CASE REPORT
Finding the Person Behind the Pain: Chronic Pain Management in a Patient With Traumatic Brain Injury Romayne Gallagher, MD, CCFP, Elisabeth Drance, MD, FRCP(C), and Susan Higginbotham, RN Chronic pain is common after a traumatic brain injury. Cognitive impairment post injury may be a consequence of the brain injury alone, or in combination with pain, clinical depression, and psychological and emotional factors. We present a case of a severely cognitively impaired person post–traumatic brain injury, whose behavior included social withdrawal, irritability, and agitation around direct care—which was unresponsive to
psychotropic intervention or care delivery strategies. The introduction of an opioid made a significant improvement in the cognition and quality of life of the individual. This case suggests that clinicians should consider a trial of opioid analgesics in individuals with brain injury who have significant cognitive impairment in association with other behaviors suggestive of depression and pain. (J Am Med Dir Assoc 2006; 7: 432–434)
AR is a 64-year-old woman with a history of moderate to severe schizophrenia treated with depot antipsychotic medications. She is divorced and has 2 grown children who are estranged from her. At age 50 a truck hit her while she was crossing the road at night. She was comatose with a Glasgow coma scale of 3 to 4 when found by paramedics. A computed tomography (CT) scan showed an acute subdural hematoma, hemorrhagic contusion of the left temporal lobe, and a subarachnoid hemorrhage. She underwent a left frontotemporal parietal craniotomy with evacuation of the subdural hematoma and a left anterior temporal lobectomy to control massive swelling. She developed focal seizures in the postoperative period requiring phenytoin and phenobarbital. Other injuries included right third rib fracture and lung
contusions. As she recovered, a right-sided hemiplegia became obvious. Reports noted her eyes tracking and there was some impression that she may be responding to simple commands. She did not speak. She was transferred to a residential care facility. Over the next 12 years it was noted that she would recognize frequent visitors and enjoyed music, but screamed when she was touched. Periods of “calling out” were controlled with antipsychotics. She was agitated with any kind of physical contact and thus developed contractures. She did not participate in social activities and would scream in situations with groups of people where there was significant sensory stimulation. Eleven years after living in the facility she was seen by geriatric psychiatry. An empiric diagnosis of depression was made based on social isolation, subjective unhappiness and reduced activity, and agitation around times of care. A trial of olanzapine and citalopram made no improvement in her ability to interact with people. After an education session on pain management in people with dementia, the nursing staff chose to consult with palliative care for the purpose of assessing and managing her pain. Her medications at the time were the following:
Division of Residential Care, Providence Health Care, Vancouver, BC, Canada (R.G., S.H.); Department of Family Practice, University of British Columbia, Vancouver, BC, Canada (R.G.); Department of Psychiatry, University of British Columbia, Vancouver, BC, Canada (E.D.). R.G. accepts honoraria for educational presentation by Purdue Pharma, makers of long-acting oxycodone. R.G. wrote the paper with contribution and feedback from E.D. and S.H. The patient in this case report is not capable of giving informed consent. We have consent from her daughter.
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No funding was required.
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Address correspondence to Romayne Gallagher, MD, CCFP, Division of Residential Care, Providence Health Care, 1081 Burrard Street, Vancouver, BC, Canada V6Z 1Y6. E-mail:
[email protected]
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Copyright ©2006 American Medical Directors Association
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DOI: 10.1016/j.jamda.2006.04.010
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432 Gallagher et al.
