To discover which factors contributed to recovery after surgical intracranial decompression, we reviewed the records of 82 consecutive comatose patients with traumatic acute subdural hematoma (ASDH) who were treated in a single center under a uniform protocol. The delay from injury to operation was the factor of greatest therapeutic importance. Patients who underwent surgery within the first four hours had a 30 per cent mortality rate, as compared with 90 percent in those who had surgery after four hours (P less than 0.0001). Other important prognostic variables included results of the initial neurologic examination, sex, multimodality-evoked potentials, and postoperative intracranial pressure (ICP). If all patients with traumatic ASDH were taken directly to hospitals equipped to diagnose and remove the hematoma within four hours of injury, mortality rates could be reduced considerably.

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The relationship of outcome to the appearance of the basal cisterns as seen on initial computerized tomography (CT) scanning was assessed in 218 consecutive severely head-injured patients entered into the second phase of the National Pilot Traumatic Coma Data Bank. Outcome could be directly related to the status of the basal cisterns on the initial CT scan. The mortality rates were 77%, 39%, and 22% among those with absent, compressed, and normal basal cisterns, respectively. This association between cisterns and outcome was shown to be strong after adjusting for Glasgow Coma Scale (GCS) score (p less than 0.001). The state of the cisterns was more important for those with higher GCS scores (scores 6 to 8) than for those with lower scores (scores 3 to 5). Patients with GCS scores of 6 to 8, with cisterns absent or not visualized, suffered nearly a fourfold additional risk of poor outcome, compared to those with normal cisterns. This indicates that the status of the cisterns can be used as an early noninvasive method of identifying patients at high risk of death or severe disability, in whom the initial neurological examination would potentially suggest otherwise.

A series of 51 comatose patients suffering traumatic epidural hematoma after closed head injury is reviewed. This prospective series was accumulated from the National Pilot Traumatic Coma Data Bank during a 2-year period and represents 9% of all patients entered into the Data Bank. The overall mortality was 41%, with 4% remaining in the vegetative state. Fifty per cent of these patients, all of whom were in coma, also had an associated intracerebral contusion. There was no difference in outcome with regard to sex, mode of injury, or the presence or absence of contusion or shift on the computed tomographic (CT) scan. The motor score immediately before operation was the most powerful preoperative predictor of outcome. Sixty-seven per cent or two-thirds of the patients with a motor score of 4, 5, or 6 on the Glasgow coma scale had a satisfactory outcome at last follow-up examination. In contrast, in patients with a motor score of 3 or less, two-thirds either died or remained in a vegetative state. The acute traumatic epidural hematoma is often lethal in the comatose patient. We recommend early evacuation of epidural hematomas, i.e., when they are first noted on the CT scan, rather than waiting for clinical motor deterioration.

The effect of changes in cerebrospinal fluid (CSF) concentration of magnesium ion ([Mg2+]) on pial arterioles was investigated in anesthetized cats equipped with acutely implanted cranial windows for the observation of the pial microcirculation. Increased [Mg2+] caused vasodilation, whereas decreased [Mg2+] caused vasoconstriction. The effect of [Mg2+] was dose dependent and was the same in small and larger arterioles. There was an interaction between CSF [Mg2+] and calcium ion concentration ([Ca2+]), such that the vasodilator effect of Mg2+ was greater when the [Ca2+] was lower, especially in larger vessels. The vasodilator effect of Mg2+ on pial arterioles was enhanced in the presence of the calcium antagonist verapamil (0.5 micrograms/ml), despite the fact that verapamil by itself caused a 12-13% arteriolar dilation. These results show that the vasodilator effect of Mg2+ is probably related to an interaction at the cell membrane resulting in reduction in the influx of Ca2+ into vascular smooth muscle.

To examine possible metabolic frontal lobe alterations in i.v. heroin-dependent patients with different histories of concomitant substance use, N-acetylaspartate (NAA), a putative marker of neuronal viability, was measured by (1)H-MRS. Compared with controls, NAA levels in patients were reduced by 7% in gray matter (p = 0.015) but not in white matter. To what extent comorbid conditions or substance use, including alcohol, contributed to these frontocortical metabolic changes remains to be elucidated.

