Atypical sexual behavior during sleep

OBJECTIVE: This article reports a case series of atypical sexual behavior during sleep, which is often harmful to patients or bed partners. METHODS: Eleven subjects underwent clinical evaluation of complaints of sleep-related atypical sexual behavior. Complaints included violent masturbation, sexual assaults, and continuous (and loud) sexual vocalizations during sleep. One case was a medical-legal case. Sleep logs, clinical evaluations, sleep questionnaires, structured psychiatric interviews, polysomnography, actigraphy, home electroencephalographic monitoring during sleep, and clinical electroencephalographic monitoring while awake and asleep were used to determine clinical diagnoses. RESULTS: Atypical sexual behaviors during sleep were associated with feelings of guilt, shame, and depression. Because of these feelings, patients and bed partners often tolerated the abnormal behavior for long periods of time without seeking medical attention. The following pathologic sleep disorders were demonstrated on polysomnography: partial complex seizures, sleep-disordered breathing, stage 3 to 4 non-rapid eye movement (REM) sleep parasomnias, and REM sleep behavior disorder. These findings were concurrent with morning amnesia. CONCLUSIONS: The atypical behaviors were related to different syndromes despite the similarity of complaints from bed partners. In most cases the disturbing and often harmful symptoms were controlled when counseling was instituted and sleep disorders were treated. In some cases treatment of seizures or psychiatric disorders was also needed. Clonazepam with simultaneous psychotherapy was the most common successful treatment combination. The addition of antidepressant or antiepileptic medications was required in specific cases.     

The QT interval during wake and sleep in patients with ventricular arrhythmias

Eight patients with frequent ventricular ectopy underwent continuous electrocardiographic (ECG) and polygraphic monitoring for 4 days. A complex protocol consisted of normal day-night, activity-nonactivity, cycles for 48 h (nine patients); followed by a 24-h awake bedrest; and finally by a very delayed sleep and inactivity phase in the morning before returning to a normal day-night cycle (eight patients only). ECG tracings showed that the QT intervals during rapid eye movement sleep and nonrapid eye movement sleep increased significantly when compared with active wakefulness. The Bazett's corrected QT (QTc) interval also increased from active wakefulness to rapid eye movement sleep and nonrapid eye movement sleep. Adjusted mean QT intervals computed using the RR [corrected] interval as a covariate were significantly longer during non-rapid-eye-movement (407 ms) and rapid-eye-movement (408 ms) sleep than during active wakefulness (386 ms). The RR-adjusted mean QT intervals during inactive wake were also longer (400 ms) but this clear trend did not reach statistical significance (p = 0.08). Although prolongation of the QT interval during sleep reflects inactivity that may be related to withdrawal of sympathetic tone, we postulate that sleep per se also has an effect on the interval.     

Comparison of pleural pressure and transcutaneous diaphragmatic electromyogram in obstructive sleep apnea syndrome

STUDY OBJECTIVES: Based on studies of the impact of esophageal pressure on cardiovascular variables during sleep, this signal can be used to refine the severity level in the clinical diagnosis of obstructive sleep apnea syndrome. We hypothesized that relative changes in diaphragmatic electromyogram (EMG) can reflect short-term changes in esophageal pressure durng obstructive apneas and hypopneas. DESIGN: Diaphragmatic EMG was sampled at 0.25 kHz; diaphragmatic EMG waveform was band-pass filtered and digitally converted; the electrocardiogram artifact was eliminated; using a gating procedure, the waveform was fast-Fourier transformed and digitally rectified; and a moving average of 200 milliseconds was calculated. For each inspiratory effort during apnea or hypopnea, we calculated maximum diaphragmatic EMG and esophageal pressure. Data were normalized calculating the percentage difference between the first obstructed and each subsequent inspiratory effort during the respiratory event. SETTING: Sleep disorders laboratory. PATIENTS: 9 patients with moderate obstructive sleep apnea syndrome presenting with apneas and hypopneas during sleep. INTERVENTION: None. MEASUREMENTS AND RESULTS: 861 respiratory events were scored, and the evolution between esophageal pressure and diaphragmatic EMG were compared. Normalized data showed a good correlation between the 2 measures during apneas and hypopneas. There was a significant difference between the percentage increase in esophageal pressure and diaphragmatic EMG for apneas and hypopneas (esophageal pressure, apnea: 118.1% +/- 118.5%, hypopnea: 76.1% +/- 74.3%, P = .000; diaphragmatic EMG, 123.5% +/- 131.7%, hypopnea: 73.3% +/- 74.2%, P = .000). No significant differences for apnea or hypopnea were noted between the 2 measures under investigation. CONCLUSION: Diaphragmatic EMG may be clinically useful to describe relative changes in respiratory effort under conditions of apnea and hypopnea during sleep and to reliably dissociate central from obstructive events where esophageal pressure monitoring is not readily available.     

