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Perspectives in Psychiatric Care

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Biological Perspectives Pain: It’s Not All in Your Head Peter C. Kowalski, MD, Jonathan S. Dowben, MD, and Norman L. Keltner, EdD, CRNP Peter C. Kowalski, MD, is a Child Psychiatrist in private practice in Fort Worth, Texas, USA; Jonathan S. Dowben, MD is a Staff Psychiatrist, Pediatric and Adolescent Behavioral Health Service, Brooke Army Medical Center (BAMC), Fort Sam Houston, Texas, USA; and Norman L. Keltner, EdD, CRNP, is a Professor, School of Nursing, University of Alabama at Birmingham, Birmingham, Alabama, USA Search terms: Depression, pain, pain pathways Author contact: [email protected], with a copy to the Editor: [email protected] Disclaimer: The views expressed in this article do not represent the views of Brooke Army Medical Center or the U.S. Army. doi: 10.1111/ppc.12051

Emotions are emitted from pain like warmth from flame, slow and constant like a candle or blazing like a furnace blast. Pain and Its Transmission A simple but incomplete biological model for pain transmission and processing includes these elements: 1. Peripheral nerve endings with cell bodies in the dorsal root ganglia or trigeminal ganglia that synapse directly onto neurons in the spinal cord. An injury involving mechanical pressure or change in temperature sends a “pain message” via a volley of nervous impulses that travel through the cell body of the nerve located to the side of the spinal column, and then enters the spinal cord to deliver the message by means of the release of a chemical neurotransmitter, that is, it forms a synaptic connection with receiving neurons. 2. Interneurons and projection neurons at the level of the dorsal horn of the spinal column that convey ascending nociception to higher brain areas, such as nuclei in medulla, pons, midbrain, and thalamus. Processing the pain message at this level involves the interplay of a variety of signals from neurons from the outside of the spinal cord, neurons which reside only at the level of the site of entry (interneurons), and neurons from higher brain levels. The gate theory of pain reflects the interrelated coordination, enhancement, and suppression of pain signals that take place here, before the message is relayed to the next synaptic connection in the thalamus. 3. Thalamic neurons that relay nociceptive signals to the somatic sensory cortex, the anterior cingulate cortex, insula, medial and orbital prefrontal cortices, amygdala, ventral striatum, and hippocampus. This is the regional warehouse for pain messages before their final delivery to specific brain areas. The thalamus receives input from the spinal cord and Perspectives in Psychiatric Care 50 (2014) 3–6 © 2013 Wiley Periodicals, Inc.

projects to widespread targets in the brain, and also helps enhance or inhibit the strength of the pain messages it conveys. Other similar passageways exist to deliver the message from spine to brain areas, such as the spinoreticular tract, which complement the spinothalamic tract. 4. The “pain matrix” of perceptual, alerting and arousalenhancing, attentional, affective and behavioral systems that comprise the psychochemical interplay of conscious pain recognition and response. The brain receives the pain message in the somatosensory cortices, anterior cingulated gyrus, amygdala, insula, hypothalamus, and other brain areas to mobilize a response to enhance survival. This results in identification and discrimination of pain, the affective responses to pain, the autonomic activation necessary to promote rapid responses by the body, and memory systems to record what is happening for future purposes of avoidance. 5. The descending modulatory pathways that terminate at the dorsal horn to reduce or augment nociceptive signaling (Brooks & Tracy, 2005). The brain creates its own analgesic system to reduce the perception of pain, which directly reduces the pain message to a lower level. Nerves that originate from prefrontal cortices travel to the spinal level and release neurotransmitters that inhibit transmission of pain at the spinal column. The central perception and responses to pain vary according to the circumstances of its occurrence, its chronicity, and individual traits, including the personality, temperament, and affective state of the individual who is experiencing it. Because it is not measurable by objective tests or biological markers, the subjective nature of the pain message often causes misunderstanding and apprehension on the part of the sufferer and treater alike. Pain is not simply nociception. It is the integration of nociception with mental processes such as sensation, localization and discrimination, affect, memory, executive and 3

