The objective of this research was to evaluate the effect of an education program using the meaningful learning approach on sleep knowledge and habits of 12th grade students. Thirty-four student volunteers (aged 16.8 ± 0.6 years) were divided into intervention (Sleep Education Program – SEP) and control groups. Sleep knowledge and habits were assessed by the “health and sleep” questionnaire. Also, the students filled out a sleep diary and the Karolinska Sleepiness Scale by one week (Stage 1). These procedures were repeated 3 weeks after the SEP (Stage 2) that was evaluated by a questionnaire. The SEP consisted of five 50-minute classes to discuss the physiological and behavioral processes of sleep and healthy lifestyle. At Stage 2, the intervention group increased the percentage of correct responses in 63% of the questions. On weekdays, they increased time in bed by 26 min, woke up 11 min later and showed a tendency to go to bed 18 min earlier (P = 0.07). On weekends, they advanced bedtime and wake-up times. These changes were associated with decreased irregularity at bedtimes and wake up times. These results were not observed in the control group, except the advance on wake up time on weekends. The frequency and duration of naps and daytime sleepiness levels did not differ between the stages for both groups. The SEP increased knowledge and contributed to positive changes in the adolescents' sleep-wake cycle (SWC). However, daytime sleepiness levels remained unchanged probably due to an insufficient reduction on sleep deprivation to decrease its negative consequences.

Neurobiological mechanisms determining a possibility of parsimonious descriptions of the continuous sleep process as a sequence of a few all-or-nothing variables called “sleep stages” remain unknown. We tested a suggestion that stage 1 sleep (“drowsy sleep”) corresponds to a rapid decay of a wake-promoting process and that the boundary with stages 2 separates this decay from a rapid buildup of a sleep-promoting process. The analyzed dataset included power spectra calculated from the electroencephalographic (EEG) records obtained during attempts of 15 adults to stay permanently awake for 43–61 h and during multiple napping attempts of nine sleep-deprived, nine sleep-restricted, and 11 sleep-unrestricted adults. The time courses of scores on the 1st and 2nd principal components of the EEG spectra reflected the suggested phase relationships between rapid changes in the sleep- and wake-promoting processes, respectively. The 1st principal component score was permanently attenuated during wakefulness and stage 1 sleep but started to build up on the boundary with stage 2. In contrast, the 2nd principal component score started to fall down near the wake-sleep boundary but remained unchanged across stage 2. We concluded that stage 1 sleep corresponds to the decay phase of the wake-promoting process that precedes the buildup phase of the sleep-promoting process during stage 2.

We want to evaluate the effect of sertraline on polysomnogram (PSG) and clinical variables in depression. An 8-week and open-label trial (n = 31) was applied. The primary outcome was mean baseline-to-visit changes in PSG variables. The secondary outcomes were clinical improvement, side-effects, and the subjective sleepiness. Rapid eye movement (REM) latency was prolonged significantly over the course of the study. The arousal index reached the highest level on the 1st day (13.8 ± 7.2). From the 14th day onward, the sleep latency (SL) and wake after sleep onset (WASO) decreased significantly. The percentage of stage 3 sleep increased in this trial. The Hamilton Rating Scale for Depression (HRSD) and Clinical Global Impression (CGI) scores on the 14th, 28th, and 56th days were significantly lower than baseline. Furthermore, a significant correlation was shown between the decreasing score rate of HRSD on the 56th day and the decreasing score rate of REM latency on the 1st day (r = −0.733, P = 0.003). The effectiveness of sertraline positively correlated with the reduction of REM latency. The final clinical improvement could be predicted by the extent of the prolongation of REM latency on the first night.

Rapid eye movement (REM) sleep behavior disorder (RBD) is a parasomnia characterized by the loss of muscle atonia during paradoxical (REM) sleep (PS). The neuronal dysfunctions responsible for RBD are not known. In the present review, we propose an updated integrated model of the mechanisms responsible for PS and explore different hypotheses explaining RBD. We propose that RBD appears based on a specific degeneration of PS-on glutamatergic neurons localized in the caudal pontine sublaterodorsal tegmental nucleus or the glycinergic/GABAergic premotoneurons localized in the medullary ventral gigantocellular reticular nucleus.

