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Sleep disturbances in depression and anxiety: Issues in childhood and adolescence
Journalo/Psychosomatic Research. Vol. 38, Suppl. I. pp. 61 67, 1994 Elsevier Science Ltd Printed in Great Britain 0022 3999/94 $7.00 + 00
Pergamon
0022-3999(94)00044-1
SLEEP D I S T U R B A N C E S IN DEPRESSION A N D ANXIETY: ISSUES IN C H I L D H O O D A N D A D O L E S C E N C E PETER HILL
CHILDHOOD is not a homogeneous developmental period, babies obviously differ from 12yr olds. The same point needs to be made about adolescence: 13 yr olds are different from 18 yr olds. Generalizing about sleep and its associations with emotional disorders in childhood and adolescence is therefore necessarily a crude procedure. Sleep architecture and some of the disorders of sleep show changes of form and emphasis which link to development within childhood and within adolescence. There is always, in any aspect of childhood psychopathology and physiopathology, a need to take a developmental perspective not just within the lifespan generally but within childhood and adolescence themselves and this is equally true of sleep research. The amount of sleep research in children and adolescence is very small. There are a number of reasons, ranging from practical considerations (for example, most children and teenagers with depression or anxiety disorders are treated in their own homes and are not easily accommodated in sleep laboratories) to issues of nosology. This last point is important. The classification of psychiatric disorders in childhood is not very satisfactory. It is only the emergence of operational diagnostic criteria, particularly in DSM III and its successors which has enabled findings in groups of similarly affected children to be replicated. Yet the diagnostic rules used in DSM lII and DSM III-R do not include severity criteria and in general have been developed for adults, rather than arising from epidemiology applied to young populations. Thus there is a growing realisation that DSM III criteria for major depressive disorder identifies many adolescents with only moderate depression and the large number of possible anxiety disorders which exist in DSM III and its revised version produce artificial separations within the general group of overanxious children. The simplest statement that one can make is that studies of polysomnographic or EEG findings in depressed children and adolescents yield inconsistent results. But closer examination of published studies in this age group reveals greater consistency, suggesting that differences in criteria for diagnosis and variations in age may obscure consistent trends. For instance, Weinberg's [1] criteria for the diagnosis of depression or the application of broad RDC or DSM III criteria are almost certainly too overselective in children and young adolescents so that some studies relying on these [24] yield negative findings when depressed children are compared with controls (usually healthy normals). If cases are selected by RDC specifically for endogenous depression St G e o r g e ' s H o s p i t a l M e d i c a l S c h o o l , L o n d o n .
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or if multiple criteria are used to supplement the Weinberg criteria, then positive findings emerge. Although overall, Puig-Antich et al. [3] found no differences between depressed children and normals when the depressed children were divided into those with endogenous features (by RDC) and those without trends emerged towards longer sleep latency, decreased REM latency and decreased SWS in the endogenously depressed group. This issue was specifically taken up by Appleboom-Fondu et al. [5] who compared nine adolescents with RDC major depressive syndrome with 12 who had a minor depressive syndrome. Though the REM latency of both major and minor depressives showed a trend to be lower than controls it did not differ between the two depressed groups. But the major depressives had lower sleep efficiency and a higher number of wakenings than did the minor depressives. Kutcher et al. [6], selecting adolescents who fulfilled the criteria for DSM III major depression, endogenous subtype, found depressed adolescents (age 15 19) to have decreased REM latency and increased sleep latency compared with normal controls. Selecting for endogenous depression helps provide distinctions. Similarly, if the depressed children are drawn from a population of in-patients (presumably a proxy indicator for severity) then positive findings are more likely than when depressed out-patients are studied. Emslie et al. [7, 8] showed shortened REM latency, increased sleep latency and increased REM activity in one group of in-patient depressed adolescents compared with normal data and pursued this in a controlled study [8] which showed depressed prepubertal and pubescent children who were in-patients to have shorter REM latency, increased sleep latency and increased REM time. Dahl et al. [9] reported no difference in sleep variables between depressed and normal adolescents until analysis of subgroups showed decreased REM latency among in-patient depressed adolescents and higher REM density among suicidal depressed adolescents. This was echoed by the study of Goetz et al. [10] on 16-25 yr olds with RDC major depression who found only prolonged sleep latency to distinguish the depressed group from normal controls. But when those who were in-patients and those who were suicidal were separately studied, a shorter REM latency emerged within the in-patients and a higher REM density among the suicidal depressives. There is also an interaction with age. Puig-Antich et al. [3] and Young et al. [4] who studied depressed prepubertal children and Goetz et al. [11] in a study on adolescents (11 18 yr olds, mean age 15) found no significant differences from normal controls, though the latter study shows a non-significant trend towards reduced REM latency and prolonged sleep latency in the depressed group. Yet Lahmeyer et al. [12], with somewhat older adolescents (11-19, mainly 18 and 19 yr olds) was able to demonstrate significantly lower REM latency and higher REM density in the depressed group as were Appleboom-Fondu et al. [5] with 11-20 yr olds and Kutcher et al. [6] with 15-19 yr olds. Similarly Riemann and Schmidt [13] were able to show decreased REM latency in depressed 14 20yr olds compared with controls even though they used DSM III criteria for selection. The same workers had earlier [14] described the inability of shortened REM latency to discriminate depressed young adults (18 35) from controls although the discriminatory ability did apply to a total population (age 18 65). This suggests an interaction with age and genetic loading or severity.