Pain: It’s Not All in Your Head

autonomic functions. These are respectively served by the primary and secondary somatosensory cortices, the amygdala, ventral striatum, insular cortex, hippocampus, and orbitomedial and dorsolateral prefrontal cortices. How pain shapes the patient and how the patient shapes pain is our topic. We will attempt to contrast the integration of pain and personality in our case reports, illustrating the interweaving of adaptation and dysfunction in the whole person, using the most recent insights in pain research. Case Report One A 53-year-old surgeon was referred by his neurologist for the aftermath of several progressive physical conditions and their negative effects on his professional and family life. He had worked overtime in many capacities as clinician and educator in spite of many years of chronic severe low back pain from widespread multilevel lumbar spondylosis with sacroiliac joint dysfunction, and radicular symptoms from foraminal stenoses at multiple lumbar sites. He underwent lumbar decompression 8 years previously with relief of his then current radicular pain but experienced no relief of local low back pain. He also experienced bilateral carpal tunnel syndrome, left greater than right, and had recently been diagnosed with hereditary sensory autonomic neuropathy type I. At the time of his lumbar decompression, numbness of his right lateral foot and left medial foot emerged. This sensation slowly progressed to include paresthesia (“pins and needles”), burning, and allodynia (the perception of pain by a non-pain-inducing stimulus), and he became sensitive to even light touch. The affected area had progressed to above his ankles by the time of his presentation and made the manipulation of foot pedals impossible for him. He had begun dropping instruments as the neuropathy had progressed to his hands. No surgical correction was available to him, and his nociceptive and neuropathic symptoms were treated with a variety of tricyclic antidepressants, serotonin noradrenergic reuptake inhibitors, anticonvulsants, and analgesics. His deteriorating physical condition prevented him from continuing to practice surgery. That professional challenge, together with conflicts with his family members, contributed to the emergence of a major depressive disorder, single episode, moderate. His psychiatric symptoms consisted of a continual depressed mood, daily insomnia and daytime fatigue, excessive feelings of guilt and diminished self-worth, social and family withdrawal and periods of isolation by perceived rejection, worry and rumination about his physical incapacity and ability to provide for his family, habitual checking, forgetfulness and diminished abilities to attend and concentrate, and although never suicidal, having a sense of a foreshortened future. 4

Case Report Two A self-described “hebephilic” (sexually attracted to pubescent youth) 40-year-old homosexual with a chronic history of depression and multiple drug use including benzodiazepines, marijuana, and opiates sought treatment for his difficulties in forming intimate attachments and discontent in his sense of identity. He was sexually assaulted at age 9 by a gang of adolescent boys. He reported that his mother began sexually fondling him beginning around 4 to 5 years of age, and that his father occasionally took action to stop this. A tumultuous adolescence without much adult supervision led to sexual misadventures, and drug abuse. He claims to have witnessed multiple deaths of associates involved in drug dealings. Although sexually active with both sexes in the past, mostly adolescents or adults of his same age, the patient never acted upon his sexual attractions to children or adolescents. He had engaged in procuring animated or cartoon representations of child sex, which he guiltily disposed of after achieving sexual gratification. Only one or two similarly inclined associates knew of this interest, and the patient had constant fear of discovery and legal prosecution, aggravated by media reports describing the activities of discovered pedophiles. He experienced several cycles of opiate relapse, detoxification and rehabilitation, then relapse until his early 30s. The patient had consulted a fatherly psychiatrist periodically from age 11 until the psychiatrist’s retirement, who then transferred his care to a younger colleague. This psychiatrist had provided the patient a regular prescription of pentazocine and naloxone for a number of years until the patient admitted himself for detoxification. He was opiate free for many years before consulting the new psychiatrist. At the first visit and for the first time, he related his overwhelming and incredibly distressing preoccupation with boys who were on the verge of entering puberty. He began a process of mostly supportive psychotherapy with exploration of traumatic life events according to his comfort level. His progress was slow. The patient reported multiple sites of osteoarthritic pain in the lumbar spine and knees from earlier accidents and incisional pain from an abdominal hernia repair. Five days after the death of his father, the patient relapsed back into opiate use. He persuaded his psychiatrist to write a prescription of hydrocodone and acetaminophen until he could return to his primary care physician. His father’s death had upended his life, and he stopped attending his regular appointments. His request for refills was continued for additional weeks, which turned into months as the patient delayed his return to his primary care physician for pain medication, and resisted referrals for pain management. After 5 months, the psychiatrist finally refused any more opiate refills and provided clonidine to assist him in opiate withdrawal. The patient made no more mention of opiate use until 3 years later. Perspectives in Psychiatric Care 50 (2014) 3–6 © 2013 Wiley Periodicals, Inc.

