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One hundred and forty-three soldiers who received ballistic injury were actively treated at U.S. Army Seventh Corps hospitals during Operation Desert Storm. Ninety-five percent were wounded by fragments, 5% by bullets. Many had wounds of several body parts, including 17.3% who received a head wound; 4.3% a neck wound; 5.8% a chest wound; 9.3% an abdominal wound; and 90% who had extremity wounds. Three hospital deaths occurred--a 2.1% mortality rate. Only two soldiers sustained a brain wound; in both, the missile entered below the skull area protected by the Kevlar helmet. One brainwounded individual was treated and lived; the other died from hemorrhage and shock from concomitant traumatic lower-extremity amputations. The current U.S. helmet appears to provide significant protection from fragmenting ordnance as does the armored vest. Hemorrhage from proximal extremity wounds caused hospital deaths. Treatment of such wounds will have to be improved to reduce future combat mortality.

Lipid second messengers such as arachidonic acid and its metabolites and diacylglycerols (DAG5) are affected in brain injury. Therefore, changes in the pool size and the fatty acid composition of free fatty acids (FFAs) and DAGs were analyzed in different rat brain areas 4 and 35 days after traumatic injury. Cortical impact injury of low-grade severity was applied in the right frontal somatosensory cortex. Four days after injury, FFAs and DAGs were increased by three-and twofold, respectively, in the injured cortex and to a lesser extent in the contralateral cortex compared with sham-operated animals. Docosahexaenoic acid followed by stearic acid, and arachidonic acid, displayed the greatest changes in both FFAs and DAGs. By day 35, free stearic, oleic, and arachidonic acids remained elevated in the damaged cortex (1.5-fold each). DAGs showed the greatest change, reaching values 2.7-fold higher than sham in all frontal and occipital cortical areas, including brainstem. Oleoyl-and arachidonoyl-DAGs (four-and threefold increase, respectively) followed by docosahexaenoyl-DAGs (twofold) contributed to the DAG accumulation. These results reveal that traumatic brain injury triggers a sustained and time-dependent activation of phospholipase-mediated signaling pathways leading to membrane phospholipid degradation and targeting, early on, docosahexaenoyl phospholipid-enriched excitable membranes. Key Words: Free fatty acids-Diacylglycerols-Phospholipase A 2-Phospholipase C-Phospholipase D-Traumatic brain injury.

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Eighty-six patients with brain abscesses were seen at the University of Minnesota Hospitals from 1946-1965, and 46 died, a 53% mortality. Multiple and brain stem abscesses accounted for several fatalities, while delayed and missed diagnosis accounted for one third of the deaths. Evidence of infection was often minimal in patients with brain abscess. Lumbar puncture as a diagnostic tool was inaccurate and occasionally fatal. Brain scan, electroencephalography, and angiography were the best diagnostic tests. Drainage and excision were each associated with approximately a 20% mortality. The most pertinent correlation regarding treatment, however, was that of increasing mortality with deteriorating preoperative neurological status. Postoperative deaths were due to failure in locating the abscess at surgery or untoward events such as cerebritis, edema, or excessive bleeding at the operative site.KEY WORD brain abscess E

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Summary: Purpose:To assess the effect of vagus nerve stimulation (VNS) on interictal epileptiform activity in the human hippocampus. Clinical studies have established the efficacy of vagus nerve stimulation in patients with epilepsy (VNS Study Group, 1995), although the electrophysiologic effects of VNS on the human hippocampus and mesial temporal lobe structures remain unknown.Methods: We report a case study in which a patient with an implanted VNS underwent intracranial electrode recording before temporal lobectomy for intractable complex partial seizures. Epileptiform spikes and sharp waves were recorded from a depth electrode placed in the patient's left hippocampus. Spike frequencies and sharp-wave frequencies before and during VNS were compared using both a 5-and a 30-Hz stimulus. Different stimulation rates were tested on different days, and all analyses were performed using a Student's t test.Results: We found no significant differences in spike frequency between baseline periods and stimulation at 5 and 30 Hz. In contrast, stimulation at 30 Hz produced a significant decrease in the occurrence of epileptiform sharp waves compared with the baseline, whereas stimulation at 5 Hz was associated with a significant increase in the occurrence of epileptiform sharp waves.Conclusions: VNS produces a measurable electrophysiologic effect on epileptiform activity in the human hippocampus. Although a clinical response to VNS did not occur in our patient before surgery, 30-Hz VNS suppressed interictal epileptiform sharp waves that were similar in appearance to those seen during the patient's actual seizures. In contrast, 5-Hz stimulation appeared to increase the appearance of interictal sharp waves. Key Words: Vagus nerve stimulationHippocampal depth electrodes-Epileptiform activitySpikes-Sharp waves.Vagus nerve stimulation (VNS) using the NeuroCybernetic Prosthesis (NCP; Cyberonics, Inc., Houston, TX, U.S.A.) was approved by the Food and Drug Administration (FDA) in July 1997 for use as an adjunctive therapy for adults or adolescents older than 12 years with medically refractory partial onset seizures. Although its efficacy is well established (1,2), the exact mechanism of action of VNS remains unknown. Animal studies have shown that stimulation of the cervical portion of the vagus nerve can terminate electrographic seizures caused by either topical cortical or systemic strychnine or pentylenetetrazol (PTZ) (3). VNS can also block the development of kindled seizures (4).McLachlan (5) found that electrical stimulation of the left vagus nerve reduced or abolished penicillin-induced interictal cortical spikes in Wistar rats during and immediately after stimulation. In his study, stimulation consisted of square-wave pulses of 0.01-1.2 mA at 20 or 50 Hz. Woodbury and Woodbury (6) studied the effects of different stimulus parameters and found that stimulation of unmyelinated (C) vagus nerve fibers in male SpragueDawley rats could inhibit electrically or chemically induced seizures. They concluded that the optimal stimulus ...