Case Study Delayed Sleep Phase Disorder after Traumatic Brain Injury SCOTI B. PATIEN, M.D.,
AND
W. MARK LAUDERDALE, M.D., F.R.C.P.(C)
Abstract. Sleep-wake schedule disorder is defined by DSM-lIl-R as a mismatch between the normal sleepwake schedule for a person 's environment and his or her circadian sleep-wake pattern. The authors report a case in which a sleep-wake schedule disorder arose after a closed head injury . Sleep-wake schedule disorder has not been described as an outcome of closed head injury. As patients with sleep-wake schedule disorders may present with insomnia, this case suggests the possibility that some of the insomnia that frequently follows closed head injury may represent sleep-wake schedule disorders. J. Am. Acad. Child Adolesc. Psychiatry, 1992, 31, I: 100-102. Key Words: sleep disorder, sleep, adolescence, school phobia, head injuries. Sleep-wake schedule disorder is defined by DSM-III-R as a "mismatch between the normal sleep-wake schedule for a person's environment and his or her circadian sleep-wake pattern, resulting in a complaint of either insomnia or hypersomnia" (American Psychiatric Association, 1987). The disorder includes several subtypes, including advanced or delayed types, disorganized type, or frequently changing type. The factors most frequently associated with the onset of sleep-wake schedule disorders are travel through different time zones and shift work schedules. The delayed type of sleep-wake schedule disorder occurs when an individual cannot get to sleep until later than usual, but then sleeps normally for a normal amount of time. The pathophysiology of the delayed type of sleep-wake schedule disorder is believed to be related to a reduced ability, on the part of these patients, to phase advance their sleep-wake schedule as well as the presence of environmental synchronizing cues that prevent resynchronization by phase retardation (Czeisler et al., 1981). Sleep schedule disturbances have been described in both adults and children (Ferber, 1987). In children and adolescents, the disorder is particularly troublesome because it produces somnolence, fatigue, and irritability during hours when the affected individual is expected to be attending school. The authors have recently seen a 13-year-old boy who developed a sleep-wake schedule disorder of the delayed type soon after suffering a closed head injury. The case is of interest because head injury has not been described as a cause of sleep-phase schedule disorder.
Case Report l.W. was a 13-year-old seventh grade student with severe Accepted June 27, 1991. Dr. Patten is Clinical Fello w, Alberta Heritage Foundation for Medical Research, University ofCalgary, and Dr. Lauderdale is Clinical Assistant Professor, Department ofPsychiatry, University of Calgary. Reprint requests to Dr. Patt en, Department of Community Health Sciences, Faculty ofMedicin e, The University ofCalgary, 3330 Hosp ital Drive N. W., Calgary, Alberta T2N 4N1 . 0890-8567/92/3101-100$03 .OO/O© 1992 by the American Academy of Child and Adolescent Psychiatry.
