No abstract

Femoral and abdominal adipose tissue cellularity and metabolism as well as muscle morphology and metabolism were examined in women with Cushing's syndrome and compared with those in nonobese women and obese women with the android and gynoid types of fat distribution. Cushing's syndrome was characterized by abdominal obesity and enlarged abdominal fat cells, with adipose tissue lipoprotein lipase activity elevated 2-3 times that in normal women and low lipolytic capacity. Muscle tissue in women with Cushing's syndrome had a relatively low proportion of type I (30%) and a high proportion of type IIB (32%) muscle fibers, similar to those in android obesity (45% and 25%, respectively) and in contrast to fiber composition in gynoid obesity (55% and 12%, respectively). Glycogen synthase activity in the lateral vastus muscle was very low. We suggest that the enlargement of abdominal fat depots in women with Cushing's syndrome is at least partially due to elevated adipocyte lipoprotein lipase activity and low lipolytic activity. Furthermore, the abnormal muscle fiber composition might be caused by the corticosteroid excess. Such muscle is known to be relatively insulin insensitive and might thus contribute to the marked insulin resistance that occurs during chronic corticosteroid excess.

External hydrocephalus means abnormal fluid accumulation in the subarachnoid space under increased pressure with no or slight widening of the ventricles. 9 children were investigated because of pathologically increasing head circumference and abnormal transillumination. PEG and/or CT showed widened sulci frontally, parietally and interhemispherically but no widening of the ventricles. 7 patients were subjected to exploratory craniotomy which disclosed a deep arachnoid space. 2 patients were shunted . All follow-up CT examinations showed normal conditons. We suggest that infants with clinical signs of hydrocephalus and CT picture of external hydrocephalus should not be treated with shunt. The widening of the subarachnoidal space will normalize. The rate of headgrowth will also normalize.

Cranial nerve dysfunction and headache may occur with unruptured aneurysms of the cavernous and supraclinoid portions of the internal carotid artery. Nerve deformation (mass effect) and transmitted pulsations have been suggested as pathogenetic mechanisms. Differentiation may be possible by studying effects of endovascular treatment with Guglielmi detachable coils. Symptoms and signs of cranial neuropathy were retrospectively contrasted with angiographic aneurysm volumes before and after treatment in 10 patients. Mean follow-up was 36 months. Symptoms improved in three of four patients with cranial nerve dysfunction and in all patients with headache. None of the other patients, one with cranial nerve dysfunction, and three who were asymptomatic, developed any new symptoms after treatment. Aneurysm volume ranged from 0.1 to 2.7 cm(3 )before and 0.2 to 5.7 cm(3) after treatment; the size thus increased by 15 to 110%, a change which was statistically significant (P=0.004). The consistent increase in aneurysm volume with treatment is not associated with clinical deterioration, suggesting that deformation and displacement play a minor role in cranial neuropathy and that transmitted pulsations may be more important.

In an earlier study in dogs we found a reduced cerebral blood flow measured intermittently during the first hours after an intravenous injection of E. coli endotoxin. Within 5 min after the endotoxin injection, a temporarily reduced cerebrospinal fluid pressure was seen irrespective of changes in arterial blood pressure. One possible explanation for this could be an early reduction of the blood flow in the brain. To test this hypothesis, the initial flow reaction was evaluated by measurement of the blood flow in the superior sagittal sinus using an electromagnetic probe around the intact sinus. In five animals following E. coli endotoxin 1.0-1.5 mg/kg intravenously, the superior sagittal sinus blood flow decreased within 2 min, followed by increasing flows within 15 min and thereafter continuously decreasing values up to 60 min, thus giving a two-phase vascular reaction. In all animals there was a marked initial increase in cerebrovascular resistance and the fall in blood flow was thus not a mere consequence of blood pressure changes. In three other animals pretreated with methysergide, a serotonin antagonist, no increase in cerebrovascular resistance was seen during the initial phase. Later, the reaction was similar in all eight animals.