The survey results demonstrate that there is significant uncertainty as to the optimal surgical technique for primary evacuation of ASDH. The fact that the majority of the respondents are willing to become collaborators in the planned RESCUE-ASDH trial highlights the relevance of this important subject to the neurosurgical community in the UK and Ireland.
Isoflurane exposure can protect the mammalian brain from subsequent insults like ischemic stroke. However, this protective preconditioning effect is sexually dimorphic, with isoflurane preconditioning decreasing male while exacerbating female brain damage in a mouse model of cerebral ischemia. Emerging evidence suggests that innate cell sex is an important factor in cell death, with brain cells having sex-specific sensitivities to different insults. We used an in vitro model of isoflurane preconditioning and ischemia to test the hypothesis that isoflurane preconditioning protects male astrocytes while having no effect or even a deleterious effect in female astrocytes following subsequent oxygen and glucose deprivation (OGD). Sex-segregated astrocyte cultures derived from postnatal day 0 to 1 mice were allowed to reach confluency before being exposed to either 0% (sham preconditioning) or 3% isoflurane preconditioning for 2 hours. Cultures were then returned to normal growth conditions for 22 hours before undergoing 10 hours of OGD. Twenty-four hours following OGD, cell viability was quantified using a lactate dehydrogenase assay. Isoflurane preconditioning increased cell survival following OGD compared to sham preconditioning independent of innate cell sex. More studies are needed to determine how cell type and cell sex may impact on anesthetic preconditioning and subsequent ischemic outcomes in the brain.
Simultaneous recordings of intracranial pressure (ICP) from a single-lumen subdural screw and a ventricular catheter were compared in 10 patients with severe head injury. Forty-one percent of the readings corresponded within the same 10 mm Hg ranges, while 13% of the screw pressure measurements were higher and 46% were lower than the associated ventricular catheter measurements. In 10 other patients, also with severe head injury, pressure measurements obtained with the Leeds-type screw were similarly compared with ventricular fluid pressure. Fifty-eight percent of the dual pressure readings corresponded, while 15% of the screw measurements were higher and 27% were lower than the ventricular fluid pressure, within 10-mm Hg ranges. It is concluded that subdural screws may give unreliable results, particularly by underestimating the occurrence of high ICP.
Objectives-(1) To establish the feasibility of myotatic reflex measurement in patients with head injury. (2) To test the hypothesis that cerebral dysfunction after head injury causes myotatic reflex abnormalities through disordered descending control. These objectives arise from a proposal to use reflex measurements in monitoring patients with head injury. Methods-The phasic stretch reflex of biceps brachii was elicited by a servopositioned tendon hammer. Antagonist inhibition was evoked by vibration to the triceps. Using surface EMG, the amplitude of the unconditioned biceps reflex and percentage antagonist inhibition were measured. After standardisation in 16 normal adult subjects, the technique was applied to 36 patients with head injury across the range of severity. Objective (1) was addressed by attempting a measurement on each patient without therapeutic paralysis; three patients were also measured under partial paralysis. Objective (2) was addressed by preceding each of the 36 unparalysed measurements with an assessment of cerebral function using the Glasgow coma scale (GCS); rank correlation was employed to test a null hypothesis that GCS and reflex indices are unrelated. Results-In normal subjects, unconditioned reflex amplitude exhibited a positive skew requiring logarithmic transformation. Antagonist inhibition had a prolonged time course suggesting presynaptic mechanisms; subsequent measurements were standardised at 80 ms conditioning test interval (index termed "TI 80 ").Measurements were obtained on all patients, even under therapeutic paralysis (objective (1)). The unconditioned reflex was absent in most patients with GCS less than 5; otherwise it varied little across the patient group. TI 80 fell progressively with lower GCS, although patients' individual GCS could not be inferred from single measurements. Both reflex indices correlated with GCS (p<0.01), thereby dismissing the null hypothesis (objective (2)). Conclusion-Cerebral dysfunction in head injury is reflected in myotatic reflex abnormalities which can be measured at the bedside. With greater reproducibility, reflex measurements may assist monitoring of patients with head injury. (J Neurol Neurosurg Psychiatry 2000;68:581-588)
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