Polysomnographicfindings in depression
63
Briefly alluding to adult findings, Ulrich et al. [15] showed sleep efficiency, REM latency and the amount of SWS in depressed adults all to show strong correlations with age. Gillin et al. [16] also showed REM latency, TST, the amount of SWS and sleep efficiency to decrease with age in both normals and depressives and Coble et al. [17] showed an age effect comparing depressed 18 30 yr olds with 38 50 yr olds. In their study there were no differences in the clinical symptomatology between age groups but sleep efficiency, amount of SWS and REM latency were all lower in the older group. Normative data on sleep demonstrate a lessening of SWS with age beginning in late adolescence and a small decrease in REM latency with age, these being a continuation of age-related changes detectable in prepubertal children [18]. Changes are age related rather than related to pubertal staging: pubertal status has little effect on normal sleep measures [19]. No study on depressed children or adolescents has found any relationship with pubertal stage but a general association with increased age has been referred to above. What can we draw from this? I suggest three statements. 1. Differences comparable to those found in adult depression can be demonstrated in the young, though are usually of lesser degree. The most replicated finding is decreased REM latency. 2. Differences are more easily demonstrated when the subjects are a. severely depressed as indexed by inpatient status b. affected by depression with an endogenous picture c. older 3. No effect has been shown for sex or pubertal status In general, there seems to be an interaction between severity of depression, endogenicity and age. The polysomnographic abnormalities found in depression in the young appear to be extremes of those which occur in ageing. INSOMNIA IN ADOLESCENCE It is sometimes assumed that adolescents who complain of insomnia are essentially healthy or at any rate within the mainstream of adolescent development. In part this derives from the common observation that adolescents go to bed late when allowed to and sleep late in the mornings when they have the opportunity, in part because it is a common issue [20], and partly because mental health professionals are extremely tolerant of psychological deviations in adolescence because they believe (wrongly) that adolescence is necessarily a period of emotional turmoil. But adolescents who complain of difficulty getting off to or maintaining sleep, or describe themselves as having poor quality or insufficient sleep, are not likely to be healthy and in fact have symptoms suggestive of emotional conditions. Between 5 and 12°/,, of teenagers surveyed in general population studies complain of insomnia [21, 22]. It is the complaint of insomnia which is relevant--most individuals with low total sleep times have no reservations about their sleep and indeed it is normal for total sleep time to fall during adolescence. Adolescents who complain of insomnia have high rates of symptoms of depression and tension. In a study of 639 American school-age teenagers, Price et al. [22] found that those with insomnia in terms of difficulties getting off to sleep or waking for
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long periods during the night were more likely to be female, to worry more, to have personal and family problems, to have low self-esteem and feel m o o d y and dispirited. These findings are comparable to studies on medical students [23] and on young adults [24] suggesting that young adolescents are not qualitatively different from people a little older. In conclusion there are no grounds for thinking that the association of emotional pathology with a complaint of insomnia in adolescence differs from that in young adults. The complaint has much the same connotations. 1 emphasise the point because of colloquial assumptions that adolescence in its own right explains disturbances of sleep. It does not and in the case of insomnia there seems to be a particular association with m o o d or anxiety disorder. The direction of the association can be questioned. There are grounds for thinking that many or most Western teenagers are sleep-deprived [25] or are living a sleep wake cycle out of phase with convention and that this may have an effect on m o o d in its own right. Certainly this is a feature of some cases of the so-called sleep-phase syndrome [26] within which a teenager has become accustomed to going to bed at 3 or 5 a.m. ANXIETY The nosology of anxiety disorders in the young is unsatisfactory. There are too many conditions of uncertain validity which rely on subjective judgement and clinical preconception. Anxiety is, of course both a symptom and a disorder in its own right. As a symptom it is prominent in a number of reactions in childhood and can be regarded as the most prominent feature. There is thus a large number of so-called childhood anxiety disorders in both ICD-10 and DSM-IV (as proposed) and the picture is too confused for a simple statement to be made. Perhaps the most straightforward source of information about an association between an anxiety disorder and disturbances of sleep in