Amplitude Of Cortical Somatosensory Evoked Potentials Research Articles

Cortical somatosensory evoked potential amplitudes and clinical outcome after cardiac arrest: a retrospective multicenter study

ObjectiveBilaterally absent cortical somatosensory evoked potentials (SSEPs) reliably predict poor outcome in comatose cardiac arrest (CA) patients. Cortical SSEP amplitudes are a recent prognostic extension; however, amplitude thresholds, inter-recording, and inter-rater agreement remain uncertain.MethodsIn a retrospective multicenter cohort study, we determined cortical SSEP amplitudes of comatose CA patients using a standardized evaluation pathway. We studied inter-recording agreement in repeated SSEPs and inter-rater agreement by four raters independently determining 100 cortical SSEP amplitudes. Primary outcome was assessed using the cerebral performance category (CPC) upon intensive care unit discharge dichotomized into good (CPC 1–3) and poor outcome (CPC 4–5).ResultsOf 706 patients with SSEPs with median 3 days after CA, 277 (39.2%) had good and 429 (60.8%) poor outcome. Of patients with bilaterally absent cortical SSEPs, one (0.8%) survived with CPC 3 and 130 (99.2%) had poor outcome. Otherwise, the lowest cortical SSEP amplitude in good outcome patients was 0.5 µV. 184 (42.9%) of 429 poor outcome patients had lower cortical SSEP amplitudes. In 106 repeated SSEPs, there were 6 (5.7%) with prognostication-relevant changes in SSEP categories. Following a standardized evaluation pathway, inter-rater agreement was almost perfect with a Fleiss’ kappa of 0.88.InterpretationBilaterally absent and cortical SSEP amplitudes below 0.5 µV predicted poor outcome with high specificity. A standardized evaluation pathway provided high inter-rater and inter-recording agreement. Regain of consciousness in patients with bilaterally absent cortical SSEPs rarely occurs. High-amplitude cortical SSEP amplitudes likely indicate the absence of severe brain injury.

Added value of somato-sensory evoked potentials amplitude for prognostication after cardiac arrest

AimsBilateral absence of cortical somato-sensory evoked potentials (SSEPs) robustly predicts poor outcome after cardiac arrest (CA), but it is uncertain if SSEP amplitudes provide additional information. Here, we examined the prognostic value of cortical SSEP amplitude in comparison with other known outcome predictors. MethodsWe retrospectively determined SSEP amplitudes in a prospective CA registry, identified an amplitude cut-off for worst Cerebral Performance Category (CPC) within three months, and examined correlations of SSEP amplitude with pupillary light reflex (PLR), myoclonus, peak serum neuron specific enolase (NSE), and 24–36 h and 36–72 h EEG (reactivity, epileptiform features). ResultsAmong 158 patients, 54% awoke. Amplitudes correlated with EEG findings, present PLR, myoclonus, NSE. A cut-off for cortical SSEP ≤ 0.41 μV was 100% specific for poor outcome (95% CI: 96–100%); sensitivity increased marginally vs. SSEPs absence [47% (35–59%) vs 46% (34–58%)] for CPC 4–5. Adding SSEPs ≤0.41 μV to a multimodal prognostic model including EEG, clinical features, and NSE improved prediction for mortality, but not for CPC 3–5 at three months. No statistical correlation between amplitudes and good outcome was observed. SSEP amplitudes correlated inversely with CPC at three months in the overall cohort (r = −0.332; p < 0.0001) but not in the subgroup with present SSEPs (r = −0.102; p = 0.256). ConclusionDecreased SSEPs amplitudes are associated with poor outcome after cardiac arrest; however, adding this to a multimodal prognostic approach including EEG, clinical and blood biomarkers, improves slightly prediction of mortality, but not of poor or good outcome.

Early-SEPs' amplitude reduction is reliable for poor-outcome prediction after cardiac arrest?

