Brain perfusion abnormalities in patients with compromised venous outflow.

Elevated intracranial intravenous pressure is not routinely measured in clinical practice. Indirect evidence of increased venous pressure is reflected in the size change of the cerebral sinuses and the presence of venous infarctions. The purpose of this study is to evaluate the role of brain perfusion venous time-density curves in the diagnosis of cerebral venous hypertension. A retrospective review of four cases in which increased cerebral intravenous pressure was reflected in abnormal time-density curves on CT brain perfusion studies was completed. The abnormal venous time-density curves correlated with clinically increased intravenous pressure and normalized after treating the underlying pathology. Abnormal venous outflow affects brain perfusion. This could be identified on a CT brain-perfusion study based on characteristic venous time-density curves. These curves may appear quite similar even when the underlying etiologies are different. Normalization of the venous time-density curves may be observed after the underlying pathology was treated.

Detectable levels of cytochrome C and activated caspase-9 in cerebrospinal fluid after human traumatic brain injury.

BACKGROUND: The intrinsic pathway of apoptosis has been proposed as one mechanism of cell death after traumatic brain injury (TBI). This study tested the hypothesis that cytochrome c and activated caspase-9 are released into the cerebrospinal fluid (CSF) after severe TBI and that their presence correlates with mitochondrial injury and severity of neurologic outcome. METHODS: Nine adult patients with severe TBI (GCS < or = 8) underwent placement of intraventricular catheters for monitoring and management of intracranial pressure. CSF was sampled at catheter insertion (2-26 h after injury) and at intervals of 24, 48, and 72 h thereafter. Control samples were obtained from patients undergoing spinal anesthesia (ASA1). CSF levels of cytochrome c and activated caspase-9 were measured using ELISA. RESULTS: Cytochrome c was detected in 18 (51.4%) samples, in the range of 0.08-5 ng/ml; mean value for cytochrome c was 0.44 ng/ml (SD +/- 0.632). Activated caspase-9 was detected in 10 samples (28.6%); mean value was 0.28 ng/ml (SD +/- 0.39). R (s) between cytochrome c and Glasgow outcome score (GOS) was -0.25 (P = 0.14), and between GOS and activated caspase-9 was -0.35 (P = 0.04). R calculated based on linear regression of activated caspase-9 and cytochrome c concentrations was 0.18. Control CSF samples had no detectable levels of either marker (detection level for cytochrome c was 0.08 ng/ml and 0.20 for activated caspase-9). CONCLUSIONS: We concluded that activated caspase-9 and cytochrome c are present in the CSF of patients with severe TBI. Activated caspase-9 shows weak correlation with poor neurologic outcome.

Role of transcranial Doppler in optimizing treatment of cerebral vasospasm in subarachnoid hemorrhage.

This study was undertaken to evaluate the role of transcranial Doppler ultrasonography in arterial blood pressure management during hypervolemia/hypertension/ hemodilution therapy in patients with vasospasm from subarachnoid hemorrhage and correlate this data with neurologic outcome. The study included 18 adult patients, Hunt and Hess grades III-IV. Complete neurologic assessment was performed. Transcranial Doppler indices were calculated by standard formulas. On the basis of our results, resistance area product can be used to estimate the optimal arterial blood pressure in hypervolemia/hypertension/hemodilution therapy. An increase in the cerebral blood flow index was associated with better performance on neurologic examination. Estimated cerebral perfusion pressure from transcranial Doppler data analysis showed poor correlation with cerebral perfusion pressure derived from direct measurement of intracranial pressure in patients with cerebral vasospasm (rho = 0.15; 95% CI, 0.11-0.39; P = .2590).