Rem sleep brady-arrhythmias: an indication to pacemaker implantation?

OBJECTIVES: Important adjustments in the autonomic nervous system occur during sleep. Bradycardia, due to increased vagal tone, and hypotension, caused by reduction of sympathetic activity, may occur during non rapid eye movement (REM) sleep (NREM). Increased sympathetic activity, causing increased heart rate, is conversely a feature of phasic REM sleep. During REM sleep, sinus arrests and atrioventricular (AV) blocks unrelated to apnea or hypopnea have been described. These arrhythmias are very rare and only a few cases have been reported in the literature. PATIENTS/METHODS: Following an ECG performed for other reasons, two patients with no history of sleep complaints nor symptoms of heart failure or heart attack were referred to our center for nocturnal brady-arrhythmias. RESULTS: 24h ECG Holter recorded several episodes of brady-arrhythmia with sinus arrest in the first patients and brady-arrhythmias with complete AV block in the second patient. In both patients, episodes of brady-arrhythmia were prevalent in the second part of the night. Nocturnal polysomnography (PSG) demonstrated that episodes occurred only during REM sleep, particularly during phasic events. Treatment with pacemaker was considered only for the patient with complete AV blocks. CONCLUSIONS: These types of brady-arrhythmias are usually detected accidentally due to their lack of symptoms. It has been suggested that in some patients they may lead to sudden unexpected death. Thus, the identification of predisposing factors is mandatory in order to prevent potentially dangerous arrhythmic events.

Prevalence of 'poor sleep' among patients with multiple sclerosis: an independent predictor of mental and physical status.

BACKGROUND: Patients with multiple sclerosis (MS) report sleep disturbances more frequently than the general population. Besides specific sleep disturbances, many other conditions could impair nocturnal rest in this population. In addition, information regarding the role of disrupted sleep on quality of life (QoL) in MS patients is lacking. This study was performed to bridge this gap. METHODS: A total of 120 patients with MS were enrolled into the study. Demographic, socioeconomic and clinical characteristics (clinical course and duration of MS, EDSS score, therapeutic information, presence of pain, presence of sexual and/or bladder dysfunction, localization of demyelinating plaques, and presence of anxiety and depression) were collected. The Pittsburgh Sleep Quality Index (PSQI), the Charlson Comorbidity Index (CCI) and the Italian version of the 36-item Short Form (SF-36) were used to assess quality of sleep, comorbidity and QoL, respectively. RESULTS: Nearly half (47.5%) of MS patients were classified as "poor sleepers," having significantly higher EDSS (3.1+/-1.4 vs. 2.3+/-1.4, p=0.009) and CCI scores (0.19+/-0.4 vs. 0.03+/-0.2, p=0.009) than "good sleepers." In addition, pain due to MS was more common among "poor sleepers" (33.3% vs. 17.7%, p=0.05). Scores for each domain of the SF-36, and the mental component summary (MCS) and physical component summary (PCS) scores were significantly lower in poor sleepers than in good sleepers (p<0.001 for each score). Of the different variables associated with MCS, the only independent predictors of mental status were: presence of sexual and/or bladder dysfunction and global PSQI score. The independent predictors for physical status (PCS) were age, EDSS score and global PSQI score. CONCLUSIONS: Poor sleep is common in patients with MS, representing an independent predictor of QoL. Patients with MS who are poor sleepers should receive immediate assessment and treatment, bearing in mind that, in addition to specific sleep disturbances, other clinical conditions (both related and unrelated to MS) can disrupt nocturnal sleep.

Sleep disturbances in elderly: a subjective evaluation over 65.

Sleep in elderly people shows progressive changes caused by general aging processes. Several alterations are described in medical literature: changes of sleep/wake rhythm and modifications both in sleep duration and in sleep architecture. The aim of our study was to evaluate sleep disturbances in elderly people, with and without cognitive impairment,through a sleep questionnaire. Our population included 1000 subjects, over 65 years of age, stratified by sex and age. The first 600 interviews were included in this report. All patients underwent a mini mental state examination (MMSE) and a questionnaire concerning excessive daytime sleepiness. In our total sample, we found a high prevalence of excessive daytime sleepiness, insomnia, nighttime awakenings, snoring, restlessness and periodic leg movements during sleep. Patients with cognitive dysfunctions showed less difficulty in falling asleep and fewer nighttime awakenings; they snored less frequently and were the only ones to present enuresis and to fall off the bed. Moreover, patients with cognitive impairment presented excessive daytime sleepiness with variable intensity and frequency. In conclusion, our results indicate significant differences in sleep disorders between healthy subjects and patients cognitively impaired. Besides, our subjective evaluation seems to be a useful method to perform an assessment of sleep disturbances in elderly people.

Sleep and sleep deprivation as EEG activating methods.

