A centenary is often an excuse for reminding people of la fin des siècles, and there seems to be recurrent revivals of interest in the psychological, the mysterious, and their related medical syndromes. Only history will tell if the same occurred at the turn of the millennium, but to date there does not appear to be a flood of novels equivalent to, for example, Dr. Jekyll and Mr. Hyde, in which the two opposing poles of the human psyche are laid out with dramatic effect. At that time there was much interest in hypnosis, automatisms, sonambulism, and their relationship to human happenstance. However, there have been recent novels about Tourette syndrome, such as Johnathan Letham's Motherless Brooklyn. There may also be a revival of interest about epilepsy, and two recently published novels are of particular neuropsychiatric relevance. The first is Lauren Slater's Spasm, and the second Mark Salzman's Lying Awake.

The subtitle of Spasm hints at what is to come. It is a “Memoir With Lies.” Chapter 1 begins with the words “I exaggerate.” The tale is an autobiographical account of the growing up of a young girl with seizures, diagnosed as epilepsy, and who is put through all the traumas associated with the disorder. With auras of strange smells and seizure descriptions that would be called partial and secondarily generalized seizures, she gets examined by her pediatrician, given phenobarbital (600 mg!), has psychotherapy, and goes to a special school run by nuns. However, her seizures are relentless, she sees a neurologist who stimulates her cortex and recommends that she has a corpus callosotomy, which she then undergoes.

The decision to devote this issue of CNS Spectrums to sleep disorders was two-fold. First, sleep disorders are of relatively high prevalence in the population with a significant impact on public health and safety. Unfortunately, their significance has been underestimated. Hence, the training of subspecialists capable to deal competently with the diagnosis and treatment of these disorders that afflict all age groups has lagged behind the training of other subspecialists. Second, the presence of psychiatric symptoms in many individuals afflicted with these disorders and the bona fide psychiatric comorbidity of many such patients have been underestimated. Psychiatric comorbidity raises some compelling issues about the need that at least selected patients presenting with a sleep problem should undergo a thorough psychiatric evaluation along with a specialized evaluation, if deemed necessary.

Although the majority of patients with sleep disorder would benefit from an initial psychiatric evaluation, such a practice may not be available at all sleep centers. A psychiatric evaluation should first assess the nature and origin of psychiatric symptoms and determine the presence of a primary or secondary psychiatric disorder. Once a reliable diagnosis has been established, the proper course of treatment can be outlined. As with most other psychiatric conditions, a combined course of pharmacotherapy and psychotherapy has the best chance of restoring functionality and preventing relapses. Thus, the role the psychiatrist can play in optimizing the care of patients with a sleep disorder cannot be overemphasized.

What should clinicians know about sleep disorders? This article briefly introduces the reader to sleep medicine and succinctly reviews common sleep disorders. First, the authors describe the diagnostic tools unique to sleep medicine: the over-night polysomnogram and the multiple sleep latency test. Next, the authors review essential features of a subset of the sleep, described in the International Classification of Sleep Disorders-Revised, that sleep disorder specialists commonly evaluate, diagnose, and treat. The disorders reviewed include the intrinsic and circadian rhythm subsets of the dyssomnias group and the parasomnia group of sleep disorders. The authors identify the core signs and symptoms, polysomnogram findings, multiple sleep latency test findings, and treatment of these disorders.

Are symptoms of daytime sleepiness relevant among patients with insomnia? Patients with insomnia frequently report daytime consequences secondary to their difficulty initiating and maintaining sleep. The purpose of this study was to determine the frequency of daytime sleepiness as defined by a self-reported measure of daytime sleepiness (the Epworth Sleepiness Scale). In addition, the study characterized the patients' psychological status using the Symptom Checklist-90-Revised. The study corroborated a relatively high frequency of excessive daytime sleepiness and psychiatric conditions among patients with insomnia. Furthermore, the results of the study suggest variation in psychological distress levels, according to the different levels of sleepiness/alertness.