100
sleep disturbance. Specifically, he was unable to get to sleep until 5 or 6 o'clock in the morning and then would sleep normally until 3 o'clock in the afternoon. The symptoms dated back to a motorcycle accident 13 months before. l.W. was wearing a helmet that "split" when he fell off the bike. He was unconscious for about 5 minutes, followed by a headache and drowsiness. His physical examination in the emergency room was normal. No abnormalities were noted in his mental state except that he was somewhat " vague." Skull, neck, chest, and pelvic x-rays were all normal. A computed tomographic scan showed only a small calcification along the parasagittal region on the right side. An EEG was normal. He remained in hospital for 2 days for observation. In the weeks after the injury, l .W. suffered from vertigo, bilateral throbbing headaches, and an inability to sleep until later and later at night. His performance at school declined because of fatigue and inability to concentrate. Eventually, he was unable to get up to go to school, and he began taking correspondence courses at home. In the 13 months after the injury, the vertigo and headache decreased in severity, duration, and frequency (1-2 per month). He was seen by several neurologists and neuropsychologists for the persisting sleep problem and school absence. All neurological examinations were normal. Neuropsychological testing showed no impairments in cognitive functioning. He showed average ability in both verbal and visual-spatial areas, and his memory was generally above average. Measures of frontal lobe function were normal. His school grades had been above average in the early years, average in Grade 6, and below average or failing in Grade 7 before the accident. Once he began correspondence courses, however, he achieved above average grades again, which he attributed to being able to work alone and at his own pace. He disliked having to be at school by 8:30 A.M. Before psychiatric evaluation, chronotherapy schedules and medication with nitrazepam were tried, and both were only temporarily successful. Behavioral ratings or sleep logs were not done. At psychiatric examination, l.W. appeared older than his stated age. He was slightly overweight with a large frame. Both height and weight were above the 95th percentile for his age, but there was no history of appetite change or weight J. Am. Acad. Child Adolesc. Psychiatry, 31:1, January 1992
SLEEP PHASE DISORDER AFrER HEAD INJURY
gain since the accident. His mood was euthymic with normal range of expression. He stated that he was motivated to proceed with the treatment to normalize his sleep pattern. There was no fatigue, anxiety, nightmares, reexperiencing of the trauma, phobias, or emotional numbing that would suggest the presence of post-traumatic stress disorder (Silverman, 1986). Speech, perception, and cognition were normal. He seemed self-confident and generally satisfied with his family life. J.W. had no previous medical or psychiatric history. His mother had epilepsy, for which she was receiving medications. J.W.'s biological father had died when J.W. was 3 years old, but he is said to have been an alcoholic and to have spent time in prison because of felony convictions. One paternal uncle had committed suicide. There was no other psychiatric history in the family. The authors' evaluation and management of J.W. included a number of sessions with his family in which there was evidence of dysfunction. J.W.'s stepfather was unsupportive and disengaged, and his mother seemed to have difficulty defining limits and imposing structure on her children's behavior. She therefore may have had difficulty providing the environmental structure that would have been ideal for the enforcement of the chronotherapy schedules. The parents also found it difficult to bring J.W. to sessions regularly because of the distance they had to travel and their working hours. J.W.'s response to the treatment course was less than might have been hoped. Various approaches were used over a 4-month period, and J.W. was reasonably compliant in performing instructions. Initially, because chronotherapy had been previously unsuccessful, there was an attempt to remove the reinforcers for staying up at night. He was reassured that even after his schedule returned to normal he could continue with correspondence courses. His household chores, outdoor exercise, schoolwork, television watching, and other entertainment were restricted to daytime hours, while at night he was to practice self-relaxation techniques and remain inactive. With a poor response to these interventions, hypnosis was added to help him gain a more positive attitude toward sleeping restfully and the ordeal of hourly calisthenics was prescribed if he had not yet fallen asleep. With only temporary improvement of a few days, this approach was replaced by chronotherapy . J.W. was asked to stay up 1 hour later each day until his schedule was normalized. Phase advancing was successful for the first week but then reverted to the original pattern when J.W. was unable to fall asleep at midday. After 2 months of minimal improvement, l.W. was asked to stay up all night and the next day if he was not asleep within 1 hour of going to bed at 10:30 P.M. Over a 3-week period, it was necessary for J.W. to stay up all night on three occasions, but his sleep schedule was more or less normal. During this time, l.W. seemed to be in a good mood and was making plans for a summer job and helping his mother work in the garden. However, his mother developed a number of somatic complaints after a conflict with her husband, and in the following weeks l.W. stopped using the approach J.Am.Acad. Child Adolesc.Psychiatry, 31:1, January1992
