Arousal from sleep shortens sympathetic burst latency in humans. (1/1232)

1. Bursts of sympathetic activity in muscle nerves are phase-locked to the cardiac cycle by the sinoaortic baroreflexes. Acoustic arousal from non-rapid eye movement (NREM) sleep reduces the normally invariant interval between the R-wave of the electrocardiogram (ECG) and the peak of the corresponding sympathetic burst; however, the effects of other forms of sleep disruption (i.e. spontaneous arousals and apnoea-induced arousals) on this temporal relationship are unknown. 2. We simultaneously recorded muscle sympathetic nerve activity in the peroneal nerve (intraneural electrodes) and the ECG (surface electrodes) in seven healthy humans and three patients with sleep apnoea syndrome during NREM sleep. 3. In seven subjects, burst latencies were shortened subsequent to spontaneous K complexes (1.297 +/- 0.024 s, mean +/- s. e.m.) and spontaneous arousals (1.268 +/- 0.044 s) compared with latencies during periods of stable NREM sleep (1.369 +/- 0.023 s). In six subjects who demonstrated spontaneous apnoeas during sleep, apnoea per se did not alter burst latency relative to sleep with stable electroencephalogram (EEG) and breathing (1.313 +/- 0.038 vs. 1.342 +/- 0.026 s); however, following apnoea-induced EEG perturbations, burst latencies were reduced (1.214 +/- 0.034 s). 4. Arousal-induced reduction in sympathetic burst latency may reflect a temporary diminution of baroreflex buffering of sympathetic outflow. If so, the magnitude of arterial pressure perturbations during sleep (e.g. those caused by sleep disordered breathing and periodic leg movements) may be augmented by arousal.  (+info)

Recognizing problem sleepiness in your patients. National Center on Sleep Disorders Research Working Group. (2/1232)

Normal sleep is required for optimal functioning. Normal wakefulness should be effortless and free of unintended sleep episodes. Problem sleepiness is common and occurs when the quantity of sleep is inadequate because of primary sleep disorders, other medical conditions or lifestyle factors. Medications and substances that disturb sleep, such as caffeine and nicotine, or those that have sedating side effects, may also cause problem sleepiness. This condition can lead to impairment in attention, performance problems at work and school, and potentially dangerous situations when the patient is driving or undertaking other safety-sensitive tasks. However, problem sleepiness is generally correctable when it is recognized. Asking a patient and his or her bed partner about the likelihood of drowsiness or of falling asleep during specific activities, as well as questions that uncover factors contributing to the sleepiness, helps the physician to recognize the disorder. Accurate diagnosis of specific sleep disorders may require evaluation by a specialist. The primary care physician is in an ideal position to identify signs and symptoms of problem sleepiness and initiate appropriate care of the patient, including educating the patient about the dangers of functioning while impaired by sleepiness.  (+info)

Hypoglycemia and torpor in Siberian hamsters. (3/1232)

We tested whether reduced blood glucose concentrations are necessary and sufficient for initiation of torpor in Siberian hamsters. During spontaneous torpor bouts, body temperature (Tb) decreases from the euthermic value of 37 to <31 degrees C. Among hamsters that displayed torpor during maintenance in a short-day length (10 h light/day) at an air temperature of 15 degrees C, blood glucose concentrations decreased significantly by 28% as Tb fell from 37 to <31 degrees C and increased during rewarming so that by the time Tb first was >36 degrees C, glucose concentrations had returned to the value preceding torpor. Hamsters did not display torpor when maintained in a long-day length (16 h light/day) and injected with a range of insulin doses (1-50 U/kg body mass), some of which resulted in sustained, pronounced hypoglycemia. We conclude that changes in blood glucose concentrations may be a consequence rather than a cause of the torpid state and question whether induction of torpor by 2-deoxy-D-glucose is due to its general glucoprivic actions.  (+info)

Considerations in pharmaceutical conversion: focus on antihistamines. (4/1232)

The practice of pharmaceutical conversion, which encompasses three types of drug interchange (generic, brand, and therapeutic substitution), is increasing in managed care settings. Pharmaceutical conversion has numerous implications for managed care organizations, their healthcare providers, and their customers. Although drug cost may be a driving consideration in pharmaceutical conversion, a number of other considerations are of equal or greater importance in the decision-making process may affect the overall cost of patient care. Among these considerations are clinical, psychosocial, and safety issues; patient adherence; patient satisfaction; and legal implications of pharmaceutical conversion. Patient-centered care must always remain central to decisions about pharmaceutical conversion. This article discusses the issues related to, and implications of, pharmaceutical conversion utilizing the antihistamines class of drugs as the case situation.  (+info)

Effects of fluoxetine on the polysomnogram in outpatients with major depression. (5/1232)

