Cerebral oxidative metabolism and evoked potential deterioration after severe brain injury: new evidence of early posttraumatic ischemia.

BACKGROUND: We commonly observe progressive deterioration in somatosensory evoked potentials (SSEPs) after severe head injury. We had previously been unable to relate this deterioration to raised intracranial pressure but had noted a relationship with decreasing transcranial oxygen extraction (arteriovenous oxygen difference [AVDO2]). The purpose of this study was twofold: to prove the hypothesis that deterioration in SSEP values is associated with decreasing AVDO2 and to test the subsidiary hypotheses that deteriorating SSEPs were the result of either ischemia/reperfusion injury or failure of oxygen extraction/utilization. METHODS: Monitoring of 97 patients with severe traumatic brain injury (Glasgow Coma Scale scores of < or = 8 after resuscitation) included twice daily AVDO2 measurement and hourly SSEP recording for an average of 5 days. The last 51 patients also underwent 12-hourly measurement of cerebral blood flow (CBF), with calculation of the cerebral metabolic rate of oxygen. Cluster analysis was used to classify patients based on initial AVDO2 values and subsequent SSEP trends. The time courses of CBF, SSEPs, AVDO2, and cerebral metabolic rate of oxygen were examined in the groups defined by the cluster analysis. The clinical outcomes considered were survival or nonsurvival and the Glasgow Outcome Scale scores obtained at 3 months or more after injury. RESULTS: Cluster analysis confirmed the association between high initial AVDO2 values and subsequent SSEP deterioration. Patients in this category initially had significantly higher AVDO2, lower CBF, and higher cerebral metabolic rates of oxygen but recovered to adequate levels within 24 to 36 hours after injury. SSEP values were initially identical in the patients with normal AVDO2 values and those with elevated AVDO2 but differed significantly at 60 hours after injury and beyond. CONCLUSION: The findings of increased oxygen utilization and lowered CBF in the patients with deteriorating SSEPs strongly imply that early ischemia rather than failure of O2 extraction or utilization is responsible for the associated SSEP deterioration. This issue of defining thresholds for ischemia based on AVDO2 is confounded by the dependency of CBF and AVDO2 values on the time after injury.

Clinical significance of CSF glutamate concentrations following severe traumatic brain injury in humans.

Glutamate excitotoxicity is a putative mechanism of secondary damage after traumatic brain injury (TBI). No relationship between glutamate release and clinical status has been shown in humans, however. We hypothesize a dose-response relationship between CSF glutamate concentrations and severity of injury, electrophysiological deterioration as measured by somatosensory evoked potential amplitudes, and clinical outcome. From August 1991 to March 1996, intensive monitoring of 55 patients with severe TBI (GCS < or = 8 after resuscitation) included twice daily CSF glutamate levels and hourly somatosensory evoked potentials (SSEPs) for an average of 5 days. Clinical outcomes were survival/nonsurvival and Glasgow outcome score (GOS) at 3 months or more post-injury. Glutamate levels were not associated with severity of injury, electrophysiological deterioration, or clinical outcome. Neither peak nor mean glutamate levels significantly improved a simple logistic regression model which used only age and presence of bilaterally unreactive pupils to predict survival. Using this methodology CSF glutamate concentrations did not display a dose-response relationship to severity of injury, electrophysiological deterioration, or predict clinical outcomes following TBI in a group of 55 patients. An early effect of glutamate, an effect dependent on time of exposure to glutamate or other modulating effects cannot be ruled out.

Monitoring severe head injury: a comparison of EEG and somatosensory evoked potentials.

We report on our experience with long-term monitoring of the EEG power spectrum and somatosensory evoked potentials (SSEPs) in 103 patients with severe closed head injury (Glasgow Coma Scale-GCS < or = 8). Patients were monitored for an average of 5 days post injury and monitoring was terminated when they died, regained consciousness or their intracranial physiologic parameters (primarily intracranial pressure-ICP) were stable for 2-3 days. Patients were treated according to a standard protocol that included mechanical ventilation, sedation, and neuromuscular blockade. At 7 of 9 twelve hour time intervals post injury, SSEPs were significantly (p < .05) different between outcome groups using the Glasgow Outcome Score collapsed to 3 categories. The percent slow (delta) activity in the EEG was not significantly different between outcome groups at any time point, post injury. The total power in the EEG power spectrum differed only at the last time epoch post injury (108 hr.). Based on the superior prognostic capabilities of the SSEP, we routinely base critical management decisions on SSEP values. We have not been able to rely on EEG parameters for these same decisions due to the lack of clear distinction between good and poor prognosis groups based on common EEG parameters.