because of the continued necessity to regularly stay up all night. In the end, in view of J.W.'s satisfactory academic performance and personal and social adjustment his parents were reluctant to force him to change to a more "normal" sleep schedule. He continued in follow-up for another year with no significant change in this pattern. Difficulties in the parents' marriage continued to occur periodically. His stepfather resisted attempts to engage in therapy. Discussion
The authors have described a case in which a sleep-wake schedule disorder had its onset after a head injury involving loss of consciousness. Closed head injury has not been described as a cause of sleep-wake schedule disorder. There was no suggestion in this case that the sleep disturbance was initiated by other factors that might have impaired sleep onset, such as the headaches experienced by this patient. Furthermore, as is typical of sleep-wake schedule disorders, the patient's sleep was qualitatively normal during the time when he was asleep. Ideally, a polysomnographic recording could have been performed to document the normality of sleep but was not performed in this case. It should also be noted that the circadian disturbances characteristic of the sleep-wake schedule disorders can be documented with sleep logs and temperature charts. In this case, the reports of the patient and his family were used to make the diagnosis. Although changes in the physiology of sleep occur during adolescence (Carskadon et aI., 1983), no such changes would be expected to result in the occurrence of sleep-wake schedule disorders. Secondary gain was probably a significant factor in maintaining the symptom. J.W. was having academic difficulty, which the correspondence approach seemed to resolve, and he preferred to be somewhat socially isolated anyway. Also, the parents' marriage was marred by emotional distance and occasional conflict that compromised their ability to provide the support J.W. needed to change his behavior. Perhaps J.W.'s school avoidance was an unconscious means of staying home to protect and support his mother. The typical signs of separation anxiety disorder (school phobia) were not present, however (Gittelman-Klein, 1975). The sleep disturbance was not an isolated symptom in this patient; he complained of vertigo and headaches as well. Thus, the clinical features in this case have a resemblance to the so-called postconcussion syndrome. The patient was an adolescent, and descriptions of the postconcussion syndrome in nonadults are scarce in the literature. However, the published reviews have generally concluded that the postconcussion syndrome does occur in childhood, although the clinical presentation may be modified (Dillon and Leopold, 1961; Gerring, 1986). Although insomnia is a very common aspect of the postconcussion syndrome, insomnia related to sleep schedule disturbance has not been described. It is possible that a proportion of patients suffering from insomnia after a head injury actually suffer from sleep-wake schedule disorders. The postconcussion syndrome is controversial. Although various symptoms are common after minor closed head in101
PATIEN AND LAUDERDALE
jury, these tend to resolve spontaneously within a few months (Levin et al., 1987). In those cases where symptoms persist, psychological factors are deemed to be important in their perpetuation (Kay et al., 1971). Nevertheless, the relative importance of organic and psychological factors remains undefined (Robertson, 1988). Some published studies, based on neuropsychological testing (Jakobsen et al., 1987) and cerebral blood flow measurements (Pogacnik, 1989), have argued for an organic origin of postconcussional symptoms, whereas the failure of auditory brain stem response abnormalities to predict outcome after head injury has been cited as an argument against an organic basis for the postconcussion syndrome (Schoenhuber and Gentilini, 1986). The ambiguities related to the origin of the postconcussion syndrome are evident in this case, as they have been in previously reported cases of postconcussion syndrome in children (Nylander and Rydelius, 1988). The sleep disturbance is explicable in terms of an organic lesion because the regulation of circadian rhythms has an anatomic basis in the hypothalamus (Stephan and Zucker, 1972), and closed head trauma may be capable of producing widespread microscopic brain damage such as axon "fracturing" in the white matter (Robertson, 1988; Taylor, 1967). Thus, the disorder may have been caused by organic damage related to the suprachiasmatic nucleus of the hypothalamus. The computed tomographic scan did not show any hypothalamic damage but would only be expected to detect relatively gross lesions. Nonorganic factors may have also played a role in the presentation of this case. For example, secondary gain was achieved by not having to go to school. A syndrome of motivated sleep phase delay has been described in adolescents (Ferber and Boyle, 1983). The authors were unable to find any previous reports linking the occurrence of sleep-wake schedule disorders to head injury. However, there have been a few reports of other types of sleep disturbance related to head or neck injury. One author reported the onset of sleep related respiratory difficulties in eight patients after' 'whiplash" injuries (Guilleminault, 1982). There are also single case reports of "sleep attacks" occurring in relation to atlantoaxial dislocation (Hall and Danoff, 1975) and jactatio nocturna after head injury (Drake, 1986). Despite the apparently high rate of sleep disturbance in individuals who have experienced closed head trauma, the literature linking specific sleep disorders to head injury is rudimentary. A greater understanding of these' disturbances may allow for more effective treatment. Research in this area should be encouraged.