This study investigated the effects of open-label fluoxetine (20 mg/d) on the polysomnogram (PSG) in depressed outpatients (n = 58) who were treated for 5 weeks, after which dose escalation was available (< or = 40 mg/d), based on clinical judgment. Thirty-six patients completed all 10 weeks of acute phase treatment and responded (HRS-D < or = 10). PSG assessments were conducted and subjective sleep evaluations were gathered at baseline and at weeks 1, 5, and 10. Of the 36 subjects who completed the acute phase, 17 were reevaluated after 30 weeks on continuation phase treatment and 13 after approximately 7 weeks (range 6-8 weeks) following medication discontinuation. Acute phase treatment in responders was associated with significant increases in REM latency, Stage 1 sleep, and REM density, as well as significant decreases in sleep efficiency, total REM sleep, and Stage 2 sleep. Conversely, subjective measures of sleep indicated a steady improvement during acute phase treatment. After fluoxetine was discontinued, total REM sleep and sleep efficiency were found to be increased as compared to baseline.  (+info)

Intracerebroventricular injection of TNF-alpha promotes sleep and is recovered in cervical lymph. (6/1232)

Recent studies have shown that the central nervous system (CNS) communicates with the periphery by the drainage of cerebrospinal fluid and brain interstitial fluid into blood and lymph. We hypothesized that tumor necrosis factor (TNF)-alpha would not only influence the CNS by promoting sleep but also would be directly transmitted into the peripheral immune system. Five hundred nanograms of 125I-labeled TNF-alpha were injected into the lateral ventricles of the brain of six sheep and sampled in venous blood and cervical and prescapular lymph every 30 min for 6 h. 125I-TNF-alpha was measured in lymph nodes and control fat, skin, and muscle tissues 6 h postinjection. 125I-TNF-alpha was detected in the cervical lymphatics within the first 30 min and peaked within 2-3 h. 125I-TNF-alpha counts were elevated in the nodes of the head and neck region. Polysomnographic recordings of four animals showed that TNF-alpha induced a significant increase in slow-wave sleep at postinjection hours 4 and 5. CNS TNF-alpha and its direct drainage into the lymphatic system may influence both the sleeping/waking brain and peripheral immune functions.  (+info)

Application of a rheolytic thrombectomy device in the treatment of dural sinus thrombosis: a new technique. (7/1232)

We present a novel application of a transvascular rheolytic thrombectomy system in the treatment of symptomatic dural sinus thrombosis in a 54-year-old woman with somnolence and left-sided weakness. The diagnosis of bilateral transverse and superior sagittal sinus thrombosis was made and the patient was treated with anticoagulant therapy. After an initial period of improvement, she became comatose and hemiplegic 8 days after presentation. After excluding intracerebral hemorrhage by MR imaging, we performed angiography and transfemoral venous thrombolysis with a hydrodynamic thrombectomy catheter, followed by intrasinus urokinase thrombolytic therapy over the course of 2 days. This technique resulted in dramatic sinus thrombolysis and near total neurologic recovery. Six months after treatment, the patient showed mild cognitive impairment and no focal neurologic deficit. Our preliminary experience suggests that this technique may play a significant role in the endovascular treatment of this potentially devastating disease.  (+info)

Study of cardiac repolarization in healthy volunteers performed with mizolastine, a new H1-receptor antagonist. (8/1232)

AIMS: The occurrence of serious dysrhythmias, such as torsades de pointes, with terfenadine and astemizole had led to a reexamination of the potential effect of H1 antihistamines on cardiac repolarization. Mizolastine is a potent, selective, nonsedating peripherally acting H1-receptor antagonist which is registered for rhinitis and urticaria at a recommended dose of 10 mg once daily. The present study was carried out to investigate the effects of therapeutic and supratherapeutic doses of mizolastine, on ventricular repolarization in healthy volunteers. METHODS: Twenty-four healthy young volunteers participated in a double-blind, placebo-controlled, randomised study with three parallel groups. Each group consisted of 2 way cross-over 7 day treatment periods where mizolastine (10, 20 or 40 mg) and placebo were randomly administered. On day 1 and day 7, 12-lead ECG recordings were performed prior and 0.5, 1, 2, 3, 4, 6, 8, 12, 16, and 20 h after dosing and from day 2 to day 6, before dosing and 1, 2, 3, and 4 h after. RESULTS: Whatever the analysis used (raw data, changes from baseline, incidence of individual out-of-range values) no significant differences were observed at any dose level vs placebo, on any of ECG parameters (HR, PR, QRS, QT, and QTc). In particular, no effect of mizolastine vs placebo was shown on QT and QTc although 95% CIs were wide. The only subject who exhibited a QTc>/=450 ms received placebo for 7 days. CONCLUSIONS: This study found no evidence of an effect of mizolastine up to 40 mg (four times the therapeutic dose) on ventricular repolarization in healthy volunteers.  (+info)