Pain: It’s Not All in Your Head

He disclosed a rapid relapse on opiates from diverted sources of 4 months duration, which started when he received a prescription of hydrocodone from a hotel physician on a trip out of town. His daily usage increased from 100 mg of hydrocodone shortly after he received this prescription, to 155 mg daily in the month preceding his self-disclosure, to 260 mg per day in the few days prior to this event. He was admitted to detoxification and rehabilitation and discharged on buprenorphine for opioid maintenance, which his psychiatrist continued. The patient maintained that his sexual fantasies were diminished by the opiates. He had struggled nightly with a powerful tendency to retreat into fantasy with a recurrent theme in which a sexually traumatized boy was forced to leave his rejecting family and make his way in the world, until he found a sexually attractive “squire,” an older middle-aged man who would protect and nurture him. Various sexual elements and themes were interwoven into this archetypal fantasy, with traumatic and painful memories and elaboration of actual traumatic memories incorporated in equal measure. Case Reports One and Two: Synopsis and Discussion The first patient’s premorbid personality was alloplastic, the tendency to change the external environment in a crisis, as opposed to autoplastic,the tendency to change one’s one internal environment. As a “take-charge” type, he had an extreme external locus of control over events in his environment. The second patient’s personality from the earliest was passively dependent, with very little sense of control over his environment, for which he compensated by procrastination and delay as a substitute for activity, and relegation of powerful others into servant-like status. The first patient was confronted with an uncontrollable and progressively debilitating disease with severe pain as its primary manifestation. His defenses of “fight or flight” mobilized his sympathetic nervous system as analgesia and distraction to modulate his sense of pain. He was only partly successful for a time before these defenses began to break, and depression acutely emerged. The second patient’s physical pain was secondary to his psychic distress in actual intensity, but served as a representation and measure of his psychological discomfort and vulnerability. It is objectively impossible to confirm whether his pedophilic fantasies were directly remitted by the presence of opiates. He continued to report freedom from these fantasies while being prescribed bupenorphine and other opiates by a pain management physician. Gabbard (2000) describes the experience of sexual activity with children (or in this case, the fantasy) as involving, “the unconscious . . . fusion with an ideal object or the restoration Perspectives in Psychiatric Care 50 (2014) 3–6 © 2013 Wiley Periodicals, Inc.

of a youthful idealized self. Anxiety about death or dying may be warded off through sexual activity with children.” The same theme is conveyed in Thomas Mann’s Death In Venice. The patient’s pain signaled the deterioration of his body. Its relief lightened, eased the psychological need for fusion. “Neuroplastic transformation” can be defined as the process mediating how personality characteristics are reinforced by chronic pain and how personality characteristics are changed by chronic pain. It involves the aforementioned pain matrix integrating with personality traits and individual temperament to create a new homeostasis. Well known to reinforce psychopathology, chronic pain enhances anxiety and environmental surveillance for paincausing activities, with subsequent avoidance of all activities. Depression emerges and deepens with pain. Persistent irritability and periods of overt anger swell, and constant preoccupation with the body and pain are likely. A reinforcement of passivity and feelings of vulnerability, combined with diminished self-worth and failure leads to a feeling of being interminably punished (Smith, 2007). Regression to earlier internal object relations results in splitting, transference, and countertransference reactions including sadism and hatred, primitive projections involving idealization and devaluation or scapegoating, and as mentioned above, intrapsychic fusion, all of which strain the working alliance between the treater, the patient, and others involved in his life. Walking through the minefield of chronic pain is a delicate crossing for all. Case Report Three Mrs. Smith was a 67-year-old woman from rural Nebraska who was referred for evaluation of an“intractable”pain disorder related to a diagnosis of shingles. She was briefly hospitalized on the acute care psychiatric unit of a nationally recognized psychiatric facility. Mrs. Smith’s family physician forwarded his treatment notes that indicated that Mrs. Smith had sustained herpetic whitlow lesions on her hands and feet approximately 8 months prior to hospitalization that had healed. She had been prescribed opiate analgesics as her pain persisted. She had become largely bedridden and wheelchair bound. Mrs. Smith was noted to continuously complain and moan about her pain. Drafts of air or even someone touching her sheets or blankets would induce spasms of pain. Mrs. Smith and her husband, both of whom were fairly religious, were not sure what she or they had done to “anger God” to provoke the pain that was torturing Mrs. Smith and, by extension, her husband, adult children, grandchildren, and concerned neighbors. While opiate analgesics were helpful to some degree, she became tolerant to the effect of this type medication, and increasing doses made her become “mildly demented,” constipated, and even incontinent, a further scourge, that was also evidence of “God’s wrath.” 5

