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Overview
Of all human experience, pain is, as long as it lasts, the most absorbing; it is the only human experience that when it comes to an end, automatically confers a sense of relief and joy. Moreover, by its very nature it is solitary. Despite its intensity and its unequalled power over mind and body, pain can be difficult to recall once it subsides.
The International Association for the Study of Pain (IASP) has defined pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage.” This definition recognizes the fact that pain has both an acute nociceptive aspect and an emotional-affective dimension; these factors suggest that psychiatrists can have a significant role in the treatment of the pain patient. Conceptualizing pain in this manner underscores the fact that pain is an important and complicated sensation, one that may present in a multitude of ways.
In this chapter, the pathophysiology of pain, along with common pain syndromes and terminology are reviewed. In addition, the role of the psychiatric consultant along with psychiatric assessment of the pain patient will be discussed. Furthermore, general principles of pain therapy, including medications commonly used for symptomatic pain management, as well as approaches to the treatment of pain behavior are outlined.
Pathophysiology of Pain
To understand pain one needs to know about the pathophysiology of nociception and to realize that the threshold, intensity, quality, time course, and perceived location of pain are determined by CNS mechanisms. For example, neurosurgeons have shown that interruption of the specific pain pathways often does not eliminate pain; numbness does not confer analgesia. Peripheral nerve damage may result in changes in the receptive fields and recruitment of neurons at multiple levels of the nervous system (from the dorsal horn to the brainstem, and to the thalamus and cortex). Somatic therapies directed only at nociceptive input may be ineffective.
Detection of noxious stimuli (i.e., nociception) starts with the activation of peripheral nociceptors (somatic pain) or with the activation of nociceptors in bodily organs (visceral pain). Somatic pain is usually well localized, attributable to certain structures or areas, and described as stabbing, aching, or throbbing. In contrast, visceral pain may be poorly localized, not necessarily attributable to the involved organ (i.e., as is the case with referred pain), and is characteristically described as dull and crampy.
Tissue injury stimulates the nociceptors by the liberation of prostaglandins, arachidonic acid, histamine, and bradykinin. Subsequently, axons transmit the pain signal to the spinal cord (to cell bodies in the dorsal root ganglia; Figure 18-1 ).
Three different types of axons are involved in the transmission of a painful stimulus from the skin to the dorsal horn. A-β fibers are the largest and most heavily myelinated fibers that transmit awareness of light touch. A-δ fibers and C fibers are the primary nociceptive afferents. A-δ fibers are 2–5 µm in diameter and are thinly myelinated. They conduct immediate, rapid, sharp, and brief pain (first pain) with a velocity of 20 m/second. C fibers are 0.2–1.5 µm in diameter and are unmyelinated. They conduct prolonged, burning, and unpleasant pain (second pain) at a speed of 0.5 m/second. A-δ and C fibers enter the dorsal root and ascend or descend one to three segments before synapsing with neurons in the lateral spinothalamic tract (substantia gelatinosa in the gray matter).
Substance P, an 11-amino-acid polypeptide, considered to be a major pain neurotransmitter, is released from the fibers at many of these synapses. Capsaicin, which is extracted from red hot peppers, inhibits nociception by inhibiting substance P. Inhibition of nociception in the dorsal horn is functionally quite important. Stimulation of the A-δ fibers not only excites some neurons but also inhibits others. This inhibition of nociception through A-δ fiber stimulation may explain effects of acupuncture and transcutaneous electrical nerve stimulation (TENS). The lateral spinothalamic tract crosses the midline and ascends toward the thalamus. At the level of the brainstem more than half of this tract synapses in the reticular activating system (in an area called the spinoreticular tract ), in the limbic system, and in other brainstem regions (including centers for autonomic nervous system). Another site of projections at this level is the periaqueductal gray (PAG; Figure 18-2 ), which plays an important role in the brain's endogenous analgesia system. After synapsing in the thalamic nuclei, pain fibers project to the somatosensory cortex, located posterior to the Sylvian fissure in the parietal lobe (Brodmann's areas 1, 2, and 3).