childhood is the study of trauma victims. Children who have been involved in shipping disasters, group kidnappings or other catastrophes show a high rate of extreme anxiety reactions including patterns of signs conforming to DSM III-R/ICD-10 criteria for posttraumatic stress disorder. Among groups of children and young adolescents who have been exposed to such disasters, high levels of general anxiety and panic attacks are c o m m o n and there are prominently raised rates of problems settling to sleep, frequent waking, parasomnias, enuresis and nightmares have been reported [27]. The specific association between anxiety and sleep disturbance has not been explored in detail but the two phenomena are common and coexist. Levy [28] drew attention to the post-traumatic nightmare as being recurrent, literal in its depiction of the trauma and intensely anxiety-provoking. He compared dreams following alarming surgical procedures in children and combat neurosis in adults. In the early studies of disaster and children, Terr [29] was able to extend his description of dreams in terrorized children in her controlled study of 5 14-yr-old children who were the victims of a group kidnap and live burial. She described t h e onset of parasomnias, particularly sleep terrors, in previously unaffected children. With the passage of time, the content of nightmares was modified gradually and underwent what seemed to be partial symbolic change, particularly the inclusion of
Polysomnographic findings in depression
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personally dying during the recalled drama. Subsequent studies, well reviewed by Udwin [27] have documented the general increase in disturbances of sleep initiation and maintenance as well as an increased incidence of parasomnias and enuresis but the functional links between these remain unexplored. Conversely, most children presenting with parasomnias as a primary complaint do not seem overtly anxious
[301. Within such reports is usually an item which refers to difficulties settling to sleep. These are of course, common in young children and commonly relate to difficulties separating from an attachment figure. The complexity here is that the attachment relationship is a key element in anxiety management. Proximity to an attachment figure relieves anxiety (as well as providing relief from fear, pain or tension) and bedtime can be associated with various fears: of separation itself, of the dark or of bad dreams. The child clings, resisting separation from a parent because the parent's proximity assists anxiety reduction and allows sleep. Yet sleep is itself a separation from the attachment figure. Anxiety in middle childhood, or indeed in adolescence, activates the anxiety management strategies of earlier childhood and anxious schoolchildren commonly cling to their parents in an attempt to reduce their own anxiety. This in its own right can produce difficulties settling to sleep because of the child's attempts to maintain the proximity of a parent. Or the unavailability of a parent at bedtime can produce anxiety which can prolong sleep latency. The importance of drawing attention to this is that what may be measured as an apparent physiological variable (sleep latency) might well be a reflection of a psychological process. On the other hand, some objective study of sleep maintenance in childhood anxiety disorders might elucidate whether there really is a problem with sleep maintenance. It is a common complaint made by the parents of anxious children that the child wakes frequently during the night. Yet what is not known is whether there is a true increase in night waking or whether what is happening is that anxious children who wake are unable to settle themselves back to sleep on their own. This would be in contrast to those who wake and subsequently settle back to sleep without waking their parents. There is some circumstantial evidence that this may be the case [31, 32]. In parallel with insomnia, what becomes the focus of clinical interest in whether the waking is the subject of a complaint made by parents because they are themselves woken by a crying or intruding child. This is different from the physiological problem of waking yet numerous doctors attempt to treat night-waking in children with sedatives rather than recognise the key point, that it is a failure to re-settle rather than waking itself which is the problem. Associations between difficult temperament (emotional, active, resisting imposed change, withdrawing from novelty etc.) and sleep difficulties in small children have been found [33]. The difficulty is knowing the direction of the association. Certainly infants with difficult temperaments are more likely to react to stressors such as the birth of a sibling [34] but there is also the possibility that sleep deprivation because of settling or waking problems can cause difficulties of moodiness, irritability and poor acceptance of novelty during the day of the type described by temperament questionnaires. Various clinicians have made the point that establishing adequate settling and sleep routines improves daytime behaviour and the possibility of bidirectional causality needs to be made.
