Search

In this paper we examine the relationship between melatonin suppression and reduction of sleepiness through light by comparing three different data sets. In total 36 subjects participated in three studies and received 4 h of bright light either from midnight till 4:00 hours (experiments A and B) or from noon till 16:00 hours (experiment C). In experiment A (night-time light, partial illumination of the retina, pupil dilated) subjects were exposed to either 100 lx of ocular light on the temporal, 100 lx on the nasal part of the retina, or <10 lx of dim light on the whole retina. In experiments B (night-time light, whole retina, pupil not dilated) and C (daytime light, whole retina, pupil not dilated) subjects were exposed either to bright (5000 lx) or to dim light (<10 lx). Subjective sleepiness/fatigue and melatonin concentrations in saliva were assessed hourly in all three experiments. For experiment A, a significant suppression of melatonin due to nasal and temporal illumination of the retina was found, that was not accompanied by a detectable reduction of subjective sleepiness/fatigue. For experiment B we found a suppression of melatonin that was paralleled with a significant reduction in subjective sleepiness, but not in fatigue. During experiment C we found no melatonin suppression but a reduction of subjective sleepiness, but also no effect on fatigue. From these data we conclude that the effects of light on sleepiness/fatigue are not mediated by melatonin and that the influence of endogenous melatonin concentration on sleepiness/fatigue is restricted.

Adolescents and young adults are often excessively sleepy. This excessive sleepiness can have a profound negative effect on school performance, cognitive function, and mood and has been associated with other serious consequences such as increased incidence of automobile crashes. In this article we review available scientific knowledge about normal sleep changes in adolescents (13-22 years of age), the factors associated with chronic insufficient sleep, the effect of insufficient sleep on a variety of systems and functions, and the primary sleep disorders or organic dysfunctions that, if untreated, can cause excessive daytime sleepiness in this population.

There are strong associations between childhood sleep disorders and behavioural, concentration and mood problems. Sleep disorders caused and maintained by behavioural factors (eg, sleep-onset association disorder) are common in young children, and have a significant impact on families. Evaluation should include a medical history, a physical, neurological and developmental examination, a description of any nocturnal events or daytime effects of the child's disturbed sleep, and a good understanding of the family situation and parental management of the child. Management involves recognising the developmental age of the child and the family dynamics, and educating and supporting families in applying behavioural techniques to establish good sleep hygiene. Children with parasomnias (eg, night terrors) also benefit from good sleep hygiene, while those with respiratory or neurological causes of sleep disturbance should be referred for specialist treatment.

In this review, narcolepsy is described based on personal experience of the author with this disease, especially with imperative day-somnolence and cataplexy. Narcolepsy is frequently underestimated and repressed. The economical (disability) and ethical (traffic accidents) implications of the disease may be significant. Optimal treatment and changes of behaviour are important.

Objective: To describe health and functional status in treated narcolepsy patients and to compare it with normative data and with patients with another cause of sleepiness, the obstructive sleep apnea/hypopnea syndrome (OSAHS) patients., Methods: A functional status survey in narcolepsy patients and in symptomatic untreated and CPAP treated OSAHS patients with an apnea-hypopnea index (AHI) >5 was assessed using the UK Short Form 36 (SF-36) questionnaire, the Functional Outcomes of Sleep Questionnaire (FOSQ) and the Epworth Sleepiness Scale (ESS). SF-36 scores in narcoleptics were compared to age and sex matched controls. Narcolepsy patients also replied to a psychosocial aspects questionnaire. Health history and demographic data were obtained via a review of medical records and postal survey., Results: Forty-nine treated narcolepsy patients, 56 untreated OSAHS and 48 CPAP treated OSAHS patients attending the sleep disorders clinic were recruited for this study. Narcoleptics presented significantly lower scores in all SF-36 domains compared to normative data. No difference in SF-36 scores was found between narcoleptics and untreated OSAHS patients but narcoleptics were sleepier and had lower FOSQ scores. These treated narcolepsy patients had lower scores in two dimensions of the SF-36 and in all FOSQ domains compared to CPAP-treated OSAHS patients., Conclusions: Functional status in treated narcoleptics is poor.