The bilateral absence of cortical Somatosensory Evoked Potentials (SEPs), after cardiac arrest (CA), is a high reliable predictor of poor outcome but it is present in no more than 40% of patients. An amplitude reduction of cortical SEPs was found in about 30% of subjects, but few papers analysed its prognostic significance. The aim of our study is to identify a value of SEP amplitude reduction below which all the CA patients had poor outcome and the relationship between SEP and Electroencephalogram (EEG) patterns. We analysed comatose patients in whom SEPs and EEG were recorded at 6-12 hours after CA. We evaluated the sensitivity at specificity of 100% of SEP amplitude in predicting the non-recovery of consciousness by plotting Receiver Operating Characteristic (ROC) curves. We also analysed the relationship between SEP amplitude and EEG patterns. Outcome was evaluated at 6 months by Glasgow Outcome Scale. We analysed 119 subjects. According to the ROC analysis (area under the curve = 0.95/CI 0.91-0.99), all patients with a cortical SEP amplitude <0.65 μV did not recover consciousness (GOS 1-2), with a sensitivity of 71.8%. Severe EEG abnormalities (suppression and burst-suppression patterns) were also observed in all these patients. Not only the absence but also a bilateral amplitude reduction of cortical SEPs (<0.65 μV) is associated with ominous prognosis (death or non-recovery of consciousness) with a very high predictive value. However, we emphasize that great caution should be applied before adopting amplitude reduction as a criterion for the poor prognosis of CA patients.

F108. The prognostic value of median nerve SSEP after cardiac arrest: Evaluation of severity of hypoxic-ischemic encephalopathy by brain autopsies

Introduction The severity of hypoxic-ischemic encephalopathy (HIE) strongly determines outcome after cardiac arrest (CA). Bilaterally absent cortical median nerve somatosensory evoked potentials (SSEPs) have been shown to accurately predict poor prognosis. However, self-fulfilling prophecy due to withdrawal of life-sustaining therapy is an important bias in prognostication studies on CA patients. Brain autopsies in patients who died after CA provide a unique opportunity to verify prognostic parameters such as SSEPs. Methods We retrospectively identified CA patients from university hospitals in Berlin, Germany, Lund, Sweden and Arhus, Denmark, who died after initially successful resuscitation and for whom SSEPs for neuro-prognostication and brain autopsy were available. We blindly determined presence/absence and, if applicable, cortical peak-to-peak SSEP amplitudes from original recordings. Severity of HIE was quantified histopathologically according to the selective eosinophilic neuronal death (SEND) score. Results We identified 58 CA autopsy patients who had been investigated with SSEP. All 21 patients with bilaterally absent SSEP and all 5 with cortical SSEP amplitudes below 0.5 μV had severe HIE (SEND 2–4 in cortical regions). The highest cortical SSEP amplitude in a patient with severe HIE was 2.7 μV, all 11 patients with higher amplitudes had no/moderate HIE (SEND 0–1 in cortical regions). Conclusion We did not find evidence for a self-fulfilling prophecy in the prediction of poor neurological outcome by SSEP after cardiac arrest. Bilaterally absent cortical SSEP and very low SSEP amplitudes indicated histopathologically severe HIE whereas cortical SSEP amplitudes above 2.7 μV indicated absence of severe HIE.

Effect of early evaluation of CSEP and DNEP on spinal cord ischemic injury: an experimental study

