Narcolepsy might be a particular interesting clinical model to investigate the interaction of sleep and metabolism, because this rare sleep disorder involves central deficiency of orexins, known to be essential in sleep regulation and regulation of food intake and body weight. Moreover, obesity is a well-known feature of narcolepsy and reports suggest an increased incidence of type-II-diabetes. 82 patients of the German Narcolepsy Society were included. Blood glucose, HbA1c, cholesterol, LDL, HDL, triglyceride, uric acid, lipoprotein A and homocysteine levels were assessed in the morning. Anthropometric data were collected. To date, narcolepsy was confirmed in 62 patients (41F: 42±16y, BMI 29.3±7kg/m2; 21M: 49±16y, BMI 30.4±5kg/m2). Abnormal HDL levels were found in 16 patients (25.8%; mean±SD 58±17mg/dl). Parameter for homocysteine (10.4±3.3µmol/l), triglyceride (148±141mg/dl) and glucose (94±16mg/dl) in 14 patients (22.6%), LPA in 12 patients (19.4%, 21.6±32mg/dl), uric acid in 11 patients (17.7%, 5.1±1.4mg/dl), LDL in 9 patients (14.5%, 122±35mg/dl), cholesterol (199±40mg/dl) and HbA1c (5.4±0.5mg/dl) in 5 patients (8.1%) were also found to be abnormal. 21 patients (33.9%, 9F,12M) met the criteria for the metabolic syndrome as defined by the IDF. Our results suggest a high prevalence of individual metabolic abnormalities and the metabolic syndrome in narcoleptic patients. To clarify the clinical relevance, a comparison with a large non-narcoleptic population is planned.
Pregnant women have an increased risk of experiencing restless legs syndrome (RLS). Aim of this study was to elucidate the relationship between pregnancy-related hormonal and metabolic changes and RLS symptomatology.Blood measurements and overnight polysomnography were performed during the third trimester of pregnancy and again 3 months after delivery. We investigated blood hormonal levels (estradiol, prolactin, progesterone, testosterone, follicle-stimulating hormone [FSH], luteinizing hormone [LH], iron, ferritin, hemoglobin) and polysomnographic sleep parameters. Subjective sleep quality and RLS symptoms were evaluated using the Pittsburgh Sleep Quality Index (PSQI) and the International RLS study group (IRLSSG) rating scale.Sleep laboratory.Ten pregnant women fulfilling the IRLSSG criteria for RLS diagnosis and 9 pregnant healthy controls underwent the protocol.N/A.Women with RLS showed higher levels of estradiol during pregnancy compared to controls (34,211 +/- 6397 pg/mL vs. 25,475 +/- 7990 pg/mL, P<0.05). Patients also showed more periodic limb movements (PLMs) before and after delivery, particularly during sleep stage 1 and wakefulness (P<0.05). PLMs decreased postpartum in subjects with RLS only (P<0.05); sleep efficiency increased in women without RLS and remained unchanged in patients (P<0.05). No significant differences were found between groups before or after delivery in plasma concentrations of prolactin, progesterone, testosterone, FSH, LH, iron, ferritin or hemoglobin.RLS in pregnant women goes along with transiently increased estradiol levels and PLM indices suggesting that estrogens play a pathophysiological role for triggering RLS symptoms during pregnancy.
Obesity is a common feature of narcolepsy. In addition, an increased occurrence of non-insulin dependent diabetes has been reported. So far, it is not known whether glucose metabolism in narcolepsy is disturbed due to, or independently of obesity.Case-control study.Sleep medicine clinic at a research institute.We studied 17 patients with narcolepsy/cataplexy compared to 17 healthy controls matched for age, sex, and body mass index (BMI).A 75-g oral glucose tolerance test was performed.Glucose tolerance was determined by computing plasma glucose curve following oral glucose challenge for 240 minutes; insulin sensitivity and insulin secretion by homeostasis model assessment and minimal model analysis.Standard outcome measures and indices of the oral glucose tolerance test did not differ between the patient group and the group of control subjects.In this study, no clinically relevant pathologic findings in the glucose metabolism of narcoleptic patients compared to weight matched controls were found. Thus, narcolepsy is unlikely to be a risk factor per se for impaired glucose tolerance or diabetes.
The neural mechanisms of panic disorder (PD) are only incompletely understood. Higher sensitivity of patients to unspecific fear cues and similarities to conditioned fear suggest involvement of lower limbic and brainstem structures. We investigated if emotion perception is altered in remitted PD as a trait feature.We used blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging (fMRI) to study neural and behavioural responses of 18 remitted PD patients and 18 healthy subjects to the emotional conflict paradigm that is based on the presentation of emotionally congruent and incongruent face/word pairs. We observed that patients showed stronger behavioural interference and lower adaptation to interference conflict. Overall performance in patients was slower but not less accurate. In the context of preceding congruence, stronger dorsal anterior cingulate cortex (dACC) activation during conflict detection was found in patients. In the context of preceding incongruence, controls expanded dACC activity and succeeded in reducing behavioural interference. In contrast, patients demonstrated a dropout of dACC and dorsomedial prefrontal cortex (dmPFC) recruitment but activation of the lower limbic areas (including right amygdala) and brainstem.This study provides evidence that stimulus order in the presentation of emotional stimuli has a markedly larger influence on the brain's response in remitted PD than in controls, leading to abnormal responses of the dACC/dmPFC and lower limbic structures (including the amygdala) and brainstem. Processing of non-panic related emotional stimuli is disturbed in PD patients despite clinical remission.
To study the brain’s activity during sleep, functional MRI in combination with simultaneous polysomnographic recordings has been used in the last decade as a combination of methods with high spatial and temporal resolution. Recent data analysis tools have opened a window to determine cerebral functional networking in task-free fMRI data, ideally suited for an application in sleeping subjects. Data are discussed which are derived from complementary analyses. We describe how reorganization of functional cerebral communication may further our understanding of phenomena like fading of consciousness during sleep, and how information reprocessing during sleep may be linked to global flow of information in light sleep and more local reprocessing in deep sleep.
Recent studies have focused on the interaction between sleep regulation and metabolism, owing to the important role of the orexin system in sleep regulation and pathophysiology of narcolepsy. To address this issue we performed glucose tolerance tests in narcoleptic patients. We have examined 7 male and 2 female patients with narcolepsy and cataplexy (mean age 34.4±10.8y; mean BMI 25.8±3.2kg/m2) and 9 healthy controls matched for sex, age and BMI. Blood glucose, insulin, HbA1c, cortisol, ACTH, cholesterol, triglyceride levels were assessed. At 0800h the subjects were offered either a 75g/300ml glucose or a similar sorbitol sweetened drink, followed by drawing blood samples for glucose at 0, 30, 60, 120, 180, 240min. 4 of the 9 narcoleptic but no healthy subjects had a 120min blood glucose level above 140mg/dl indicating a pathological glucose tolerance. The AUC for the glucose condition was significantly higher in patients suffering from narcolepsy than in healthy controls (28248.3 vs. 25676.7min·mg/dl; t[8]=2.662; p=0.029; effects size d=0.8). The percentage of HbA1c was found to be significant higher in narcoleptic patients than in controls (5.41% vs. 5.01%, t[8]=2.353; p=0.049; effects size d=0.7), however the other metabolic and endocrine parameters did not differ between the groups. The glucose tolerance in narcoleptic patients is impaired. HbA1c shows a slight but significant increase in that group. Disturbed glucose metabolism might be a genuine feature of narcolepsy.
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