28 research outputs found

    The Neuropsychological and Emotional Profile of Adults with Parasomnia: A Case Series

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    Although parasomnias are nocturnal phenomena occurring during sleep or during arousals from sleep, there is increasing evidence that they are associated with daytime dysfunction as well. However, systematic studies in this field are scarce. The aim of the current case series was to investigate the sleep–wake, neuropsychological and emotional profiles of patients with parasomnias. Thirty patients with parasomnia (13 NREM, 17 REM) and 30 healthy subjects matched for age, sex and educational status were included. All participants underwent comprehensive neuropsychological, cognitive and behavioral evaluation. We found that parasomnia patients scored higher in all neuropsychological, emotional, sleep–wake and quality of life scales compared to healthy subjects. The presence of a parasomnia was associated with major impact on daytime functioning across several domains with increased levels of fatigue (FSS > 4) in 56%, sleepiness (ESS > 10) in 47%, depressive symptoms (BDI > 20) in 17%, anxiety (PSWQ > 52) in 17%, anger expression out (STAXI A > 16) in 27% and anger expression in (STAXI B > 16) in 23%, as well as a reduced average quality of life score (RAND derived from SF-36). Sleep–wake disturbances were significantly correlated with QoL scores. In the intergroup analysis between REM/NREM, we found that the REM group had worse cognitive performance and lower levels of fatigue/energy compared to NREM patients. These findings suggest that parasomnia is associated with difficulties in several aspects of daytime functioning (cognitive, affective/emotional and physical) and, therefore, parasomnia diagnostic workup should not be limited only to nocturnal phenomena

    Sleep disorders in myotonic dystrophy

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    Introduction: The aim of this study was to document in detail the sleep disorders in patients with myotonic dystrophy (MD). Material and Method: Thirty-five (14 women, 21 men) consecutive patients with genetically confirmed MD (34 MD1, 1-MD2) were participated. All participants were ambulatory? A detailed history of the disease and a sleep history were obtained. All participants completed the Epworth Sleepiness Scale (ESS) and the Beck Depression Inventory scale. The severity of the disease was assessed with the muscular disability rating scale (MDRS). Blood gases were assessed and patients with hypercapnia were excluded. An overnight polysomnography was followed. Results: Patients mean age was 39±13 years and the mean duration of the disease was 13±9 years. The severity of the disease was mild to moderate in the 94% of the patients and the 6% was asymptomatic. The 57% of the participants were overweighted (BMI >25 kgr/m²). No one had signs of severe depression (BDI 10.4±6.6). The 69% of patients reported symptoms indicative of disordered sleep. The most prevalent complains were difficulty in morning awakening (60%), daytime sleepines (26%) and prolonged sleep periods (26%). The 11.5% reported non refreshing sleep episodes. The PSG revealed fragmented sleep in the 23.7% (>15 arousals/hour) mainly due to apnoea-hypopnoea episodes. The 57% had apnoea-hypopnoea index (AHI)>10/hour mainly due to episodes of apnoea-hypopnoea of obstructive type. Increased AHI was accompanied by reduction of the hypnic period (r=-35) increased stage wake and stage 1 (r=0.36) and decreased stages 2 (r=65) and REM (r=51). Increased BMI and years of disease were associated with increased AHI (r=0.54 and r=0.46 respectively). Patients with AHI>10 had higher BMI (27±4.5) compared to those with AHI25 kgr/m² ΔΣΜ). Κανένας δεν είχε ενδείξεις σοβαρής καταθλιπτικής συνδρομής (BDI 10.4±6.6). Το 69% των ασθενών ανέφερε συμπτώματα ενδεικτικά διαταραχής ύπνου με συχνότερα την δυσχέρεια στην πρωινή έγερση (ΔΠΕ-60%) την υπνηλία την ήμερα (ΥΥΗ 26%) και την παρατεταμένη περίοδο ύπνου (ΠΠΥ-26%). Στο 11.5% η υπνηλία είχε επεισοδιακό μη αναζωογονητικό χαρακτήρα. Το 54.2% παρουσίαζε κατακερματισμένο ύπνο (>15 αφυπνίσεις/ώρα ύπνου) κυρίως λόγω επεισοδίων άπνοιας υπόπνοιας. Το 57% παρουσίαζε παθολογικό δείκτη υπό απνοικών επεισοδίων (AHI) κυρίως αποφρακτικής αιτιολογίας. Η αύξηση του AHI συνοδεύτηκε από ελάττωση της υπνικής περιόδου (r=-0.35), από αύξηση του σταδίου εγρήγορσης και του σταδίου 1 (r=0.36) και ελάττωση των σταδίων 2 (r=-0.65) και REM (r=0.51). Ο AHI ήταν μεγαλύτερος στα υπέρβαρα άτομα (r=0.54) και στα άτομα με περισσότερα έτη νόσου (r=0.46). Τα άτομα με ΑΗΙ>10 είχαν υψηλότερο ΔΣΜ (27±4.5) σε σχέση με αυτά με ΑΗΙ<10 (r=0.016). Η αύξηση του ΔΣΜ συνοδευόταν από αύξηση των εγέρσεων που σχετίζονται με αναπνευστική διαταραχή (r=0.40). Το 50% των ασθενών εμφάνιζε περιοδική αναπνοή και κεντρικές άπνοιες, ιδιαίτερα στα πρώτα σταδία του ύπνου και μετά από έγερση. Τα άτομα με περιοδική αναπνοή ήταν πιο ηλικιωμένα (r=0.011) και παρουσίαζαν μικρότερο ποσοστό σταδίου REM (r=0.045). Συζήτηση-Συμπεράσματα: Η πλειονότητα των ασθενών με ΜΔ1 παρουσιάζει συμπτωματολογία που παραπέμπει σε υπνική διαταραχή. Η συμπτωματολογία ομοιάζει με ιδιοπαθή υπερύπνια με παρατεταμένες περιόδους ύπνου ένδειξη δυσλειτουργίας των κέντρων ύπνου. Παρόλα αυτά η πολυσωματοκαταγραφική μελέτη αναδεικνύει σημαντικά κατακερματισμένο ύπνο εξαιτίας υπό απνοικών επεισοδίων κυρίως αποφρακτικού χαρακτήρα ακόμα και σε ασυμπτωματικούς ασθενείς. Συνυπάρχουν περιοδική αναπνοή και κεντρικές άπνοιες, ένδειξη δυσλειτουργίας των κέντρων της αναπνοής. Η βαρύτητα του κατακερματισμού αυξάνεται με την αύξηση του ΔΣΜ, την ηλικία του ασθενή, τη χρονιότητα της νόσου