102
References American Psychiatric Association (1987), Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised. Washington, DC: American Psychiatric Association Press. Carskadon, M. A., Orav, E. J. & Dement, W. C. (1983), Evolution of sleep and daytime sleepiness in adolescents. In: Sleep/Wake Disorders: Natural History. Epidemiology, and Long Term Evolution, ed. C. Guilleminault & E. Lugaresi. New York: Raven Press, pp. 201-216. Czeisler, C. A., Richardson, G. 5., Coleman, R. M., Zimmerman, J. C., Moore-Ede, M. c., Dement, W. C. & Weitzman, E. D. (1981), Chronotherapy: resetting the circadian clocks of patients with delayed sleep phase insomnia. Sleep, 4:1-21. Dillon, H. & Leopold, R. L. (1961), Children and the post-concussion syndrome. JAMA, 175:110-116. Drake, M. E. (1986), Jactatio nocturna after head injury. Neurology, 36:867-868. Ferber, R. (1987), Circadian and schedule disturbances. In: Sleep and Its Disorders in Children, ed. C. Guilleminault, New York: Raven Press, pp. 165-175. - - Boyle, M. P. (1983), Delayed sleep phase syndrome versus motivated sleep phase delay in adolescents. Sleep Research, 12:239. Gerring, J. P. (1986), Psychiatric sequelae of severe closed head injury. Pediatr. Rev., 8:115-121. Gittelman-Klein, R. (1975), Pharmacotherapy and management of pathological separation anxiety. In: Recent Advances in Child Psychopharmacology, ed. R. Gittelman. New York: Human Sciences Press, pp. 257-262. Guilleminault, C. (1982), Sleep and breathing. In: Sleeping and Waking Disorders: Indications and Techniques, ed. C. Guilleminault. Menlo Park: Addison-Wesley Publishing Company, pp. 155-182. Hall, C. W. & Danoff, D. (1975), Sleep attacks-apparent relationship to atlantoaxial dislocation. Arch. Neurol., 32:57-58. Jakobsen, J., Baadsgaard, S. E., Thomsen, S. & Henriksen, P. B. (1987), Prediction of post-concussional sequelae by reaction time test. Acta Neurol. Scand., 75:341-345. Kay, D. W., Kerr, T. A. & Lassman, L. P. (1971), Brain trauma and the post-concussional syndrome. Lancet, 2:1052-1055. Levin, H. 5., Mattis,S., Ruff, R. M. et al. (1987), Neurobehavioural outcome following minor head injury: a three center study. J. Neurosurg., 66:234-243. Nylander, I. & Rydelius, P. A. (1988), Post-concussion syndrome. Acta Paediatr. Scand., 77:475-477. Pogacnik, T. (1989), Characteristics of regional cerebral blood flow in patients with concussion. Psychiatry Res., 29:313-316. Robertson, A. (1988), The post-concussional syndrome then and now. Aust. s.z. J. Psychiatry, 22:396-403. Schoenhuber, R. & Gentilini, M. (1986), Auditory brain stem responses in the prognosis of late postconcussional symptoms and neuropsychological dysfunction after minor head injury. Neurosurgery, 19:532-534. Silverman, J. J. (1986), Post-traumatic stress disorder. Adv. Psychosom. Med., 16:115-140. Stephan, F. K. & Zucker, I. (1972), Circadian rhythms in drinking behaviour and locomotor activity of rats are eliminated by hypothalamic lesions. Proc. Natl. Acad. Sci., USA 69:1583-1586. Taylor, A. R. (1967), Post-concussional sequelae. Br. Med. J. [Clin Res] 3:67-71.