Rapid eye movement (REM) sleep behavior disorder (RBD) and hypnagogic hallucinations are salient symptoms of abnormal and dissociated REM sleep that are frequently associated in serious neurological diseases. RBD is a strong, independent risk factor for hallucinations in narcolepsy (odds ratio: 4.3) and in Parkinson's disease (odds ratio: 2.7). In Parkinson's disease, RBD also predicts incident hallucinations and psychosis in prospective cohorts. Status dissociatus (a mixture of hallucinations, RBD, and dissociated sleep–wake states) is observed in patients with Guillain-Barré when hallucinating, but also in Lewy bodies dementia, delirium tremens, fatal familial insomnia, and Morvan's chorea. This co-occurrence of RBD and visual hallucinations suggests a common, extensive lesion within REM sleep executive systems.

Rapid eye movement sleep behavior disorder (RBD) frequently occurs in synucleinopathies including multiple system atrophy, Parkinson's disease, and dementia with Lewy bodies despite the clinical course of RBD being different between these disorders. Comparatively, the existence of RBD symptoms is relatively rare in patients with progressive supranuclear palsy, a tauopathy showing atypical parkinsonism compared with Parkinson's disease. Moreover, in patients with Alzheimer's disease, which is another tauopathy, RBD symptoms are less frequent than dementia with Lewy bodies, although both disorders share commonalities in terms of the existence of cortical dementia. Thus, RBD is thought to be relatively specific to synucleinopathies.

Rapid eye movement sleep behavior disorder (RBD) is a parasomnia characterized by dream enactment behavior during rapid eye movement sleep, which is generally related to damage of pontomedullary structures. Idiopathic RBD is a well-established risk factor for neurodegenerative disease; at least 40–65% of patients with idiopathic RBD will develop a defined neurodegenerative phenotype over 10 years. This is almost always a “synucleinopathy” (Parkinson's disease, dementia with Lewy bodies, or multiple system atrophy). Often, patients develop a syndrome with overlapping parkinsonism and cognitive impairment. The ability of RBD to predict disease has major implications for development of neuroprotective therapy, by providing a high-risk prodromal group for neuroprotective trials. In addition, it allows testing of other predictive markers of neurodegeneration. Recent prospective studies found that idiopathic RBD patients with abnormal olfaction at baseline had a 65% 5-year risk of developing neurodegenerative disease, compared with a 14% risk in those with normal olfaction. Those with abnormal color vision had a 74% risk of neurodegenerative disease compared with 26% in those with normal vision. Additionally, neuroimaging markers of the substantia nigra including dopaminergic functional imaging and transcranial ultrasound have been able to predict imminent development of defined neurodegenerative disease in RBD, although sensitivity and lead time have not been established. Future studies will continue to expand the list of predictive markers of neurodegeneration and will better define specificity, sensitivity, and lead time of prodromal markers.

Rapid eye movement (REM) sleep behavior disorder (RBD) is characterized by dream-enacting behavior and impaired motor inhibition during REM sleep (REM sleep without atonia, RSWA). RBD is commonly associated with Parkinsonian disorders, but is also reported in narcolepsy. Most patients with narcolepsy with cataplexy lack the hypocretin neurons in the lateral hypothalamus. In contrast, RBD, RSWA, and hypocretin deficiency are rare in narcolepsy without cataplexy. Phasic motor activity in REM and non-REM (NREM) and dream-enacting behavior (RBD) coexist with cataplexy in narcolepsy because of hypocretin deficiency. Thus, hypocretin deficiency is linked to the two major disturbances of REM sleep motor regulation in narcolepsy: RBD and cataplexy. Moreover, it is likely that hypocretin deficiency independently predicts periodic limb movements in REM and NREM sleep, probably via involvement of the dopaminergic system. This supports the hypothesis that an impaired hypocretin system causes general instability of motor regulation during wakefulness, REM and NREM sleep in human narcolepsy. We propose that hypocretin neurons are centrally involved in motor tone control during wakefulness and sleep in humans and that hypocretin deficiency causes a functional defect in the motor control involved in the development of cataplexy during wakefulness and RBD/RSWA/phasic motor activity during REM sleep.

Narcolepsy with cataplexy (NC) is caused by the loss of hypothalamic neurons that produce hypocretins (also known as orexins). The hypocretin system plays a crucial role in sleep, wakefulness, and energy homeostasis. Behavioral, anatomical and neurophysiological studies in animals have shown that hypocretins are involved in reward and addictive behaviors. Recently neuroimaging and behavioral studies indicated that reward-processing and decision-making networks are also altered in hypocretin-deficient narcoleptic patients. These evidences offer new research directions to our understanding of the role of hypocretins in reward and addiction.