Objective To investigate the effect of early evaluation of cortical somatosensory evoked potentials(CSEP)and desending neurogenic motor evoked potentials(DNEP)in spinal cord ischemic injury by observing the early change characteristics of CSEP and DNEP of spinal cord ischemia in rabbits. Methods To establish a rabbit model with different degree of permanent spinal cord ischemic injury through the ligation of different levels of lumbar arteries. The rabbits were divided into 5 groups(ligation of the left renal artery and the different levels of lumbar arteries between arterial bifurcations respectively, including 1 to 5-artery group). After modeling, CSEP and DNEP were continuously recorded for 60 min. After 2 days, the samples of ischemic central area were selected for HE staining. The motor function score Tarlov criteria were used to assess the motor function. The relationship between the amplitude variation of CESP and DNEP and the motor function after ligation were analyzed. Results There were statistical significance in the percentages of the CSEP amplitude and preoperative baseline amplitude between the 4- and 5-artery groups compared with before ligation(P 0.05). There were statistical differences in the percentages of the DNEP amplitude and preoperative baseline amplitude among the 3-, 4- and 5 artery groups compared with before ligation(all P 0.05). Compare with before ligation, there were statistical significances in the motor function 2 days after ligation between the 4- and 5-artery group(all P 0.05). The amplitude variation of CSEP and DNEP was positively correlated with the motor function 2 days after ligation of blood vessels(r=0.97, P<0.001; r=0.95, P<0.001). Conclusions Both CSEP and DNEP can predict the motor function after spinal cord injury. DNEP is more sensitive to spinal cord ischemic injury and is more specific to motor function. It can find ischemic injury in the early spinal cord ischemia. Key words: Spinal cord ischemia; Evoked potentials, somatosensory; Evoked potentials, motor; Rabbits

Amplitudes of cortical somatosensory evoked potentials and outcome prediction after cardiac arrest

Bilaterally absent cortical somatosensory evoked potentials (SSEPs) predict poor outcome after cardiac arrest. A threshold for the amplitude of early cortical SSEPs above which patients may survive with good outcome has not been determined. Thus, tolerable noise levels for the interpretation of cortical SSEPs are poorly defined. Furthermore, it has not been systematically investigated whether high amplitudes of cortical SSEPs may exclude severe hypoxic encephalopathy incompatible with re-awakening.

Susceptibility of Transcranial Electric Motor-evoked Potentials to Varying Targeted Blood Levels of Dexmedetomidine during Spine Surgery

Dexmedetomidine has been increasingly used as an adjunct to opioid-propofol total intravenous anesthesia (TIVA). The authors tested the hypothesis and found that clinically relevant blood levels of dexmedetomidine do not produce significant attenuation of the amplitude of transcranial electric motor-evoked potentials either independently or by interaction with propofol in a dose-dependent manner. The authors planned to recruit 72 patients with idiopathic scoliosis who had posterior spine fusion surgery during propofol and remifentanil TIVA with dexmedetomidine as an adjunct. However, the authors terminated the study after enrolling 44 patients because of change in surgical technique. Before administering dexmedetomidine, baseline transcranial electric motor-evoked potentials were acquired during TIVA with remifentanil and propofol. Patients were randomized to varying targeted blood levels of dexmedetomidine (0.4, 0.6, and 0.8 ng/ml) and propofol (2.5, 3.75, and 5 microg/ml) using a factorial design. The primary outcome variable was amplitude of transcranial electric motor-evoked potential. The secondary outcome was amplitude of cortical somatosensory-evoked potentials. Of the 44 recruited patients, 40 completed the study, and their data were analyzed. The administration of dexmedetomidine in increasing doses as an adjunct to propofol-based TIVA caused a clinically and statistically significant attenuation of amplitudes of transcranial electric motor-evoked potentials. The authors conclude that under the stimulation conditions used, dexmedetomidine as an anesthetic adjunct to propofol-based TIVA at clinically relevant target plasma concentrations (0.6-0.8 ng/ml) can significantly attenuate the amplitude of transcranial electric motor-evoked potentials.