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In s u m m a r y , there are v i r t u a l l y n o d a t a o n d i s t u r b a n c e s o f sleep a n d a n x i e t y d i s o r d e r s in c h i l d h o o d a n d a d o l e s c e n c e b e y o n d the r a t h e r special case o f t r a u m a p r e c i p i t a t e d a n x i e t y w h i c h suggests a g e n e r a l a r o u s a l - r e l a t e d d i s t u r b a n c e o f D I M S , n i g h t m a r e s , p a r a s o m n i a s a n d enuresis. N e v e r t h e l e s s t h e r e is an i n t e r e s t i n g issue as to h o w the a t t a c h m e n t r e l a t i o n s h i p influences b o t h sleep i n i t i a t i o n , re-settling a l t e r n o r m a l n i g h t w a k i n g a n d a n x i e t y r e d u c t i o n w h i c h m i g h t h a v e s o m e p a r a l l e l s in a d u l t h o o d . In this area, as in the w o r k o n d e p r e s s i o n , the p o s s i b i l i t y t h a t m o o d d i s t u r b a n c e m a y be b o t h c a u s e a n d c o n s e q u e n c e o f sleep d i s t u r b a n c e arises. Sleep r e s e a r c h is o n e o f the few a r e a s o f e n q u i r y w h i c h has t a k e n n o t e o f ager e l a t e d c h a n g e s w i t h i n a d u l t life. We are b e c o m i n g m o r e a w a r e t h a t d e v e l o p m e n t d o e s n o t s t o p at 18 o r 21 b u t c o n t i n u e s for m u c h o f life. D e v e l o p m e n t is a m o r e c o m p l e x n o t i o n t h a n a g e - r e l a t e d c h a n g e b u t sleep r e s e a r c h is an a r e a w h i c h c a n a c c o m m o d a t e this, b r i d g i n g n o t o n l y p h y s i o l o g y a n d p s y c h o p a t h o l o g y b u t o f f e r i n g an o p p o r t u n i t y for a g e n u i n e d e v e l o p m e n t a l p s y c h o p a t h o l o g i c a l a p p r o a c h t o o .
REFERENCES 1. WEINBERGWA, RUTMANJ, SULLIVANL, et al. Depression in children referred to an educational diagnostic center. Pediat 1973; 83: 1065-1072. 2. KUPFERD J, COBLEP, KANEJ, et al. Imipramine and EEG sleep in children with depressive symptoms. Psychopharmacology 1979; 60:117 123. 3. PUIG-ANTICH JR GOETZR, HANLON C, DAVIES M, THOMPSONJ, CHAMBERSW J, TABRIZI M, WEITZMAN ED. Sleep architecture and REM sleep measures in prepubertal children with major depression. Arch Gen Psychiat 1982; 39: 932-939. 4. YOUNG W, KNOWLESJB, MACLEANAW BOAG L, McCoNVILLE BJ. The sleep of childhood depressives: comparison with age matched controls. Biol Ps)ehiat 1982; 17:1163 1168. 5. APPELBOOM-FONDUJ, KERKHOFS M, MENDLEWICZ J. Depression in adolescents and young adults polysomnographic and neuroendocrine aspects. J Affec! Disord 1988; 14: 35~,0. 6. KUTCHER S, WILL1AMSONP, MARTON P, SZALA1J. REM latency in endogenously depressed adolescents. Br J Psychiat 1992; 161: 399402. 7. EMSLIEG J, ROFFWARGI/P, RUSH A J, WEINBERGWA, PARKIN-FEIGENBAUML. Sleep LEG findings in depressed children and adolescents. Am J Psychiat 1987; 144: 668-670. 8. EMSL1E G J, RUSH A J, WEINBERG WA, RINTELMANN JW, ROFFWARG, HP. Children with major depression show reduced rapid eye movement latencies. Arch Gen Psyehiat 1990; 47: 119-124. 9. DAHL RE, PUIG-ANTICH J, RYAN ND, NELSON B, DACHILLE S, CUNNINGHAM SL, TRUBNICK L, KLEPPER TP. EEG sleep in adolescents with major depression: the role of suicidality and inpatient status. J AffEct Disord 1990; 19:63 75. 10. GOETZRR, PUIG-ANTICHJ, DAHL RE, RYANND, ASNISGM, RABINOVICHH, NELSONB. LEG sleep of young adults with major depression: a controlled study. J AJJect Disorders 1991; 22:91 100. 11. GOETZ RR, PU1G-ANTICH J, RYAN N, RABINOVICH H, AMBROSINI PJ, NELSON B, KRAWIEC V. Electroencephalographie sleep of adolescents with major depression and normal controls. Arch Gen Psychiat 1987; 44: 61-68. 12. LAHMEYERHW, POZNANSKIEO, BELLURS. LEG sleep in depressed adolescents. Am J Psychiat 1983; 140: 1150-1153. 13. R1EMANN D, SCHMIDT MH. REM sleep distribution in adolescents with major depression and schizophrenia. Sleep Res 1993; 22: 554. 14. LAUERCJ, RIEMANND, W1EGAND M, ]3ERGERM. From early to late adulthood: changes in LEG sleep of depressed patients and healthy volunteers. Biol Psychiat 1991; 29:979 993. 15. ULRICHR, SHAW DH, KUPPER DJ. The effects of aging on sleep. Sleep 1980; 3: 3140. 16. GILLIN JC, DUNCANWC, MURHY DL, et al. Age related changes in sleep in depressed and normal subjects. Psychiat Res 1981; 4: 73-78. 17. COBLE P, McPARTLAND RJ, SILVA WJ, et al. Is there a first night effect? Biol Psychiat 1974; 9: 215-219. 18. COBLEPA, KUPEER DJ, REYNOLDSCF, HOUCKP. LEG sleep of healthy children 6 12 years of age. In Sleep and its Disorders in Children (Edited by GUILLEM1NAULTC), pp. 29~41. New York: Raven Press, 1987.
