Harvey Moldofsky

Tourette syndrome : a follow-up study

We describe a long-term follow-up study (1–15 years) of 33 patients with Tourette syndrome who were treated with pimozide (2–18 mg), haloperidol (2–15 mg), or no drugs. Both drugs produced comparable relief of symptoms at follow up; however, significantly more patients on haloperidol (eight of 17), compared with those on pimozide (one of 13), discontinued treatment (p ⩽ 0.05). Haloperidol produced significantly more acute dyskinesias/dystonias than pimozide (p ⩽ 0.03); otherwise, the adverse effect profile was similar for the two drugs. In particular, we found no increased incidence of ECG abnormalities in patients treated with pimozide. A prospective, randomized, double-blind crossover trial is required to determine whether there are significant differences in efficacy between pimozide and haloperidol in treatment of Tourettes disorder.

Dysthymic disorder and rheumatic pain modulation disorder (fibrositis syndrome): a comparison of symptoms and sleep physiology

It has been suggested that “fibrositis” or rheumatic pain modulation disorder (RPMD) is a varient of depressive illness. Both disorders are associated with abnormalities in sleep physiology. Since the clinical features of RPMD do not meet all the criteria for a major depressive disorder, the symptoms and sleep phsyiology in subjects with dysthmic disorder (DSM III criteria) (N = 6), and RMPD (N = 6) were compared, in order to determine the similarity between the two groups. The sleep physiology in dysthymic disorder was first examined over three consecutive nights since a systematic evaluation of the sleep physiology in this group of disorders has not yet been reported. All dysthymic patients showed episodic bursts of high-amplitude (75–150 microvolts) theta (3–5 Hz) bursts in stage 2 sleep, and REM onset latency was abbreviated only on night 2. The theta bursts have not been previously reported, and may be an early marker of disorganization of non-REM sleep in the dysthymic subjects. The comparison of the two groups revealed that RPMD subjects reported more pre- and post-sleep pain (p < 0.01), lighter sleep (p < 0.01), and more physical ailments during sleep (p < 0.01), and had more alpha (7–11.5 Hz) in non-REM sleep (p < 0.01). The dysthymic subjects who reported deeper sleep (p < 0.01), had a greater sleep continuity disturbance with longer stage 2 onset latency (p < 0.05), fewer hours of sleep (p < 0.05), more wakefulness after sleep onset (p < 0.05), more awakenings per hour of sleep (p < 0.01) and more stage changes per hour of sleep (p < 0.01), and showed theta bursts in stage 2 (p < 0.01). The distinctive symptoms and sleep physiologies in the two groups suggest that the two disorders are not related.

Sleep, cytokines and immune function.

Bi-directional communication pathways exist between the brain and the cytokine-immune-endocrine systems. The hypothalamic-pituitary axis, the efferent neuronal hypothalamus-autonomic nervous system axis, and the direct drainage of macromolecules from the brain into the blood and the lymphatic system provide a network by which the sleeping/waking brain influence bodily functions. Similarly, changes in cytokine levels in the periphery modulate the central nervous system either directly or via the vagal nerve and influence the sleeping/waking brain. In humans, circadian nocturnal sleep-daytime wakefulness is associated with changes in peripheral cytokines, cellular immune functions, and endocrines. Progesterone levels influence sleep and cellular immune functions during the menstrual cycle. The interaction between the circadian sleeping/waking brain and the cytokine-immune-endocrine system are integral to preserving homeostasis. Disorganization or loss of sleep disrupts the harmonious integration of the circadian cytokine-immune-endocrine system. However, the mechanisms of circadian sleep/wakefulness-related cytokine-immune-endocrine functions in host defence against disease remain to be determined.

The contribution of sleep medicine to the assessment of the tired patient.

Tiredness is one of the most common complaints that confront the clinician. Yet the nature of the symptom and its implications for sleep-related disorders is poorly understood. This review provides the clinician with an understanding of the difficulties inherent in assessing the tired patient. The complaint of tiredness is commonly an expression of sleepiness and fatigue that arises as the result of sleep-wake–related disorders. Behavioural and physiological procedures are described in the assessment and management of sleepiness and fatigue in primary sleep disorders and sleep-related medical and psychiatric disorders. Improvement in the diagnosis and management of the fatigued or sleepy patient requires that residents in psychiatry and neurology be exposed to the behavioural and physiological techniques of sleep medicine as part of their post-graduate training programs.