Developments in imaging technology have been helpful in understanding the relationship between pain pathways and cortical and limbic areas. These findings may help explain the relationship between emotions, cognition, and pain modulation that we observe in clinical practice as heightened pain perception in depressed patients and high rates of depression in those with chronic pain. Functional imaging studies utilizing both functional MRI (fMRI) and positron emission tomography (PET) study have shown that acute traumatic nociceptive pain activates the hypothalamus and the PAG in addition to the prefrontal cortex (PFC), insular cortex, anterior cingulate cortex (ACC), posterior parietal cortex, primary motor/somatosensory areas, supplementary motor area (SMA), thalamus, and cerebellum. Additionally, functional imaging studies have helped clinicians understand cognitive and emotional modulation of pain perception. Researchers have shown that with hypnotic suggestion the activity in the ACC is dependent on the intensity of the suggestion (i.e., same stimulus with the suggestion of “highly unpleasant” induces significantly more ACC activation than when suggestions are less unpleasant). In another study, when subjects were distracted during a painful stimulus, pain perception was attenuated in somatosensory regions and the PAG. The short-acting opioid, remifentanil, as well as placebo analgesia, have been shown to activate the ACC, which is rich in opioid receptors. It is of interest that analgesia induced by both opioids and placebos was reversed with the opioid antagonist naloxone. These findings suggest that cortical areas may exert control over lower brain areas involved in opioid analgesia.
Endogenous analgesic systems involve at least 18 endogenous peptides with opiate-like activity in the CNS (e.g., endorphins, enkephalins, and dynorphins). Different opiate receptors are involved in different effects of opiates.
Mu (µ)-receptors are involved in the regulation of analgesia, respiratory depression, constipation, and miosis. Mu receptors (located in the PAG, rostral ventral medulla, medial thalamus, and dorsal horn of the spinal cord) are the receptors that are mainly responsible for supraspinal analgesia.
Kappa (κ)-receptors are involved in spinal analgesia, sedation, and miosis. They are located in the dorsal horn (spinal analgesia), deep cortical areas, and other locations; pentazocine preferentially acts on these receptors.
Delta (δ)-receptors, like κ-receptors, mediate spinal analgesia, hypotension, and miosis. Enkephalins have a higher affinity for these receptors than do opiates. They are located in the limbic system, the dorsal horn, and other locations unrelated to pain. δ-Receptors also mediate psychotomimetic effects (i.e., psychosis) in the CNS. Their effects are not reversed by naloxone, an opiate antagonist.
In terms of anatomic organization, the centers involved in endogenous analgesia include, in addition to PAG, the rostral ACC, amygdala, parabrachial plexus in the pons, and rostral ventromedial medulla.
The descending analgesic pain pathway starts in the PAG (which is rich in endogenous opiates), projects to the rostral ventral medulla, and from there descends through the dorsolateral funiculus of the spinal cord to the dorsal horn. The neurons in the rostral ventral medulla use serotonin to activate endogenous analgesics (enkephalins) in the dorsal horn. This effect inhibits nociception at the level of the dorsal horn since neurons that contain enkephalins synapse with spinothalamic neurons.
Additionally, there are noradrenergic neurons that project from the locus coeruleus (the main noradrenergic center in the CNS) to the dorsal horn and inhibit the response of dorsal horn neurons to nociceptive stimuli. The effect of tricyclic antidepressants (TCAs) and other newer antidepressants is thought to be related to an increase in serotonin and norepinephrine that inhibits nociception at the level of the dorsal horn.
Pain Terminology
Acute pain is usually related to an identifiable injury or to a disease; it is self-limited, and resolves over hours to days or in a time frame that is associated with healing. Acute pain is usually associated with objective autonomic features (e.g., tachycardia, hypertension, diaphoresis, mydriasis, or pallor).
