8 1998 Martin Dunitz Ltd

international Journal of Psychiatry in Clinical Practice 1998 Volume 2 Pages 143 - 145

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The treatment of sleep disorders in people with learning disabilities using light therapy

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CA SHORT’ AND PK

CARPENTER^

’Senior Registrar in Child and Adolescent Psychiatry, Downend Clinic; and ’Consultant Psychiatrist in Learning Disabilities, Hanham Hall Hospital, Bristol, LJK

CorrespondenceAddress Dr Clare Short, Senior Registrar in Child and Adolescent Psychiatry, Department of Child and Adolescent Psychiatry,Downend Clinic, Buckingham Gardens, Bristol BS16 5rW, UK Tel: +44 (0) 117 9566025 Fax: +44 (0) 117 9561907

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Light therapy is a recognized treatment for sleep phase disorders in the general population. Exposure to natural light can be a powerful means of correcting people’s sleep/wake pattern. Although sleep problems in the learning-disabled population are common, research is limited Light therapy has not to our knowledge been studied in this population. We report the case of a m a n with profound learning disabilities and poor visual acuity who was successfully treated with natural light for chronic sleep disturbance. Light therapy is safe, cheap and relatively easy to carry out. I t may prove helpful in subjects with learning disabilities who have sleep problems, even ifthey do not fulfill the criteriafor a particular sleep disorder. (Int J Psych Clin Pruct 1998; 2: 143 - 145)

Received 19 November 1997; accepted for publication 23 December 1997

INTRODUCTION leep problems are thought to be very common among S patients with learning disabilities and yet, as Espie and Tweedie’ report in their literature review for this population, research is limited, especially regarding electroencephalographic studies and reports based on informants. This may be because many individuals with learning disabilities are unable to communicate their sleep difficulties, and sleep problems among this group are therefore usually diagnosed only when they become a problem to the carers.l Polysomnographic sleep studies on individuals with learning disabilities have reported impoverished rapid eye movement (REM) sleep, with fewer eye movements during REM sleep2’ and lower REM sleep rates than normal controls. The quantity of REM sleep seems to relate positively to higher intelligence.’-‘ It has also been shown that this population sleeps for longer periods than normal controls, although they are more prone to night-time It is wise to interpret these results with caution, as most reports do not appear to have adequately controlled for the over-representation of individuals with epilepsy in the learning disability population. Epilepsy and anti-epileptic medication may. alone account for the reported differences.’ Sleep disorders among the learning-disabled are of great importance because they can impair both intellectual

functioning and behaviour. Disturbed or fragmented sleep can compromise the patient’s already impaired level of functioning. Drug therapy is often unsatisfactory, as it can cause daytime sedation and cognitive impairment as well as physical dependency. It may also depress REM sleep, which may already be compromised. Behavioural methods used for the non-impaired population are also being used for the learning-disabled, to retrain the patient’s sleep pattern through the reinforcement of social cues that prompt times of sleeping and waking. So far, the effectiveness of such approaches does not seem to have been evaluated in this population. One might, however, expect these behavioural methods to be more difficult to apply in the learning-disabled population, as they rely on staff awareness and a consistency in keeping the patients active through the day. This is often difficult to achieve in institutional settings.

CASE REPORT We report the case of a 34-year-old man with congenital hydrocephaly and subsequent profound learning disability, as well as very poor visual acuity, due to optic atrophy acquired as a child. He presented with an acute disruption of his sleep pattern, particularly a difficulty in getting off to sleep, and waking frequently during the early hours of the morning. He subsequently developed excessive daytime

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CA Short and PK Carpenter

drowsiness and lethargy. He had a past history of sleep problems of a similar nature, which had been treated with short-acting benzodiazepines, with limited success. A behavioural approach was adopted which aimed at improving sleep hygiene by reinforcing normal social cues and preventing any positive reinforcement of his night-time wakefulness. He was woken in the mornings at appropriate times, and dressed. Daytime sleeping was discouraged, but it was dlfficult to prevent it completely, due to staffing problems. The approach had little therapeutic effect. The introduction of a range of different hypnotics, including temazepam and zopiclone, in conjunction with the behavioural programme also proved ineffective over a 3month period; the patient in fact developed recognized side-effects from zopiclone. All hypnotic medication was stopped, and a new regime of direct exposure to natural light was introduced, to try to resynchronize the patient’s sleep/wake cycle. He was woken at a set time in the morning and exposed to direct natural light for a minimum of 2 hours. This was achieved either by taking him outdoors or by sitting him next to a window where he would receive maximum light exposure indoors. The behavioural approach continued alongside the introduction of light exposure. Within 2 weeks of implementing the light regime, his sleep pattern was back to normal and remained stable thereafter.

