AMONG THE RESIDUAL SEQUELAE of traumatic brain. Cognitive Behavioral Therapy for Insomnia Associated With Traumatic Brain Injury: A Single-Case Study

Size: px

Start display at page:

Download "AMONG THE RESIDUAL SEQUELAE of traumatic brain. Cognitive Behavioral Therapy for Insomnia Associated With Traumatic Brain Injury: A Single-Case Study"

William Ferguson
6 years ago
Views:

1 1298 Cognitive Behavioral Therapy for Insomnia Associated With Traumatic Brain Injury: A Single-Case Study Marie-Christine Ouellet, MPs, Charles M. Morin, PhD From the École de Psychologie, Centre d Étude des Troubles du Sommeil, Université Laval, Québec City, QC, Canada. Presented in part at the Association of Professional Sleep Societies meeting, June 2002, Seattle WA. Supported by the Fonds de la Recherché en Santé du Québec. No commercial party having a direct financial interest in the results of the research supporting this article has or will confer a benefit upon the author(s) or upon any organization with which the author(s) is/are associated. Reprint requests to Marie-Christine Ouellet, MPs, École de Psychologie, Université Laval, Québec City, QC G1K 7P4, Canada, mcouellet@psy.ulaval.ca /04/ $30.00/0 doi: /j.apmr ABSTRACT. Ouellet M-C, Morin CM. Cognitive behavioral therapy for insomnia associated with traumatic brain injury: a single-case study. Arch Phys Med Rehabil 2004;85: Objective: To test the efficacy of a cognitive behavioral therapy (CBT) for insomnia with a patient with traumatic brain injury (TBI). Design: Single-case study. Setting: Outpatient rehabilitation center. Participant: A man in his late thirties who sustained a moderate TBI in a motor vehicle crash and who developed insomnia. He complained of difficulties falling asleep and staying asleep, despite pharmacotherapy with zopiclone. Interventions: Eight weekly individual CBT sessions. Treatment included stimulus control, sleep restriction, cognitive therapy, and sleep hygiene education. Main Outcome Measures: Sleep diary and polysomnography data. Results: Sleep onset decreased from 47 to 18 minutes, and nocturnal awakenings dropped from 85 to 28 minutes on average at posttreatment. Sleep efficiency also increased substantially (58% to 83%). Polysomnography evaluations corroborated the diary data by showing a decrease in total time awake (63.2 to 26.3min) and in the number of awakenings (21 to 7.5). The majority of gains were well maintained at 1- and 3-month follow-up assessments. Conclusions: These preliminary results suggest that sleep disturbances after TBI can be alleviated with a nonpharmacologic intervention. CBT for post-tbi insomnia is a promising therapeutic avenue deserving more scientific and clinical attention. Key Words: Behavior therapy, cognitive; Brain injuries; Insomnia; Rehabilitation by the American Congress of Rehabilitation Medicine and the American Academy of Physical Medicine and Rehabilitation AMONG THE RESIDUAL SEQUELAE of traumatic brain injury (TBI), sleep disturbances have received little scientific attention despite the fact that they are reported by more than 50% of patients. 