Chronic pain (i.e., pain that persists beyond the normal time of healing or lasts longer than 6 months) may have a neurologic origin, involving lowered firing thresholds for spinal cord cells that modulate pain (triggering pain more easily); anatomic plasticity and recruitment of a wide range of cells in the spinal cord (so that touch or movement causes pain); convergence of cutaneous, vascular, muscle, and joint inputs (where one tissue refers pain to another); or aberrant connections (electric short-circuits between the sympathetic and sensory nerves that produce causalgia). Muscle pains often add to the pain experience. Vascular and other visceral mechanisms share features with neurologic mechanisms, however these mechanisms involved are not mutually exclusive. Table 18-1 summarizes the clinical implications of the mechanisms of chronic pain. Characteristic features include vague descriptions of pain and an inability to describe the pain's timing and localization. Unlike acute pain, chronic pain lacks signs of heightened sympathetic activity. Depression, anxiety, and premorbid personality problems are common in this patient population. Usually the major issue is a lack of motivation and incentive to improve. It is usually helpful to determine the presence of a dermatomal pattern ( Figure 18-3 ), determine the presence of neuropathic pain, and assess pain behavior.
TABLE 18-1
Chronic Pain: Nervous System Pathophysiology
| NEUROLOGIC MECHANISMS | PHYSIOLOGIC EFFECTS | CLINICAL IMPLICATIONS |
|---|---|---|
| Neuroplasticity |
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| Neurotoxins | Excitotoxic (e.g., quinolinic acid) Neuropathy |
AIDS pain: anti-epileptic drugs, serotoninergic/noradrenergic agents, free radical scavengers |
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| Sympathetic pain | Mechano-allodynia, swelling Dystrophic changes |
Sympathetic blockade and/or α-blocking drugs may be useful in CRPS, trauma, facial pain, arthritis |
| Monoamines (5-HT, NE, dopamine) |
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| Psychiatric illness | Decreased sleep Decreased muscle relaxation Alienation, anxiety |
Differential diagnosis of psychiatric conditions and appropriate treatments |
NMDA, N -methyl-D-aspartate; GABA, γ-aminobutyric acid; CRPS, complex regional pain syndrome; 5-HT, 5-hydroxytryptamine; NE, norepinephrine; SSRIs, selective serotonin re-uptake inhibitors.
Continuous pain in the terminally ill tends to originate from well-defined tissue damage due to terminal illness (e.g., cancer). It is a variant of nociceptive pain. Stress, sleep deprivation, depression, and premorbid personality problems may exacerbate this pain.
Neuropathic pain is caused by an injured or dysfunctional central or peripheral nervous system; it is manifest by spontaneous, sharp, shooting, or burning pain that is usually distributed along dermatomes ( Figure 18-3 ). Neuropathic pain is often observed in deafferentation pain, complex regional pain syndrome (CRPS), diabetic neuropathy, central pain syndrome, trigeminal neuralgia, or postherpetic neuralgia.
Terms commonly used to describe neuropathic pain include: hyperalgesia (an increased response to stimuli that are normally painful); hyperesthesia (an exaggerated pain response to noxious stimuli, e.g., pressure or heat); allodynia (pain with a stimulus not normally painful, e.g., light touch or cool air); and hyperpathia (pain from a painful stimuli with a delay and a persistence that is distributed beyond the area of stimulation).
CRPS is a syndrome of sympathetically maintained pain, or pain in an extremity that is mediated by sympathetic overactivity. The syndrome is usually caused by injury; however, the cause is unknown in approximately 10% of cases. Any type of trauma, such as a sprain, a fracture, or a contusion, may cause it; iatrogenic causes include amputation, lesion resection, myelography, and intramuscular (IM) injections. CRPS may be disease-related (e.g., due to myocardial infarction, shoulder-hand syndrome, herpes zoster, cerebrovascular accidents, diabetic neuropathy, disc herniation, degenerative disc disease, neuraxial tumors or metastases, multiple sclerosis, or poliomyelitis). CRPS is divided into two types. In type I CRPS, which typically develops after minor trauma or fracture, no overt nerve lesion is detectable. In type II CRPS, a definable nerve injury is present. Per diagnostic criteria set forth by the IASP, the diagnosis of CRPS can be made if the following criteria are met:
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Preceding noxious event without (CRPS I) or with obvious nerve lesion (CRPS II);
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Spontaneous pain or hyperalgesia/hyperesthesia not limited to a single nerve territory and disproportionate to the inciting event;
- 3.
