysgranular zone (DZ) in S1 of rats and mice. Our results demonstrate that squirrels have both similar and unique features of M1 organization compared with those described in rats and mice, and that changes in 3a/DZ borders appear to have occurred in both lineages.     

Somatosensory cortectomy induces motor cortical hyperexcitability and scoliosis: an experimental study in developing rats

Background contextDysfunctions in sensorimotor integration, reminiscent to those described in idiopathic dystonia, have been found in idiopathic scoliosis (IS) and might be involved in its pathogenesis. Studying the effects of experimental disruption of sensory cortex may shed further insight into the etiopathology of IS.PurposeTo evaluate whether disruption of central sensorimotor integration through partial ablation of the somatosensory cortex leads to scoliosis in developing rats and to describe the effects of such an intervention on motor cortico-cortical inhibition and facilitation.MethodsFifty Wistar rats aged 3 weeks were used in the study. Twenty-four rats underwent craniotomy and electrocoagulation of the sensory cortex (PAR1) in the right hemisphere. A second group of 16 rats underwent a sham operation with craniotomy but no electrocoagulation. A third group of 10 rats was used as intact controls. Four weeks after surgery, motor cortical excitability was assessed with paired-pulse electrical cortical stimulation. Neurologic and behavioral examinations were completed serially, and 10 weeks after surgery, X-ray examinations were performed in anesthetized rats to assess spinal curvature. Electromyographic recordings of paravertebral muscle activity were performed in waking rats. At the end of the study, rats were sacrificed, and histologic examinations of brain tissue were performed to confirm the extent of the lesion. A grant from a Government Health Research Fund without salaries assignment financed the study.ResultsAlmost half of the animals with somatosensory cortectomy (46%) developed scoliosis, with an average Cobb angle of 23±8°. None of the animals in the sham or control groups developed scoliosis. Despite cortical lesions, no motor or behavioral deficits were apparent in the experimental group, and cortectomized rats were neurologically indistinguishable from sham or control animals, except for the presence of scoliosis. Cortico-cortical inhibition was significantly reduced in the hemisphere of scoliotic concavity in the cortectomized group but was normal in the other groups.ConclusionsThese findings indicate that altered sensorimotor integration may cause scoliosis without noticeable motor impairment. Reduced cortico-cortical inhibition was observed in cortectomized rats. This finding is consistent with results in adolescents with IS and suggests that alteration of cortical hemispheric balance of sensorimotor integration may play an important role in the pathogenesis of IS.     

Localization of human sensorimotor cortex during surgery by cortical surface recording of somatosensory evoked potentials

The traditional means of localizing sensorimotor cortex during surgery is Penfield's procedure of mapping sensory and motor responses elicited by electrical stimulation of the cortical surface. This procedure can accurately localize sensorimotor cortex but is time-consuming and best carried out in awake, cooperative patients. An alternative localization procedure is presented that involves cortical surface recordings of somatosensory evoked potentials (SEP's), providing accurate and rapid localization in patients under either local or general anesthesia. The morphology and amplitude of median nerve SEP's recorded from the cortical surface varied systematically as a function of spatial location relative to the sensorimotor hand representation area. These results were validated in 18 patients operated on under local anesthesia in whom the sensorimotor cortex was independently localized by electrical stimulation mapping; the two procedures were in agreement in all cases. Similar SEP results were demonstrated in an additional 27 patients operated on under general anesthesia without electrical stimulation mapping. The following three spatial relationships between SEP's and the anatomy of the sensorimotor cortex permit rapid and accurate localization of the sensorimotor hand area: 1) SEP's with approximately mirror-image waveforms are recorded at electrode sites in the hand area on opposite sides of the central sulcus (P20-N30 precentrally and N20-P30 postcentrally); 2) the P25-N35 is recorded from the postcentral gyrus as well as a small region of the precentral gyrus in the immediate vicinity of the central sulcus: this waveform is largest on the postcentral gyrus about 1 cm medial to the focus of the 20- and 30-msec potentials; and 3) regardless of component identification, maximum SEP amplitudes are recorded from the hand representation area on the precentral and postcentral gyri.     