Excessive daytime sleepiness (EDS) or somnolence is common in our patients and in society in general. The most common cause of EDS is "voluntary" sleep restriction. Other common causes include sleep-fragmenting disorders such as the obstructive sleep apnea syndrome. Somewhat less familiar to the clinician are EDS conditions arising from central nervous system dysfunction. Of these so-called primary disorders of somnolence, narcolepsy is the most well known and extensively studied, yet often misunderstood and misdiagnosed. Idiopathic hypersomnia, the recurrent hypersomnias, and EDS associated with nervous system disorders also must be well-understood to provide appropriate evaluation and management of the patient with EDS. This review summarizes the distinguishing features of these clinical syndromes of primary EDS. A brief overview of the pharmacological management of primary EDS is included. Finally, in view of the tremendous advances that have occurred in the past few years in our understanding of the pathophysiology of canine and human narcolepsy, we also highlight these discoveries.

Sleepiness, cognitive performance, and quality of life are overlapping aspects of daytime function that may be affected in patients with obstructive sleep apnoea/hypopnoea syndrome. The evidence is compatible with hypotheses that these deficits are reversible with treatment, particularly for patients with severe disease.

Disorders of excessive sleepiness are uncommon in children. When they occur, the presentation is often consistent with the developmental age of the child and does not meet either historical or laboratory criteria determined with adults in mind. Because of these differences, the true diagnosis can be missed or inadequately treated. Knowledge of the differences in presentation, diagnosis, and treatment between adult and childhood sleep disorders is imperative to prevent serious cardiac, respiratory, psychiatric, and cognitive morbidity.

Heart failure is associated with Cheyne-Stokes breathing, which fragments patients' sleep. Correction of respiratory disturbance may reduce sleep fragmentation and excessive daytime sleepiness. This randomized prospective parallel trial assesses whether nocturnal-assist servoventilation improves daytime sleepiness compared with the control. A total of 30 subjects (29 male) with Cheyne-Stokes breathing (mean apnea-hypopnea index 19.8 [SD 2.6] and stable symptomatic chronic heart failure (New York Heart Association Class II-IV) were treated with 1 month's therapeutic (n = 15) or subtherapeutic adaptive servoventilation. Daytime sleepiness (Osler test) was measured before and after the trial with change in measured sleepiness the primary endpoint. Secondary endpoints included brain natriuretic peptide levels and catecholamine excretion. Active treatment reduced excessive daytime sleepiness; the mean Osler change was +7.9 minutes (SEM 2.9), when compared with the control, the change was -1.0 minutes (SEM, 1.7), and the difference was 8.9 minutes (95% confidence interval, 1.9-15.9 minutes; p = 0.014, unpaired t test). Significant falls occurred in plasma brain natriuretic peptide and urinary metadrenaline excretion. We conclude that adaptive servoventilation produces an improvement in excessive daytime sleepiness in patients with Cheyne-Stokes breathing and chronic heart failure. This study suggests improvements in neurohormonal activation with this treatment.