J. Am. Acad. Child Adolesc. Psychiatry, 31:1, January 1992
AND
W. MARK LAUDERDALE, M.D., F.R.C.P.(C)
Abstract. Sleep-wake schedule disorder is defined by DSM-lIl-R as a mismatch between the normal sleepwake schedule for a person 's environment and his or her circadian sleep-wake pattern. The authors report a case in which a sleep-wake schedule disorder arose after a closed head injury . Sleep-wake schedule disorder has not been described as an outcome of closed head injury. As patients with sleep-wake schedule disorders may present with insomnia, this case suggests the possibility that some of the insomnia that frequently follows closed head injury may represent sleep-wake schedule disorders. J. Am. Acad. Child Adolesc. Psychiatry, 1992, 31, I: 100-102. Key Words: sleep disorder, sleep, adolescence, school phobia, head injuries. Sleep-wake schedule disorder is defined by DSM-III-R as a "mismatch between the normal sleep-wake schedule for a person's environment and his or her circadian sleep-wake pattern, resulting in a complaint of either insomnia or hypersomnia" (American Psychiatric Association, 1987). The disorder includes several subtypes, including advanced or delayed types, disorganized type, or frequently changing type. The factors most frequently associated with the onset of sleep-wake schedule disorders are travel through different time zones and shift work schedules. The delayed type of sleep-wake schedule disorder occurs when an individual cannot get to sleep until later than usual, but then sleeps normally for a normal amount of time. The pathophysiology of the delayed type of sleep-wake schedule disorder is believed to be related to a reduced ability, on the part of these patients, to phase advance their sleep-wake schedule as well as the presence of environmental synchronizing cues that prevent resynchronization by phase retardation (Czeisler et al., 1981). Sleep schedule disturbances have been described in both adults and children (Ferber, 1987). In children and adolescents, the disorder is particularly troublesome because it produces somnolence, fatigue, and irritability during hours when the affected individual is expected to be attending school. The authors have recently seen a 13-year-old boy who developed a sleep-wake schedule disorder of the delayed type soon after suffering a closed head injury. The case is of interest because head injury has not been described as a cause of sleep-phase schedule disorder.
Case Report l.W. was a 13-year-old seventh grade student with severe Accepted June 27, 1991. Dr. Patten is Clinical Fello w, Alberta Heritage Foundation for Medical Research, University ofCalgary, and Dr. Lauderdale is Clinical Assistant Professor, Department ofPsychiatry, University of Calgary. Reprint requests to Dr. Patt en, Department of Community Health Sciences, Faculty ofMedicin e, The University ofCalgary, 3330 Hosp ital Drive N. W., Calgary, Alberta T2N 4N1 . 0890-8567/92/3101-100$03 .OO/O© 1992 by the American Academy of Child and Adolescent Psychiatry.
100
sleep disturbance. Specifically, he was unable to get to sleep until 5 or 6 o'clock in the morning and then would sleep normally until 3 o'clock in the afternoon. The symptoms dated back to a motorcycle accident 13 months before. l.W. was wearing a helmet that "split" when he fell off the bike. He was unconscious for about 5 minutes, followed by a headache and drowsiness. His physical examination in the emergency room was normal. No abnormalities were noted in his mental state except that he was somewhat " vague." Skull, neck, chest, and pelvic x-rays were all normal. A computed tomographic scan showed only a small calcification along the parasagittal region on the right side. An EEG was normal. He remained in hospital for 2 days for observation. In the weeks after the injury, l .W. suffered from vertigo, bilateral throbbing headaches, and an inability to sleep until later and later at night. His performance at school declined because of fatigue and inability to concentrate. Eventually, he was unable to get up to go to school, and he began taking correspondence courses at home. In the 13 months after the injury, the vertigo and headache decreased in severity, duration, and frequency (1-2 per month). He was seen by several neurologists and neuropsychologists for the persisting sleep problem and school absence. All neurological examinations were normal. Neuropsychological testing showed no impairments in cognitive functioning. He showed average ability in both verbal and visual-spatial areas, and his memory was generally above average. Measures of frontal lobe function were normal. His school grades had been above average in the early years, average in Grade 6, and below average or failing in Grade 7 before the accident. Once he began correspondence courses, however, he achieved above average grades again, which he attributed to being able to work alone and at his own pace. He disliked having to be at school by 8:30 A.M. Before psychiatric evaluation, chronotherapy schedules and medication with nitrazepam were tried, and both were only temporarily successful. Behavioral ratings or sleep logs were not done. At psychiatric examination, l.W. appeared older than his stated age. He was slightly overweight with a large frame. Both height and weight were above the 95th percentile for his age, but there was no history of appetite change or weight J. Am. Acad. Child Adolesc. Psychiatry, 31:1, January 1992