Spinal cord contusion in the rat: somatosensory evoked potentials as a function of graded injury

A weight-drop technique was used to produce mild, moderate, or severe spinal cord contusive injury in rats. At 4 weeks after injury, somatosensory evoked potentials (SEPs) were recorded with silver ball electrodes placed over the somatosensory cortex of anesthetized rats to measure the response to sciatic nerve stimulation. Both SEP area and amplitude were measured and were highly correlated with each other. Both indices of the SEP correlated inversely with the height of the weight drop and directly with the degree of residual function assessed at 4 weeks after injury. Measures of residual function consisted of a motor score, inclined plane test, and a combined behavioral score based on several neurologic functions. No correlation between latency of the SEP with degrees of contusive injury was observed. The data indicate that the SEP can be used as one criterion in the assessment of the severity of a lesion in a rat model of a graded spinal cord injury.     

Effect of intrathecal bupivacaine on somatosensory evoked potentials following dermatomal stimulation

The effect of spinal anesthesia with 3.6 +/- 0.1 ml (mean +/- SEM) of 0.5% bupivacaine on early (less than 150 msec) somatosensory evoked potentials (SEPs) with electrical stimulation of the L1 and S1 dermatomes was examined in 12 patients. The mean level of sensory analgesia (pinprick) was T8,9 +/- 1.0 (+/- SEM) and the mean degree of motor blockade was 1.3 +/- 0.1 (Bromage scale). Intrathecal bupivacaine significantly (P less than 0.05) decreased the amplitude of all SEP components after stimulation of the L1 dermatome and most components during stimulation of the S1 dermatome. Intrathecal bupivacaine also increased the latency of SEPs (P less than 0.05) of both dermatomes. The L1 SEP disappeared in 7 and the S1 SEPs in 5 of the 12 patients during neural blockade. In three patients the SEPs disappeared at both locations. Sensory thresholds increased significantly during blockade. We found no correlation between decrease of amplitude and degree of motor blockade or level of sensory analgesia. Thus, intrathecal plain bupivacaine has a strong depressant effect on the neural afferent transmission as assessed by SEPs. However, despite clinically effective blockade as assessed by pinprick and motor blockade nerve potentials after nociceptive stimulation within the area of sensory block were often able to pass to the cerebral cortex.     

Acute and chronic changes in diffusivity measures after sports concussion

Despite negative neuroimaging findings in concussed athletes, studies indicate that the acceleration and deceleration of the brain after concussive impacts result in metabolic and electrophysiological alterations that may be attributable to changes in white matter resulting from biomechanical strain. In the present study we investigated the effects of sports concussion on white matter using three different diffusion tensor imaging (DTI) measures: fractional anisotropy (FA), mean diffusivity (MD), and axial diffusivity (AD). We compared a group of 10 non-concussed athletes with a group of 18 concussed athletes of the same age (mean age 22.5 years) and education (mean 16 years) using a voxel-based approach (VBA) in both the acute and chronic post-injury phases. All concussed athletes were scanned 1-6 days post-concussion and again 6 months later in a 3T Siemens Trio(?) MRI. Three 2×2 repeated-measures analyses of variance (ANOVAs) were conducted, one for each measure of DTI used in the current study. There was a main group effect of FA, which was increased in dorsal regions of both corticospinal tracts (CST) and in the corpus callosum in concussed athletes at both time points. There was a main group effect of AD in the right CST, where concussed athletes showed elevated values relative to controls at both time points. MD values were decreased in concussed athletes, in whom analyses revealed significant group differences in the CST and corpus callosum at both time points. Although the use of VBA does limit the analyses to large tracts, and it has clinical limitations with regard to individual analyses, our results nevertheless indicate that sports concussions do result in changes in diffusivity in the corpus callosum and CST that are not detected using conventional neuroimaging techniques.     