Patients with idiopathic rapid eye movement sleep behavior disorder have been reported to be at increased risk for developing Parkinson's disease (PD), dementia with Lewy bodies, or multiple system atrophy. 6-[18F]fluoro-l-m-tyrosine/Positron emission topography (PET) is useful for evaluating PD patients from the early stage of the disease. Substantia nigra hyperechogenicity is a marker of vulnerability to PD. Decrease in 6-[18F]fluoro-l-m-tyrosine uptake in the striatum or hyperechogenic alterations in the substantia nigra may suggest the existence of an underlying neurodegenerative disorder such as PD or dementia with Lewy bodies associated with preclinical dopaminergic dysfunction in patients with idiopathic rapid eye movement sleep behavior disorder.

One of the essential features of rapid eye movement (REM) sleep behavior disorder is REM sleep without atonia seen during nocturnal polysomnographic recordings. In this paper we provide an overview about the varied scoring criteria proposed for visual analysis of loss of atonia during REM sleep. The automatic quantification of loss of atonia overcomes many of the limitations of visual scoring and these new approaches are reviewed. Finally, the contributions of these automatic methods to the understanding of the complex mechanisms underlying muscle atonia and motor suppression during REM sleep are briefly illustrated.

While rapid eye movement (REM) sleep behaviour disorder (RBD) in animals has been associated with stuctural brain stem lesions since the very beginning of RBD research, human brain imaging of RBD did not reveal specific results at first. It was later that single cases of symptomatic RBD due to inflammatory, neoplastic or ischemic lesions were described.

Only recently, systematic voxel-based morphometry (VBM) and diffusion tensor imaging (DTI) studies for RBD have been performed. The SINBAR Sleep Innsbruck Barcelona Group investigated 26 idiopathic RBD (iRBD) patients and 14 age-matched controls with both statistical parametric mapping (SPM) and DTI. Substantial decreases of fractional anisotropy in midbrain tegmentum and rostral pons were found, and mean diffusivity was increased in midbrain and pontine reticular formation. In addition, VBM revealed an increase of gray matter densities in both hippocampi of iRBD patients. The Marburg group performed DTI in 12 iRBD and 12 controls and reported microstructural changes in the brainstem, substantia nigra, olfactory region, left temporal lobe, coronal radiata and the right visual stream. A recent study performed VBM in 20 iRBD and compared the findings to 18 age-matched controls. This study found significant gray matter volume reduction in the anterior lobes of the cerebellum, the pontine tegmentum and the left parahippocampal gyrus. In summary, the areas highlighted from these studies are in line with areas regulating features of REM sleep, and in part with evolving synucleinopathies.

Using the rapid eye movement (REM) sleep behavior disorder severity scale (RBDSS) as a reliable clinical tool we further assessed the phenomenology of REM sleep behavior disorder (RBD) in 56 Parkinson's disease patients with RBD. The scale uses phenomenological categories based on the localization of movements in the distal or proximal extremities and/or involving the trunc and on the presence or absence of vocalizations. Inter-rater reliability has been published previously. In the current study we looked into the distribution of motor and vocal phenomena. We identified a small percentage of patients with only vocalizations (4/56), and 8/56 patients with and 10/56 patients without vocalizations and small nonviolent movements of the distal extremities or facial jerks. Ten patients showed more forceful movements of the proximal extremities, 11 patients with movements involving the proximal extremities had additional vocalizations, 5 patients were recorded with axial involvement, and 12 patients with axial movements and vocalizations. These findings underline the clinical variety of RBD manifestation in Parkinson's disease patients without a certain pattern. However, both extreme variants, the mild one and the violent one, are rare. The RBDSS facilitates the risk estimate for harmful behaviors and may be recommended for comparative studies on RBD and its pharmacotherapy.

Parasomnia Overlap Disorder (POD) was described and named in 1997 with a series of 33 cases of rapid eye movement (REM) sleep behavior disorder (RBD) combined with a disorder of arousal from non-rapid eye movement (NREM) sleep (sleepwalking, sleep terrors) that emerged idiopathically or symptomatically with neurological and other disorders. POD is a subtype of RBD in the International Classification of Sleep Disorders Diagnostic and Coding Manual, second edition (ICSD-2). An updated classification of POD also includes subclinical RBD-NREM parasomnia, RBD-sleep-related eating disorder, RBD-sexsomnia, RBD-rhythmic movement disorder, and status dissociatus (SD), which is another subtype of RBD in the ICSD-2. Similar to POD, a core feature of SD is sleep motor-behavioral dyscontrol, with release of dream-related behaviors suggestive of RBD, but with nearly continuous ambiguous polygraphic sleep precluding the identification of NREM/REM sleep states. SD exemplifies extreme state dissociation. SD is always a symptomatic disorder, and is causally associated with a broad range of neurologic disorders, often with thalamic, limbic, striatal, and pontine involvement. The parasomnia behaviors associated with POD and SD – typical RBD behaviors – can often be controlled with bedtime clonazepam therapy, including the abnormal dreaming.