Does narcolepsy, a neurological disease, need to be considered when diagnosing major mental illness? Clinicians have reported cases of narcolepsy with prominent hypnagogic hallucinations that were mistakenly diagnosed as schizophrenia. In some bipolar disorder patients with narcolepsy, the HH resulted in their receiving a more severe diagnosis (ie, bipolar disorder with psychotic features or schizoaffective disorder). The role of narcolepsy in psychiatric patients has remained obscure and problematic, and it may be more prevalent than commonly believed. Classical narcolepsy patients display the clinical “tetrad”—cataplexy, hypnagogic hallucinations, daytime sleep attacks, and sleep paralysis. Over 85% also display the human leukocyte antigen marker DQB10602 (subset of DQ6). Since 1998, discoveries in neuroanatomy and neurophysiology have greatly advanced the understanding of narcolepsy, which involves a nearly total loss of the recently discovered orexin/hypocretin (hypocretin) neurons of the hypothalamus, likely by an autoimmune mechanism. Hypocretin neurons normally supply excitatory signals to brainstem nuclei producing norepinephrine, serotonin, histamine, and dopamine, with resultant suppression of sleep. They also project to basal forebrain areas and cortex. A literature review regarding the differential diagnosis of narcolepsy, affective disorder, and schizophrenia is presented. Furthermore, it is now possible to rule out classical narcolepsy in difficult psychiatric cases. Surprisingly, psychotic patients with narcolepsy will likely require stimulants to fully recover. Many conventional antipsychotic drugs would worsen their symptoms and make them appear to become a “chronic psychotic,” while in fact they can now be properly diagnosed and treated.

Is there an association between obstructive sleep apnea (OSA) and depression? OSA is a common breathing-related sleep disorder. There have been reports that depressive symptoms can be associated with this sleep disorder. A number of investigations have addressed this issue. Although some have found no correlation, most studies have concluded that there is an association between OSA and depressive symptoms. Other investigations have shown that depressive symptoms improve with treatment of OSA, and that untreated OSA may contribute to treatment resistance in some cases of mood disorders. Within the framework of current psychiatric diagnostic criteria, the depressive symptoms associated with OSA can be viewed as a combination of a mood disorder secondary to a primary medical condition and an adjustment disorder with depressed mood. The question of whether OSA causes depressive symptoms can perhaps be best answered by viewing OSA and depression as having certain symptoms that are common to both disorders.

How should sleep-related rhythmic movements in children be assessed and treated? Rhythmic movement disorder (RMD) represents an unusual variety of childhood parasomnia characterized by repetitive motion of the head, trunk, or extremities, which usually occurs during the transition from wakefulness to sleep or arises during sustained sleep. Although the condition most often affects infants and toddlers in a transient and self-limited fashion, the condition occasionally persists in a problematic fashion, which may nevertheless be amenable to treatment. Since RMD may occasionally cause injury or resemble nocturnal seizure, prompt recognition, and appropriate management on the part of the clinician is essential. This article will examine the spectrum of RMD in children, including their common clinical manifestations; data regarding their epidemiology and natural history; the role of polysomnography, electroencephalography; and other diagnostic testing. Potential causes of the condition and available methods of treatment are also examined.

What is the effect of melatonin on jet lag syndrome? Jet lag desynchronizes the internal sleep-wakefulness cycle with the environmental light/dark cycle. Advance (but not delay) of light onset is known to abolish pineal N-acetyltransferase activity and urine excretion of 6-sulphatoxymelatonin. Measurements of pineal serotonin, the substrate of melatonin biosynthesis; N-acetylserotonin (NAS), the immediate melatonin precursor; and melatonin (high-performance liquid chromatography-fluorimetric method) in the animal (rat) model of jet lag revealed that prolonged delay of darkphase onset disrupted the rhytms in comparable ways as the advance of light-phase onset. Advance of dark phase onset resulted in less severe disturbances of rhythms as compared with the advance of light phase onset. Melatonin, but not NAS, injections at the beginning of a new dark period accelerated recovery of NAS and melatonin, but not serotonin, rhythms. Spontaneously hypertensive rats were more sensitive to advance of light onset and less responsive to melatonin injections than normotensive rats. NAS and methylene blue, an inhibitor of monoamine oxidase A, attenuated light-induced disruption of NAS but not melatonin rhythms. We draw the following conclusions from our data: the beginning of the dark period may be preferable to the beginning of light period as the arrival time on eastward flights; the efficacy of melatonin in alleviating jet lag may be enchanced by administering it before, during and after rapid transition through time zones; and hypertension may exaggerate jet lag syndrome.