Cephalometric analyses and flow-volume loops in obstructive sleep apnea patients

Fifteen patients with obstructive sleep apnea syndrome (OSAS) and 10 controls were studied. Polygraphic monitoring during sleep confirmed the presence or absence of OSAS. Ten OSAS patients and five controls had cephalometric analysis and 12 OSAS patients and five controls had a flow-volume loop study during wakefulness. Seven OSAS patients were submitted to both analyses. Flow-volume loops were unable to detect extrathoracic airway obstruction in six out of 12 OSAS patients. One control was found with positive results. Six out of seven subjects with positive flow-volume loops were overweight (greater than or equal to 30% ideal weight). Cephalograms were very useful in demonstrating mandibular deficiencies in OSAS patients. The length of the soft palate and the position of the hyoid bone, together with the measurement of the posterior airway space, are criteria of great interest in OSAS patients. Cephalometric analysis is recommended in all OSAS patients scheduled for surgical procedure. None of these tests, however, whether alone or in combination, is capable of identifying all cases of OSAS.     

SPECT findings in the Kleine-Levin syndrome

STUDY OBJECTIVES: The Kleine-Levin Syndrome, is a rare disorder with onset during teenage years, but little is known on etiopathogenesis. Seven subjects with Kleine-Levin Syndrome accumulated over time had systematic SPECT studies during (n=5) and out (n=7) of the symptomatic period. SUBJECTS: Seven boys with symptom onset between 11 and 17 years of age and at least 2 episodes per year were followed for a mean of 6 years. METHODS: Electroencephalogram awake-asleep, computed tomography scan, and magnetic resonance imaging studies were performed before Tc-99m ECD single photon emission tomography (SPECT) obtained during day 4 or 5 (n=5) and at least 1 month away from the symptomatic period (n=7). RESULTS: All imaging tests except SPECT were normal. Hypoperfusion of both thalami were seen during the symptomatic period that completely disappeared during the asymptomatic period. Hypoperfusion in other regions were also noted in some, but not all subjects. They persisted during the asymptomatic period in 2 cases over the temporal lobe (2/7 cases), frontal lobe (1/7 cases), and basal ganglia (1/7 cases). The largest amount of persistent hypoperfusion was seen in the subject with longest clinical evolution. CONCLUSION: Hypoperfusion of the thalamus is a consistent finding during the symptomatic period, but perfusion abnormalities may persist even during the asymptomatic period. The longer the duration of the syndrome, the more extended the hypoperfusion regions during the asymptomatic period.     

DQB1-0602 (DQw1) is not present in most nonDR2 Caucasian narcoleptics.

Human narcolepsy is a genetically determined disorder of sleep strongly associated with the human leucocyte antigens (HLA) DR2 and DQw1. In black narcoleptic patients, susceptibility for narcolepsy is more closely related to a specific gene subtype of DQw1, DQB1-0602, than to DR2. About 30% of black narcoleptic patients are nonDR2, but all carry the HLA DQB1-0602 gene. In the present study, we have tested caucasian nonDR2 cataplectic patients (6 sporadic cases and 7 familial cases from 3 multiplex families) for the presence of the HLA DQB1-0602 and DQA1-0102 (DQw1) using a specific polymerase chain reaction (PCR)-oligotyping technique. None of the patients was DQB1-0602 or DQA1-0102 positive, thus proving that, in caucasians, DQB1-0602 and DQA1-0102 (DQw1) are not prerequisites for the diagnosis of narcolepsy. Further studies with more patients are warranted to exclude the possibility that a few caucasian patients carry rare haplotypes with DQB1-0602 independently of DR2.     