The Effects of Propofol, Small-Dose Isoflurane, and Nitrous Oxide on Cortical Somatosensory Evoked Potential and Bispectral Index Monitoring in Adolescents Undergoing Spinal Fusion

In this study we compared the effects of propofol, small-dose isoflurane, and nitrous oxide (N(2)O) on cortical somatosensory evoked potentials (SSEP) and bispectral index (BIS) monitoring in adolescents undergoing spinal fusion. Twelve patients received the following anesthetic maintenance combinations in a randomly determined order: treatment #1: isoflurane 0.4% + N(2)O 70% + O(2) 30%; treatment #2: isoflurane 0.6% + N(2)O 70% + O(2) 30%; treatment #3: isoflurane 0.6% + air + O(2) 30%; treatment #4: propofol 120 microg . kg(-1) . min(-1) + air + O(2) 30%. Cortical SSEP amplitudes measured during anesthesia maintenance with treatment #3 (isoflurane 0.6%/air) were more than those measured during maintenance with treatment #1 (isoflurane 0.4%/N(2)O 70%) (P < 0.0001) and treatment #2 (isoflurane 0.6%/N(2)O 70%) (P < 0.0052). Cortical SSEP amplitudes measured during treatment #4 (propofol 120 microg . kg(-1) . min(-1)/air) were more than treatment #1 (isoflurane 0.4%/N(2)O 70%) (P < 0.0001), treatment #2 (Iso 0.6%/N(2)O 70%) (P < 0.0007), and treatment #3 (isoflurane 0.6%/air) (P < 0.0191). In addition, average BIS values measured during treatments 1, 2, 3 and 4 were 62, 62, 61, and 44 respectively. Only treatment #4 (propofol 120 microg . kg(-1) . min(-1)/air) uniformly maintained BIS values less than 60. Our study demonstrates that propofol better preserves cortical SSEP amplitude measurement and provides a deeper level of hypnosis as measured by BIS values than combinations of small-dose isoflurane/N(2)O or small-dose isoflurane alone.

Pharmacologic and physiologic influences affecting sensory evoked potentials: implications for perioperative monitoring.

Pharmacologic and physiologic influences affecting sensory evoked potentials: implications for perioperative monitoring.

Negative myoclonus in Creutzfeldt–Jakob disease

Objective: To describe electrophysiological findings in a patient with Creutzfeldt–Jakob disease (CJD) showing negative myoclonus.Methods and results: We studied this CJD patient electrophysiologically, in comparison with two patients with cortical reflex positive myoclonus due to benign adult familial myoclonic epilepsy (BAFME). Spontaneous negative myoclonus was associated with periodic synchronous discharges (PSDs) on the electroencephalogram, but negative myoclonus could also be induced by electrical stimulation of the median nerve in the CJD patient. This patient showed giant somatosensory evoked potentials (SEPs) and enhanced C reflexes, and the duration of the induced EMG silences was found to be significantly correlated with the amplitude of cortical SEPs. The duration of silent periods (SPs) produced by magnetic stimulation of the motor cortex was extremely long. The study of recovery function of SEPs suggested that the excitability of the somatosensory cortex was decreased during a long post-stimulus period. These findings were clearly different from those of patients with BAFME.Conclusions: This CJD patient had two types of negative myoclonus; one was associated with PSDs and the other was cortical reflex negative myoclonus. The long-lasting decrease in excitability of the sensorimotor cortices after stimulation could be related to the occurrence of both types of negative myoclonus.

Effects of propofol, propofol-nitrous oxide and midazolam on cortical somatosensory evoked potentials during sufentanil anaesthesia for major spinal surgery