1-3 For people with TBI, problems falling asleep or staying asleep can exacerbate other symptoms related to the injury, such as pain, cognitive deficits, fatigue, anxiety, or depression. Insomnia can thus potentially compromise rehabilitation, complicate social reintegration or return to work, and lower the quality of life (QOL) of patients with TBI. Nonetheless, studies to evaluate the efficacy of different treatment options specifically for post-tbi insomnia have not been done. In clinical practice, hypnotics remain the most frequent treatment for insomnia. Hypnotic medications are effective for the short-term treatment of insomnia; they produce rapid benefits that last several nights and, in some cases, a few weeks. However, there are few data that document the sustained benefits when drugs are discontinued or of their continued efficacy with prolonged use. In addition, hypnotic medications can produce side effects and present some risk of dependence. 4 Several nonpharmacologic interventions have been used to treat insomnia in the general population. Research efforts have mainly been devoted to evaluating the efficacy of behavioral and, more recently, cognitive behavioral treatments. Two recent meta-analyses of the literature 5,6 (based on 60 studies) revealed that these interventions treat insomnia efficaciously. In fact, behavioral interventions such as stimulus control or sleep restriction are as effective as pharmacotherapy in the short term and even more effective in the longer term. Although most of this research has been conducted with patients who had primary insomnia (ie, insomnia unrelated to a coexisting condition), preliminary findings from less controlled studies have yielded promising results suggesting that patients with insomnia secondary to medical and psychiatric conditions, or even those using hypnotic medications, can also benefit from behavioral treatment for sleep disturbances Because patients with TBI are faced with an amalgam of emotional and environmental stressors (eg, cognitive deficits, anxiety, heavy rehabilitation schedules, financial uncertainty), psychologic factors such as emotional arousal or maladaptive habits probably have an important role in producing, exacerbating, or prolonging sleep disturbances. Psychologic treatment options that specifically target those perpetuating factors should therefore be promising. In this study, we evaluated the effectiveness of cognitive behavioral therapy (CBT) in treating insomnia in a patient with moderate TBI. METHODS The patient was a man in his late thirties with a high school education. He was married, lived with his wife and young children, and worked as a technician on an assembly line. His medical history was unremarkable until August 2000, when he was involved in a motor vehicle crash (MVC) and sustained a TBI of moderate severity. On arrival at the hospital, his Glasgow Coma Scale score was 13/15. No coma was observed but his posttraumatic amnesia lasted from 5 to 7 days. A computerized axial tomography scan performed on the day of the MVC revealed a small hemorrhage in the left lateral ventricle and a small (0.5cm) petechial zone in the right superior parietal region. There were no signs of epidural or subdural hematomas, no cerebral edema, and no apparent fracture. Other injuries included scalp lacerations and a torn ligament in the left knee. A complete neuropsychologic evaluation completed 1 month after the crash revealed a general decline in nonverbal

