Daytime sleepiness during Ramadan intermittent fasting: polysomnographic and quantitative waking EEG study

During the lunar month of Ramadan, Muslims abstain from eating, drinking and smoking from sunrise to sunset. We reported previously that Ramadan provokes a shortening in nocturnal total sleep time by 40 min, an increase in sleep latency, and a decrease in slow-wave sleep (SWS) and rapid eye movement (REM) sleep duration during Ramadan. During the same study, the effects of Ramadan intermittent fasting on daytime sleepiness were also investigated in eight healthy young male subjects using a quantitative waking electroencephalograph (EEG) analysis following the multiple sleep latency test (MSLT) procedure. This procedure was combined with subjective alertness and mood ratings and was conducted during four successive experimental sessions: (1) baseline (BL) 15 days before Ramadan, (2) beginning of Ramadan (R11) on the 11th day of Ramadan, (3) end of Ramadan (R25) on the 25th day of Ramadan, (4) recovery 2 weeks after Ramadan (AR). During each session, four 20-min nap opportunities (MSLTs) were given at 10:00, 12:00, 14:00 and 16:00 h and were preceded by rectal temperature readings. Nocturnal sleep was recorded before each daytime session. Subjective daytime alertness did not change in R25 but decreased in R11 at 12:00 h, and subjective mood decreased at 16:00 h, both in R11 and R25. During the MSLT, mean sleep latency decreased by an average of 2 min in R11 (especially at 10:00 and 16:00 h) and 6 min in R25 (especially at 10:00 and 12:00 h) compared with BL. There was an increase in the daily mean of waking EEG absolute power in the theta (5.5-8.5 Hz) frequency band. Significant correlations were found between sleep latency during the MSLT and the waking EEG absolute power of the fast alpha (10.5-12.5 Hz), sigma (11.5-15.5 Hz) and beta (12.5-30 Hz) frequency bands. Sleep latency was also related to rectal temperature. In conclusion, Ramadan diurnal fasting induced an increase in subjective and objective daytime sleepiness associated with changes in diurnal rectal temperature.     

3 Beta-hydroxysteroid dehydrogenase expression in rat spinal cord

In adult male rats, 3beta-hydroxysteroid dehydrogenase/delta5-delta4-isomerase (3beta-HSD) expressing cells were identified in the spinal cord from the cervical to the sacral segments. An in situ hybridization study, using an oligonucleotide common to the four known isoforms of rat 3beta-HSD, revealed its mRNA in gray matter. Measurements of optical densities in autoradiograms showed the following regional distribution: dorsal horn (layers I-III) > central canal (layer X) > or = ventral horn (layers VIII-IX) > ventral funiculus = lateral funiculus. At the cellular level, the number of grains was higher on the large motoneurons than on small neurons of the dorsal horn, but the grain density per cell was similar. Further evidence for the expression of 3beta-HSD in the spinal cord was obtained by western blot analysis, which revealed an immunoreactive protein of approximately 45 kDa in the dorsal and ventral parts of the spinal cord. Castration and adrenalectomy did not influence the expression of 3beta-HSD mRNA and protein. Gas chromatography/mass spectrometry measurements showed higher levels of pregnenolone and progesterone in the spinal cord than in the plasma. After castration and adrenalectomy, their levels remained elevated in the spinal cord, suggesting that these neurosteroids may be synthesized locally. The wide distribution of 3beta-HSD, and the high levels of pregnenolone and progesterone in the spinal cord even after castration and adrenalectomy, strongly suggest a potential endogenous production of progesterone and an important signalling function of this steroid in the spinal cord.     