Study Objectives: This study examined the effects of bright light exposure, as compared to dim light, on daytime subjective sleepiness, incidences of slow eye movements (SEMs), and psychomotor vigilance task (PVT) performance following 2 nights of sleep restriction., Design: The study had a mixed factorial design with 2 independent variables: light condition (bright light, 1,000 lux; dim light, < 5 lux) and time of day. The dependent variables were subjective sleepiness, PVT performance, incidences of SEMs, and salivary melatonin levels., Setting: Sleep research laboratory at Monash University., Participants: Sixteen healthy adults (10 women and 6 men) aged 18 to 35 years (mean age 25 years, 3 months)., Interventions: Following 2 nights of sleep restriction (5 hours each night), participants were exposed to modified constant routine conditions. Eight participants were exposed to bright light from noon until 5:00 pm. Outside the bright light exposure period (9:00 am to noon, 5:00 pm to 9:00 pm) light levels were maintained at less than 5 lux. A second group of 8 participants served as controls for the bright light exposure and were exposed to dim light throughout the entire protocol., Measurements and Results: Bright light exposure reduced subjective sleepiness, decreased SEMs, and improved PVT performance compared to dim light. Bright lights had no effect on salivary melatonin. A significant positive correlation between PVT reaction times and subjective sleepiness was observed for both groups. Changes in SEMs did not correlate significantly with either subjective sleepiness or PVT performance., Conclusions: Daytime bright light exposure can reduce the impact of sleep loss on sleepiness levels and performance, as compared to dim light. These effects appear to be mediated by mechanisms that are separate from melatonin suppression. The results may assist in the development of treatments for daytime sleepiness.

Complaints of insomnia, i.e. problems to fall asleep or maintain asleep and/or non-restorative sleep are very common in general practice. This article presents the clinical algorithm non-restorative sleep which was devised by the German Society for Sleep Research and Sleep Medicine. This algorithm presents a guideline for the diagnosis and the treatment of insomnia.

Disorders of sleep and daytime alertness are frequent in Parkinson's disease patients and arise from a number of diverse factors. The most common complaint of night-time sleep disturbance in Parkinson's disease is sleep fragmentation. Sleep fragmentation can be associated with recurrent parkinsonian symptoms, the effect of medications, concomitant medical disorders such as nocturia, or psychiatric disorders such as depression or anxiety. Likewise, nocturnal sleep disturbance may arise from sleep apnea, periodic limb movements of sleep, or rapid eye movement (REM) sleep behavior disorder. Nocturnal sleep deprivation may lead to excessive daytime sleepiness. Other potential sources of daytime sleepiness include the effects of medications or disruption of central sleep mechanisms due to the pathologic processes of Parkinson's disease itself. Diagnosis of sleep disturbances and daytime sleepiness requires a direct interview of the patient and the caregiver, and may involve consultation with the sleep specialist or medical physician. Treatment is aimed toward improving night-time sleep and daytime drowsiness by addressing the causative factors.

Excessive Daytime Sleepiness (EDS) is a difficult clinical problem, which is often indicative of a serious underlying physiologic condition. EDS is associated with automobile accidents, work-related injury, and increased use of the health care system, but it appears to be under-appreciated despite its common occurrence. There are many causes of EDS, ranging from insufficient sleep or inadequate sleep hygiene to drug effects and serious medical conditions. Assessment of EDS should begin with a detailed clinical history, and may also include self-rated instruments and ultimately physiologic tests to measure propensity to fall asleep or stay awake. Ultimately, evaluation in the sleep laboratory is often required in order to arrive at an accurate diagnosis and an appropriate therapeutic recommendation.

Background: Patients with winter depression, (seasonal affective disorder, SAD) frequently complain of difficulty awakening in the morning. Dawn simulation has been found effective in treating SAD, but its effect on difficulty awakening has not been assessed., Methods: Fifty medication-free patients with SAD associated with hypersomnia were randomized to receive either 1 week of dawn simulation (250 lux) or a dim (0.2-2 lux) placebo signal. The patients assessed their level of drowsiness upon awakening during the baseline week and during the treatment week using the Stanford sleepiness scale (SSS). A psychiatrist rated difficulty awakening after the baseline week and after the treatment week., Results: Dawn simulation lowered both the difficulty awakening score (P<0.05) and the SSS score (P<0.05) compared to the placebo dawn signal., Limitations: Replication is necessary. No biological markers of circadian phase were measured., Conclusions: Compared to a placebo condition, dawn simulation appears effective in decreasing both prospectively assessed morning drowsiness and retrospectively assessed difficulty awakening. The symptom of difficulty awakening is consistent with the phase delay hypothesis of SAD. Assessment of difficulty awakening could prove useful in the evaluation of SAD.