Electrophysiologic assessment of intracerebral contusions in closed head injury.

To determine whether intracerebral contusions should be evacuated in severe closed head injuries, patients with Glasgow Coma Scale scores < or = 8 and with radiologic evidence of midline shift on computed tomography admitted from 1987 through 1993 to our intensive care unit were monitored with median nerve somatosensory evoked potentials (SSEPs). A total of 44 patients and 84 hemispheres were included in the study. Initial SSEPs, calculated by a quantitative peak-peak amplitude method, were not significantly different between hemispheres that contained localized contusions > or = 2.5 cm, those that had evidence of diffuse injury or punctate lesions < 2.5 cm not considered suitable for surgical evacuation, and those without evidence of parenchymal hemorrhage (mean 14.64 microV, p = 0.43). The SSEPs deteriorated 41.2% from initial baseline levels in diffusely injured and 22.6% in contused hemispheres, whereas in normal-appearing hemispheres, SSEPs improved 51.1% (p = 0.01). The difference in SSEPs, however, was not significant between the contused and diffusely injured hemispheres. The results suggest that in severe closed head injury, cerebral hemispheres without radiologic evidence of structural damage have a high likelihood of improving after initial impact injury. Furthermore, hemispheres with localized contusions showed no more deterioration than those with more diffuse injury, implying that hemispheric electrical deterioration is not related to size of localized contusions but rather to underlying axonal damage. This indicates that surgical evacuation of localized contusions unless accompanied by mass effect is probably not warranted.

Somatosensory evoked potentials and intracranial pressure in severe head injury.

The purpose of this study was to explore the relationship between neurologic function, using a quantitative measurement of continuous somatosensory evoked potentials (SSEPs), and intracranial pressure (ICP) following traumatic brain injury. During a 6 year period, severely head-injured patients with a Glascow Coma Scale < or = 8 who were not moribund were monitored with SSEPs and ICP measurements. SSEPs from each hemisphere and ICP were recorded hourly for each patient. Neurologic outcomes were scored using the Glasgow Outcome Scale at three months post injury. Although initial SSEP amplitude did not correlate well with outcome, final SSEP summed peak to peak amplitude from both hemispheres (p = .0001), the best hemisphere (p = .0004), and the worst hemisphere (p = .0001) correlated well with the Glasgow Outcome Scale groups. Of a total of 72 patients, 40 had deteriorating SSEPs and 32 had stable or improving SSEPs. Peak ICP values were not statistically different in these groups (p = .6). Among patients with deteriorating SSEPs, 52.5% lost the greatest proportion of hemispheric electrical activity prior to ICP elevation. In the remaining patients, the percent reduction of SSEP activity after peak ICP levels was not statistically different from the percent reduction in SSEP activity prior to the peak ICP levels (p = .9). This data suggests that in a select group of patients with severe head injury, ICP does not cause SSEP deterioration, but rather is the consequence of deterioration of brain function.

A new quantitative measure for monitoring somatosensory evoked potentials.

This paper describes the development and testing of a computer algorithm to automate the process of peak identification and somatosensory evoked potential (SSEP) grading. We tested the accuracy of computerized peak detection and evaluated grading schemes using a test set of 60 SSEPs ranked from worst to best by the programmer (RJM) and a blinded grader (PO). The computer algorithm recognized 95% of peaks identified by visual inspection. Twelve percent of peaks identified by the computer were noise. Summed peak to peak amplitude gave the most accurate ranking of SSEPs. Rank correlation between computer and blinded and unblinded expert grading was r = .82 for PO, r = .92 for RJM, p < .0001 for both. Computer and manually summed amplitudes were highly correlated (Pearson r = .98, p < .0001). Correlation between the 2 expert graders was .86, p < .0001. Computer graded SSEPs were significantly related to clinical outcome at 3 months, p < .0001. Automatic grading of SSEPs using summed peak to peak amplitude is highly correlated with expert grading. The measure is objective, continuous, and well suited to statistical analysis.