健侧C7神经根移位术后患肢对应皮层体感诱发电位的变化规律

目的：对照已行健侧C7神经根移位术患者与正常人的皮层体感诱发电位(somatosensory evoked potential，SEP)，了解、分析大脑重塑过程中电生理变化特点。方法：12例左侧臂丛神经撕脱伤已行健侧C7→尺神经→正中神经重建患者，其中6例患肢感觉在健侧者为A组，感觉转到患侧者为B组；同时以12位正常人作为对照组。利用SEP技术，刺激左上肢正中神经腕部、肘部，分别记录左右两侧皮层SEP的波形，测定其潜伏期、波幅和腕→肘神经传导速度，并进行统计学比较。结果：正常人两侧皮层SEP的潜伏期、波幅之间存在差异，但潜伏期差异无显著性，而波幅差异有显著性。A组患者两侧皮层间SEP潜伏期差异有显著性，波幅差异无显著性。B组患者两侧皮层间SEP潜伏期差异无显著性，而波幅差异则存在显著性。A组与B组患者对侧皮层SEP潜伏期和波幅差异均有显著性。结论：健侧C7神经根移位术后，患肢对侧皮层发生功能重塑，两侧皮层记录的SEP潜伏期差值缩短，而波幅差异增大。患侧SEP检测可为患肢对应皮层功能重塑的“再支配”现象提供相应佐证与数据，为临床采取进一步措施促进患者肢体与大脑皮层功能的恢复提供客观依据。     

Neglect induced by thalamotomy in humans: a quantitative appraisal of the sensory and motor deficits

Stereotactic lesions for the treatment of tremor and rigidity in patients with Parkinson's disease are occasionally followed by neglect of the use of contralateral extremities for spontaneous movement when there are no specific sensory or motor deficits. A group of patients with neglected extremities was compared with a group of patients in which thalamotomy did not produce neglect. Neglect was shown by changes in motor performance, somatosensory evoked potentials (SEP) and electroencephalographic frequency induced by the lesion, as well as radiological evidence of brain atrophy and place and extension of lesions. Reaction time to both auditory and somatosensory stimuli was significantly increased only in the extremities contralateral to the lesion of patients with neglect; tremor decreased equally in both groups, and other motor abilities remained unchanged. P-200 component of SEP decreased in amplitude and increased in latency only in cases with neglect, particularly ipsilateral to the lesion; early components and mean electroencephalographic frequency remained unchanged. Brain atrophy was significant in patients with neglect, particularly for the posterior portion of the 3rd ventricle. No differences in size and location of the lesions were found between the groups. Results indicate that this type of neglect is not secondary to lesions in specific sensory of motor pathways, but to lesions of structures coupling sensorimotor functions and the process of attention and that midline thalamic nuclei atrophy precipitates the neglect, perhaps by critically decreasing the amount of reticulothalamocortical projections engaged in selective attention.     

Athletes after anterior cruciate ligament reconstruction demonstrate asymmetric intracortical facilitation early after surgery

Quadriceps dysfunction persists after anterior cruciate ligament reconstruction (ACLR), yet the etiology remains elusive. Inhibitory and facilitatory intracortical networks (ie, intracortical excitability) may be involved in quadriceps dysfunction, yet the investigation of these networks early after ACLR is sparse. The purposes of this study were to examine (a) changes in intracortical excitability in athletes after ACLR compared to uninjured athletes during the course of postoperative rehabilitation, (b) the association between intracortical excitability and quadriceps strength in athletes after ACLR. Eighteen level I/II athletes after ACLR between the ages of 18 to 30 years and eighteen healthy sex, age, and activity matched athletes were tested at three‐time points: (a) 2 weeks after surgery, (b) achievement of a “quiet knee” defined as full range of motion and minimal effusion, (c) return to running time point defined as achievement of a quadriceps index ≥80% and at least 12 weeks post‐ACLR. Short‐interval intracortical inhibition (SICI) and intracortical facilitation (ICF), measured via transcranial magnetic stimulation and isometric quadriceps strength were examined bilaterally at each time point. There was a significant group × limb interaction (P = .017) for ICF. The ACLR group demonstrated asymmetric ICF (greater in the nonsurgical limb) compared to controls and a significant relationship between SICI and quadriceps strength of the surgical limb at the quiet knee time point (P = .018). ACLR individuals demonstrate differential effects on ICF between limbs. Also, SICI is associated with isometric quadriceps strength after ACLR, suggesting increased inhibition of the motor cortex may contribute to impaired quadriceps strength following ACLR.     

Intraoperative localization of the central sulcus by cortical somatosensory evoked potentials in brain tumor. Case report.

Perplexing findings of cortical somatosensory evoked potentials (SEP's) for determining the central sulcus during a craniotomy are reported in a case of brain tumor. On stimulation of the contralateral median nerve in that patient, phase-reversal of SEP waves N1 and P2 was observed not only across the central sulcus but also across the precentral sulcus. In topographic mapping of the N1-P2 amplitude, the sulcus dividing the maximum polarity was the central sulcus; this was confirmed by the cortical stimulation-evoked motor responses. For accurate localization of the central sulcus by cortical SEP's, the distribution of potentials must be analyzed with extensive exposure of the sensorimotor cortex.     

