Morning headache in sleep apnoea: clinical and polysomnographic evaluation and response to nasal continuous positive airway pressure.

Morning headache is accepted as part of clinical findings of obstructive sleep apnoea syndrome (OSAS). The prevalence of morning headache is at variable levels from 18% to 74% in patients with OSAS. However, there is controversy over the association of morning headache and OSAS. We studied morning headache prevalence and characteristics in 101 controls with apnoea-hypnoea index (AHI) < 5 and 462 OSAS patients with AHI > or = 5. Morning headache was reported by only nine (8.9%) subjects in a control group compared with 156 (33.6%) of OSAS patients (P < 0.01). Morning headache prevalence was significantly higher in severe and moderate OSAS groups. AHI was significantly higher in OSAS patients with morning headache compared with patients without morning headaches. Oxygen saturation nadir during rapid eye movement and non-rapid eye movement sleep as well as mean oxygen saturation value during total sleep time were also found to be significantly lower in morning headache group. However, none of the sleep parameters was found to be determinants of morning headache. Morning headache was more frequently reported by patients of female gender and with primary headache history. Morning headache was totally resolved in 90% of patients treated with nasal continuous positive airway pressure. The history of OSAS should be considered in the differential diagnosis of morning headache.

Fatigue and sleep disturbance in multiple sclerosis.

Considering the association of sleep disturbance and fatigue in multiple sclerosis (MS), we investigated the presence of sleep disturbances that may be related to fatigue by using objective and subjective measures. We included 27 MS patients with fatigue, 10 MS patients without fatigue and 13 controls. The Pittsburgh sleep quality index score showed significant differences between patient groups and controls. Beck depression inventory scores were significantly higher in fatigued than non-fatigued patients. Comparison of patient groups and controls revealed significant differences for time in bed, sleep efficiency index, sleep continuity index, wake time after sleep onset, total arousal index and periodic limb movement arousal index. Our study confirms that MS causes sleep fragmentation in terms of both macro and microstructure. Fatigue in MS could be partially explained by disruption of sleep microstructure, poor subjective sleep quality and depression.

Sleep and sleepiness in patients with Parkinson's disease before and after dopaminergic treatment.

Sleep disturbances and daytime sleepiness are well-known phenomena in Parkinson's disease (PD). Fifteen previously untreated PD patients underwent clinical evaluation, subjective sleep evaluation and polysomnographic evaluation (PSG) before and after a treatment period of mean 8+/-3.1 months with dopaminergic drugs. Both mean Unified Parkinson's Disease Rating Scale (UPDRS) total score and mean subset III of the UPDRS were significantly improved with dopaminergic treatment. PSG revealed that administration of dopaminergic drugs resulted in significant increase in mean percentage of stages 1 and 2. The mean Epworth Sleepiness Scale (ESS) score was significantly increased and mean Multiple Sleep Latency Test (MSLT) score was significantly decreased after dopaminergic treatment indicating subjective and objective daytime sleepiness. The differences in MSLT scores were best explained by a higher dose of L-dopa, whereas other variables such as disease duration, treatment duration, Hoehn and Yahr stage, sleep efficiency index or dopamine agonists did not increase the significance. In contrast, any of the variables appeared to explain ESS score variability. This study demonstrates that daytime sleepiness is not present in untreated patients but emerges later during dopaminergic treatment. Total daily L-dopa dose is predictive of objective daytime sleepiness. Furthermore, subjective assessment of sleepiness may cause underestimation of the severity of daytime sleepiness.

Is there a link between the severity of sleep-disordered breathing and atherosclerotic disease of the carotid arteries?

Epidemiological studies have shown a strong association between sleep-disordered breathing (SDB) and cerebrovascular diseases. A total of 114 male patients, aged 40-65 years, referred to sleep laboratory for the evaluation of snoring and disturbed sleep were studied. Subjects were divided into three groups: habitual snoring, mild-moderate and severe obstructive sleep apnea syndrome (OSAS), respectively, determined by using three respiratory disturbance index (RDI) cut points (/=30). Measurement of intima-media thickness (IMT) and the presence of plaque were determined by ultrasonographic evaluation. Major vascular risk factors such as hypertension, diabetes, smoking, hyperlipidemia, and obesity were determined. The OSA groups had significantly higher IMT values compared with the habitual snoring group. Three groups were significantly different with regard to the presence of plaque. Age and body mass index were found to be significantly associated with IMT while age and RDI were found to be most probably predictive for plaque. There were no significant differences amongst the three groups with respect to age, prevalence of hypertension and diabetes, smoking, total cholesterol and total triglyceride levels. These findings suggested that SDB is a predisposing factor for the atherosclerotic process and precipitate plaque particularly when associated with higher RDI.

The role of mean inspiratory effort on daytime sleepiness.

This study has investigated the role of average maximum inspiratory effort in excessive daytime sleepiness in patients with obstructive sleep apnoea syndrome (OSAS) and upper airway resistance syndrome (UARS). Fifteen patients diagnosed with UARS and 32 patients with OSAS, with >5.5 h total sleep time (TST) during 8 h of nocturnal polygraphic recordings, were included in the study. Demographical data, polysomnographical data and data about daytime sleepiness, including Epworth sleepiness scale (ESS) and multiple sleep latency test (MSLT), were evaluated. In order to compute the average maximum inspiratory effort from oesophageal pressure (Poes) measurements, maximum Poes was obtained from 20 representative obstructive respiratory events (obstructive apnoeas, hypopnoeas or flow limitations) for each sleep stage in both supine and side positions. From Poes measurements during sleep, the increase in Poes (deltaPoes) during respiratory events was also calculated. The average maximum Poes, deltaPoes, respiratory disturbance index (RDI) and arousal index were significantly correlated with ESS in OSAS patients. In patients with UARS, the only significant correlation was obtained between average maximum Poes and ESS. The MSLT score did not show any significant correlation with arousal index, number of stage variations, RDI, average Poes, deltaPoes, minimum oxygen saturation (Sa,O2) and percentage of TST with an Sa,O2 <90% in both UARS and OSAS patients. The results of multiple regression analysis showed that average maximum Poes correlates best with the variance in ESS for OSAS patients. In conclusion, the data from this study indicate the possible important role of average inspiratory effort in determining subjective sleepiness in both obstructive sleep apnoea syndrome and upper airway resistance syndrome patients.

Effects of 48 hours sleep deprivation on human immune profile.

It is a common belief that sleep deprivation increases the susceptibility to diseases. In order to evaluate the effects of sleep deprivation on immune profile in humans, peripheral venous blood was obtained from sixteen healthy young male volunteers. Ten of the volunteers underwent 48 hours of sleep deprivation and the other six maintained their regular sleep schedule and acted as controls. The first blood samples were taken at the end of the first polysomnographic recording at 8:00 a.m. After this sampling, ten subjects were sleep deprived for 48 hours in sedentary conditions. The second and third blood samples were taken at the 24th and 48th hours. The subjects were recorded again to verify rebound effects of sleep deprivation after the third blood sampling. In this second polysomnographic recording, all sleep-deprived subjects showed slow wave and REM sleep rebound. The last blood samples were taken at the 72nd hour of study at 8:00 a.m. CD4, CD8, CD5, CD16, CD19 surface antigen positive lymphocyte subsets, serum IgG, IgM, and cortisol levels were assessed in all samples. Our results showed that the proportion of NK cells were decreased during sleep deprivation and returned to normal values after recovery sleep. In the control group, we did not observe any changes in the same direction as the sleep-deprived group.