Recording of cortical somatosensory evoked potentials (CSEP) enables monitoring of spinal cord function. We studied the effects of propofol, propofol-nitrous oxide or midazolam during sufentanil anaesthesia on CSEP monitoring during major spinal surgery. Thirty patients with normal preoperative CSEP were allocated randomly to one of the following anaesthesia regimens: propofol (2.5 mg kg-1 followed by 10-6 mg kg-1 h-1) with or without nitrous oxide, or midazolam (0.3 mg kg-1 followed by 0.15 mg kg-1 h-1) combined with sufentanil 0.5 microgram kg-1 h-1 in the propofol and midazolam groups, or 0.25 microgram kg-1 h-1 in the propofol-nitrous oxide group. CSEP were elicited by alternate right and left tibial posterior nerve stimulation and recorded before and after induction (15 min, 1, 2 and 3 h), and during skin closure. CSEP latencies were not significantly modified in the three groups. CSEP amplitude decreased significantly in the propofol-nitrous oxide group (from mean 2.0 (SEM 0.3) to 0.6 (0.1) microV; P < 0.05) but not in the propofol (from 1.8 (0.6) to 2.2 (0.3) microV) or midazolam (1.7 (0.5) to 1.6 (0.5) microV) groups. The time to the first postoperative voluntary motor response (recovery) delay was significantly greater in the midazolam group (115 (19) min) compared with the propofol and propofol-nitrous oxide groups (43 (8) and 41 (3) min, respectively). Consequently, the use of propofol without nitrous oxide can be recommended during spinal surgery when CSEP monitoring is required.

Comparison of the Effects of Ketamine-Midazolam with Those of Fentanyl-Midazolam on Cortical Somatosensory Evoked Potentials During Major Spine Surgery

LANGERON, O.; LILLE, F.; ZERHOUNI, O.; ORLIAGUET, G.; SAILLANT, G.; RIOU, B.; CORIAT, P. Author Information

Effects of hypothermia and sternal retractors on median nerve somatosensory evoked potentials.

Somatosensory evoked potentials (SEPs) are altered by hypothermia, which is often used during cardiopulmonary bypass (CPB). However, the effect of hypothermia on SHP amplitudes is unclear. Also, the sternal retractors used during open heart surgery are reported to cause brachial plexus distension and SEP changes. Median nerve SEPs under hypothermic CPB were studied in 29 elective patients scheduled for open heart surgery. In 23 patients who underwent left internal mammary artery (IMA) dissection, the effects of sternal retractors on cortical SEP before the initiation of CPB were investigated. A latency shift of all SEP components was detected when nasopharyngeal temperature decreased from 35.7(SD 0.4) degrees C to 27.8(SD 0.25) degrees C. The mean cortical N20 latency was increased by 39% (P < 0.0001), cervical N13 by 33% (P < 0.0001), and peripheral N9 by 27% (P < 0.0001). The latency changes were reversible when normothermia was restored. The effect of hypothermia on SEP amplitudes was more complex. The mean amplitude of N20 decreased from 2.7 microV to 2.2 microV (P < 0.05) and the amplitude of N13 from 2.5 microV to 2.0 microV (P < 0.0001). In contrast, the N9 component showed an increase from 1.4 microV to 2.1 microV (P < 0.0001) during hypothermia. The sternal retractors did not cause significant cortical SEP amplitude changes during IMA dissection or sternotomy. Also, the latency changes were small, although significant (P < 0.05). Despite the moderate amplitude changes produced by hypothermia, SEPs can be successfully monitored during hypothermia. Theoretically, the different behaviour of amplitude in peripheral and cranial components of SEP during hypothermia is interesting. Hypothermia has a more profound effect on synaptic transmission, represented by the cortical N20 latency, than on the peripheral nerve conduction velocity. Intraoperative monitoring of temperature is essential whenever SEPs are recorded. The sternal retractors were not responsible for the intraoperative SEP changes.

Comparison of the effects of ketamine-midazolam with those of fentanyl-midazolam on cortical somatosensory evoked potentials during major spine surgery