SLEEP PHASE DISORDER AFrER HEAD INJURY
gain since the accident. His mood was euthymic with normal range of expression. He stated that he was motivated to proceed with the treatment to normalize his sleep pattern. There was no fatigue, anxiety, nightmares, reexperiencing of the trauma, phobias, or emotional numbing that would suggest the presence of post-traumatic stress disorder (Silverman, 1986). Speech, perception, and cognition were normal. He seemed self-confident and generally satisfied with his family life. J.W. had no previous medical or psychiatric history. His mother had epilepsy, for which she was receiving medications. J.W.'s biological father had died when J.W. was 3 years old, but he is said to have been an alcoholic and to have spent time in prison because of felony convictions. One paternal uncle had committed suicide. There was no other psychiatric history in the family. The authors' evaluation and management of J.W. included a number of sessions with his family in which there was evidence of dysfunction. J.W.'s stepfather was unsupportive and disengaged, and his mother seemed to have difficulty defining limits and imposing structure on her children's behavior. She therefore may have had difficulty providing the environmental structure that would have been ideal for the enforcement of the chronotherapy schedules. The parents also found it difficult to bring J.W. to sessions regularly because of the distance they had to travel and their working hours. J.W.'s response to the treatment course was less than might have been hoped. Various approaches were used over a 4-month period, and J.W. was reasonably compliant in performing instructions. Initially, because chronotherapy had been previously unsuccessful, there was an attempt to remove the reinforcers for staying up at night. He was reassured that even after his schedule returned to normal he could continue with correspondence courses. His household chores, outdoor exercise, schoolwork, television watching, and other entertainment were restricted to daytime hours, while at night he was to practice self-relaxation techniques and remain inactive. With a poor response to these interventions, hypnosis was added to help him gain a more positive attitude toward sleeping restfully and the ordeal of hourly calisthenics was prescribed if he had not yet fallen asleep. With only temporary improvement of a few days, this approach was replaced by chronotherapy . J.W. was asked to stay up 1 hour later each day until his schedule was normalized. Phase advancing was successful for the first week but then reverted to the original pattern when J.W. was unable to fall asleep at midday. After 2 months of minimal improvement, l.W. was asked to stay up all night and the next day if he was not asleep within 1 hour of going to bed at 10:30 P.M. Over a 3-week period, it was necessary for J.W. to stay up all night on three occasions, but his sleep schedule was more or less normal. During this time, l.W. seemed to be in a good mood and was making plans for a summer job and helping his mother work in the garden. However, his mother developed a number of somatic complaints after a conflict with her husband, and in the following weeks l.W. stopped using the approach J.Am.Acad. Child Adolesc.Psychiatry, 31:1, January1992
because of the continued necessity to regularly stay up all night. In the end, in view of J.W.'s satisfactory academic performance and personal and social adjustment his parents were reluctant to force him to change to a more "normal" sleep schedule. He continued in follow-up for another year with no significant change in this pattern. Difficulties in the parents' marriage continued to occur periodically. His stepfather resisted attempts to engage in therapy. Discussion