Excessive somnolence is a common symptom, with a prevalence of 10 to 20% in a general population. However, physicians seldom ask their patients about sleep complaints. The internal biological clock drives the balance between sleepiness and alertness, generating circadian rhythms, with "physiological" increases of somnolence, especially at mid-day and before the habitual bed time. Excessive somnolence is a subjective feeling of an imperious need of sleep in unusual time and environmental conditions. Sleep deprivation, sleep fragmentation and to a lesser degree hypoxia are believed to be the main mechanisms leading to excessive somnolence. Excessive somnolence increases the risk of car accidents, deteriorates health status and quality of life and might increase mortality. Excessive somnolence is associated with many diseases such as obstructive sleep apnoea syndrome. Excessive sleepiness can be assessed by visual scales or questionnaires, the best known being the Epworth sleepiness scale. Objective tests in somnolent patients assess the sleep-wake balance disturbances. The most widely used tests are the multiple sleep latency test (MSLT), the maintenance of wakefulness test (MWT) and the Oxford sleep resistance (OSLER) test. These tests measure the time to sleep emergence in different conditions.

Daytime tiredness and daytime sleepiness are frequent complaints occurring in 29% and 14% of the Austrian population. Epidemiological studies demonstrate a high comorbidity between nonorganic hypersomnia and mental disorders. Especially comorbidity with affective disorders increases steadily from the general population over primary to tertiary care settings. Diagnostic criteria of nonorganic hypersomnia have been described in the International Classification of Diseases (ICD-10). Nonorganic hypersomnia can be primary or associated with a number of psychiatric disorders such as reaction to severe stress or adjustment disorders, affective disorders, other functional disorders, tolerance to or withdrawal of CNS-stimulating substances and chronic use of CNS-sedating substances. Diagnostic procedures comprise case history and symptom evaluation, sleep-specific and supplementary investigations. Concerning the latter, this article will focus on sleep questionnaires, vigilance and psychological tests as well as CNS investigations. Therapy of nonorganic hypersomnia rests on 3 pillars: psychological, somatic and pharmacological treatment. In view of the wide variety of psychiatric causes, resulting in a number of therapeutic options, it seems desirable that apart from subjective clinical assessment also objective methods be used in diagnosis and treatment. On the neurophysiological level objective measures can be obtained by means of EEG mapping during the day and polysomnography at night. Different mental disorder patients show different brain activity patterns as compared with normal controls and different classes of psychotropic substances cause different changes in neurophysiological variables. The fact that the changes in electrophysiological brain activity caused by mental disorders are exactly opposite to those induced by the psychotropic drugs used for their treatment suggests a key-lock principle in the diagnosis and treatment of nonorganic hypersomnia.

Many pharmacologic and nonpharmacologic strategies are available to treat sleep disorders successfully. Conventional stimulants and the new stimulant modafinil have roles to play in the management of narcolepsy and idiopathic hypersomnia. Knowledge of the properties and clinical effects of these drugs allows adequate doses of medications to be used with the goal of attaining as maximal alertness as possible. A range of dopaminergic agents is available to treat restless legs syndrome; other medications such as opiates, benzodiazepines, and anticonvulsants can also be used. Successful use of the dopaminergic agents depends on an understanding of the phenomena of augmentation, rebound, and tolerance. Arousal parasomnias can be treated with behavioral methods such as hypnosis and drug therapy. Clonazepam provides relief of the symptoms in most patients with REM sleep behavior disorder.