Cortical somatosensory evoked potentials (CSEP) allow monitoring of spinal cord function during surgery. Ketamine has been shown to enhance CSEP amplitude, but there is no previous study comparing its effects with those of other anaesthetic regimens. Therefore, we have compared the effects of ketamine with those of fentanyl, both combined with midazolam, on CSEP monitoring during major spine surgery. Twenty patients with normal preoperative CSEP were allocated randomly to a ketamine or fentanyl group. Anaesthesia was induced with ketamine 3 mg kg-1 or fentanyl 6 micrograms kg-1 i.v., and midazolam 0.3 mg kg-1 i.v in both groups, and maintained with continuous i.v infusion of ketamine 2 mg kg-1 h-1 or fentanyl 3 micrograms kg-1 h-1, combined in both groups with midazolam 0.15 mg kg-1 h-1 and 60% nitrous oxide in oxygen. CSEP were elicited by tibial posterior nerve stimulation and measured P1 and N1 latencies, and P1-N1 amplitude, CSEP were recorded before and after induction, at 15 min, 1 and 2 h after induction, during skin closure and after removal of nitrous oxide. Both groups were comparable in characteristics, duration of surgery, mean arterial pressure and temperature. CSEP latencies were not significantly affected in either group. CSEP amplitude decreased significantly over time in the fentanyl group (from mean 2.02 (SEM 0.41) to 0.95 (0.17) microV, P < 0.05), but not in the ketamine group (from 1.33 (0.36) to 1.05 (0.31) microV, ns). Nevertheless, we did not observe any significant differences in amplitudes or latencies between the two groups. The delay in obtaining the first voluntary postoperative motor response was significantly greater in the ketamine group (170 (54) vs 55 (17) min, P < 0.01). Both ketamine and fentanyl allowed us to obtain reliable CSEP during major spine surgery, and there were no significant difference between these two anaesthetic regimens for CSEP monitoring, but a longer delay for voluntary postoperative motor assessment was observed in the ketamine group.

Effets de l'association propofol-sufentanil sur les potentiels évoqués somesthésiques au cours de la chirurgie du rachis

Most anaesthetics depress cortical somatosensory evoked potentials (CSEPs). However, the modification of CSEPs during total intravenous anaesthesia using propofol remaining still unknown, justified this trial. Open, prospective, clinical study. Nine consecutive patients requiring CSEPs monitoring for spine surgery, were studied. Anaesthesia was induced with propofol (2.5 mg.kg-1 then 10 mg.kg-1.h-1) and sufentanil (0.50 micrograms.kg-1 then 0.25 micrograms.kg-1.h-1). Maximum positive (P40) and negative (N50) waweform latencies, and the peak to peak amplitude of CSEPs (posterior tibial nerve stimulation, cortical recording), were recorded before induction, 30 min, 1 and 2 h after induction, and at the end of surgery. Data are means +/- SD. Duration of anaesthesia was 260 +/- 73 min. Propofol induced significant lengthening of CSEPS (P40: from 37 +/- 10 up to 41 +/- 11 ms; N50: from 45 +/- 11 up to 51 +/- 14 ms), and a significant decrease in amplitude (from 1.9 +/- 0.9 down to 0.8 +/- 0.4 microV), but these changes were stable from 30 min after the induction to the end of spine surgery. A motor response was obtained 29 +/- 14 min after the end of anaesthetic administration. Total intravenous anaesthesia with propofol and sufentanil induces a small but stable lengthening of CSEPs latency and a stable decrease of its amplitude, which enable an appropriate monitoring of CSEPs during spine surgery.

Reversibility of transient focal cerebral ischemia evaluated by somatosensory evoked potentials in cats

We designed this study to determine whether somatosensory evoked potentials (SEP) could be a reliable indicator to detect development of cerebral infarction or to predict reversibility of cerebral ischemia by investigating relationship among SEP, local cerebral blood flow (1-CBF), and histological changes after transient occlusion of the middle cerebral artery (MCA) in 36 cats. In 24 cats (group I), gradual recovery of the cortical SEP was observed despite continued MCA occlusion, whereas the SEP remained lost in the remaining 12 cats (group 2). In group 1, amplitude of cortical SEP recovered completely 6 hours after recirculation following 30, 60, or 120 minutes of MCA occlusion, and only one developed cortical infarction. In six cats of group 2, the circulation was restored after 30 minutes of MCA occlusion. All showed complete recovery of SEP amplitude and none developed cortical infarction. When the MCA occlusion lasted 60 minutes in the remaining six cats, there was no recovery of the SEP amplitude and large cortical infarction was found in all six cats. Our findings suggest that SEP is a useful monitor for detecting cerebral infarction after MCA occlusion and that the critical time to avoid cerebral infarction would be 30 minutes when cortical SEP remains lost.