Cognitive impairment is a frequent feature of rapid eye movement sleep behavior disorder (RBD). The cognitive profile of RBD patients is heterogeneous, with impairments in attention, executive functions, episodic memory, and visuospatial abilities. Moreover, over 50% of RBD patients meet the diagnostic criteria for mild cognitive impairment (MCI). Although a comprehensive neuropsychological assessment remains the most sensitive way to detect MCI, three cognitive screening tests have been validated in RBD. The Montreal Cognitive Assessment was found to be the most appropriate screening test for detecting MCI in RBD. In addition, RBD in Parkinson's disease may be a risk factor for MCI and dementia.

In four of six subjects with narcolepsy, multiple sleep latency tests-examined disconjugated binocular eye movements were observed in the very beginning of multiple sleep latency test recordings. The eye movements appeared before disappearance of alpha and decrease of chin electromyography. All subjects with disconjugated eye movements had also rapid eye movement sleep without atonia and symptoms of rapid eye movement behavior disorder in their past history. Three of them (all children) had post-vaccination narcolepsy. It is not known whether such eye movements are seen in most narcoleptic subjects or whether they are more common in autoimmune/inflammatory narcolepsy with involvement of the structures that coordinate eye movements.

A sleep diary is often employed for diagnosing and treating hypersomnia. However, its reliability needs to be evaluated because overlooked chronic sleep insufficiency could be misdiagnosed as narcolepsy. In this study, we compared simultaneous sleep measurements using a sleep diary and by actigraphy in patients visiting our sleep clinic for the first time with complaints of excessive daytime sleepiness. Of the 28 patients enrolled, 24 complied with both these requirements. In this population, the results obtained using a sleep diary tended to estimate a statistically significant earlier sleep onset time and longer total sleep time than those via actigraphy. For total sleep time, this tendency was more prominent in patients with a higher Epworth Sleepiness Scale score. In 5 of the 24 (20.8%) patients, the sleep diary records indicated >6 h of total sleep time while the actigraphy records indicated <6 h of total sleep time, with a discrepancy of >1 h. These results suggested that sleep insufficiency in hypersomnia patients may be overlooked when their sleep time is assessed using only a sleep diary in the initial phase of the diagnostic procedure, and the simultaneous use of actigraphy may be preferable in this assessment.

To explore biological mechanisms underlying the association between sleep fragmentation and hypercholesterolemia, we conducted an experimental study with 36 Wistar male rats aged 7 weeks. An experimental model for 4-day subchronic sleep fragmentation was applied to rats which were fed ad libitum or were given 50% restricted amount of standard chow. Sleep fragmentation was induced by a treadmill which moved intermittently for 3 s with 30-second pauses between moves. Blood lipid and lipoprotein profiles and adiponectin, leptin, ghrelin, cortisol, epinephrine, and norepinephrine levels were compared among four groups including rats with ad libitum sleep and ad libitum intake (Control), those exposed to sleep fragmentation with ad libitum intake (SF), those with ad libitum sleep and diet restriction (DR), and those exposed to sleep fragmentation and diet restriction (SF+DR). SF and SF+DR showed a higher ratio of LDL and HDL cholesterol (184% and 132% increase, P-value for SF effects <0.001) and ghrelin (64% and 18% increase, P-value for SF effects <0.01) and lower leptin (76% and 44% decrease, P-value for SF effects <0.001) and adiponectin levels (3% and 18% decrease, P-value for SF effects <0.01) than Control. The LDL and HDL cholesterol ratio was highly correlated with leptin (rho = −0.92, P-value <0.001) and ghrelin (rho = 0.53, P-value <0.05) in Control and DR as well as with adiponectin (rho = −0.85, P-value <0.001) and leptin (rho = −0.60, P-value <0.01) in SF and SF+DR. Based on these findings, we suggest that sleep fragmentation may induce lipoprotein disturbances independent of food intake with decreased levels of adiponectin and leptin.