OBJECTIVES: We examined retrospectively 19 patients with a history of clinical seizures, but normal activity or unclear epileptiform abnormalities in wake EEG recordings and obtained preliminary data for a controlled cohort study to evaluate the effects of sleep deprivation (SD) on interictal epileptic activity. METHODS: Nineteen patients referred to our EEG department for diagnostic or follow-up purposes were divided in two groups on the basis of the different EEG protocols applied. The first group (n=5) underwent two laboratory polysomnographies during afternoon naps, after SD, but the patients failed to fall asleep in one of the two occasions. The second group (n=14) was submitted to two polysomnographies, the first without SD and the second after SD. RESULTS: The first group of patients demonstrated focal epileptic discharges in 4 patients in which wake after SD appeared to be less activated that sleep after SD. In the second group the results obtained from the waking part of the recordings suggest a lack of activating effect due to SD. CONCLUSIONS: SD does not seem to offer greater activation than sleep alone. However, a mild SD may be a convenient activating method for inducing sleep and drowsiness without using any drug.

Respiratory disorders during sleep in patients with epilepsy: effect of ventilatory therapy on EEG interictal epileptiform discharges.

OBJECTIVE: Sleep disorders are common and may coexist with a variety of diseases, including epilepsy, with important implications for the clinical management of the latter. Sleep fragmentation and deprivation, and hypoxia associated to sleep disordered breathing (SDB) may contribute to the occurrence of seizures. On the other hand, antiepileptic drugs may worsen SDB by reducing the muscle tone of the upper airways, and increasing the arousal threshold. There is evidence indicating that treatment of the SDB can reduce both frequency and intensity of seizures. This study aimed at further understanding the relationship between SDB and epilepsy, particularly the influence of SDB on epileptogenicity - as evaluated by a quantitative analysis of interictal epileptogenic activity. METHODS: Eight consecutive patients affected by partial epilepsy associated to SDB (OSAS or an association between chronic obstructive pulmonary disease-- COPD - and snoring) underwent two nocturnal polysomnographies (PSG)-- before and after ventilatory therapy with CPAP (in 6 patients with OSAS) or oxygen (in two patients with COPD and snoring). Spiking was quantified during the first sleep cycle in both PSG studies, and spiking rates were calculated both for the entire sleep cycle and for each separate sleep phase (NREM 1, NREM 2, NREM 3-4, REM and wake time after sleep onset - WASO). RESULTS: In all patients, the improvement of the SDB after ventilatory treatment--as demonstrated by a reduction of the respiratory disturbances index (RDI) - was associated to a reduction of spiking rates, both in the entire cycle and in relationship to slow wave sleep. This reduction was particularly marked in patients with higher spiking rates in baseline conditions. CONCLUSION: Our data show that SDB treatment reduces the interictal epileptogenic activity, suggesting that SDB plays a role in increasing epileptogenicity. Further studies will be necessary to clarify the mechanisms whereby this reduction in epileptogenicity occurs, although improved sleep stability seems to play an important role. The presence of an underlying SDB in patients with refractory epilepsy should be investigated.

Analysis of cystic intracranial lesions performed with fluid-attenuated inversion recovery MR imaging.

BACKGROUND AND PURPOSE: T1-, T2-, and proton density (PD)-weighted sequences are used to characterize the content of cystic intracranial lesions. Fluid-attenuated inversion recovery (FLAIR) MR sequences produce T2-weighted images with water signal saturation. Therefore, we attempted to verify whether FLAIR, as compared with conventional techniques, improves the distinction between intracranial cysts with a free water-like content versus those filled with a non-free water-like substance and, consequently, aids in the identification of these lesions as either neoplastic/inflammatory or maldevelopmental/porencephalic. METHODS: Forty-five cystic intracranial lesions were studied using T1-weighted, T2-weighted, FLAIR, and PD-weighted sequences. By means of clustering analysis of the ratio in signal intensity between the cystic intracranial lesions and CSF, the intracranial lesions were classified as filled with a free water-like content or with a non-free water-like substance. The results were compared with their true content as evaluated either histologically or on the basis of clinical, neuroradiologic, and follow-up features (necrotic material, 13 cases; accumulation of intercellular proteinaceous/myxoid material, eight cases; keratin, five cases; CSF, 19 cases). Cystic intracranial lesions were divided into two clinical groups, neoplastic/inflammatory and maldevelopmental/porencephalic, to evaluate the level of accuracy of each MR technique. The difference in absolute value signal intensity between CSF and cystic intracranial lesion content was calculated on FLAIR and PD-weighted images. RESULTS: PD-weighted and FLAIR sequences, unlike T1- and T2-weighted sequences, accurately depicted all cystic intracranial lesions containing necrotic or myxoid/proteinaceous intercellular material (non-free water-like) and most CSF-containing cystic intracranial lesions (free water-like). All imaging techniques inaccurately showed some of the keratin-containing cystic intracranial lesions and pineal cysts. The overall error rate was 22% for T1-weighted, 27% for T2-weighted, 9% for FLAIR, and 13% for PD-weighted sequences. The signal intensity difference between CSF and cystic intracranial lesion content was higher with FLAIR imaging. CONCLUSIONS: FLAIR imaging depicts far more accurately the content of cystic intracranial lesions and better reveals the distinction between maldevelopmental/porencephalic and neoplastic/inflammatory lesions than do conventional sequences. FLAIR has the added advantage of a higher signal intensity difference between cystic intracranial lesions and CSF.