2 TREATMENT OF INSOMNIA AFTER TBI, Ouellet 1299 Table 1: Neuropsychologic Test Results Test Administered Wechsler Adult Intelligence Scale III Verbal IQ Performance IQ Global IQ Verbal comprehension index Percepetual organization index Working memory index Processing speed index Hooper Visual Organization Test Tower of London Test Rey Complex Figure Test Copy Immediate recall Delayed recall Rey Auditory Verbal Learning Test Trial 1: list A Trial 2: list A Trial 3: list A Trial 4: list A Trial 5: list A Trial 5: list B Immediate recall: list A Delayed recall: list A Recognition Symbol Digit Modalities Test Oral Written Trail-Making Test Part A Part B Boston Cancellation Test Structured A Unstructured A Structured star Unstructured star Stroop Test Verbal Fluency Test Ruff2&7Selective Attention Test Speed Accuracy Range, Percentile, or SD From the Mean High average 20th 29th percentile 2 SD 25th percentile 25th percentile 2.46 SD 2.08 SD 2.11 SD 10th 20th percentile 10th percentile 7th percentile 70th percentile NOTE. This is only a summary of neuropsychologic findings. It does not represent the full extent of the neuropsychologic evaluation; interpretation of the results was also based on qualitative information and on comparisons with estimates of pretraumatic functioning. Abbreviations: IQ, intelligence quotient; SD, standard deviation. intellectual functions, a slowing of information processing, and impairments in the areas of attention, visuospatial organization, and immediate verbal memory (see table 1 for results of neuropsychologic tests). A Million Clinical Multiaxial Inventory II indicated no significant psychopathology on either Axes I or II. His medication included zopiclone (daily dose, 5 7.5mg) prescribed specifically for his sleep difficulties, and amitriptyline (25mg daily dose), prescribed mainly for pain. At the time he enrolled in the study, 1 year after the MVC, the patient was still in rehabilitation on an outpatient basis and was being evaluated for an eventual return to work. In addition to significantly increased fatigability and mild pain in the left knee, the patient complained of difficulties falling asleep and, more important, staying asleep every night. He did not report any sleep difficulties before the crash; these problems appeared shortly after the trauma and persisted despite pharmacologic intervention. When he was evaluated, the patient reported that his usual bedtime was around 10:30 PM, and his arising time was 7:00 AM. He estimated that it took on average 40 minutes to fall asleep and that he was awake for at least 2 hours at night, giving him 4 to 5 hours of sleep a night. A clinical interview, as well as data from several weeks of sleep diaries, confirmed that the patient suffered from mixed insomnia defined as (1) having a significant sleep complaint (eg, dissatisfaction with sleep or significant distress), (2) having a sleep onset latency of 30 minutes or more, and nocturnal awakenings totaling 30 minutes or more, (3) experiencing these symptoms at least 3 nights a week, (4) having a complaint of at least 2 negative daytime effects (eg, fatigue, impaired functioning, mood disturbances) attributed to poor sleep, and (5) having insomnia for at least 1 month. These criteria represent a combination of the diagnostic criteria of the International Classification of Sleep Disorders 11 and the Diagnostic and Statistical Manual of Mental Disorders. 12 Measures The patient completed 5 nights of polysomnography (PSG; 3 before and 2 after treatment) in the sleep clinic, as well as subjective measures of sleep (ie, Insomnia Severity Index 13 [ISI], Dysfunctional Beliefs and Attitudes About Sleep Scale 14 [DBAS]), fatigue (Multidimensional Fatigue Inventory 15 [MFI]), and psychologic symptoms (Beck Anxiety Inventory 16 [BAI], Beck Depression Inventory 17 [BDI]). He also completed a daily sleep diary throughout 5 weeks of baseline, 8 weeks of CBT, and 2 weeks at posttreatment and follow-up evaluations 1 month and 3 months after treatment ended. The main outcome measures used to evaluate the patient s progress were derived from the sleep diary and included sleep onset latency, time awake after sleep onset, sleep efficiency, total time awake, total sleep time, and sleep medication consumption. Treatment Treatment was based on a manualized multifactor intervention 13 and included stimulus control, sleep restriction, cognitive therapy, and sleep hygiene education. CBT was delivered by a clinical psychologist through 8 weekly face-to-face therapy sessions. The stimulus control instructions 18 are aimed at reassociating the bed, bedroom, and bedtime stimuli with sleep rather than with frustration, anxiety, or tension. The patient was instructed to (1) go to bed only when sleepy; (2) use the bed and bedroom only for sleep and sex; (3) leave the bed and go to another room if unable to fall asleep or return to sleep; (4) repeat step 3 as often as necessary throughout the night; (5) arise at the same time each morning, regardless of the amount of time slept during the night; and (6) refrain from napping during the day. The sleep restriction procedure 19 consists of limiting the time spent in bed to the actual total time spent sleeping. The patient was instructed to determine his allowable time in bed according to the total subjective sleep time he recorded in his sleep diary. The initial sleep window was restricted to this estimated sleep time. Specific bedtime and rising times were predetermined, with weekly adjustments and gradual increases in time spent in bed being contingent on objective improvement in sleep efficiency. Cognitive therapy of insomnia 13 consists of identifying, challenging, and altering a set of dysfunctional beliefs and attitudes about sleep. The objective of cognitive therapy is to break the cycle of insomnia, dysfunctional thoughts, and emotional distress that lead to further sleep disturbances.

