64 research outputs found

    Evaluation of postural balance in patients with obstructive sleep apnoea syndrome

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    Introduction. Patients with obstructive sleep apnoea syndrome (OSAS) can be more prone to accidents due to excessive daytime sleepiness which can lead to attention deficits and thereby cause balance problems. One of the tests evaluating postural balance is static posturography (SPG). In this study, we aimed to evaluate postural balance with SPG in OSAS patients.Methods. Patients who were referred to a sleep disorders outpatient clinic of a tertiary health care centre with snoring, daytime sleepiness or witnessed apnoea were enrolled consecutively in this cross-sectional study. They were grouped as the OSAS group and the control group according to the apnoea-hypopnoea index. Posturographic analyses were carried out in all subjects on a SPG platform under five different conditions: eyes open (EO), eyes closed (EC), head rotated to left (HL), head rotated to right (HR), and tandem Romberg.Results. A total of 95 patients and 23 controls were included in the study. In EO conditions, there was no difference between the OSAS group and the control group in any of the posturographic parameters. In EC conditions, change in lateral sway was significantly higher in the OSAS group which also correlated negatively with SaO2(min). HR conditions caused an i ncrease in anterior-posterior (A-P) sway velocity, and HL conditions led to an increase in change in lateral and A-P sways, sway area, and sway area velocity in the OSAS group.Conclusions. Our findings suggest that postural balance in OSAS patients is impaired even in the very first hours of the day, and that the severity of the disease has an impact on postural balance

    Early left ventricular functional alterations in patients with obstructive sleep apnea syndrome

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    Background: The knowledge regarding myocardial alterations in patients with obstructive sleep apnea syndrome (OSAS) in the absence of any known cardiovascular disorders including hypertension is limited. The aim of this study was to assess the early alterations of left ventricular (LV) functions caused by OSAS before the development of hypertension and other cardiovascular manifestations of OSAS.Methods: Eighty consecutive patients who underwent polysomnography (PSG) were enrolled in the study. Patients with hypertension, diabetes mellitus or any other known cardiac diseases were excluded from the study. Subjects were separated into two groups by their apnea/hypopnea index (AHI) (group 1: AHI < 15, and group 2: AHI ≥ 15). Fourty-three patients with normal polysomnographic examination or mild OSAS (group 1) and 37 patients with moderate to severe OSAS (group 2) were compared. After PSG examination, LV functions were assessed by using the conventional and tissue Doppler echocardiographic methods.Results: The mean age was similar between the groups. The ratio of male patients was higher in group 2 (male/female: 31/12 in group 1 vs. 34/3 in group 2, p = 0.04). Body mass index was higher in group 2 (p = 0.05). Conventional echocardiography showed that interventricular septum thickness was 9.5 ± 1.1 mm in group 1, and 10.5 ± 1.4 mm in group 2 (p = 0.02). Mean left atrial diameter was 35.6 ± 4.1 mm in group 2, and 33.8 ± 3.1 mm in group 1 (p = 0.04). Ratio of early to late transmitral diastolic velocities was lower in group 2 (p = 0.01), indicating that impairment of diastolic function was more frequent in moderate to severe OSAS patients. Tissue Doppler echocardiography showed that early diastolic myocardial velocity was lower ingroup 2 (21.1 ± 5.6 cm/s in group 1 vs. 18.3 ± 5.3 cm/s in group 2, p = 0.01).Conclusions: Left ventricular diastolic dysfunction, LV hypertrophy and left atrial dilatationoccur in patients with OSAS even before the development of hypertension and other cardiovascular diseases

    Shift Work and Shift Work Sleep Disorders: Definition, Symptoms and Treatment

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    Today, due to the rapid progress of the global industrial economy, the use of new technologies and the economic competition environment, the necessity of 24 hour interrupted job production has increased and this has caused the obligation to work with the shift system. Approximately 20% of the population is working on shifts and turns apart from the standard working hours. While the shift system has many positive effects on work and manufacture life, it also has negative effects on the life quality of employees and it brings many comorbid health and sleep problems. Shift work sleep disorder is categorized as a subgroup of circadian rhythm sleep disorders family. The primary symptoms of shift work sleep disorder are insomnia and excessive daytime sleepiness. The goal of shift work sleep disorder treatment is to improve the quality of life and work efficiency while improving the current symptoms related to sleep disturbances, and to minimize accidents by increasing attention and alertness. The goal of this review is to determine the clinical findings, diagnostic criteria, systemic outcomes, and treatment methods of shift work sleep disorder and the associated sleep disorders

    Chronic Intermittent Hypoxemia in Patients with Obstuctive Sleep Apnea Syndrome Causes Reduction of Peripheral Nerve Motor Fibers (Unit Number)

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    Objective:Obstructive Sleep Apnea syndrome (OSAS) is a chronic intermittent hypoxic process. In this study, we aimed to investigate electrophysiologically the changes in number of skeletal muscle motor unit due to chronic intermittent hypoxemia in cases followed up with the diagnosis of OSAS.Materials and Methods:According to the apnea-hypopnea index (AHI), patients divided into two groups (group 1: AHI 0.5). Maximum M mean area of nerve medianus was 50.8±20.4 (16.1-121.7) in group 1 and 48.6±20.05 (10.5-111.4) in group 2 (p=0.55). The mean MUNE values were 155.3±41.17 (46.6- 251.7) in group 1 and 127.7±40.2 (22.8-235) in group 2 (p<0.00).Conclusion:The MUNE method demonstrates that chronic intermittent hypoxemia during sleep causes reduction of the motor unit number in OSAS patients and is an independent risk factor for subclinical polyneuropathy

    The Role of Cardiac Repolarization Index for Sudden Cardiac Death Risk in Patients with Obstructive Sleep Apnea Syndrome without any Systemic Disesae

