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THE TREATMENT OF SLEEP DISORDERS WITH MELATONIN

Since sleep requires neurological control, it is not surprising that disorders of the brain may be associated with severe sleep disturbance (Okawa el al. 1986). Neurologically multiply disabled children can experience chronic sleep-wake rhythm difficulties (Okawa et al. 1987, Quine 1991), which often respond poorly to strict bedtime scheduling, various psychological measures and sedatives. In fact sedatives may cause agitation or provide the desired effect for only a few days, and physicians often cannot offer successful
treatment. Some of these children have difficulty falling asleep, some sleep in a totally fragmented fashion for minutes or hours, while others seem to require only a few hours of sleep. When they are awake they tend to fuss, cry, play and demand attention from their exhausted parents, to the point where the sleep disturbance itself can become the major reason for parental exhaustion and the introduction of foster care. The prevalence of chronic neurological disabilities has significantly increased during the last decade, because markedly preterm infants and children with severe brain damage have survived due to advances in medical care (Alberman et al. 1992,Robinson and Jan 1993). Sleep disorders have also appeared to be increasing in this population. Melatonin plays an important role in the induction of sleep. It is produced by pinealocytes in the pineal gland. Tryptophan is converted to serotonin then to N-acetylserotonin and finally to melatonin (N-acetyl-5-methoxytryptamine).The secretion of melatonin is controlled by an endogenous rhythm-generating system in the brain which is synchronised by the light-dark cycle, so that melatonin levels are high in darkness and low in light; this is why it is called the ‘hormone of
darkness’ (Utinger 1992). The process begins at the retina, from where the signal goes to the suprachiasmatic nucleus of the hypothalamus, the reticular system, the spinal cord, cervical ganglia and through the postganglionic sympathetic fibres to the pineal gland (Rusak 1977). Recently, the suprachiasmatic nucleus has been found to be a major sleep regulator, and melatonin appears to influence this structure (Cassone el al. 1986,Vanecek et 01. 1987). When it is damaged, as demonstrated in studies with rodents, sleep difficulties develop which are intensified in a darkened environment. Melatonin has been synthesised, and the oral form is now available for investigational use. Its usefulness in regulating sleep has been noted for shift-workers (Weitzman et al. 1981), jet-lag (Arendt 1987),chronic insomnia (MacFarlane et al. f991) and delayed sleep-phase syndrome (Dahlitz er 01. 1991). Blind adults with free-running sleep-wake rhythms may also benefit from it (Sack el al. 1991). Voordouw et al. (1992) gave 300 mg of melatonin daily for four months to women, and found that it inhibited ovarian function. Yet even with such large doses, adverse side-effects were not noted by these or any of the other investigators.We became interested in melatonin treatment on compassionate grounds because a blind, neurologically multiply disabled child was referred to the Visually Impaired Program with a severe and chronic sleep disorder which did not respond to conventional treatment. His parents were sleep-deprived and in crisis. The treatment was successful, so we began to use it for other children with and without visual impairment

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