Acetaminophen 1 g 3 times a day Alendronate 70 mg once weekly Baclofen 10 mg twice a day Calcium carbonate 1250 mg twice a day Citalopram 40 mg daily Olanzapine 5 mg at bedtime Phenobarbital 60 mg twice a day Phenytoin 250 mg daily JAMDA – September 2006
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Vitamin D 1000 units per day
In view of her symptoms of screaming with any physical care and her history of trauma it was felt that she may have chronic pain and that acetaminophen was not potent enough to give pain relief. A trial of long-acting oxycodone was started at 10 mg every 12 hours, and the staff was instructed that the dose was to be titrated upward as tolerated while monitoring behavior. The clinical “end point” was persistent drowsiness or other intolerable side effects of opioids. Two weeks after starting the pain medication, on a dose of 20 mg every 12 hours, AR greeted the staff with a “good morning” as they came in to give medications. Staff noted that she still complained of pain all over but seemed calmer, responded with more complex words, and her care was slightly easier. As the dose continued to be titrated up, AR began to answer staff questions with appropriate answers and when asked how she was she would say “so-so” or “better” rather than “awful” or “lousy” as before. With increased doses, staff reported her looking better and being much easier to engage in social activities. She started attending some exercise classes and although not participating, she appears to enjoy the passive involvement in the group environment. She recently participated in her first trip outside the facility in 12 years. She now makes eye contact when talking and is able to make more complex statements, such as “I don’t want to hurt you by saying no, but I don’t want it” in response to offers of dentures. AR takes 60 mg of long-acting oxycodone controlled release every 8 hours with short-acting oxycodone available for breakthrough pain. Increasing the oxycodone controlled release above this dose resulted in drowsiness. The major side effect has been constipation controlled with a bowel regime of stimulants, softeners, and osmotic agents. Geriatric psychiatry changed her antidepressant to venlafaxine and increased the olanzapine at bedtime. AR is brighter and has been better able to define her pain as being a headache with painful leg spasms. Since she has been seizure-free for some years the phenobarbital has been discontinued and replaced by gabapentin to see if a neuropathic adjuvant will achieve improved pain control. AR still has severe memory deficit and cannot recall being married or having children. She is able to recognize herself in a picture taken when she was a young adult but cannot recognize her husband sitting beside her or pictures of her children. DISCUSSION A 1996 study of a tertiary pain clinic revealed that 52% of patients with moderate/severe traumatic brain injury (TBI) reported chronic pain1 with the head being the most common site. Much of the cortex of the brain and its pia-archnoid covering is insensitive to pain, but cerebral arteries, cranial and upper cervical nerves, dura at the base of the brain, periosteum and cancellous bone are pain sensitive.2 Damage to the pain-sensitive structures can induce chronic pain. Posttraumatic headache can be divided into a number of headache subtypes such as tension, migraine type, cluster like, neuroCASE REPORT
genic, and whiplash associated.3 Paradoxically, posttraumatic headache may be more common in mild as compared to severe brain injury.4 There is a network of somatosensory, limbic, and associative areas of the brain that are involved in pain processing, interpretation, and modulation.5 Dysregulation of the function of these networks is common in TBI and therefore can result in chronic pain. In addition, functioning of cholinergic and dopaminergic neurotransmitter systems are affected in brain injury.6 Motor, language, cognitive, and behavioral systems are also disrupted after brain injury and may influence the interpretation, modulation, and expression of pain, making the detection of pain very difficult. Because posttraumatic headache is so common following TBI, a high degree of suspicion of chronic headache should be entertained in anyone with significant brain injury, particularly in those who may be unable to accurately report symptoms. There is now ample evidence that chronic pain, especially head and neck pain, independent of brain injury, can impair cognitive functioning.7 Pain and cognitive performance share key neural mechanisms8 and chronic pain may have an inverse relationship with cognitive performance. This has been demonstrated in a study of community-dwelling elders with and without chronic low-back pain as a result of osteoarthritis. Their neuropsychological performance was inversely related to the intensity of the pain and the neuropsychological performance mediated the relationship between pain and physical performance.9 It is perhaps the increased attention required by interacting with other residents and staff or participating in social events that drove AR into