Due to the increased interest of the medical community in sleep disorders an experts meeting was called to establish common criteria for diagnosis, treatment and management of these disorders. Adult prevalence of sleep apnea/hypopnea syndrome (SA/HS) is about 2-4% and increases in the elderly. Snoring and excessive daytime somnolence (EDS) are habitual symptoms. Increased risk to cardiovascular disorders and traffic accidents are the major complications. Increased upper airways resistance syndrome is a recently described syndrome which also involves EDS. A standardized questionnaire was developed and its use was recommended in order to evaluate patients with respiratory sleep disorders (RSD). Polysomnography was established as gold standard in the diagnosis of RSD. Minimal requirement of split night studies and screening studies was also standardized and specific indications were summarized. Medical treatment of obesity in relationship to RSD was analyzed. Nasal continuous positive airways pressure (CPAP) was established as the first choice treatment of SA/HS. Titration of CPAP was standardized. Oral appliances with mandibular advancement could be considered in the treatment of snoring patients without SA/HS and in patients with increased upper airways resistance syndrome. Uvulopalatopharingoplasty can only be performed in snoring patients in whom the presence of SA/HS has been dismissed by polysomnography. Management of patients must include periodic clinical control. EDS must be determined by Epworth test. In order to evaluate CPAP compliance the use of time-controlled devices is highly recommended.

Objective: The differential diagnosis of primary (idiopathic) vs. psychiatric hypersomnia is challenging because of the lack of specific clinical or laboratory criteria differentiating these two disorders and the frequent comorbidity of mental disorders in patients with primary hypersomnia. The aim of this study was to assess whether polysomnography aids in the differential diagnosis of these two disorders., Methods: After excluding patients taking medication and those with an additional diagnosis of sleep-disordered breathing, we compared the nocturnal and daytime sleep of 82 consecutive patients with a diagnosis of either primary hypersomnia (N = 59) or psychiatric hypersomnia (N = 23) and normal control subjects (N = 50)., Results: During nocturnal sleep, patients with psychiatric hypersomnia showed significantly higher sleep latency, wake time after sleep onset, and total wake time and a significantly lower percentage of sleep time than patients with primary hypersomnia and control subjects (p < .05). In addition, the daytime sleep of patients with psychiatric hypersomnia was significantly higher in terms of sleep latency, total wake time, and percentage of light (stage 1) sleep and lower in terms of percentage of sleep time and stage 2 sleep than in patients with primary hypersomnia and control subjects (p < .05). The daytime sleep of patients with primary hypersomnia as compared with that of control subjects was characterized by lower sleep latency and total wake time and a higher percentage of sleep time (p < .05). Finally, a sleep latency of less than 10 minutes or a sleep time percentage greater than 70% in either of the two daytime naps was associated with a sensitivity of 78.0% and a specificity of 95.7%., Conclusions: Our findings indicate that psychiatric hypersomnia is a disorder of hyperarousal, whereas primary hypersomnia is a disorder of hypoarousal. Polysomnographic measures may provide useful information in the differential diagnosis and treatment of these two disorders.

Narcolepsy is a chronic disorder characterized by excessive daytime sleepiness, cataplexy, and other auxiliary symptoms. An interview can ascertain specific symptomatology, whereas a polysomnogram can reveal distinct clinical features. The clinical and laboratory evaluation together enable an accurate diagnosis of narcolepsy. This diagnosis includes a wide spectrum of symptom combinations. Treatment of narcolepsy should include the empathic guidance of a sleep clinician, an emphasis on sleep hygiene, and in many cases pharmacotherapy.

In aviation, it is essential that all aircrew members remain alert and contribute, by their observations and actions, to flight safety. Especially in helicopter operations, crewmembers riding in the rear of the aircraft play an integral role in many aspects of flight, such as take-offs, landings, turns, formation flights, hazard avoidance, situational awareness, military operations, and crew coordination. We present the case of a helicopter crew chief with idiopathic hypersomnia, briefly review the disorder, and give the recent U.S. military aviation experience with sleep disorders. Flight surgeons and aeromedical examiners should be active in considering and diagnosing sleep-related disorders as the aviator or crewmember may not be aware of the disease or may not volunteer the history. A directed history is important in making the diagnosis, as are reports from family and other aircrew members. Referral to a sleep specialist is required in performing objective sleep studies, establishing the diagnosis, recommending treatment, and providing a prognosis. Many sleep disorders are treatable and aeromedically waiverable.