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19. COBLE PA, KUPFER D, TASKA LS. et al. EEG sleep of normal healthy children. Part 1: Findings using standard measurement methods. Sleep 1984; 7:289 303. 20. WELSTEIN C, DEMENT WC, REDINGTON D, GUILLEM1NAULTC, MITLER MM. Insomnia in the San Francisco Bay area: a telephone survey. In Sleep~Wake Disorders: Natural Histoo,, Epidemiology and Long-Term Evolution (Edited by GUILLEMINAULTC, LUGARESI E), pp. 73--86. New York: Raven Press. 21. KARACAN I, THORNBY Jl, ANCH M, et al. Prevalence of sleep disturbance in a primarily urban Florida county. Soe Sei M e d 1976; 10:239 244. 22. PRICE VA, COATES T J, THORESON CE, GRINSTEAD OA. Prevalence and correlates of poor sleep a m o n g adolescents. Am J Dis Children 1978: 132:325 334. 23. JOHNS MW, GAY TJA, GOODYEAR M, et al. Sleep habits of healthy young adults. Br J Prey Soe Med 1971; 25:236 241. 24. KALES A, CALDWELL AB. PRESTON TA, et al. Personality patterns in insomnia. Archs Gen Psychiat 1976; 33:1128 1134. 25. WEBB W, AGNEW H. Are we chronically sleep-deprived? Bull Psyehonom Soe 1975; 6 : 4 7 48. 26. WCITZMANN ED, CZEISLER CA, COLEMAN RM, SPEILMAN AJ, ZIMMERMAN J, DEMENT WC. Delayed sleep phase syndrome. Arch Gen Psyehiat 1981: 38:737 746. 27. UDWlN O. Children's reactions to traumatic events. J Child Psyehol Psyehiat 1993; 34:115 127. 28. LEVY D. Psychic trauma of operations in children and a note on combat neurosis. Am J Dis Childhood 1945; 69: 7-25. 29. TERR LC. Nightmares in children. In Sle~7) and its Disorders in Children (Edited by GUILLEMINAULT C), pp. 231 242. New York: Raven Press. 30. GUILLEMINAULTC. Somnambulism and night terrors. In Sleep and its Disorders #~ Children (Edited by GUILLEMINAULTC), pp. 243 252. New York: Raven Press. 31. ANDERST. Home-recorded sleep in two nine-month old infants. J Am Chihl Psyehol 1978; 17: 421~432. 32. SCOTT G, RICHARDS MPM. Night waking in infants: effects of providing advice and support for parents. J Child Psyehol Psyehiat 1990; 31:551 567. 33. RICHMAN N. Surveys of sleep disorders in children. In Sleep and its Disorders b~ Children (Edited by GUILLEMINAULT C), pp. 115 127. New York: Raven Press. 34. DUNN J, KENDRICK C. Siblings: Love, Em T and Understanding. London: Grant Mclntyre, 1982. 35. KUPFER DJ, ULRICIt RF, COBLE PA. Electroencephalographic sleep of young depressives. Areh Gen Psychiat 1985; 42:806 810. 36. PUIG-ANTICH J, GOETZ R, HANLON C, TABRIZI M, DAVIES M, WE1TZMANED. Sleep architecture and R E M sleep measures in prepubertal major depressives. Areh Gen Psyehiat 1983; 40:187 192.
