Thirty patients were treated surgically for spinal epidural hematoma (SEH). Twelve of these cases resulted from spinal surgery, seven from epidural catheters, four from vascular lesions, three from anticoagulation medications, two from trauma, and two from spontaneous causes. Pain was the predominant initial symptom, and all patients developed neurological deficits. Eight patients had complete motor and sensory loss (Frankel Grade A); six had complete motor loss but some sensation preserved (Frankel Grade B); and 16 had incomplete loss of motor function (10 patients Frankel Grade C and six patients Frankel Grade D). The average interval from onset of initial symptom to maximum neurological deficit was 13 hours, and the average interval from onset of symptom to surgery was 23 hours. Surgical evacuation of the hematoma was performed in all patients; 26 of these improved; four remained unchanged, and no patients worsened (mean follow up 11 months). Complete recovery (Frankel Grade E) was observed in 43% of the patients and functional recovery (Frankel Grades D or E) was observed in 87%. One postoperative death occurred from a pulmonary embolus (surgical mortality 3%). Preoperative neurological status correlated with outcome; 83% of Frankel Grade D patients recovered completely compared to 25% of Frankel Grade A patients. The rapidity of surgical intervention also correlated with outcome; greater neurological recovery occurred as the interval from symptom onset to surgery decreased. Patients taken to surgery within 12 hours had better neurological outcomes than patients with identical preoperative Frankel grades whose surgery was delayed beyond 12 hours. This large series of SEH demonstrates that rapid diagnosis and emergency surgical treatment maximize neurological recovery. However, patients with complete neurological lesions or long-standing compression can improve substantially with surgery.

Human obesity is known to be a familial disorder. We studied 130 nondiabetic adult southwestern American Indians (74 men and 56 women) from 54 families to determine whether the resting metabolic rate, as measured by indirect calorimetry, is a familial trait that is independent of individual differences in fat-free mass (estimated mass of metabolically active tissue), age, and sex. We found that most of the variance in the resting metabolic rate (83 percent, P less than 0.0001) was accounted for by three covariates--fat-free mass, age, and sex--and that fat-free mass was the most important determinant. Family membership accounted for an additional 11 percent (P less than 0.0001) of the variance in the resting metabolic rate. Thus, resting metabolic rate is a familial trait in this population, and it is independent of differences in fat-free mass, age, and sex. We also found that persons from families with lower resting metabolic rates were no more obese than persons from families with higher metabolic rates. This finding may be partly explained by the close correlation between fat-free mass and percentage of body fat (r = 0.81, P less than 0.0001), which indicates that the resting metabolic rate, as adjusted for fat-free mass, is already partly adjusted for obesity. Only prospective studies will elucidate whether the familial dependence of the resting metabolic rate is a contributing mechanism to the familial predisposition to obesity.

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To investigate the role of angiogenesis in the pathogenesis of dural arteriovenous malformations (AVMs), 40 rats underwent common carotid artery-external jugular vein (CCA-EJV) anastomosis, bipolar coagulation of the vein draining the transverse sinus, and sagittal sinus thrombosis to induce venous hypertension. Fifteen rats underwent a similar surgical procedure, but venous hypertension was not induced. The 55 rats were divided into seven groups. Four groups, each containing 10 rats, underwent induced venous hypertension. The other three groups, each containing five rats, did not undergo induced venous hypertension. After 1, 2, or 3 weeks, dura mater was obtained from one group of hypertensive rats and from one group of nonhypertensive rats and was assayed for angiogenic activity (rabbit cornea bioassay). The remaining group of 10 hypertensive rats was not assayed to determine if sampling affected dural AVM formation. Unlike rats without CCA-EJV anastomosis, rats with CCA-EJV anastomosis had significantly increased postoperative sagittal sinus pressures (p < 0.0001). Mean angiogenesis indices were significantly greater in rats with venous hypertension than in rats without venous hypertension (p = 0.004). Dural AVMs formed in 42% of the 55 rats and facial AVMs formed in 51%. Angiogenic activity correlated positively with venous hypertension (p = 0.74). Development of dural AVMs correlated positively with both venous hypertension (p = 0.0009) and angiogenic activity (p = 0.04). These data indicate that venous hypertension may induce angiogenic activity either directly or indirectly by decreasing cerebral perfusion and increasing ischemia, and that dural AVM formation may be the result of aberrant angiogenesis.

There is no single ideal treatment for the obliteration of DAVMs. The management of each case is best considered individually. The results of this review serve as a rational starting point for the selection of treatment options.