ABSTRACT. Cerebral high energy phosphates were studied in the intact rabbit brain using nuclear magnetic resonance spectroscopy. The effect of hypothermia on degradation kinetics in total ischemia due to circulatory arrest was examined, measuring phosphocreatine, adenosine triphosphate, and inorganic phosphate as a function of time at three different temperatures (35, 24, 21" C). Phosphocreatine-and ATP-decays followed single exponential functions at all three temperatures. The half-life times increased by approximately a factor of three upon lowering the temperature from 35 to 21" C with activation energies of 15-20 kcal/mol, which corresponds to values of Qlo between 2.4 and 3.2. In the temperature range studied, no critical temperature was found below which metabolism would stop completely. We conclude that nuclear magnetic resonance spectroscopy allows, in the intact animal, quantitative assessment of the influence of hypothermia on energy metabolism in the brain. This influence is a major concern in the field of cardiac surgery in infants and children who are often operated in total circulatory arrest under deep hypothermia. (14) have investigated the effect of hypothermia on the degradation kinetics of cerebral high energy phosphates after total circulatory arrest using NMR spectroscopy. These studies were performed on isolated and perfused neonatal rat brain. Several other authors have shown that NMR spectroscopy of the cerebral phosphates can also be performed in humans and in intact animals under varied conditions (I 5-29).As there are however no reports of kinetic studies in intact Received January 10, 1986: accepted April 25, 1986. Correspondence N. Herschkowitz, Department of Pediatrics, University of Bern, animals under deep hypothermia, we have chosen to investigate degradation of cerebral high energy phosphates by NMR spectroscopy in the hypothermic rabbit. MATERIALS AND METHODSMale New Zealand rabbits (average body weight 3.4 kg, range 3.0-3.7) were anaesthetized with 0.85 g/kg Urethane intraperitoneal, 30 min later with the same dose intravenous in an ear vein. The neck, thorax, and abdomen were then shaved, tracheostomy performed, and a 3.5-mm tube inserted. An internal jugular vein was catheterized with an umbilical vein catheter (Pharmaseal, CH 5, AHS Herstal, Belgium). The catheter was filled with saline, the syringe remained attached to the catheter without flushing. A femoral artery was prepared and a catheter (Vygon intravenous catheter G 18, Steriflex O.R.X., Ecouen, France) inserted up to the abdominal aorta. This catheter was connected via a transducer to a monitor displaying the arterial blood pressure curve, systolic, mean and diastolic pressure as well as heart rate (Tektronix 414). A temperature probe was inserted through the mouth into the pharynx and the temperature was displayed on the same monitor. Preparation of the animal lasted for an average of 41 min (ranae 30-55) and was similar for all temperaturegroups. ~u r i n g thise procebures, the animal was breathing spontaneousl...

Of 366 consecutive patients with severe head injury, treated and managed by a uniform protocol, 61 (17%) were admitted with signs of severe brain-stem dysfunction. Forty-three of the 61 patients (70%) had surgical mass lesions and 30% had diffuse brain damage. Twelve of the 61 patients (20%) survived, but only six patients made a good to moderately disabled recovery. All six of these patients had a traumatic acute subdural hematoma (SDH). The records of the 20 comatose patients with an acute SDH and severe brain-stem dysfunction were reviewed to discover which factors contributed to functional recovery. The average survivor was operated on within 2 1/2 hours after injury and the nonsurvivors within 4 1/2 hours. Prompt surgical intervention and prudent control of postoperative intracranial pressure were major factors in preventing permanent brain-stem damage, with a significance of p less than 0.05 and p less than 0.02, respectively. Measurement of multimodality evoked potentials in the early postoperative period correctly distinguished between reversible and irreversible brain-stem dysfunction in six of the seven patients.