Is sleep-disordered breathing an independent risk factor for hypertension in the general population (13,057 subjects)?

Objective: Sleep-disordered breathing has been hypothesized to have a close relationship with hypertension but previous studies have reported mixed results. This is an important health issue that requires further clarification because of the potential impact on the prevention and control of hypertension.Methods: The relationship between hypertension and three forms of sleep-disordered breathing (chronic snoring, breathing pauses and obstructive sleep apnea syndrome (OSAS)) was assessed using representative samples of the non-institutionalized population of the UK, Germany and Italy (159 million inhabitants). The samples were comprised of 13,057 individuals aged 15–100 years who were interviewed about their sleeping habits and their sleep symptoms over the telephone using the Sleep-EVAL system.Results: OSAS was found in 1.9% (95% CI: 1.2% to 2.3%) of the UK sample, 1.8% (95% CI: 1.4% to 2.2%) of the German sample and 1.1% (95% CI: 0.8% to 1.4%) of the Italian sample. OSAS was an independent risk factor (odds ratio (OR): 9.7) for hypertension after controlling for possible confounding effects of age, gender, obesity, smoking, alcohol consumption, life stress, and, heart and renal disease.Conclusions: Results from three of the most populated countries in Western Europe indicate that OSAS is an independent risk factor for hypertension. Snoring and breathing pauses during sleep appeared to be non-significant predictive factors.     

Aging,respiratory efforts during sleep,and pulsus paradoxus

Forty patients with either obstructive sleep apnea syndrome or a clinical complaint of daytime sleepiness with measured nocturnal increase in upper airway resistance and snoring were investigated during sleep for the presence of pulsus paradoxus, which is defined as a decrease in systolic blood pressure (SBP) of at least 10 mmHg during inspiration. Two thirds of the subjects presented pulsus paradoxus. Age, lowest oxygen saturation (SaO₂), and negative inspiratory esophageal pressure nadir (an index of inspiratory effort) were the only studied variables which could statistically dissociate patients presenting pulsus paradoxus. We then divided the patient population into three different subgroups of equal number based upon the degree of decrease in SBP (i.e., >20 mmHg, <20 but >10 mmHg, and <10 mmHg). In this second analysis, age was the only significant variable that separated the three groups. Lowest SaO₂ could not be used to statistically separate subjects with mild to moderate pulsus paradoxus from those without it; and negative inspiratory esophageal pressure measurements could only significantly identify subjects with severe pulsus paradoxus (i.e., >20 mmHg) from those without any pulsus paradoxus. The variable which correlated best with age was negative inspiratory esophageal pressure nadir (R = 0.83). Our interpretation is that as age increased, negative inspiratory esophagel pressure became less negative, due to the known impact of aging on muscles, and pulsus paradoxus was no longer observed. Offprint requests to: C. Guilleminault     

Abnormalities of pulmonary artery wedge pressures in sleep-induced apnea

Six patients with sleep apnea syndrome were studied with continuous hemodynamic monitoring during sleep. Sleep apnea had been previously documented with an average number of apneas per hour of sleep ranging from 23 to 93 (mean 63). There was a significant decrease in heart rate during sleep (82 ± 5 to 69 ± 6, P < 0.01). There was a significant rise in systemic blood pressure (103 ± 2 mm Hg to 116 ± 6 mm Hg, P < 0.05) and pulmonary artery pressure (20 ± 1 mm Hg to 32 ± 5 mm Hg) during sleep. In addition, pulmonary artery wedge pressure increased (12 ± 2 mm Hg to 20 ± 3 mm Hg, P < 0.05) during sleep and 5 of the 6 patients developed an abnormal pulmonary wedge pressure. There was a significant decrease in P_O2 during sleep (71 ± 3 mm Hg to 49 ± 2 mm Hg, P < 0.005). These findings suggest that increases in pulmonary wedge pressures may be contributing to increase in pulmonary artery pressures in these patients during sleep.