No abstract

It could be expected that the various stages of sleep were reflected in variation of the overall level of cerebral activity and thereby in the magnitude of cerebral metabolic rate of oxygen (CMRO2) and cerebral blood flow (CBF). The elusive nature of sleep imposes major methodological restrictions on examination of this question. We have now measured CBF and CMRO2 in young healthy volunteers using the Kety-Schmidt technique with 133Xe as the inert gas. Measurements were performed during wakefulness, deep sleep (stage 3/4), and rapid-eye-movement (REM) sleep as verified by standard polysomnography. Contrary to the only previous study in humans, which reported an insignificant 3% reduction in CMRO2 during sleep, we found a deep-sleep-associated statistically highly significant 25% decrease in CMRO2, a magnitude of depression according with studies of glucose uptake and reaching levels otherwise associated with light anesthesia. During REM sleep (dream sleep) CMRO2 was practically the same as in the awake state. Changes in CBF paralleled changes in CMRO2 during both deep and REM sleep.

Results obtained by the 133Xe clearance method with external detectors and by transcranial Doppler sonography (TCD) suggest that dynamic exercise causes an increase of global average cerebral blood flow (CBF). These data are contradicted by earlier data obtained during less-well-defined conditions. To investigate this controversy, we applied the Kety-Schmidt technique to measure the global average levels of CBF and cerebral metabolic rate of oxygen (CMRO2) during rest and dynamic exercise. Simultaneously with the determination of CBF and CMRO2, we used TCD to determine mean maximal flow velocity in the middle cerebral artery (MCA Vmean). For values of CBF and MCA Vmean a correction for an observed small drop in arterial PCO2 was carried out. Baseline values for global CBF and CMRO2 were 50.7 and 3.63 ml.100 g-1.min-1, respectively. The same values were found during dynamic exercise, whereas a 22% (P < 0.0001) increase in MCA Vmean was observed. Hence, the exercise-induced increase in MCA Vmean is not a reflection of a proportional increase in CBF.

The effect of hyperinsulinemia on glucose blood-brain barrier (BBB) transport and cerebral metabolism (CMRglc) was studied using the intravenous double-indicator method and positron emission tomography using [18F]fluorodeoxyglucose as tracer (PET-FDG). Sixteen normal healthy control subjects (25 +/- 4 years old) were studied twice during a euglycemic and a euglycemic-hyperinsulinemic condition. Our hypothesis was that high physiologic levels of insulin did not affect the BBB transport or net metabolism of glucose. During insulin infusion, arterial plasma insulin levels increased from 48.5 to 499.4 pmol/l. The permeability-surface area products for glucose and FDG BBB transport obtained with the double-indicator method remained constant during hyperinsulinemia. Similarly using PET-FDG, no changes were observed in the unidirectional clearance of FDG from blood to brain. k2* (FDG transport from brain to blood) increased significantly by 15 and 18% (gray and white matter, respectively), and k4* (dephosphorylation of FDG) increased by 18%. The increase in k2* may be caused by insulin inducing a decrease in the available FDG brain pool. The increase in k4* may be related to an increased loss of labeled products during insulin fusion. Irrespective of these changes, CMRglc remained unchanged in all brain regions. We conclude that hyperinsulinemia within the normal physiologic range does not affect BBB glucose transport or net cerebral glucose metabolism.

Among 873 consecutive patients who had undergone a total of 1021 spinal anaesthesias involving puncture of the lumbar dura, 75 (7.35%) complained of Postdural Puncture Headache (PDPH). The severity of each patient's PDPH was categorized, on a scale from mild to severe, on the basis of the onset, duration, severity of the headaches, and the degree to which they were accompanied by auditory and vestibular symptoms. In the patients who developed PDPH, 65% developed symptoms within 24 hours of the lumbar punctures and 92% developed symptoms within 48 hours. For the patients who recovered spontaneously the mean duration of the PDPHs was 5 days, with a range of 1-12 dyas. PDPH was characterized by headaches that were influenced by the patient's posture and the severity of PDPH was categorized as follows: Mild PDPH resulted in a slight restriction of their physical activity. These patients were not confined to bed and had no associated symptoms. Moderate PDPH forced the patient to stay in bed for part of the day, and resulted in restricted physical activity. Associated symptoms were not necessarily present. Severe PDPH. Patients were bedridden for the entire day and made no attempt to raise their head or to stand. Associated symptoms were always present. Forty-five of the PDPH patients (60%) recovered spontaneously. Of these, 8 patients (11%) were categorized as mild cases of PDPH, 14 (19%) as moderate, and 23 (30%) patients as severe cases of PDPH. Thirty of the PDPH patients (40%) were treated with an autologous epidural blood patch (AEBP). Of these, 27 patients (36%) were classified as severe and 3 patients (4%) as moderate PDPH.(ABSTRACT TRUNCATED AT 250 WORDS)