Sleep syndromes

Familial advanced and delayed sleep phase syndromes can both be attributed to mammalian per mutations in a region of the PER protein, presumably a CKIe binding domain (Ebisawa et al 2001, Toh et al 2001). Because a phosphorylation disorder might cause some sleep syndromes, the establishment of a system with which to assay post-translational modifications of PER protein has recently received considerable focus. 

Sleep disorders are common, and are generally underdiagnosed. The two major complaints related to sleep are insomnia ( I can t sleep ) and excessive daytime sleepiness (EDS, I can t stay awake ). EDS is a relatively nonspecific symptom. It can be the end result of any factor that causes sleep disruption, and it can be caused by primary or intrinsic sleep disorders. Insomnia of any cause can result in sleep deprivation and subsequent EDS. The most common cause of EDS in the general population is self-imposed sleep deprivation, or insufficient sleep syndrome. By contrast, the most common causes of EDS seen in a sleep center are primary (intrinsic) disorders of EDS. The American Academy of Sleep Medicine (AASM, formerly the American Sleep Disorders Association) classification of sleep disorders includes over 80 diagnoses that are associated with EDS, but the majority of patients evaluated at sleep centers have sleep apnea, narcolepsy, idiopathic hypersomnia, or periodic limb movements of sleep. 

Absence Epilepsies are a group of epileptic syndromes typically starting in childhood or adolescence and characterized by a sudden lack of attention and mild automatic movements for some seconds to minutes. Absence epilepsies are generalized, i.e. the whole neocortex shifts into a state of sleep-like oscillations. 

Measurement of muscle activity, usually measured by electrodes placed on the skin. The EMG is used in sleep research to aid in the discrimination of sleep stages, and also as part of diagnosis of sleep disorders such as periodic limb movements and restless legs syndrome. 

Restless legs syndrome, also known as Ekbom s syndrome, causes unpleasant sensations in the legs such as tingling, discomfort and sometimes pain. Symptoms are usually worse at night and disturb sleep. Resting usually makes symptoms worse and activity relieves the condition. The cause of the condition is currently unknown but it is common and usually occurs in middle age. There are currently few treatments in place. 

Antiemetics and antivertigo drag s are used cautiously in patients with glaucoma or obstructive disease of the gastrointestinal or genitourinary system, those with renal or hepatic dysfunction, and in older men with possible prostatic hypertrophy. Piromethazine is used cautiously in patients with hypertension, sleep apnea, or epilepsy. Trimethobenzamide is used cautiously in children with a viral illness because it may increase the risk of Reye s syndrome... 

A rebound sleep disturbance has been found after only 7—10 days of treatment with therapeutic doses of triazolam (Greenblatt et al. 1987). Others have described a withdrawal syndrome after substitution of a short-acting benzodiazepine for a long-acting benzodiazepine (Conell and Berhn 1983). Rebound insomnia may occur with zolpidem. 

Patients with IBS may experience comorbidities outside the gastrointestinal tract such as fibromyalgia, sleep disturbances, headaches, dyspareunia, and temporomandibular joint syndrome. 

S = Sleep disturbances (insomnia, rapid eye movement sleep behavioral disorder, restless legs syndrome)... 

Describe the mechanisms of the sleep disorders covered in this chapter, including insomnia, narcolepsy, restless-legs syndrome, obstructive sleep apnea, and parasomnias. 

Restless-legs syndrome treatment involves suppression of abnormal sensations and leg movements and consolidation of sleep. Dopaminergic and sedative-hypnotic medications are prescribed commonly. 

Restless-legs syndrome occurs in 5% to 15% of the population, making it a common sleep disorder.11,12 The prevalence of RLS increases with age and in various medical conditions such as end-stage renal disease (ESRD), pregnancy, and iron deficiency.13 RLS appears to be more common in women than in men and has a genetic link. The majority of RLS patients (63% to 92%) report a positive family history.14... 

Restless-Legs Syndrome and Periodic Limb Movements of Sleep (PLMS)... 

FIGURE 38-1. Primary assessment and initial treatment for complaint of excessive daytime sleepiness. RLS, restless-legs syndrome NPSG, nocturnal polysomnography OSA, obstructive sleep apnea DA, dopamine agonist MSLT, multiple sleep latency test BZDRA, benzodiazepine receptor agonist SNRI, serotonin and norepinephrine reuptake inhibitor TCA, tricyclic antidepressant CPAP, continuous positive airway pressure. 

OSA obstructive sleep apnea Hening WA, Allen RP, Earley CJ, et al. Restless Legs Syndrome Task... 

Garcia-Borreguero D., Larrosa O., Saiz T. et al. (2001). Circadian variation in neuroendocrine response to the administration of L-dopa in patients with restless legs syndrome a pilot study. Sleep 24(suppl.), (A16-A17). 

A number of clinical studies have now made use of the phase advancing property of melatonin for treating delayed sleep phase syndrome (DSPS). Melatonin, at a 5 mg dose, has been found beneficial in advancing the sleep onset time and wake time in DSPS subjects (Dahlitz et al. 1991 Nagtegaal et al. 1998 Kayumov et al. 2001). Melatonin was found to be effective when given five hours before its endogenous onset or seven hours before sleep onset. 

Dahlitz, M., Alvarez, B., Vignau, J. et al. (1991). Delayed sleep phase syndrome response to melatonin. Lancet 337, 1121-4. 

Kayumov, L., Brown, G., Jindal, R., Buttoo, K. Shapiro, C. M. (2001). A randomized, double-blind, placebo-controlled crossover study of the effect of exogenous melatonin on delayed sleep phase syndrome. Psychosom. Med. 63, 40-8. 

Nagtegaal, J. E., Kerkhof, G. A, Smits, M. G., Swart, A. C. van der Meer, Y. G. (1998). Delayed sleep phase syndrome A placebo-controlled cross-over study on the effects of melatonin administered five hours before the individual dim light melatonin onset. J. Sleep Res. 7, 135-43. 

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