Night workers complain of sleepiness, reduced performance and disturbed sleep due to lack of adjustment of the circadian rhythm. In simulated night-work experiments scheduled exposure to bright light has been shown to reduce these complaints. Here we studied the effects of bright light treatment on the adaptation to 14 days of consecutive night work at an oil platform in the North Sea, and the subsequent readaptation to day life at home, using the Karolinska sleep/wake diary. Bright light treatment of 30 min per exposure was applied during the first 4 nights of the night-shift period and the first 4 days at home following the shift period. The bright light exposure was scheduled individually to phase delay the circadian rhythm. Bright light treatment modestly facilitated the subjective adaptation to night work, but the positive effect of bright light was especially pronounced during the re-adaptation back to day life following the return home. Sleepiness was reduced and the quality of day was rated better after exposure to bright light. The modest effect of bright light at the platform was, possibly, related to the finding that the workers seemed to adapt to night work within a few days even without bright light. These results suggest that short-term bright light treatment may help the adaptation to an extended night-work period, and especially the subsequent re-adaptation to day life.

Sleep disorders are very prevalent in the general population and are associated with significant medical, psychological, and social disturbances. Insomnia is the most common. When chronic, it usually reflects psychological/behavioral disturbances. Most insomniacs can be evaluated in an office setting, and a multidimensional approach is recommended, including sleep hygiene measures, psychotherapy, and medication. The parasomnias, including sleepwalking, night terrors, and nightmares, have benign implications in childhood but often reflect psychopathology or significant stress in adolescents and adults and organicity in the elderly. Excessive daytime sleepiness is typically the most frequent complaint and often reflects organic dysfunction. Narcolepsy and idiopathic hypersomnia are chronic brain disorders with an onset at a young age, whereas sleep apnea is more common in middle age and is associated with obesity and cardiovascular problems. Therapeutic naps, medications, and supportive therapy are recommended for narcolepsy and hypersomnia; continuous positive airway pressure, weight loss, surgery, and oral devices are the common treatments for sleep apnea.

When it is not due to an extrinsic origin, somnolence may be the main symptom of various diseases. Among these causes of excessive daytime sleepiness, obstructive sleep apnea syndrome is noteworthy for its very important prevalence, estimated at 4% in adult males. Due to repeated upper airway obstructions during sleep, this disease is efficiently treated by continuous positive airway pressure applied through a nasal masks during sleep. Another syndrome, periodic limb movements during sleep may also lead to a sleep fragmentation at the origin of daytime sleepiness. Its treatment is principally based on dopaminergic agonists. Narcolepsy-cataplexy and idiopathic hypersomnia are two causes of excessive daytime sleepiness in young people. The first is as frequent as multiple sclerosis and the second is ten times less frequent. The treatment of these two diseases is now based on a new French drug: modafinil(Modiodal). Sleep pathology still has only a small place in medical training. Excessive daytime sleepiness is therefore often misdiagnosed. In addition to their major risk of work or road accidents, numerous untreated patients continue to suffer from this very unpleasant symptom, at the origin of a major social handicap.

Sixteen patients with winter seasonal affective disorder and 13 healthy controls were exposed to 3300 lx of cool-white fluorescent light for either 1 hour or 15 min in the morning for 2 weeks during the winter. Subjective sleepiness, melatonin concentration in saliva, and serum 25-hydroxyvitamin D(3) concentration were measured before and after the 2-week trial as well as the following summer when the patients were well. There were no significant differences in the baseline values between the patients and healthy subjects. No significant differences in the outcome measures were observed in the patients or the controls in the two groups of each after the trial. The exposure to bright light resulted in a significant decrease in subjective sleepiness early in the evening in the patients but not in the control subjects. The reduction of depressive symptoms was associated with the decrease in subjective sleepiness but not with the changes in the melatonin or vitamin D concentrations.