DISCUSSION The natural endogenous circadian cycle in humans is longer than 24 hours, and therefore the human brain needs to be retrained each day to the 24-hour cycle demanded by society. The retraining of the ‘free-running’ endogenous sleep/wake cycle relies on a combination of external cues, which include the length of exposure to natural light as well as social contacts and consistent rising times. Without these cues, sleep rhythms can become impaired. Totally blind people, for example, have been shown to run on an endogenous sleep/wake rhythm and commonly report sleep difficulties.6,7 The use of exposure to light in this case was inspired by the treatment of delayed sleep phase syndrome. In the general population, light therapy is used to resynchronize the circadian sleeplwake cycle as treatment for sleep phase disorder syndromes. The sleeplwake cycle can be shortened or lengthened according to the time of exposure to bright light. The resynchronization is presumably mediated by the pineal hormone, melatonin, which has a high affinity for receptors in the suprachiasmatic nucleus of the hypothalamus and the secretion of which is inhibited by exposure to light falling on the retina.’ Delayed sleep phase syndrome was first described by Weitzman in 1979.’ He defined it as initial insomnia and difficulty in waking at conventional times, but undisturbed late sleep on vacations. The International Classification of Sleep Disorders” demands a minimum of a month of excessive

sleepiness in conjunction with sleep log evidence of delayed sleep consistent with 24-hour polysomnoPPhY. Treatment of this disorder has been through a mixture of chronotherapy and light exposure. Chronotherapy involves the gradual shifting forward of bedtimes and getting-up times over a period of time until the subject achieves the desired sleep schedule, whereafter times are fixed.9 More recently, the importance of daytime light illumination to help reset the internal circadian rythmn has been recognized. Lewry et al” first recommended the use of exposure to early morning light to treat delayed sleep syndrome. The case we have described does not exactly fulfil the criteria for delayed sleep phase syndrome, in that despite daytime drowsiness and a tendency to sleep well past his usual rising time if allowed to, the patient was persistently waking in the early hours of the morning. Nor was it possible to conduct 24-hour polysomnography, as the patient would not have tolerated it. Individuals with ‘learning disabilities have very few social cues to reset the internal sleep/wake clock, especially if they have sensory impairment. Those who live in institutions may also be less responsive to behavioural programmes that rely on reinforcement of social cues. Morgan et all’ reported a study of institutionalized psychiatric patients whose circadian temperature peaks reflected the season of the year rather than the social schedule. This suggests that light exposure may play a more important role than social cues, in this setting; such patients may therefore have more need of natural light exposure to augment behavioural cues. A significant proportion of the learning-disabled also suffer from diminished visual acuity, which may impair the resetting of the endogenous sleep/wake cycle. No research (to our knowledge) has been conducted among the visually-impaired learning-disabled population to identify whether this particular group have a higher incidence of

Sleep disorders and learning disabilities

sleep disruption than the learning-disabled with normal vision, and if so, whether sleep disruption in this group responds to exposure to natural light. Since this treatment is safe, cheap and relatively easy to carry out, we recommend that it be considered in patients with learning disabilities whose sleep timing is disturbed, even if they do not fulfil the criteria for a particular sleep disorder.

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ACKNOWLEDGEMENT We would like to thank Mrs S Wilson for her helpful comments on the paper.

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REFERENCES 1. Espie CA, Tweedie FM (1991) Sleep patterns and sleep problems amongst people with mental handicap. J Ment Deficiency Res 35: 25-36. 2. Feinberg I (1968) Eye movement activity during sleep and intellectual function in mental retardation. Science 159: 1256. 3. Castaldo V, Krynicki V (1973) Sleep pattern and intelligence in functional mental retardation. J Ment Deficiency Res 17: 231 -5. 4. Clausen J, Sersen EA, Lidsky A (1977) Sleep patterns in mental retardation: Down’s syndrome. Electoencephalogr Clin Neurophysiol 43: 83-91. 5. Petre-Quadens 0 (1972) Sleep in mental retardation. In: Sleep and the maturing nervous system (ed CP Clemente, DP Purpura and FE Mayer) 383-417. Academic Press, New York. 6. Sasaki H, Nakata H, Murakami S et a1 (1992) Circadian sleep-waking rhythm disturbance in blind adolescence.Jpn J Psychiatry Neurol 46: 209. 7. Okawa M, Nanami T, Wada S et a1 (1987) Four congenitally blind children with circadian sleep-wake rhythm disorder. Sleep 10: 101-10.

8. Short RV (1993) Melatonin. Hormone of darkness. Br Med J 307: 952-3. 9. Regestin QR, Monk TH (1995) Delayed sleep phase syndrome: a review of its clinical aspects. Am J Psychiatry 152: 602-8. 10. Diagnostic Classification Steering Committee (1990) International Classificationof Sleep Disorders, 128- 133American Sleep Disorder Association, Rochester, MN. 11. Lewy AJ, Sack R, Singer C (1985) Immediate and delayed effects of bright light on human melatonin production: shifting “dam” and “dark” shifts the dim light melatonin onset. Ann hT Acad Sci 453: 253 - 9. 12. Morgan R, Minors DS, Waterhouse JM (1980) Does light rather than social factors synchronise the temperature rhythm of psychiatric patients? Chronobiologica 7: 331- 5.

The treatment of sleep disorders in people with learning disabilities using light therapy.

Light therapy is a recognized treatment for sleep phase disorders in the general population. Exposure to natural light can be a powerful means of corr...
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