Pergamon
0022-3999(94)00044-1
SLEEP D I S T U R B A N C E S IN DEPRESSION A N D ANXIETY: ISSUES IN C H I L D H O O D A N D A D O L E S C E N C E PETER HILL
CHILDHOOD is not a homogeneous developmental period, babies obviously differ from 12yr olds. The same point needs to be made about adolescence: 13 yr olds are different from 18 yr olds. Generalizing about sleep and its associations with emotional disorders in childhood and adolescence is therefore necessarily a crude procedure. Sleep architecture and some of the disorders of sleep show changes of form and emphasis which link to development within childhood and within adolescence. There is always, in any aspect of childhood psychopathology and physiopathology, a need to take a developmental perspective not just within the lifespan generally but within childhood and adolescence themselves and this is equally true of sleep research. The amount of sleep research in children and adolescence is very small. There are a number of reasons, ranging from practical considerations (for example, most children and teenagers with depression or anxiety disorders are treated in their own homes and are not easily accommodated in sleep laboratories) to issues of nosology. This last point is important. The classification of psychiatric disorders in childhood is not very satisfactory. It is only the emergence of operational diagnostic criteria, particularly in DSM III and its successors which has enabled findings in groups of similarly affected children to be replicated. Yet the diagnostic rules used in DSM lII and DSM III-R do not include severity criteria and in general have been developed for adults, rather than arising from epidemiology applied to young populations. Thus there is a growing realisation that DSM III criteria for major depressive disorder identifies many adolescents with only moderate depression and the large number of possible anxiety disorders which exist in DSM III and its revised version produce artificial separations within the general group of overanxious children. The simplest statement that one can make is that studies of polysomnographic or EEG findings in depressed children and adolescents yield inconsistent results. But closer examination of published studies in this age group reveals greater consistency, suggesting that differences in criteria for diagnosis and variations in age may obscure consistent trends. For instance, Weinberg's [1] criteria for the diagnosis of depression or the application of broad RDC or DSM III criteria are almost certainly too overselective in children and young adolescents so that some studies relying on these [24] yield negative findings when depressed children are compared with controls (usually healthy normals). If cases are selected by RDC specifically for endogenous depression St G e o r g e ' s H o s p i t a l M e d i c a l S c h o o l , L o n d o n .
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or if multiple criteria are used to supplement the Weinberg criteria, then positive findings emerge. Although overall, Puig-Antich et al. [3] found no differences between depressed children and normals when the depressed children were divided into those with endogenous features (by RDC) and those without trends emerged towards longer sleep latency, decreased REM latency and decreased SWS in the endogenously depressed group. This issue was specifically taken up by Appleboom-Fondu et al. [5] who compared nine adolescents with RDC major depressive syndrome with 12 who had a minor depressive syndrome. Though the REM latency of both major and minor depressives showed a trend to be lower than controls it did not differ between the two depressed groups. But the major depressives had lower sleep efficiency and a higher number of wakenings than did the minor depressives. Kutcher et al. [6], selecting adolescents who fulfilled the criteria for DSM III major depression, endogenous subtype, found depressed adolescents (age 15 19) to have decreased REM latency and increased sleep latency compared with normal controls. Selecting for endogenous depression helps provide distinctions. Similarly, if the depressed children are drawn from a population of in-patients (presumably a proxy indicator for severity) then positive findings are more likely than when depressed out-patients are studied. Emslie et al. [7, 8] showed shortened REM latency, increased sleep latency and increased REM activity in one group of in-patient depressed adolescents compared with normal data and pursued this in a controlled study [8] which showed depressed prepubertal and pubescent children who were in-patients to have shorter REM latency, increased sleep latency and increased REM time. Dahl et al. [9] reported no difference in sleep variables between depressed and normal adolescents until analysis of subgroups showed decreased REM latency among in-patient depressed adolescents and higher REM density among suicidal depressed adolescents. This was echoed by the study of Goetz et al. [10] on 16-25 yr olds with RDC major depression who found only prolonged sleep latency to distinguish the depressed group from normal controls. But when those who were in-patients and those who were suicidal were separately studied, a shorter REM latency emerged within the in-patients and a higher REM density among the suicidal depressives. There is also an interaction with age. Puig-Antich et al. [3] and Young et al. [4] who studied depressed prepubertal children and Goetz et al. [11] in a study on adolescents (11 18 yr olds, mean age 15) found no significant differences from normal controls, though the latter study shows a non-significant trend towards reduced REM latency and prolonged sleep latency in the depressed group. Yet Lahmeyer et al. [12], with somewhat older adolescents (11-19, mainly 18 and 19 yr olds) was able to demonstrate significantly lower REM latency and higher REM density in the depressed group as were Appleboom-Fondu et al. [5] with 11-20 yr olds and Kutcher et al. [6] with 15-19 yr olds. Similarly Riemann and Schmidt [13] were able to show decreased REM latency in depressed 14 20yr olds compared with controls even though they used DSM III criteria for selection. The same workers had earlier [14] described the inability of shortened REM latency to discriminate depressed young adults (18 35) from controls although the discriminatory ability did apply to a total population (age 18 65). This suggests an interaction with age and genetic loading or severity.