The authors have described a case in which a sleep-wake schedule disorder had its onset after a head injury involving loss of consciousness. Closed head injury has not been described as a cause of sleep-wake schedule disorder. There was no suggestion in this case that the sleep disturbance was initiated by other factors that might have impaired sleep onset, such as the headaches experienced by this patient. Furthermore, as is typical of sleep-wake schedule disorders, the patient's sleep was qualitatively normal during the time when he was asleep. Ideally, a polysomnographic recording could have been performed to document the normality of sleep but was not performed in this case. It should also be noted that the circadian disturbances characteristic of the sleep-wake schedule disorders can be documented with sleep logs and temperature charts. In this case, the reports of the patient and his family were used to make the diagnosis. Although changes in the physiology of sleep occur during adolescence (Carskadon et aI., 1983), no such changes would be expected to result in the occurrence of sleep-wake schedule disorders. Secondary gain was probably a significant factor in maintaining the symptom. J.W. was having academic difficulty, which the correspondence approach seemed to resolve, and he preferred to be somewhat socially isolated anyway. Also, the parents' marriage was marred by emotional distance and occasional conflict that compromised their ability to provide the support J.W. needed to change his behavior. Perhaps J.W.'s school avoidance was an unconscious means of staying home to protect and support his mother. The typical signs of separation anxiety disorder (school phobia) were not present, however (Gittelman-Klein, 1975). The sleep disturbance was not an isolated symptom in this patient; he complained of vertigo and headaches as well. Thus, the clinical features in this case have a resemblance to the so-called postconcussion syndrome. The patient was an adolescent, and descriptions of the postconcussion syndrome in nonadults are scarce in the literature. However, the published reviews have generally concluded that the postconcussion syndrome does occur in childhood, although the clinical presentation may be modified (Dillon and Leopold, 1961; Gerring, 1986). Although insomnia is a very common aspect of the postconcussion syndrome, insomnia related to sleep schedule disturbance has not been described. It is possible that a proportion of patients suffering from insomnia after a head injury actually suffer from sleep-wake schedule disorders. The postconcussion syndrome is controversial. Although various symptoms are common after minor closed head in101
PATIEN AND LAUDERDALE
jury, these tend to resolve spontaneously within a few months (Levin et al., 1987). In those cases where symptoms persist, psychological factors are deemed to be important in their perpetuation (Kay et al., 1971). Nevertheless, the relative importance of organic and psychological factors remains undefined (Robertson, 1988). Some published studies, based on neuropsychological testing (Jakobsen et al., 1987) and cerebral blood flow measurements (Pogacnik, 1989), have argued for an organic origin of postconcussional symptoms, whereas the failure of auditory brain stem response abnormalities to predict outcome after head injury has been cited as an argument against an organic basis for the postconcussion syndrome (Schoenhuber and Gentilini, 1986). The ambiguities related to the origin of the postconcussion syndrome are evident in this case, as they have been in previously reported cases of postconcussion syndrome in children (Nylander and Rydelius, 1988). The sleep disturbance is explicable in terms of an organic lesion because the regulation of circadian rhythms has an anatomic basis in the hypothalamus (Stephan and Zucker, 1972), and closed head trauma may be capable of producing widespread microscopic brain damage such as axon "fracturing" in the white matter (Robertson, 1988; Taylor, 1967). Thus, the disorder may have been caused by organic damage related to the suprachiasmatic nucleus of the hypothalamus. The computed tomographic scan did not show any hypothalamic damage but would only be expected to detect relatively gross lesions. Nonorganic factors may have also played a role in the presentation of this case. For example, secondary gain was achieved by not having to go to school. A syndrome of motivated sleep phase delay has been described in adolescents (Ferber and Boyle, 1983). The authors were unable to find any previous reports linking the occurrence of sleep-wake schedule disorders to head injury. However, there have been a few reports of other types of sleep disturbance related to head or neck injury. One author reported the onset of sleep related respiratory difficulties in eight patients after' 'whiplash" injuries (Guilleminault, 1982). There are also single case reports of "sleep attacks" occurring in relation to atlantoaxial dislocation (Hall and Danoff, 1975) and jactatio nocturna after head injury (Drake, 1986). Despite the apparently high rate of sleep disturbance in individuals who have experienced closed head trauma, the literature linking specific sleep disorders to head injury is rudimentary. A greater understanding of these' disturbances may allow for more effective treatment. Research in this area should be encouraged.