The drosophila per gene homologs are expressed in mammalian suprachiasmatic nucleus and heart as well as in molluscan eyes

This study presents evidence for the conservation of Drosophila per gene homologs in mammalian DNA and for their expression in a number of tissues which are involved in various aspects of circadian timekeeping. Distinct 5 kb sequences, which hybridized to a non repetitive fragment of the Drosophila per gene under stringent conditions, were detected by Southern blotting. Sequences homologous to per gene of Drosophila were also amplified from rat and mouse brain cDNA libraries and from a mouse anterior hypothalamus and human hypothalamus libraries. Degenerate PCR primer design was based on conserved segments of the per protein. The per homologs were shown directly (by RT-PCR) to be expressed in hamster and mouse SCN, in hamster heart and in Aplysia and Bulla eyes.

Fiscal and service analyses in general hospital psychiatry.

Fiscal matters were analyzed in four specialized programmes of the Department of Psychiatry at the Toronto Western Hospital in order to plan for service and academic activities. The resultant analysis allowed for the establishment of criteria for growth and the evaluation of clinical service performance and goals.

Book Review: Sleep and Sleeplessness in Advanced AgeSleep and Sleeplessness in Advanced Age by René Spiegel in Advances in Sleep Research, Volume 5. New York: SP Medical & Scientific Books, 272 pp.,

chapter states that the present evidence supports the idea that the hypothalamus is inhibitory to prolactin secretion and that dopamine might be the prolactin inhibitory factor (PI F). Small amounts of dopamine prevent the secretion of prolactin by direct action on the pituitary and alphamethylparatyrosine (AMPT), which inhibits dopamine synthesis and elevates plasma prolactin levels. However, Neill also reports that the neurotransmitters histamine, serotonin and melatonin all indirectly stimulate prolactin release and that acetylcholine has been found by different investigators to either inhibit or stimulate prolactin secretion. The neuroendocrine picture of prolactin secretion is therefore far from clear. The thyroid gland has fascinated psychiatrists since the famous paper on myxoedema madness was published by the Clinical Society of London, England, in 1880. The more recent observations by Prange in depressed subjects has once again given it a prominent place in psychiatric thinking. Thyroid-stimulating hormone (TSH or thyrotropin) is secreted by the anterior pituitary gland and is responsible for the control of normal human thyroid function. The hypothalamus has a dominant stimulatory action overTSH synthesis and release, and the thyroid gland hormones have a negative feedback control over TSH synthesis and secretion. Recent work according to Scanlon et al. indicates that central dopamine has an inhibitory effect in the control of TSH secretion in man, and circumstantial evidence suggests a similar role for somatostatin (growth hormone [GH] release inhibiting hormone [GHRIH]). It becomes very evident then, as the authors point out, that hypothalamic control over TSHsynthesis and release in man is a much more complicated event than previously thought and has both stimulating and inhibitory components. Also to be considered is the evidence that estrogens and glucocorticoids may also have a role in hypothalamic-pituitary-thyroid function and this must be taken into account in the overall picture of TSH regulation. There are many other interesting chapters such as the hormone interaction and regulation during the menstrual cycle; the role of the third ventricle in fluid and electrolyte balance, arterial pressure regulation and hypertension; neurotensin; growth hormone regulation and the endorphins. The authors continually point out that newlaboratory techniques have made it possible to demonstrate that hormones once considered to be found only in the hypothalamus and pituitary gland are also located in other brain areas, the peripheral nervous system, the retina and the gastrointestinal tract. After reading the book one is left with the impression that much has been accomplished in the field of neuroendocrinology but also that much more remains to be discovered before we have a comprehensive understanding of the complex interactions of the brain hormones and their effects on behaviour. However it is a good reference text and value for the

35.00, 1981.

39.50 retail price.