Polysomnographicfindings in depression
63
Briefly alluding to adult findings, Ulrich et al. [15] showed sleep efficiency, REM latency and the amount of SWS in depressed adults all to show strong correlations with age. Gillin et al. [16] also showed REM latency, TST, the amount of SWS and sleep efficiency to decrease with age in both normals and depressives and Coble et al. [17] showed an age effect comparing depressed 18 30 yr olds with 38 50 yr olds. In their study there were no differences in the clinical symptomatology between age groups but sleep efficiency, amount of SWS and REM latency were all lower in the older group. Normative data on sleep demonstrate a lessening of SWS with age beginning in late adolescence and a small decrease in REM latency with age, these being a continuation of age-related changes detectable in prepubertal children [18]. Changes are age related rather than related to pubertal staging: pubertal status has little effect on normal sleep measures [19]. No study on depressed children or adolescents has found any relationship with pubertal stage but a general association with increased age has been referred to above. What can we draw from this? I suggest three statements. 1. Differences comparable to those found in adult depression can be demonstrated in the young, though are usually of lesser degree. The most replicated finding is decreased REM latency. 2. Differences are more easily demonstrated when the subjects are a. severely depressed as indexed by inpatient status b. affected by depression with an endogenous picture c. older 3. No effect has been shown for sex or pubertal status In general, there seems to be an interaction between severity of depression, endogenicity and age. The polysomnographic abnormalities found in depression in the young appear to be extremes of those which occur in ageing. INSOMNIA IN ADOLESCENCE It is sometimes assumed that adolescents who complain of insomnia are essentially healthy or at any rate within the mainstream of adolescent development. In part this derives from the common observation that adolescents go to bed late when allowed to and sleep late in the mornings when they have the opportunity, in part because it is a common issue [20], and partly because mental health professionals are extremely tolerant of psychological deviations in adolescence because they believe (wrongly) that adolescence is necessarily a period of emotional turmoil. But adolescents who complain of difficulty getting off to or maintaining sleep, or describe themselves as having poor quality or insufficient sleep, are not likely to be healthy and in fact have symptoms suggestive of emotional conditions. Between 5 and 12°/,, of teenagers surveyed in general population studies complain of insomnia [21, 22]. It is the complaint of insomnia which is relevant--most individuals with low total sleep times have no reservations about their sleep and indeed it is normal for total sleep time to fall during adolescence. Adolescents who complain of insomnia have high rates of symptoms of depression and tension. In a study of 639 American school-age teenagers, Price et al. [22] found that those with insomnia in terms of difficulties getting off to sleep or waking for
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long periods during the night were more likely to be female, to worry more, to have personal and family problems, to have low self-esteem and feel m o o d y and dispirited. These findings are comparable to studies on medical students [23] and on young adults [24] suggesting that young adolescents are not qualitatively different from people a little older. In conclusion there are no grounds for thinking that the association of emotional pathology with a complaint of insomnia in adolescence differs from that in young adults. The complaint has much the same connotations. 1 emphasise the point because of colloquial assumptions that adolescence in its own right explains disturbances of sleep. It does not and in the case of insomnia there seems to be a particular association with m o o d or anxiety disorder. The direction of the association can be questioned. There are grounds for thinking that many or most Western teenagers are sleep-deprived [25] or are living a sleep wake cycle out of phase with convention and that this may have an effect on m o o d in its own right. Certainly this is a feature of some cases of the so-called sleep-phase syndrome [26] within which a teenager has become accustomed to going to bed at 3 or 5 a.m. ANXIETY The nosology of anxiety disorders in the young is unsatisfactory. There are too many conditions of uncertain validity which rely on subjective judgement and clinical preconception. Anxiety is, of course both a symptom and a disorder in its own right. As a symptom it is prominent in a number of reactions in childhood and can be regarded as the most prominent feature. There is thus a large number of so-called childhood anxiety disorders in both ICD-10 and DSM-IV (as proposed) and the picture is too confused for a simple statement to be made. Perhaps the most straightforward source of information about an association between an anxiety disorder and disturbances of sleep in childhood is the study of trauma victims. Children who have been involved in shipping disasters, group kidnappings or other catastrophes show a high rate of extreme anxiety reactions including patterns of signs conforming to DSM III-R/ICD-10 criteria for posttraumatic stress disorder. Among groups of children and young adolescents who have been exposed to such disasters, high levels of general anxiety and panic attacks are c o m m o n and there are prominently raised rates of problems settling to sleep, frequent waking, parasomnias, enuresis and nightmares have been reported [27]. The specific association between anxiety and sleep disturbance has not been explored in detail but the two phenomena are common and coexist. Levy [28] drew attention to the post-traumatic nightmare as being recurrent, literal in its depiction of the trauma and intensely anxiety-provoking. He compared dreams following alarming surgical procedures in children and combat neurosis in adults. In the early studies of disaster and children, Terr [29] was able to extend his description of dreams in terrorized children in her controlled study of 5 14-yr-old children who were the victims of a group kidnap and live burial. She described t h e onset of parasomnias, particularly sleep terrors, in previously unaffected children. With the passage of time, the content of nightmares was modified gradually and underwent what seemed to be partial symbolic change, particularly the inclusion of