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    Introduction: Obstructive sleep apnea syndrome (OSAS) is associated with sudden cardiac death (SCD). In this study we aimed to evaluate the ventricular recovery time in OSAS patients without chronic systemic diseases, such as hypertension, diabetes, thyroid dysfunction, electrolyte imbalance, cardiac disease and the relationship of OSAS with SCD. Materials and Methods: In the study, between January 2008-January 2010, we analyzed 170 patientswith a mean age of 44.45±10.1 (21-75) years, who were clinically suspected of having OSAS. Following overnight polysomnography (PSG), 12 lead surface electrocardiogram (ECG), recordings were perforned and QT minimum, QT maximum and QT dispersion were computed from ECG. Results: The patients were divided into to the following 4 groups; AHI (apnea-hypopnea index) ≤5, 5< AHI ≤15, 15< AHI <30, and AHI ≥30. The mean QTD was 3.8±2 (0.40-9.7) msn in all patients and 3.5±1.8 (0.6-8.9) msn in normal group (AHI ≤5), and 4.5±1.9 (0.4-9.7) msn in severe group (AHI ≥30). It is shown that QTD increases significanty when AHI rises. Discussion: We showed that the patients with OSAS without chronic systemic disorder have higher SCD risks due to increased QT dispersion

    Loss-of-function variants in the KCNQ5 gene are implicated in genetic generalized epilepsies

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    Summary Background De novo missense variants in KCNQ5, encoding the voltage-gated K+ channel KV7.5, have been described to cause developmental and epileptic encephalopathy (DEE) or intellectual disability (ID). We set out to identify disease-related KCNQ5 variants in genetic generalized epilepsy (GGE) and their underlying mechanisms. Methods 1292 families with GGE were studied by next-generation sequencing. Whole-cell patch-clamp recordings, biotinylation and phospholipid overlay assays were performed in mammalian cells combined with homology modelling. Findings We identified three deleterious heterozygous missense variants, one truncation and one splice site alteration in five independent families with GGE with predominant absence seizures; two variants were also associated with mild to moderate ID. All missense variants displayed a strongly decreased current density indicating a loss-of-function (LOF). When mutant channels were co-expressed with wild-type (WT) KV7.5 or KV7.5 and KV7.3 channels, three variants also revealed a significant dominant-negative effect on WT channels. Other gating parameters were unchanged. Biotinylation assays indicated a normal surface expression of the variants. The R359C variant altered PI(4,5)P2-interaction. Interpretation Our study identified deleterious KCNQ5 variants in GGE, partially combined with mild to moderate ID. The disease mechanism is a LOF partially with dominant-negative effects through functional deficits. LOF of KV7.5 channels will reduce the M-current, likely resulting in increased excitability of KV7.5-expressing neurons. Further studies on network level are necessary to understand which circuits are affected and how this induces generalized seizures. Funding DFG/FNR Research Unit FOR-2715 (Germany/Luxemburg), BMBF rare disease network Treat-ION (Germany), foundation ‘no epilep’ (Germany)

    Diagnosis of comorbid migraine without aura in patients with idiopathic/genetic epilepsy based on the gray zone approach to the International Classification of Headache Disorders 3 criteria

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    BackgroundMigraine without aura (MwoA) is a very frequent and remarkable comorbidity in patients with idiopathic/genetic epilepsy (I/GE). Frequently in clinical practice, diagnosis of MwoA may be challenging despite the guidance of current diagnostic criteria of the International Classification of Headache Disorders 3 (ICHD-3). In this study, we aimed to disclose the diagnostic gaps in the diagnosis of comorbid MwoA, using a zone concept, in patients with I/GEs with headaches who were diagnosed by an experienced headache expert.MethodsIn this multicenter study including 809 consecutive patients with a diagnosis of I/GE with or without headache, 163 patients who were diagnosed by an experienced headache expert as having a comorbid MwoA were reevaluated. Eligible patients were divided into three subgroups, namely, full diagnosis, zone I, and zone II according to their status of fulfilling the ICHD-3 criteria. A Classification and Regression Tree (CART) analysis was performed to bring out the meaningful predictors when evaluating patients with I/GEs for MwoA comorbidity, using the variables that were significant in the univariate analysis.ResultsLonger headache duration (&lt;4 h) followed by throbbing pain, higher visual analog scale (VAS) scores, increase of pain by physical activity, nausea/vomiting, and photophobia and/or phonophobia are the main distinguishing clinical characteristics of comorbid MwoA in patients with I/GE, for being classified in the full diagnosis group. Despite being not a part of the main ICHD-3 criteria, the presence of associated symptoms mainly osmophobia and also vertigo/dizziness had the distinguishing capability of being classified into zone subgroups. The most common epilepsy syndromes fulfilling full diagnosis criteria (n = 62) in the CART analysis were 48.39% Juvenile myoclonic epilepsy followed by 25.81% epilepsy with generalized tonic-clonic seizures alone.ConclusionLonger headache duration, throbbing pain, increase of pain by physical activity, photophobia and/or phonophobia, presence of vertigo/dizziness, osmophobia, and higher VAS scores are the main supportive associated factors when applying the ICHD-3 criteria for the comorbid MwoA diagnosis in patients with I/GEs. Evaluating these characteristics could be helpful to close the diagnostic gaps in everyday clinical practice and fasten the diagnostic process of comorbid MwoA in patients with I/GEs

    Juvenil myoklonik epilepsilerde;klinik,nörofizyolojik ve nörogörüntüleme yöntemleri

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    TEZ4905Tez (Uzmanlık) -- Çukurova Üniversitesi, Adana, 2004.Kaynakça (s. 62-68) var.68 s. ; 30 cm.
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