    Does nasal decongestion improve obstructive sleep apnea?

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    Whether nasal congestion promotes obstructive sleep apnea is controversial. Therefore, we performed a randomized placebo-controlled cross-over trial on the effects of topical nasal decongestion in patients with obstructive sleep apnea syndrome (OSA) and nasal congestion. Twelve OSA patients with chronic nasal congestion (mean +/- SD age 49.1 +/- 11.1 years, apnea/hypopnea index 32.6 +/- 24.5/h) were treated with nasal xylometazoline or placebo for 1 week each. At the end of treatment periods, polysomnography including monitoring of nasal conductance by an unobtrusive technique, vigilance by the OSLER test, and symptom scores were assessed. Data from xylometazoline and placebo treatments were compared. Mean nocturnal nasal conductance on xylometazoline was significantly higher than on placebo (8.6 +/- 5.3 versus 6.3 +/- 5.8 mL s(-1)Pa(-1), P &lt; 0.05) but the apnea/hypopnea index was similar (29.3 +/- 32.5/h versus 33.2 +/- 32.8/h, P = NS). However, 30-210 min after application of xylometazoline, at the time of the maximal pharmacologic effect, the apnea/hypopnea index was slightly reduced (27.3 +/- 30.5/h versus 33.2 +/- 33.9/h, P &lt; 0.05). Xylometazoline did not alter sleep quality, sleep resistance time (33.6 +/- 8.8 versus 33.4 +/- 10.1 min, P = NS) and subjective sleepiness (Epworth score 10.5 +/- 3.8 versus 11.8 +/- 4.4, P = NS). The reduced apnea/hypopnea index during maximal nasal decongestion by xylometazoline suggests a pathophysiologic link but the efficacy of nasal decongestion was not sufficient to provide a clinically substantial improvement of OSA. ClinicalTrials.gov Identifier is NTC006030474

    Dementia as presenting symptom of primary hyperparathyroidism: Favourable outcome after surgery

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    The case of a 76-year-old female patient is presented with a two-year history of progressive dementia, apathy and gait impairment. Initially, Alzheimer’s disease was diagnosed and she was given donepezil for one year with no significant improvement. An extensive blood and biochemical control revealed high serum calcium and parathormone levels, and normal thyroid hormones and anti-thyroid antibodies. Ultrasound of thyroid and parathyroid glands revealed an adenoma of the right parathyroid. The detailed investigation for causes of secondary hyperparathyroidism was negative. Due to the absence of clinical hyperparathyroidism she was initially treated conservatively. At referral, the neurological picture consisted of. mild signs of parkinsonism, moderate dementia (MMSE = 15) and severe behavioural disturbances. Because of the continuous aggravation of the cognitive deficit, parathyroidectomy was decided although there were no clinical or laboratory signs of involvement from other organs. Three weeks after the operation the neurological picture showed dramatical improvement. Parkinsonism and behavioural disorders were remarkably reduced and the MMSE score raised to 25. In summary we report an exceptional case of primary hyperparathyroidism (PHPT) presenting as dementia and treated successfully by parathyroidectomy. (C) 2008 Elsevier B.V. All rights reserved
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