3 1300 TREATMENT OF INSOMNIA AFTER TBI, Ouellet Fig 1. Sleep onset latency and time awake after sleep onset as reported on the sleep diary (averaged over weeks). Sleep-hygiene education consists of teaching patients about the impact on sleep of certain lifestyle habits (eg, diet, drug use, exercise) and the influence of some environmental factors (eg, light, noise, temperature). 20 The CBT treatment package, 13 typically used for primary insomnia, was adapted to some extent to account for some dimensions of TBI. The adaptation consisted of (1) providing information on physiologic, psychologic, and environmental factors contributing to insomnia after a TBI; (2) adapting the treatment material for possible cognitive limitations such as reducing the information and providing written documentation; (3) including fatigue management skills training; (4) discussing issues related to return to work; and (5) working on the acceptance of a newly acquired vulnerability to insomnia because of the TBI. RESULTS Figures 1 to 4 show that CBT induced substantial improvements in sleep parameters in our patient. Sleep onset latency, which averaged 47 minutes before treatment, dropped to 18 minutes, and time spent awake after sleep onset decreased from to 85 minutes to an average of 28 minutes posttreatment (fig 1). Fig 2. Total sleep time and total time awake as reported on the sleep diary (averaged over weeks).

4 TREATMENT OF INSOMNIA AFTER TBI, Ouellet 1301 Fig 3. Sleep efficiency as reported in the sleep diary (averaged over weeks). These values fell below the clinical criterion of 30 minutes that is used to determine the clinical significance of insomnia symptoms. Sleep efficiency was markedly increased, from 58% to 83% (fig 3). Total sleep time decreased slightly with the CBT (probably because of the sleep restriction procedure), but then increased once treatment was completed (fig 2). The PSG evaluations corroborated the improvements seen in the diary data by showing a decrease in total time awake (63.2 to 26.3min) and in the number of awakenings (from 21 to 7.5). Improvements in sleep were maintained at 1- and 3-month follow-ups in terms of sleep efficiency, total sleep time, and total time awake, yet some deterioration was noted for sleep onset latency and time awake after sleep onset, especially at the 3-month follow-up. As indicated by the medication consumption data (fig 4), at 1-month follow-up, the patient had initiated a gradual tapering of zopiclone, with the help of his physician. This may explain the deterioration in sleep onset latency and time awake after sleep onset because tapering with this type of medication may induce withdrawal symptoms and rebound insomnia. Insomnia severity as measured by the ISI dropped from a clinically significant score (18) to a subclinical level (12). Measures of psychopathology (BDI, BAI) indicated low levels of depression and anxiety and did not vary much throughout the study (see table 2). Dysfunctional cognitions decreased, as indicated by the scores on the DBAS. Scores on the fatigue scale were decreased slightly at posttreatment and at 3-month follow-up compared with the pretreatment level (62 to 52); yet, it remains unclear whether this change was clinically significant because the patient still complained of fatigability. DISCUSSION These preliminary results suggest that sleep disturbances after TBI can be alleviated with a psychologic intervention. This study represents the first demonstration that CBT for post-tbi insomnia is a promising therapeutic avenue that deserves more scientific and clinical attention. As for other patients with medical conditions, it may be assumed that patients with TBI would not benefit from a cognitive behavioral intervention for insomnia perhaps because Fig 4. Zopiclone consumption as reported in the sleep diary (averaged over weeks).