sensory “overload” and caused the screaming. Emotional and psychological stress associated with pain can impair cognitive functioning.10 Thus, the enormous changes resulting from the accident, in addition to her chronic mental illness, could have had an impact on her cognitive functioning as well as her interpretation and expression of pain. A number of studies have now documented a relationship between chronic pain and depression. A study of more than 5000 primary care patients showed that disabling chronic pain was present in 41% of depressed patients but only in 10% of nondepressed people.11 The relationship seems even more so in elders, with an earlier study demonstrating 79% of elders with depression or dysthymia reporting disabling pain.12 The use of opioids in chronic non– cancer pain and in elders is slowly gaining credibility with evidence of its efficacy and safety in these populations.13 The starting dose should be low and titrated slowly up to achieve the best analgesia with the fewest side effects. In those unable to communicate adequately, significant sedation would be the limiting side effect encountered first. Opioids with few or no clinically significant active metabolites are likely the best to be trialed in older individuals with or without renal impairment.14 Meperidine and morphine would not be drugs of first choice for a trial of therapy. The goal of therapy is to improve function and quality of life. In patients with TBI it is a challenge to determine which of the pain, brain injury, depression, or emotional and psychological stressors are contributing to the cognitive impairment Gallagher et al. 433
and behavioral challenges. Unfortunately, in nonverbal patients with severe cognitive impairment there are no behaviors that are specifically associated with pain or standardized behavior tools available yet.15 People with severe brain injury suffer when the potentially reversible components of their cognitive impairment and behavioral challenge are not teased out from the overall picture. In AR’s situation, treatment of depression alone was inadequate, and only when satisfactory pain management was also achieved did AR experience her greatest gains both functionally and subjectively. In teasing out the person behind the TBI, the clinician must carefully assess the person for all conditions that are treatable. Because chronic pain is common with TBI and it can be confounding in its expression, the consideration of a trial of analgesics is warranted in each individual with brain injury who has significant cognitive impairment and other behaviors suggestive of pain and or depression. Since chronic pain with TBI can be severe, a satisfactory trial of analgesics must not stop at nonopioids and the clinical end point should be intolerable side effects from 1 or 2 strong opioids. REFERENCES 1. Lahz S, Bryant R. Incidence of chronic pain following traumatic brain injury. Arch Phys Med Rehabil 1996;77:889 – 891. 2. Bonica J, Loeser J. Applied anatomy relevant to pain. In: Loeser J, ed. Bonica’s Management of Pain. Philadelphia, PA: Lippincott Williams & Wilkins, 2001:196 –221.
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3. Uomoto J, Esselman P. Traumatic brain injury and chronic pain: Differential types and rates by head injury severity. Arch Phys Med Rehabil 1993;74:61– 64. 4. Martelli M, Zasler M, Bender M, Nicholson K. Psychological, neuropsychological, and medical considerations in assessment and management of pain. J Head Trauma Rehabil 2004;19:10 –28. 5. Apkarian AV, Bushnell C, Treede R-D, Zubieta J-K. Human brain mechanisms of pain perception and regulation in health and disease. Eur J Pain 2005;9:463– 484. 6. Walker W. Pain pathoetiology after TBI: Neural and nonneural mechanisms. J Head Trauma Rehabil 2004;19:72– 81. 7. Hart R, Martelli M, Zasler N. Chronic pain and neuropsychological functioning. Neuropsychol Rev 2000;10:131–149. 8. Wiech K, Seymour B, Kalisch R, et al. Modulation of pain processing in hyperalgesia by cognitive demand. Neuroimage 2005;27:59 – 69. 9. Weiner D, Rudy T, Morrow L, Sloboda T, Liebers S. The relationship between pain, neuropsychological performance and physical function in community-dwelling older adults with chronic back pain. Pain Med 2006;7:60 –70. 10. Hart R, Wade J, Martelli M. Cognitive impairment in patients with chronic pain: The significance of stress. Curr Pain Headache Rep 2003; 7:116 –126. 11. Arnow B, Hunkeler E, Blasey C, et al. Comorbid depression, chronic pain and disability in primary care. Psychsom Med 2006;68:262– 268. 12. Unutzer J, Ferrell B, Lin E, Marmon T. Pharmacotherapy of pain in depressed older adults. J Am Geriatr Soc 2004;52:1916 –1922. 13. AGS Panel on Persistent Pain in Older Persons. The management of persistent pain in older persons. J Am Geriatr Soc 2002;50:S205–S224. 14. Dean M. Opioids in renal failure and dialysis patients. J Pain Symptom Manage 2004;28:497–504. 15. Herr K, Bjoro K, Decker S. Tools for assessment of pain in non-verbal older adults with dementia: A state-of-the-science review. J Pain Symptom Manage 2006;31:170 –192.
JAMDA – September 2006