While biological sleep changes in adolescents have been investigated, the contribution of culture has scarcely been addressed. This study explored sleep patterns and related behaviors in male and female Israeli adolescents of Arab and Jewish cultures. The School Sleep Habits Survey was completed by 143 Arab (mean age: 14.7 ± 0.5; 46 males) and 92 Jewish (mean age: 14.7 ± 0.5; 45 males) 9th grade adolescents in Israel. The survey assessed sleep and wake times, sleep latency and total sleep time (TST) on weekends and weekdays, daytime sleepiness, sleep-related problem behaviors, mood and chronotype. Findings revealed that, compared to Arab adolescents, Jewish adolescents went to bed later (P ≤ 0.006) and fell asleep faster (P < 0.001), woke up later on weekdays (P = 0.002), had an evening tendency (P < 0.001), yet lower levels of daytime sleepiness (P = 0.011). TST did not differ between groups. Compared to females, males went to bed later on weekdays (P = 0.014) and weekends (P = 0.010), and slept less on weekends (P = 0.039). No culture–gender interactions were found. In conclusion, different sleep patterns are apparent in Arab and Jewish adolescents of the same region. Earlier bedtimes and longer sleep latencies in Arab adolescents possibly demonstrate a conflict between cultural and biological factors affecting sleep. Whereas TST did not differ between groups, suggesting a common biological sleep need, chronotype, usually considered a marker of circadian phase, showed marked group differences. Gender differences were partially consistent with previous reports. Findings bear implications for purveying culture-specific public health messages.

Empirical evidence indicates that persistent insomnia is a risk factor for developing depression. A personal variable shown to be related to both insomnia and depressive symptoms is perfectionism. However, results of previous studies do not allow to understand how perfectionism influences the relationship between these two clinical conditions. The aim of the present study is to evaluate, through a prospective design, whether perfectionism mediates the relationship between insomnia and depressive symptoms. A community sample of 819 participants filled the Achenbach depression scale, the Pittsburgh Sleep Quality Index and the Frost's Perfectionism scale (F-MPS) and 720 were interviewed again after three months. Analyses of Structural Equation Modeling evidence that insomnia symptoms influence depressive symptoms both directly and indirectly, through the mediation of the negative aspects of perfectionism Concerns over Mistakes and Doubts about Actions. This pattern of relationship is present in both the cross-sectional and prospective models. Results imply that clinical interventions could benefit from targeting perfectionism and insomnia in the treatment of depression.

Homeostatic and circadian changes that occur during adolescence can result in chronic sleep reduction. This may particularly be true for adolescents with Delayed Sleep Phase Disorder (DSPD), which is associated with late Dim Light Melatonin Onset (DLMO). This study assessed the influence of melatonin treatment on chronic sleep reduction in adolescents with DSPD and examined whether adolescents with DSPD suffer from more chronic sleep reduction than adolescents from the general population before and after melatonin treatment. Adolescents with DSPD (n = 145; 55.9% boys; mean age 15,5 years; mean DLMO = 22:32 h) completed a questionnaire concerning chronic sleep reduction at baseline. From these, 53 adolescents also completed this questionnaire after on average 10 weeks of melatonin treatment. At baseline adolescents with DSPD reported significantly more symptoms of chronic sleep reduction than adolescents from the general population, whereas after treatment they reported significantly less symptoms. DLMO did not influence the effect of treatment. The improvement of chronic sleep reduction after treatment is an important finding, considering the negative consequences of chronic sleep reduction for adolescents' daytime functioning.

We examined the effects of unilateral and bilateral nucleus basalis (NB) lesion in rat on sleep/wake states, and sleep/wake state-related electroencephalographic (EEG) frequency relative amplitude distributions. We aimed this study to identify the possible EEG markers for the onset and progression of cortical cholinergic neurodegeneration in rats. NB lesion was performed by ibotenic acid (IBO) microinfusion, and identified by NADPH-diaphorase histochemistry. Sleep/wake states related EEG relative amplitude analysis was done using the Probability Density Estimate (PDE) routine supplied with MATLAB 6.5. Bilateral NB lesion transiently altered gross sleep/wake states topography 14 days following lesion. While control rats exhibited equivalent durations of Wake, NREM and REM, as determined by sensorimotor versus motor cortex EEG, bilateral NB lesion decreased Wake duration in both cortices, with NREM duration increased within sensorimotor cortex, and REM duration increased within motor cortex. Also, Wake, NREM and REM theta relative amplitude was lower in motor versus sensorimotor cortex in all groups of animals. In sensorimotor cortex bilateral NB lesion increased only REM theta relative amplitude from 14–21 days following lesion, and returned to control value 28 days following lesion. In motor cortex both Wake and REM theta relative amplitude transiently increased 14 days following unilateral and bilateral NB lesion, and returned to control values 21 days after lesions. We demonstrated at functional level, for the first time, the topographically specific impact of NB cholinergic cortical afferent system dysregulation on sleep/wake states, REM and Wake EEG theta relative amplitude.