There has been a great development in sleep medicine during the past 20-25 years and the International Classification of Sleep Disorders now lists about 90 relatively well-defined conditions related to sleep. Several of them are severely underdiagnosed. This review considers frequent and/or disabling sleep disorders, in particular disorders for which treatment is available.

Disturbances of sleep are a hallmark of seasonal affective disorders (SAD), as they are of other mood disorders. Fall/winter SAD patients most often report hypersomnia. Among responses of 293 SAD patients on a symptom questionnaire, complaints of winter hypersomnia (80%) greatly exceeded insomnia (10%), hypersomnia plus insomnia (5%), or no sleep difficulty (5%). Increased sleep length in fall/winter is not unique to SAD. Among 1571 individuals across four latitudes surveyed at random from the general population, winter sleep increases of < or = 2 hr/day relative to summer were reported by nearly half. However, hypersomnia had a low correlation (r = 0.29) with the total number of other SAD symptoms that were reported in this sample. Ten SAD patients kept daily sleep logs across 1 yr that showed increases in fall and winter (sleeping most in October; least in May) whose maximum averaged 2.7 hr per day more weekend sleep than in spring and summer. These winter increases might have been somewhat attenuated since most received light therapy during part of the winter. Nocturnal EEG recordings of depressed SAD patients in winter showed decreased sleep efficiency, decreased delta sleep percentage, and increased REM density (but normal REM latency) in comparison with recordings: (1) from themselves in summer; (2) from themselves after > or = 9 days of light therapy; or (3) from age- and gender-matched healthy controls. Thus, the extent of fall/winter oversleeping recorded by our SAD patients did not differ dramatically from that reported by the general population, but sleep complaints of our SAD patients have been accompanied by features of sleep architecture that are different from healthy controls and are reversed by summer or by bright-light therapy.

Healthy sleeping habits is a complex balance between behaviour, environment and circadian rhythm. The quality of sleep can be improved by behaviour, e.g. eating tryptophan and carbohydrate rich foods, physical exercise in the afternoon or a cold shower just before going to bed. Total sleep time is maximal in thermoneutrality and decreases above and below the thermoneutrality zone. Thermoneutrality is reached for an environmental temperature of 30-32 degrees C without night clothing or of 16-19 degrees with a pyjama and at least one sheet. Noise also modifies sleep structure and above 50dB shortens total sleeping time. Although subjects do become subjectively accustomed to noise, vegetative cardiovascular reactivity to environmental noise remains unchanged. The spontaneous circadian awake/sleep cycle is 25 hours, slightly longer than the body temperature cycle, but when subjects are exposed to environmental synchronization, the two cycles coincide. In individuals undergoing temporal isolation, the two rhythms become independent often leading to subjective discomfort and fatigue. Certain factors including age can favour internal desynchronization. Other factors may include social contact, stress due to mental work load, and constant lighting which could lengthen the awake/sleep cycle. Caffeine blocks the receptors of adenosine, and thus its effects of inhibiting neurotransmission. Intake 30 to 60 minutes before sleeping shortens total sleep time and increases the duration of stage 2 and shortens stage 3 and 4. Alcohol may act as a relaxing, sedative agent when consumed just before sleeping but can also lead to night-time awakening due to sympathetic activation which does not return to baseline levels until the blood alcohol levels have returned to 0. Nicotine has a biphasic effect on sleep: at low concentrations, it leads to relaxation and sedation and at high concentrations inhibits sleep. A careful study of sleeping habits is the first step in evaluating complains of insomnia or hypersomnia. Before relying on drugs, treatment should start with attention to the sleep environment and personal habits.