Effects of induced hypothermia on somatosensory evoked potentials in patients with chronic spinal cord injury.

We have investigated the effects of mild whole body hypothermia on the amplitude and latency of somatosensory evoked potentials (SEPs) in control subjects (n = 12) and patients (n = 15) with chronic compressive or contusive spinal cord injury (SCI). Mild hypothermia (-1 degree C) was induced by controlled circulation of propylene glycol through a 'microclimate' head and vest garment while reductions in oral and limb temperatures were monitored. Cooling induced a delayed onset and reduced amplitude of tibial nerve SEPs in control subjects. All SCI patients with recordable SEPs (n = 11) showed similarly delayed onset of the cortical response. In contrast to the controls, nine of the 11 SCI patients showed an increase in amplitude of cortical SEPs. In three of these patients the increase in amplitude exceeded 100% of the precooling values. The cooling-induced changes in SEP amplitude and latency reversed on rewarming for both groups. The cooling-induced increases in cortical SEP amplitude support the a priori hypothesis that cooling would enhance central conduction in some SCI patients with conduction deficits due to focal demyelination.

EFFECTS OF MIDAZOLAM ON MEDIAN NERVE SOMATOSENSORY EVOKED POTENTIALS

We have studied the effect of i.v. midazolam on median nerve somatosensory evoked potentials (SSEP) in 10 unpremedicated adults. Anaesthesia was induced with midazolam by bolus administration (0.2 mg kg-1) followed by infusion (5 mg h-1). The latency and amplitudes of the SSEP responses over the second cervical vertebrae (SC2) and sensory cortex (P17, N20, P25) were recorded before and for 10 min after induction. Data were analysed over that period for time-related alterations. Small but statistically significant increases in latency of the cortical N20 (P less than 0.005) and P25 (P less than 0.001) waves and interwave conduction times of SC2 to P25 (P less than 0.005) and N20 to P25 (P less than 0.021) were observed. Cortical amplitude (N20-P25) decreased significantly (P less than 0.012), to approximately 60% of baseline. These results demonstrated that midazolam produced a depression of cortical SSEP amplitude without clinically significant alterations in latency.

Chronic brain ischemia in the monkey assessed by somatosensory evoked potentials and local blood flow measurements

Physiological changes occurring in experimentally induced chronic ischemic areas of the brain in monkeys have been investigated by measuring local cerebral blood flow (1CBF) and recording somatosensory evoked potentials (SEPs) to median nerve stimulation in the cortex and thalamus (VPL). Ischemia was produced by occlusion of the middle cerebral artery (MCA). Its development was followed for weeks in the unanesthetized monkey. SEPs in VPL and cortex were shown to be useful indicators of neuronal activity in the course of brain ischemia. The most reliable parameters were found to be the amplitude of components P10, P12 and P20 of the cortical SEP, generated around the central sulcus. The relationship between the changes in spontaneous recovery of the SEPs, 1CBF and behavioral signs, in the course of time, revealed characteristic patterns. Different components of the cortical SEP provide useful information on the localization of the ischemic cortical area. In addition, the amplitude of the VPL SEP may also change significantly after the occlusion of the MCA. Clear evidence for the phenomenon of diaschisis in terms of SEPs, was found in only one animal. An analysis of the relationship between 1CBF and the amplitude of the SEPs showed that cortical SEPs could be measured at local CBF levels as low as 15 ml/100 g · min. The relationship between 1CBF and cortical SEP amplitude was approximately linear in the range from about 60 ml/100 g · min down to 15 ml/100 g · min.