Steroid synthesis and metabolism in the nervous system: Trophic and protective effects

Steroids influence the activity and plasticity of neurons and glial cells during early development, and they continue to exert trophic and protective effects in the adult nervous system. Steroids are produced by the gonads and adrenal glands and reach the brain, the spinal cord and the peripheral nerves via the bloodstream. However, some of them, named neurosteroids, can also be synthesized within the nervous system. They include pregnenolone, progesterone, dehydroepiandrosterone and their reduced metabolites and sulfate esters. Little is known concerning the regulation of steroid synthesis in the nervous system, which involves interactions between different cell types. For example, the synthesis of progesterone by Schwann cells in peripheral nerves is regulated by a diffusible neuronal signal. Neurotrophic and neuroprotective effects of steroids have been documented both in cell culture and in vivo. PROG plays an important role in the neurological recovery from traumatic injury of the brain and spinal cord by mechanisms involving protection from excitotoxic cell death, lipid peroxydation and the induction of specific enzymes. After transection of the rat spinal cord, PROG increases the number of nitric oxide synthase expressing astrocytes immediately above and below the lesion. PROG also plays an important role in the formation of new myelin sheaths. This has been shown in the regenerating mouse sciatic nerve after lesion and in cocultures of sensory neurons and Schwann cells. PROG promotes myelination by activating the expression of genes coding for myelin proteins. The modulation of neurostransmitter receptors, in particular the type A -aminobutyric acid, the N-methyl-D-aspartate and the sigma 1 receptors, is involved in the psychopharmacological effects of steroids and allows to explain their anticonvulsant, anxiolytic, antidepressive and sedative effects as well as their influence on memory. Pregnenolone sulfate has been shown to reverse age-related deficits in spatial memory performance and to have protective effects on memory in different models of amnesia.     

Brainstem ischemia and preeclampsia.

Diffuse neurological manifestations of preeclampsia are due to endothelial involvement that lead to ischemia, hemorrhage, or edema. We analyzed clinical and radiological features and the course of brainstem ischemic strokes in a preeclampsia patient. We report a case of severe preeclampsia in a 30-year-old woman who was admitted 10 hr after a vaginal delivery at home. The pregnancy was at 39 wk, with no prenatal care. At her admission, she was conscious, and she had tetraparesia, swinging deep tendon reflex testing, drowsiness, and dysarthria; the BP was at 160/100 mmHg and 4 + proteinuria; magnetic resonance imaging revealed brainstem ischemic stroke. The evolution was favorable with symptomatic treatment. The patient was discharged on the 16th day; 2 months later she had a normal recovery. Brainstem strokes are rare. They are frequently due to hemorrhage; sometimes, they can also be ischemic. Their course is favorable.     

Lack of benefit of an active pectoral pulse generator on atrial defibrillation thresholds

INTRODUCTION: Atrial defibrillation can be achieved with standard implantable cardioverter defibrillator leads, which has led to the development of combined atrial and ventricular devices. For ventricular defibrillation, use of an active pectoral electrode (active can) in the shocking pathway markedly reduces defibrillation thresholds (DFTs). However, the effect of an active pectoral can on atrial defibrillation is unknown. METHODS AND RESULTS: This study was a prospective, randomized, paired comparison of two shock configurations on atrial DFTs in 33 patients. The lead system evaluated was a dual-coil transvenous defibrillation lead with a left pectoral pulse generator emulator. Shocks were delivered either between the right ventricular coil and proximal atrial coil (lead) or between the right ventricular coil and an active can in common with the atrial coil (active can). Delivered energy at DFT was 4.2 +/- 4.1 J in the lead configuration and 5.0 +/- 3.7 J in the active can configuration (P = NS). Peak current was 32% higher with an active can (P < 0.01), whereas shock impedance was 18% lower (P < 0.001). Moreover, a low threshold (< or = 3 J) was observed in 61% of subjects in the lead configuration but in only 36% in the active can configuration (P < 0.05). There were no clinical predictors of the atrial DFT. CONCLUSION: These results indicate that low atrial DFTs can be achieved using a transvenous ventricular defibrillation lead. Because no benefit was observed with the use of an active pectoral electrode for atrial defibrillation, programmable shock vectors may be useful for dual-chamber implantable cardioverter defibrillators.