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personally dying during the recalled drama. Subsequent studies, well reviewed by Udwin [27] have documented the general increase in disturbances of sleep initiation and maintenance as well as an increased incidence of parasomnias and enuresis but the functional links between these remain unexplored. Conversely, most children presenting with parasomnias as a primary complaint do not seem overtly anxious
[301. Within such reports is usually an item which refers to difficulties settling to sleep. These are of course, common in young children and commonly relate to difficulties separating from an attachment figure. The complexity here is that the attachment relationship is a key element in anxiety management. Proximity to an attachment figure relieves anxiety (as well as providing relief from fear, pain or tension) and bedtime can be associated with various fears: of separation itself, of the dark or of bad dreams. The child clings, resisting separation from a parent because the parent's proximity assists anxiety reduction and allows sleep. Yet sleep is itself a separation from the attachment figure. Anxiety in middle childhood, or indeed in adolescence, activates the anxiety management strategies of earlier childhood and anxious schoolchildren commonly cling to their parents in an attempt to reduce their own anxiety. This in its own right can produce difficulties settling to sleep because of the child's attempts to maintain the proximity of a parent. Or the unavailability of a parent at bedtime can produce anxiety which can prolong sleep latency. The importance of drawing attention to this is that what may be measured as an apparent physiological variable (sleep latency) might well be a reflection of a psychological process. On the other hand, some objective study of sleep maintenance in childhood anxiety disorders might elucidate whether there really is a problem with sleep maintenance. It is a common complaint made by the parents of anxious children that the child wakes frequently during the night. Yet what is not known is whether there is a true increase in night waking or whether what is happening is that anxious children who wake are unable to settle themselves back to sleep on their own. This would be in contrast to those who wake and subsequently settle back to sleep without waking their parents. There is some circumstantial evidence that this may be the case [31, 32]. In parallel with insomnia, what becomes the focus of clinical interest in whether the waking is the subject of a complaint made by parents because they are themselves woken by a crying or intruding child. This is different from the physiological problem of waking yet numerous doctors attempt to treat night-waking in children with sedatives rather than recognise the key point, that it is a failure to re-settle rather than waking itself which is the problem. Associations between difficult temperament (emotional, active, resisting imposed change, withdrawing from novelty etc.) and sleep difficulties in small children have been found [33]. The difficulty is knowing the direction of the association. Certainly infants with difficult temperaments are more likely to react to stressors such as the birth of a sibling [34] but there is also the possibility that sleep deprivation because of settling or waking problems can cause difficulties of moodiness, irritability and poor acceptance of novelty during the day of the type described by temperament questionnaires. Various clinicians have made the point that establishing adequate settling and sleep routines improves daytime behaviour and the possibility of bidirectional causality needs to be made.
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In s u m m a r y , there are v i r t u a l l y n o d a t a o n d i s t u r b a n c e s o f sleep a n d a n x i e t y d i s o r d e r s in c h i l d h o o d a n d a d o l e s c e n c e b e y o n d the r a t h e r special case o f t r a u m a p r e c i p i t a t e d a n x i e t y w h i c h suggests a g e n e r a l a r o u s a l - r e l a t e d d i s t u r b a n c e o f D I M S , n i g h t m a r e s , p a r a s o m n i a s a n d enuresis. N e v e r t h e l e s s t h e r e is an i n t e r e s t i n g issue as to h o w the a t t a c h m e n t r e l a t i o n s h i p influences b o t h sleep i n i t i a t i o n , re-settling a l t e r n o r m a l n i g h t w a k i n g a n d a n x i e t y r e d u c t i o n w h i c h m i g h t h a v e s o m e p a r a l l e l s in a d u l t h o o d . In this area, as in the w o r k o n d e p r e s s i o n , the p o s s i b i l i t y t h a t m o o d d i s t u r b a n c e m a y be b o t h c a u s e a n d c o n s e q u e n c e o f sleep d i s t u r b a n c e arises. Sleep r e s e a r c h is o n e o f the few a r e a s o f e n q u i r y w h i c h has t a k e n n o t e o f ager e l a t e d c h a n g e s w i t h i n a d u l t life. We are b e c o m i n g m o r e a w a r e t h a t d e v e l o p m e n t d o e s n o t s t o p at 18 o r 21 b u t c o n t i n u e s for m u c h o f life. D e v e l o p m e n t is a m o r e c o m p l e x n o t i o n t h a n a g e - r e l a t e d c h a n g e b u t sleep r e s e a r c h is an a r e a w h i c h c a n a c c o m m o d a t e this, b r i d g i n g n o t o n l y p h y s i o l o g y a n d p s y c h o p a t h o l o g y b u t o f f e r i n g an o p p o r t u n i t y for a g e n u i n e d e v e l o p m e n t a l p s y c h o p a t h o l o g i c a l a p p r o a c h t o o .
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