Pain: It’s Not All in Your Head

Mrs. Smith was prescribed low-dose mesoridazine (Serentil) and her opiates were gradually tapered to a more conservative level. She participated in group therapy and art therapy, and was “locked out” of fleeing by wheelchair into her hospital bedroom during “normal waking hours,” which initially made her angry. She was introduced to hypnosis and began to benefit from hypnotherapy for pain management after the hospital chaplain helped convince her it was not “an immoral voodoo” practice. Mrs. Smith was able to return to home continuing to be in chronic, although more tolerable pain. She continued to receive psychotherapy, a treatment that she had previously believed was for “imbeciles,” with a therapist who gave her confidence, after she ascertained the therapist was a fellow “cornhusker.”

Fortunately, we are beginning to learn that our brains and central nervous systems are plastic in a positive sense as well. Gardens do worse with herbicide and better with fertilizer. Similarly, recovery from brain stresses such as depression show increased production of neural growth factors (Schmidt & Duman, 2007) and reversal of atrophic changes in hippocampus (Phillips et al., 2012), in response to medication, physical exercise, stress management, meditation, and a positive environment. We do not know how much brain recovery can occur in chronic pain. But there appears to be every reason to hope for favorable outcomes as we continue to gather information about neural recovery and the practices that can make this occur.

Summary

References

Neuroanatomy correlates with the psychological changes of pain. Neuroplastic transformation appears in the reduction of gray matter volume, or shrinkage in the top-down cortical areas vital for working memory, problem solving, sequencing and discrimination of different information and cognitive modulation of pain via the descending pain modulatory tracts and control over other cortical areas involved in the emotional perception of pain. These latter areas become more active, thereby intensifying the susceptibility to negative affect associated with pain (Geha & Apkarian, 2006). An animal model of chronic neuropathic pain was associated with impairment in the firing activity of the locus coeruleus and its expression of noradrenaline in ascending and descending pathways, which plays roles in not only pain perception, but mood, anxiety, attention and concentration, the sympathetic nervous system, and the activity of the hypothalamic–pituitary–adrenal axis, which serves to mobilize an organism’s survival by the expression of cortisol in an immediate survival circumstance.

Brooks, J., & Tracy, I. (2005). From nociception to pain perception: Imaging the spinal and supraspinal pathways. Journal of Anatomy, 207, 22–24. Gabbard, G. O. (2000). Psychodynamic psychiatry in clinical practice (3rd ed., pp. 307–308). Arlington, VA: American Psychiatric Press. Geha, P. Y., & Apkarian, A. V. (2006). Pain and neuroanatomical effects: Evidence for cortical reorganization. Psychiatric Times, February, 22–24. Phillips, J. L., Batten, L. A., Aldosary, F., Tremblay, P., & Blier, P. (2012). Brain-volume increase with sustained remission in patients with treatment-resistant depression. Journal of Clinical Psychiatry, 73(5), 625–631. Schmidt, H. D., & Duman, R. S. (2007). The role of neurotrophic factors in adult hippocampal neurogenesis, antidepressant treatments and animal models of depressive-like behavior. Behavioral Pharmacology, 18, 391–418. Smith, M. B. (2007). Chronic pain and psychopathology: One psychiatrist’s view. Primary Psychiatry, 14, 50–64.

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Perspectives in Psychiatric Care 50 (2014) 3–6 © 2013 Wiley Periodicals, Inc.

Biological perspectives: pain: it's not all in your head.

Neuroanatomy correlates with the psychological changes of pain. Neuroplastic transformation appears in the reduction of gray matter volume, or shrinka...
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