Oxidative stress is one of the pathophysiological pathways suggested for the development of cardiovascular diseases in obstructive sleep apnea. The recurrent nocturnal episodes of hypoxia/reoxygenation observed in patients with obstructive sleep apnea (OSA) appear to be partly responsible for the increased oxidative stress. We investigated the relationship between lipid peroxidation and DNA damage in OSA patients with or without metabolic syndrome (MetS). 117 patients that had recently diagnosed OSA with or without MetS, and 25 control subjects were studied. Plasma malondialdehyde (MDA) levels in fasting blood samples were measured by a high-performance liquid chromatography method and urine 8-hydroxydeoxyguanosine (8-OHdG) was accessed by a competitive ELISA kit method. The levels of MDA and 8-OHdG were significantly higher in total apnea patients than in the controls (P < 0.0001 and P < 0.005, respectively). Apnea patients with metabolic syndrome had slightly higher MDA and lower 8-OHdG levels than those in the patients without metabolic syndrome. The values of 8-OHdG was correlated with T%SaO₂ < 90, T%SaO₂ < %85, mean SaO₂ (%), and the lowest SaO₂ (%) (R = 0.511, P = 0.000, R = 0.420, P = 0.001, R = -0.448, P = 0.000, and R = -0.437, P = 0.001, respectively) in the severe apnea patients. Significant increases in the levels of MDA and 8-OHdG support the studies suggesting possible involvement of oxidative stress in OSA. According to the state of the MetS, there is no significant difference in the levels of oxidative stress markers in OSA patients with or without MetS. High correlations between 8-OHdG and oxygen saturation levels in severe apnea group indicate the role of hypoxia/reoxygenation in DNA damage.

The aim of the present study was to demonstrate the effects of a short nap (20 min) and bright light (>2000 lux) in the afternoon on task switching ability (i.e., switch cost and mixing cost) and error-related negativity (Ne/ERN). The effects of a short nap and bright light on task switching performance have been less reported despite the importance and frequency of task switching as a common activity in many occupational situations. Sixteen volunteers performed a switching task twice a day (1200–1330 h and 1430–1600 h). Participants completed a total of four experimental conditions (control, short nap, bright light, and short nap with bright light). A short nap was taken during the break between the first and second tasks. During the second task, bright light treatment was applied in two of the four conditions. A short afternoon nap improved task-switching performance (i.e., switch cost) and enlarged Ne/ERN amplitude. No effects were found for light conditions on task-switching performance and Ne/ERN amplitude. The results suggest that: (i) a short afternoon nap improves executive functions and self-monitoring that involve the prefrontal cortex; and (ii) the effect of bright light on task-switching performance is smaller compared to a short nap.

We aimed to assess the effect of Type D personality on subjective sleep quality in patients with irritable bowel syndrome (IBS). Ninety-seven patients and 39 healthy controls were enrolled. The Type D Scale (DS14), Pittsburgh Sleep Quality Index (PSQI), and Hospital Anxiety and Depression Scale were used. IBS patients with a Type D personality were found to score higher on sleep latency, sleep disturbance, and global sleep quality domains of PSQI than patients without a Type D personality. Poor sleeping was more prevalent among patients with a Type D personality than those without (50.0% vs 33.9%; P < 0.01).

Our objective was to report the co-occurrence of seizures during sleep and epilepsy during the menstrual period in a patient. We observed a 22-year-old woman with seizures during sleep; the seizures were related to menstruation. The episodes were of partial onset and secondarily generalized. She was under drug control. The patient's neurological examination and magnetic resonance imaging (MRI) were normal. Hormonal determination was within normal range for progesterone and estrogens. The polysomongraphy-electroencephalogram (PSG-EEG) disclosed discharges in the left fronto-temporal area. Based on our observations, we recommend serial PSG-EEG to identify discharges in patients with catamenial-sleep epilepsy for a more comprehensive diagnosis.