Peter J. Hauri’s research while affiliated with Mayo Clinic - Rochester and other places

This chapter gives an overview of the Second Edition of the International Classification of Sleep Disorders (ICSD-2). This revision of ICSD was commissioned and supervised by the Board of the American Academy of Sleep Medicine. ICSD-2 abandoned the hope for a common framework to classify all sleep disorders. Some of these eight categories are based on a common complaint such as insomnia or hypersomnia. Others are grouped around the organ system from which the problems arise, such as the sleep-related breathing disorders and the sleep-related movement disorders. Still others are grouped around a presumed common etiology, such as the problems with the biological clock that are thought to underlie circadian rhythm disorders. ICSD-2 distinguishes the following eight categories of sleep disorders: (1) Insomnias, (2) Sleep-related breathing disorders, (3) Hypersomnias of central origin not due to a circadian rhythm sleep disorder, sleep-related breathing disorder, or other cause of disturbed sleep, (4) Circadian rhythm sleep disorders, (5) Parasomnias, (6) Sleep-related movement disorders, (7) Isolated symptoms, apparently normal variants and unresolved issues, and (8) Other sleep disorders. Many sleep disorders are multifactorial. In accordance with the rules developed by the World Health Organization (WHO) for the International Classification of Diseases (ICD), these different factors are classified separately.

Investigators have suggested using pupillometry to assess alertness in hypersomnolent patients. In this study we assessed hypersomnolent patients and normal volunteers by using pupillometry and examined the usefulness of this technique for the diagnosis of pathologic sleepiness in individual patients. Forty-nine patients were examined by pupillometry and their sleepiness was assessed by using the multiple sleep latency test (MSLT). Thirty-three normal well-rested volunteers were also examined by pupillometry. The patients were classified as having 'mild', 'moderate', or 'severe' sleepiness, based on their mean MSLT sleep latency. Several dynamic variables of pupil diameter were calculated from the pupillograms and correlated with the mean MSLT sleep latency, and were compared between severity groups of patients and the well-rested normal subjects. All but two pupillometric variables were significantly correlated with sleep latency. All except the same two pupillometric variables of the sleepiest group were significantly different from those of normal subjects. However, only 51% of patients with mean sleep latencies less than 10 min and 35% of patients with mean sleep latencies of less than 5 min could be correctly identified by pupillometry. Pupillometry is clearly associated with differences in alertness between groups of patients. However, pupillometric assessment cannot substitute for the MSLT in most cases.

This study reports on the sleep evaluation and follow-up of a professional woman who, in her 30s and 40s, had a decade of severe episodic fluctuations in the length of her sleep (12 vs. 4 h). Severe psychogenic fluctuations in the duration of sleep have not previously been described except in bipolar disorders. Psychological and medical history and a total of 29 polysomnogram nights are presented, as well as a 30-year follow-up interview. Long sleep episodes (>10 h) were characterized by excessive stage 1 sleep and a stage we called 'very light sleep' (over 50% alpha waves mixed with 5-10% delta waves). Long sleeps were also associated with hyperphagia and hypersexuality. Short sleeps (<4 h) emphasized delta and REM sleep. Sleep normalized spontaneously after about a decade of severe fluctuations. In this patient, the recurrent hypersomnia/hyposomnia episodes may have been based mainly on psychiatric factors.

p y r i g h t 2 0 0 2 P h y s i c i a n s P o s t g r a d u a t e P r e s s , I n c . O n e p e r s o n a l c o p y m a y b e p r i n t e d Psychological and Psychiatric Issues in Insomnia Primary Care Companion J Clin Psychiatry 2002;4 (suppl 1) 17 onsiderable progress in understanding the causes of insomnia has been achieved throughout the past 20 Excessive arousal (both psychological and physiologic) may be the main factor in the etiology of insomnia. Hyperarousal may be the final common pathway in moving the sleep/wake balance toward excessive wakefulness and away from sleep. Psychiatric and psychological factors play a major role in increasing this hyperarousal. Most clinical forms of depression and anxiety disorders are clearly associated with severe insomnia, but stress, learning, and conditioning are also crucial parameters related to insomnia. Depression, anxiety, and stress appear to cause insomnia, not vice versa. The vul-nerability of an individual to a specific stress may be a mediating variable, explaining why some per-sons develop severe insomnia when stressed, while others do not. (Primary Care Companion J Clin Psychiatry 2002;4[suppl 1]:17–20) From the Mayo Clinic, Rochester, Minn.

Insomnia is a condition which affects millions of individuals, giving rise to emotional distress, daytime fatigue, and loss of productivity. Despite its prevalence, it has received scant clinical attention. An adequate evaluation of persistent insomnia requires detailed historical information as well as medical, psychological and psychiatric assessment. Use of a classification system for sleep disorders and familiarity with major diagnostic groups will facilitate the clinician's evaluation and treatment. Thorough assessment also requires attention to the unique aspects of presentation and specific set of etiologies which are associated with particular age groups.

Insomnia is a condition which affects millions of individuals, giving rise to emotional distress, daytime fatigue, and loss of productivity. Despite its prevalence, it has received scant clinical attention. An adequate evaluation of persistent insomnia requires detailed historical information as well as medical, psychological and psychiatric assessment. Use of a classification system for sleep disorders and familiarity with major diagnostic groups will facilitate the clinician's evaluation and treatment. Thorough assessment also requires attention to the unique aspects of presentation and specific set of etiologies which are associated with particular age groups.

This paper reviews the evidence regarding the efficacy of nonpharmacological treatments for primary chronic insomnia. It is based on a review of 48 clinical trials and two meta-analyses conducted by a task force appointed by the American Academy of Sleep Medicine to develop practice parameters on non-drug therapies for the clinical management of insomnia. The findings indicate that nonpharmacological therapies produce reliable and durable changes in several sleep parameters of chronic insomnia sufferers. The data indicate that between 70% and 80% of patients treated with nonpharmacological interventions benefit from treatment. For the typical patient with persistent primary insomnia, treatment is likely to reduce the main target symptoms of sleep onset latency and/or wake time after sleep onset below or near the 30-min criterion initially used to define insomnia severity. Sleep duration is also increased by a modest 30 minutes and sleep quality and patient's satisfaction with sleep patterns are significantly enhanced. Sleep improvements achieved with these behavioral interventions are sustained for at least 6 months after treatment completion. However, there is no clear evidence that improved sleep leads to meaningful changes in daytime well-being or performance. Three treatments meet the American Psychological Association (APA) criteria for empirically-supported psychological treatments for insomnia: Stimulus control, progressive muscle relaxation, and paradoxical intention; and three additional treatments meet APA criteria for probably efficacious treatments: Sleep restriction, biofeedback, and multifaceted cognitive-behavior therapy. Additional outcome research is needed to examine the effectiveness of treatment when it is implemented in clinical settings (primary care, family practice), by non-sleep specialists, and with insomnia patients presenting medical or psychiatric comorbidity.