We examined hypersomnolence as experienced among individuals meeting standardized diagnostic criteria for Seasonal Affective Disorder (SAD). Data were available from 115 individuals attending a mood disorders clinic specializing in treatment of this disorder. Three modes of assessment were employed: retrospective self-reports (Seasonal Patterns Assessment Questionnaire), cross-sectional interviews (Standardized Interview Guide for the Hamilton Depression Scale, SAD Version), and prospective sleep diaries. Results indicated that self-reported total hours of sleep varied significantly across the seasons, with longest sleep occurring in winter and shortest sleep in summer. Seasonal sleep changes, as indicated by the SPAQ did not correlate significantly, however, with severity of depressive symptoms as indicated by the Hamilton scale. Multiple regression analyses indicated that only social activity levels (one of seven SPAQ items) was significantly and uniquely related to the severity of depression. When data obtained by the three instruments were compared, self-reported hours of sleep (whether measured by SPAQ or Hamilton interview) were significantly higher than indicated by prospective sleep diaries. We conclude that hypersomnolence may not be a central feature of SAD and that the validity of the SPAQ as an index of this disorder requires further investigation.

Subjects with isolated complaints of chronic daytime sleepiness are usually classified as "idiopathic hypersomniacs" and treated symptomatically. A group of these subjects was investigated during nocturnal sleep and daytime naps. In a subgroup of them, sleep was fragmented by very short alpha EEG arousals throughout the sleeping period. These short arousals are usually ignored in sleep analyses, but their impact is significant (in the 15 subjects identified with the syndrome, the mean sleep latency in multiple sleep latency tests was 5.1 +/- 1 min). These arousals are directly related to an abnormal increase in respiratory efforts during sleep (the mean peak inspiratory esophageal pressure measured in our subjects in the respiratory cycle just preceding a transient arousal was -33 +/- 7 cm H2O). Typically, an arousal occurs within one to three breaths of flow limitation associated with abrupt but limited reduction in tidal volume (ie, abnormal increase in upper airway resistance during sleep). The arousal restores normal breathing. Snoring was noted in association with these transient arousals in 10 of the 15 subjects; however, snoring was neither sufficient nor necessary for the identification of the clinical syndrome. Both sexes were equally represented in the affected group. All studied subjects had upper airway anatomy that was mildly abnormal. Nasal continuous positive airway pressure, used as an experimental tool, eliminated the daytime sleepiness (multiple sleep latency mean score = 13.5 min), the transient arousals (mean alpha EEG arousal index decreased from 31.3 +/- 12.4 to 8 +/- 2 per hour of sleep), and the abnormal upper airway resistance. Chronic daytime sleepiness is a major cause of social, economic, and medical impairment. Recognition of this syndrome and its cause is important, as specific treatments can be developed to eliminate the problem.

Excessive daytime somnolence is a major neurological problem involving about 4% of the general population. Its treatment is based on accurate etiological dissection. Sleep-disordered breathing is a major cause of EDS. Stimulant medication is helpful in many other instances.

The Kleine-Levin syndrome is a rare and probably underdiagnosed syndrome. It is characterized by periodic attacks of the triad: hypersomnia, vegative disturbances such as hyperphagia and hypersexuality, psychopathological changes in the level of consciousness and control of emotions. Boys and young men in the age group 10-20 years are most commonly affected. Spontaneous remission with a tendency to remission is observed and the disease "burns out" after a prolonged period of years. The etiology and pathogenesis are unknown. Theories have been propounded suggesting dysfunction of the hypothalamus. No pathognomonic findings have been observed in the early phase of sleep during the daylight hours. Central stimulating drugs have been reported to have some effect on the hypersomnia. The diagnosis is based on the clinical picture. Frequently, a long period can elapse before the diagnosis is established and some cases are never diagnosed. The literature is reviewed and is illustrated by two case reports.

A case of adverse side effects of co-trimoxazole (Biseptol) was observed, with predominance of neurological changes in the clinical picture. Attention is called to the infrequent occurrence of such side effects of this drug and to the necessity of prompt diagnostic and therapeutic management of such cases.