SUMMARY Three groups of patients who had suffered head injury were compared with matched control subjects on reaction time (RT) tasks. Group I consisted of outpatients previously hospitalised for head injury ofwide ranging degrees of severity, assessed at varying intervals after injury. Group II was composed of non-hospitalised mildly concussed patients. Group III was made up of head injured patients of varying degrees of severity assessed 7-10 months after initial hospitalisation for their injury. The reaction time tests were graded in difficulty, from a simple RT response to a complex choice RT test. In addition, subjects were compared in their ability to ignore redundant information during one of the choice RT tests. The findings indicate that traumatic brain injury causes slower information processing, deficits in divided attention, an impairment of focused attention, and inconsistency of performance.Reaction time (RT) tests have consistently revealed slowness ofinformation processing, a deficit in divided attention after head injury.' In this study, we addressed four specific issues concerning the effects of head injury on reaction time.The question of fatigue was examined by using the same simple RT test at the beginning and end of experimental sessions to see if head injured patients and normal control subjects changed their performance differently across the session.A second question addressed the nature of the attentional deficit. While "There can be no controversy... about the presence of DADs [divided attention deficit] in head injury",2 there has been less success in identifying a specific impairment in focused attention.< Focused attention is tested by evaluating the ability to ignore distracting stimuli. A selective involvement of frontal lobe areas has been suggested in head injury7"'1 and deficits in focused attention using

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This study demonstrates residual mental deficits in patients who have apparently recovered after closed head injury. Twenty closed head injury patients were compared to 20 normal control subjects matched for age, sex, handedness, education, language, and IQ. All received a series of neuropsychological tests. Discriminant function analysis significantly differentiated the two groups. Correct classification of individuals as having suffered a head injury or not was 85%. The head injury patients did have primary impairment on tests of divided attention. Litigation was not a factor. We propose that this impairment of information processing reflects residual brain damage secondary to the closed head injury.

Loss of spinal alignment can lead to neurological compromise in individuals with unstable spine injuries. We compared the ability of the Roto-Rest bed and the Stryker frame to immobilize an unstable cervical and lumbar segment in a cadaver. The Roto-Rest bed was superior to the Stryker frame in the immobilization of both cervical and lumbar fractures.

Genetic risk factors for intracranial aneurysm (IA) are not yet fully understood. Genomewide association studies have been successful at identifying common variants; however, the role of rare variation in IA susceptibility has not been fully explored. In this study, we report the use of whole exome sequencing (WES) in seven densely-affected families (45 individuals) recruited as part of the Familial Intracranial Aneurysm study. WES variants were prioritized by functional prediction, frequency, predicted pathogenicity, and segregation within families. Using these criteria, 68 variants in 68 genes were prioritized across the seven families. Of the genes that were expressed in IA tissue, one gene (TMEM132B) was differentially expressed in aneurysmal samples (n=44) as compared to control samples (n=16) (false discovery rate adjusted p-value=0.023). We demonstrate that sequencing of densely affected families permits exploration of the role of rare variants in a relatively common disease such as IA, although there are important study design considerations for applying sequencing to complex disorders. In this study, we explore methods of WES variant prioritization, including the incorporation of unaffected individuals, multipoint linkage analysis, biological pathway information, and transcriptome profiling. Further studies are needed to validate and characterize the set of variants and genes identified in this study.

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VP-16 100 mg/m2 was given intravenously to 10 patients undergoing surgical resection of intracerebral tumors, and the drug was assayed in resected tumor using high pressure liquid chromatography. VP-16 concentrations varied from undetectable (less than .1 microgram/g) to 5.9 micrograms/g (mean, 1.4 microgram/g). VP-16 concentrations in tumors were lower than concurrent plasma concentrations. In addition, intracerebral tumors had a lower concentration of VP-16 than did extracerebral tumors (mean VP-16 concentration, 3.9 micrograms/g) from 7 patients receiving VP-16 50-100 mg/m2 intravenously. Plasma pharmacokinetics of VP-16 were different in our patients with intracerebral tumors than in previously studied patients with extracerebral tumors and it is unclear what role this may played in variability of tumor VP-16 concentrations. VP-16 concentrations were similar in glioblastomas and brain metastases. Specimens from patients with small cell undifferentiated carcinoma of the lung had the highest VP-16 concentrations. A patient who had both viable and necrotic tumor resected during an occipital lobectomy had a higher drug concentration in the necrotic than in the viable area of tumor. In addition, VP-16 concentration decreased as a function of distance into brain from the tumor. Based on our data, VP-16 might be expected to have less activity against intracerebral than against extracerebral human tumors.