102
References American Psychiatric Association (1987), Diagnostic and Statistical Manual of Mental Disorders, Third Edition, Revised. Washington, DC: American Psychiatric Association Press. Carskadon, M. A., Orav, E. J. & Dement, W. C. (1983), Evolution of sleep and daytime sleepiness in adolescents. In: Sleep/Wake Disorders: Natural History. Epidemiology, and Long Term Evolution, ed. C. Guilleminault & E. Lugaresi. New York: Raven Press, pp. 201-216. Czeisler, C. A., Richardson, G. 5., Coleman, R. M., Zimmerman, J. C., Moore-Ede, M. c., Dement, W. C. & Weitzman, E. D. (1981), Chronotherapy: resetting the circadian clocks of patients with delayed sleep phase insomnia. Sleep, 4:1-21. Dillon, H. & Leopold, R. L. (1961), Children and the post-concussion syndrome. JAMA, 175:110-116. Drake, M. E. (1986), Jactatio nocturna after head injury. Neurology, 36:867-868. Ferber, R. (1987), Circadian and schedule disturbances. In: Sleep and Its Disorders in Children, ed. C. Guilleminault, New York: Raven Press, pp. 165-175. - - Boyle, M. P. (1983), Delayed sleep phase syndrome versus motivated sleep phase delay in adolescents. Sleep Research, 12:239. Gerring, J. P. (1986), Psychiatric sequelae of severe closed head injury. Pediatr. Rev., 8:115-121. Gittelman-Klein, R. (1975), Pharmacotherapy and management of pathological separation anxiety. In: Recent Advances in Child Psychopharmacology, ed. R. Gittelman. New York: Human Sciences Press, pp. 257-262. Guilleminault, C. (1982), Sleep and breathing. In: Sleeping and Waking Disorders: Indications and Techniques, ed. C. Guilleminault. Menlo Park: Addison-Wesley Publishing Company, pp. 155-182. Hall, C. W. & Danoff, D. (1975), Sleep attacks-apparent relationship to atlantoaxial dislocation. Arch. Neurol., 32:57-58. Jakobsen, J., Baadsgaard, S. E., Thomsen, S. & Henriksen, P. B. (1987), Prediction of post-concussional sequelae by reaction time test. Acta Neurol. Scand., 75:341-345. Kay, D. W., Kerr, T. A. & Lassman, L. P. (1971), Brain trauma and the post-concussional syndrome. Lancet, 2:1052-1055. Levin, H. 5., Mattis,S., Ruff, R. M. et al. (1987), Neurobehavioural outcome following minor head injury: a three center study. J. Neurosurg., 66:234-243. Nylander, I. & Rydelius, P. A. (1988), Post-concussion syndrome. Acta Paediatr. Scand., 77:475-477. Pogacnik, T. (1989), Characteristics of regional cerebral blood flow in patients with concussion. Psychiatry Res., 29:313-316. Robertson, A. (1988), The post-concussional syndrome then and now. Aust. s.z. J. Psychiatry, 22:396-403. Schoenhuber, R. & Gentilini, M. (1986), Auditory brain stem responses in the prognosis of late postconcussional symptoms and neuropsychological dysfunction after minor head injury. Neurosurgery, 19:532-534. Silverman, J. J. (1986), Post-traumatic stress disorder. Adv. Psychosom. Med., 16:115-140. Stephan, F. K. & Zucker, I. (1972), Circadian rhythms in drinking behaviour and locomotor activity of rats are eliminated by hypothalamic lesions. Proc. Natl. Acad. Sci., USA 69:1583-1586. Taylor, A. R. (1967), Post-concussional sequelae. Br. Med. J. [Clin Res] 3:67-71.
J. Am. Acad. Child Adolesc. Psychiatry, 31:1, January 1992
