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.
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 < 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. RESUME: Surveillance des trauniatismes craniens severes: comparaison de I'EEG et des potentiels evoques somesthesiques. Nous rapportons notre experience de surveillance a long terme du spectre de puissance EEG et des potentiels eVoques somethesiques (PESs) chez 103 patients ayant subi un traumatisme cranien ferine (echelle de coma de Glasgow < 8). Nous avons surveillS les patients pendant en moyenne 5 jours apres la lesion et la surveillance 6tait interrompue au d£ces, si le patient reprenait conscience ou si leurs parametres physiologiques intracranients (principalement la pression intracranienne -PIC) 6taient stables dupuis 2 ou 3 jours. Les patients Staient trails selon un protocole standard qui incluait la ventilation mecanique, , la sedation et le blocage neuromusculaire. Au septieme du neuf intervalles de 12 heures apres la lesion, les PESs dtatent significativemenl difKrents (p < 0.05) entre les groupes selon leur Evolution eValuee au moyen de l'6chelle de Glasgow reduite a trois categories. Le pourcentage d'activit6 lente (delta) n'etait pas significativement different entre les groupes selon leur evolution, quelque soit le dernier intervalle de temps apres le lesion (108 hrs). Comme la valeur pronostique des PESs est superieure, nos decisions critiques de traitement sont habituellement basees sur les valeurs de PESs. Nous n'avons pas pu nous fier sur les parametres EEG pour prendre ces decisions a cause de l'absence de distinction claire entre le groupe avec un bon pronostic et celui avec un mauvais pronostic sur la base de parametres EEG communs.Can. J. Neurol. Sci. 1998; 25: S7-S11 Given the limitations of the clinical neurological examination in comatose head injury patients, an objective, reliable measure of neurologic functio...
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.
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 headinjured patients with a Glascow Coma Scale < 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.Resume: Potentiels evoques somesthesiques et pression intracranienne dans les traumatismes craniens severes. Le but de cette etude etait d'explorer, au moyen d'une mesure quantitative des potentiels eVoqufis somesthesiques (PESs) continus, la relation entre la fonction neurologique et la pression intracranienne suite a un traumatisme cranien.
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.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.