5 1302 TREATMENT OF INSOMNIA AFTER TBI, Ouellet Table 2: Results of Subjective Measures of Sleep, Fatigue, and Mood Assessment Pre- Post- 1-Month Follow-Up 3-Month Follow-Up ISI MFI (total score) BDI NA DAI NA DBAS NA Abbreviation: NA, not available. of cognitive limitations or because a purely physiologic etiology may be attributed to post-tbi sleep disturbances. Maladaptive habits, thoughts, and beliefs about sleep are probably the main factors in the perpetuation or exacerbation of sleep problems after TBI, and these can be addressed successfully with a short cognitive behavioral intervention. As for cognitive limitations, our patient had no difficulty understanding the rationale of the procedures involved in the treatment and had adequate insight and disclosure during therapy sessions, despite some documented neuropsychologic deficits. Although severe memory, attention, or executive deficits could compromise the implementation of therapy, mild or moderate cognitive limitations should not influence clinicians to disregard the potential utility of CBT for insomnia. The behavioral recommendations proposed are simple and straightforward, but strict adherence to these principles is the key to a successful outcome. As such, patients with behavior or motivational disorders may find it more difficult to adhere to the treatment protocol. Further research will perhaps determine what variables predict the success of CBT for insomnia in TBI patients. In this study, the long-term efficacy of CBT for insomnia was somewhat obscured by the fact that the patient began tapering of his sleep medication. Indeed, although he did not return to a pretreatment level, some deterioration was noted for sleep onset latency and time awake after sleep onset when the patient lowered his medication regimen. A follow-up at 6 months or 1 year could have provided information on the patient s sleep quality after he stopped taking his sleep medication. However, this initiative can also be interpreted as a positive effect of the treatment because the patient was encouraged enough by his progress with CBT that he decided to reduce his medication intake. One goal of CBT for insomnia is to teach the patient self-management skills to cope with residual sleep difficulties when treatment is completed. Sporadic therapist guidance could have enhanced our patient s adherence to treatment recommendations and helped him to maintain therapeutic gains throughout the tapering process. CONCLUSIONS Even though the present data are limited to 1 patient, we hope our results will stimulate interest in both the scientific and clinical realms in nonpharmacologic treatment options for insomnia in patients with TBI. CBT for insomnia involves simple procedures that could easily be implemented during rehabilitation by mental health professionals, either as a therapeutic or as a preventive tool. Improving patient s ability to sleep may facilitate the rehabilitation process, as well as the patient s QOL. References 1. Perlis ML, Artiola L, Giles DE. Sleep complaints in chronic postconcussion syndrome. Percept Mot Skills 1997;84: Beetar JT, Guilmette TJ, Sparadeo FR. Sleep and pain complaints in symptomatic traumatic brain injury and neurologic populations. Arch Phys Med Rehabil 1996;77: Cohen M, Oksenberg A, Snir D, Stern MJ, Groswasser Z. Temporally related changes of sleep complaints in traumatic brain injured patients. J Neurol Neurosurg Psychiatry 1992;55: Morin CM, Wooten V. Psychological and pharmacological approaches to treating insomnia: critical issues in assessing their separate and combined effects. Clin Psychol Rev 1996;16: Morin CM, Culbert JP, Schwartz SM. Nonpharmacological interventions for insomnia: a meta-analysis of treatment efficacy. Am J Psychiatry 1994;151: Murtagh DR, Greenwood KM. Identifying effective psychological treatments for insomnia: a meta-analysis. J Consult Clin Psychol 1994;63: Chambers MJ, Alexander SD. Assessment and prediction of outcome for a brief behavioral insomnia treatment program. J Behav Ther Exp Psychiatry 1992;23: Dashevsky BA, Kramer M. Behavioral treatment of chronic insomnia in psychiatrically ill patients. J Clin Psychiatry 1998;59: Jacobs GD, Benson H, Friedman R. Perceived benefits in a behavioral-medicine insomnia program: a clinical report. Am J Med 1996;100: Morin CM, Stone J, McDonald K, Jones S. Psychological management of insomnia: a clinical replication series with 100 patients. Behav Ther 1994;25: American Sleep Disorders Association. The international classification of sleep disorders: diagnostic and coding manual. Rochester (MN): ASDA; American Psychiatric Association. Diagnostic and statistical manual of mental disorders. Washington (DC): APA; Morin CM. Insomnia: psychological assessment and management. New York: Guilford Pr; Morin CM, Stone J, Trinkle D, Mercer J, Remsberg S. Dysfunctional beliefs and attitudes about sleep among older adults with and without insomnia complaints. Psychol Aging 1993;8: Smets EM, Garssen B, Bonke B, De Haes JC. The multidimensional fatigue inventory (MFI) psychometric qualities of an instrument to assess fatigue. J Psychosom Res 1995;39: Beck AT, Epstein N, Brown G, Steer RA. An inventory for measuring clinical anxiety: psychometric properties. J Consult Clin Psychol 1988;56: Beck AT, Steer RA, Garbin MG. Psychometric properties of the Beck Depression Inventory: twenty-five years of evaluation. Clin Psychol Rev 1988;8: Bootzin RR, Epstein D, Wood JM. Stimulus control instructions. In: Hauri P, editor. Case studies in insomnia. New York: Plenum Pr; p Spielman AJ, Saskin P, Thorpy MJ. Treatment of chronic insomnia by restriction of time in bed. Sleep 1987;10: Hauri PJ, editor. Case studies in insomnia. New York: Plenum Pr; 1991.

Cognitive Behavioral Therapy for Insomnia. Melanie K. Leggett, PhD, CBSM Duke University Medical Center

Cognitive Behavioral Therapy for Insomnia Melanie K. Leggett, PhD, CBSM Duke University Medical Center Disclosures I have no relevant financial relationship with the manufacturers of any commercial products