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The article discusses the results of a prospective, observational study aimed at evaluating the incidence and clinical significance of cerebral vasospasm in patients with moderate to severe traumatic brain injury (TBI). It mentions that posttraumatic vasospasm (PTV) occurred in nearly 50% of patients while 29% with PTV developed ischemic infarcts during their hospital course. A figure showing a study protocol and a table showing the characteristics of the patient population are presented.

Object: The purpose of this study was to identify predictors of shunt-dependent hydrocephalus after aneurysmal subarachnoid hemorrhage (SAH)., Methods: The authors evaluated the incidence of shunt-dependent hydrocephalus in a consecutive cohort of 580 patients with SAH who were admitted to the Neurological Intensive Care Unit of Columbia University Medical Center between July 1996 and September 2002. Patient demographics, 24-hour admission variables, initial CT scan characteristics, daily transcranial Doppler variables, and development of in-hospital complications were analyzed. Odds ratios and 95% CIs for candidate predictors were calculated using multivariate nominal logistic regression., Results: Admission glucose of at least 126 mg/dl (adjusted OR 1.6; 95% CI 1.0-2.6), admission brain CT scan with a bicaudate index of at least 0.20 (adjusted OR 1.43; 95% CI 1.0-2.0), Fisher Grade 4 (adjusted OR 2.71; 95% CI 1.2-5.7), fourth ventricle hemorrhage (adjusted OR 1.78; 95% CI 1.1-2.7), and development of nosocomial meningitis (adjusted OR 2.2; 95% CI 1.4-3.7) were independently associated with shunt dependency., Conclusions: These data suggest that permanent CSF diversion after aneurysmal SAH may be independently predicted by hyperglycemia at admission, findings on the admission CT scan (Fisher Grade 4, fourth ventricle intraventricular hemorrhage, and bicaudate index ≥ 0.20), and development of nosocomial meningitis. Future research is needed to assess if tight glycemic control, reduction of fourth ventricle clot burden, and prevention of nosocomial meningitis may reduce the need for permanent CSF diversion after aneurysmal SAH.

Background: In vivo models of traumatic brain injury (TBI) demonstrate increased cerebral perfusion, decreased cerebral hypoxia, reduced cerebral edema, and improved neurologic recovery with propranolol administration. The purpose of this study was to determine the effect of different propranolol doses and timing on cerebral perfusion in a murine TBI model., Methods: Fifteen minutes after TBI, three groups of mice (four mice per group) were randomized to receive intravenous injections of placebo, 4 mg/kg propranolol, or 1 mg/kg propranolol. Two delayed treatment groups were randomized to receive placebo or 4 mg/kg propranolol 60 minutes after TBI. Cerebral perfusion was then imaged by micropositron emission tomography., Results: With placebo injection 15 minutes after TBI, the standard uptake value (SUV) mean was 0.395 +/- 0.01; with 4 mg/kg propranolol, the SUV mean was 0.515 +/- 0.04; and with 1 mg/kg propranolol, the SUV mean was 0.46 +/- 0.01. Animals receiving 4 mg/kg propranolol demonstrated significant improvement (p < 0.01) in cerebral perfusion compared with placebo and compared with 1 mg/kg propranolol. With placebo injection at 60 minutes after TBI, the SUV mean was 0.26 +/- 0.03; and with 4 mg/kg propranolol, the SUV mean was 0.43 +/- 0.02. After 60 minutes, animals receiving 4 mg/kg propranolol demonstrated significant improvement (p < 0.01) in cerebral perfusion compared with placebo., Conclusion: In a murine model of TBI, higher doses of propranolol were preferable to lower doses and both early and late propranolol administration improved cerebral perfusion. Potential mechanisms and therapeutic potential require further research.

Spontaneous spinal CSF leaks are best known as a cause of orthostatic headache, but may also be the cause of coma. The authors encountered a unique case of a spontaneous spinal CSF leak causing coma 2 days after craniotomy for clipping of an unruptured aneurysm. This 44-year-old woman with autosomal dominant polycystic kidney disease underwent an uneventful craniotomy for an incidental anterior choroidal artery aneurysm. No intraoperative spinal CSF drainage was used. Two days after surgery the patient became comatose with a left oculomotor nerve palsy. Computed tomography scanning revealed a right extraceberal hematoma and loss of gray-white matter differentiation. The hematoma was evacuated and a diagnosis of hemodialysis disequilibrium syndrome was made. Continuous hemodialysis and hyperosmolar therapy were instituted without any improvement. The CT scans were then reinterpreted as showing sagging of the brain, and the patient was placed in the Trendelenburg position which resulted in prompt improvement in her level of consciousness. A CT myelogram demonstrated an upper thoracic CSF leak that eventually required surgical correction. The patient made a complete neurological recovery. Neurological deterioration after craniotomy may be caused by brain sagging caused by a spontaneous spinal CSF leak, similar to intracranial hypotension due to intraoperative lumbar CSF drainage.