Abnormal activation of the motor cortical network in idiopathic scoliosis demonstrated by functional MRI

The aetiology of idiopathic scoliosis (IS) remains unknown, but there is growing support for the possibility of an underlying neurological disorder. Functional magnetic resonance imaging (fMRI) can characterize the abnormal activation of the sensorimotor brain network in movement disorders and could provide further insights into the neuropathogenesis of IS. Twenty subjects were included in the study; 10 adolescents with IS (mean age of 15.2, 8 girls and 2 boys) and 10 age-matched healthy controls. The average Cobb angle of the primary curve in the IS patients was 35° (range 27°–55°). All participants underwent a block-design fMRI experiment in a 1.5-Tesla MRI scanner to explore cortical activation following a simple motor task. Rest periods alternated with activation periods during which participants were required to open and close their hand at an internally paced rate of approximately 1 Hz. Data were analyzed with Statistical Parametric Mapping (SPM5) including age, sex and laterality as nuisance variables to minimise the presence of bias in the results. Compared to controls, IS patients showed significant increases in blood oxygenation level dependent (BOLD) activity in contralateral supplementary motor area when performing the motor task with either hand. No significant differences were observed when testing between groups in the functional activation in the primary motor cortex, premotor cortex and somatosensory cortex. Additionally, the IS group showed a greater interhemispheric asymmetry index than the control group (0.30 vs. 0.13, p < 0.001). This study demonstrates an abnormal pattern of brain activation in secondary motor areas during movement execution in patients with IS. These findings support the hypothesis that a sensorimotor integration disorder underlies the pathogenesis of IS.     

Intraoperative somatosensory evoked potential monitoring in scoliosis

During surgical correction of scoliosis, 63 patients had somatosensory evoked potential (SEP) monitoring of the spinal cord. Tibial nerves were unilaterally stimulated, and the potentials were recorded from the midcervical spine with surface and epidural needle electrodes. Over 85% had no significant change in their SEP and no postoperative neurologic deficits. Eleven percent had a significant change in their potential (amplitude decrease of greater than 60% and/or latency increase of greater than 2.5 msec) with no neurologic complications. One patient had a significant potential change and temporary postoperative sensory deficits did occur. One additional patient experienced postoperative neurologic complications but had no SEP change. This single false negative case, however, was clinically significant only for motor dysfunction, which is not monitored by the SEP. When changes in patient core temperature were compared to changes in SEP amplitude and latency, an intraoperative decrease in core temperature increased SEP latency and decreased amplitude, which may explain in part the false positive rate of the procedure.     

Effects of thiopental, fentanyl, and etomidate on upper extremity somatosensory evoked potentials in humans

The effects of three anesthetic induction agents on somatosensory evoked potentials (SEP) were assessed in unpremedicated patients who were without neurologic abnormality of the upper extremities. SEP was assessed by stimulation of the nondominant median nerve and responses were recorded over Erbs point (N10), second cervical vertebra (N14), and the contralateral cortex (P15, N20, P23 latencies, and P15-N20 and N20-P23 amplitudes). Nine patients received thipental (4 mg/kg, iv bolus), nine patients received fentanyl (25 micrograms/kg, iv bolus), and nine patients received etomidate (0.4 mg/kg, iv bolus). SEP was assessed before and after drug administration at motor threshold stimulus intensity. Thiopental increased the latency of N10, N14, and N20. The amplitudes of N10-, N14-, and scalp-recorded waves were not altered by thiopental. Fentanyl increased N20 and P23 latency and decreased the amplitude of P15-N20. Etomidate increased latency of N20 and P23 without alteration of latencies of N10 or N14 and increased the amplitude of P15-N20 and N20-P23, while the amplitude of N10 was unchanged and the amplitude of N14 was decreased. It is concluded that thiopental or fentanyl causes only modest alterations in early waves of upper extremity SEP, whereas etomidate increases the amplitude of scalp-recorded waves. The effect of etomidate on SEP may make diagnosis of neurologic injury more difficult because of the changing waveform.