Objective-To determine whether nonconvulsive electrographic post-traumatic seizures result in increases in intracranial pressure and microdialysis lactate/pyruvate ratio. Design-Prospective monitoring with retrospective data analysis.Setting-Single center academic neurologic intensive care unit.Patients-Twenty moderate to severe traumatic brain injury patients (Glasgow Coma Score 3-13). HHS Public Access Author Manuscript Author ManuscriptAuthor Manuscript Author ManuscriptMeasurements and Main Results-Continuous electroencephalography and cerebral microdialysis were performed for 7 days after injury. Ten patients had seizures and were compared with a matched cohort of traumatic brain injury patients without seizures. The seizures were repetitive and constituted status epilepticus in seven of ten patients. Using a within-subject design, post-traumatic seizures resulted in episodic increases in intracranial pressure (22.4 ± 7 vs. 12.8 ± 4.3 mm Hg; p < .001) and an episodic increase in lactate/pyruvate ratio (49.4 ± 16 vs. 23.8 ± 7.6; p < .001) in the seizure group. Using a between-subjects comparison, the seizure group demonstrated a higher mean intracranial pressure (17.6 ± 6.5 vs. 12.2 ± 4.2 mm Hg; p < .001), a higher mean lactate/pyruvate ratio (38.6 ± 18 vs. 27 ± 9; p < .001) compared with nonseizure patients. The intracranial pressure and lactate/pyruvate ratio remained elevated beyond postinjury hr 100 in the seizure group but not the nonseizure group (p < .02).Conclusion-Post-traumatic seizures result in episodic as well as long-lasting increases in intracranial pressure and microdialysis lactate/pyruvate ratio. Intracranial pressure (ICP) remains one of the principal treatment targets for traumatic brain injury (TBI) (1). Elevation of ICP is due to brain edema, mass effect from hemorrhagic lesions, and possibly from disrupted pressure autoregulation. The treatments for ICP have been focused on these pathophysiologic mechanisms. While the treatment principals for elevated ICP have been codified into guidelines and practiced by many intensivists, ICP often remains refractory to treatment. Indeed, treatment failure resulting in herniation and death occurs frequently. The mechanisms for persistently elevated ICP have not been well elucidated, but candidate mechanisms include sustained hyperemia, excitotoxicity, and osmotic rebound. In contrast, little attention has been paid to the adverse effects of epileptic activity upon the extent or duration of elevated ICP after TBI.In recent years, post-traumatic seizures have been documented to occur frequently after human TBI (2). Indeed, seizures are frequent after a variety of hemorrhagic injuries to the brain (3, 4). The incidence of seizures increases as a function of the severity of injury, and other selected features of the injury such as the presence of hemorrhagic contusions. Posttraumatic seizures previously have been associated with increased glycolysis in both animal and human metabolic imaging studies (5, 6) and have been associated with alterat...

Objective-To determine whether nonconvulsive electrographic post-traumatic seizures result in increases in intracranial pressure and microdialysis lactate/pyruvate ratio. Design-Prospective monitoring with retrospective data analysis.Setting-Single center academic neurologic intensive care unit.Patients-Twenty moderate to severe traumatic brain injury patients (Glasgow Coma Score 3-13).

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This study reports that elevated levels of glutamate are found in the perihematomal region after ICH and are decreased during hematoma drainage. Conversely, ischemic LPRs are not found in perihematomal regions and were unchanged during hematoma drainage. These data suggest that excitotoxicity related to glutamate may have an important impact on secondary injury. The data failed to support the role of ischemia in secondary perihematomal damage.

Proton nuclear magnetic resonance (H-NMR) spectroscopic analysis of cerebral spinal fluid provides a quick, non-invasive modality for evaluating the metabolic activity of brain-injured patients. In a prospective study, we compared the CSF of 44 TBI patients and 13 non-injured control subjects. CSF was screened for ten parameters: β-glucose (Glu), lactate (Lac), propylene glycol (PG), glutamine (Gln), alanine (Ala), α-glucose (A-Glu), pyruvate (PYR), creatine (Cr), creatinine (Crt), and acetate (Ace). Using mixed effects measures, we discovered statistically significant differences between control and trauma concentrations (mM). TBI patients had significantly higher concentrations of PG, while statistical trends existed for lactate, glutamine, and creatine. TBI patients had a significantly decreased concentration of total creatinine. There were no significant differences between TBI patients and non-injured controls regarding β- or α-glucose, alanine, pyruvate or acetate. Correlational analysis between metabolites revealed that the strongest significant correlations in non-injured subjects were between β- and α-glucose (r = 0.74), creatinine and pyruvate (r = 0.74), alanine and creatine (r = 0.62), and glutamine and α-glucose (r = 0.60). For TBI patients, the strongest significant correlations were between lactate and α-glucose (r = 0.54), lactate and alanine (r = 0.53), and α-glucose and alanine (r = 0.48). The GLM and multimodel inference indicated that the combined metabolites of PG, glutamine, α-glucose, and creatinine were the strongest predictors for CMRO2, ICP, and GOSe. By analyzing the CSF of patients with TBI, our goal was to create a metabolomic fingerprint for brain injury.