Edema, skin blood flow (temperature) or sudomotor abnormalities, motor symptoms, or trophic changes are present on the affected limb, in particular at distal sites;
- 4.
Other diagnoses are excluded.
The clinical course (which may last up to 6 months) starts with an acute phase that involves pain, edema, and warm skin. Subsequently, dystrophic changes dominate the picture with cold skin and trophic changes (3–6 months after the onset of the untreated acute phase). Irreversible atrophic changes (atrophy and contractures) eventually occur. There may be symptom improvement with inhibition of sympathetic output; sympathetic blockade may be both diagnostic and therapeutic.
Idiopathic pain , previously referred to as “ psychogenic pain ,” is poorly understood. The presence of pain does not imply or exclude a psychological component. Typically, there is no evidence of an associated organic etiology or an anatomical pattern consistent with symptoms. Symptoms are often grossly out of proportion to an identifiable organic pathology.
Jurisigenic pain results from perceived physical or emotional damage related to medical, personal, work, or product injury. Patients with this pain syndrome usually maintain the sick role for as long as possible to maximize financial return. It is important to recognize the existence of a conflict and to educate patients and attorneys; maintenance of a helping and neutral posture is critical.
Phantom-limb pain refers to severe and excruciating pain in the body part that is no longer present following amputation. The amputation of a limb is commonly followed by sensations that the deafferented body part is still present. These may include non-painful phantom sensations in specific positions, shapes, or movement, sensations of warmth or cold, itching, tingling, or electric sensations, and other paraesthesias. However, pain may also be present, and occurs in 50% to 80% of all amputees. Although this condition is most common after amputations of limbs, it can also occur after the surgical removal of other body parts such as the breast, rectum, penis, testicle, eye, tongue, or teeth. The pathophysiology of this pain is poorly understood, however it is likely secondary to CNS and peripheral factors (e.g., nociceptive input from the residual limb), with psychological factors influencing the course and severity of the pain. Consistent with the impact of the psyche on pain, one study showed that it is possible to induce pain in an amputee with hypnotic suggestion.
Myofascial pain can arise from one or several of the following problems: hypertonic muscles, myofascial trigger points, arthralgias, and fatigue with muscle weakness. Myofascial pain is generally used to describe muscle and connective tissue sources of pain. Myofascial pain can be a primary diagnosis (e.g., fibromyalgia) or, as more often is the case, a co-morbid diagnosis (e.g., with vascular headache or with a psychiatric diagnosis). Psychiatric symptoms are common in patients with muscle pain; other symptoms often involve decreased energy, impaired sleep, and changes in psychomotor activity. Myofascial pain syndromes may involve muscle trigger points, hypersensitive skin, a subjective sense of swelling and numbness, somatic symptom disorders, affective and anxiety disorders, non-restorative sleep, as well as pain of the head and neck. The diagnosis should be considered if there are multiple muscle trigger points in the temporalis, sternocleidomastoid, rhomboids, or trapezius muscles; if the person cannot get at least 5 hours of uninterrupted sleep; and if chronic fatigue is present. Deficient Stage 4 sleep is thought to underlie the lack of deep muscle relaxation, aching muscles, arthralgias, and general malaise.
Pain Measurement
The experience of pain is always subjective. Objective measurement of the patient's subjective response, however, is possible. Several sensitive and reliable clinical instruments for pain measurement are available. These include:
- 1.
The pain drawing . This involves having the patient draw the anatomic distribution of the pain as it is felt in his or her body. The patient draws the outline of the body, labels where the pain is, and keeps this document as part of the medical record. The drawing serves as a clue to the anatomy of the problem, to the psychological state of the patient, and to the patient's level of knowledge.
- 2.
The visual analog scale . A 100-mm visual analog scale (with 0 signifying no pain and 100 representing severe pain) is readily understood by most patients. It is also exquisitely sensitive to change; consequently, the patient can mark this scale once a day or even hourly during treatment trials, if desired. Two separate scales can be kept for the least and the greatest pain. Concurrent scales for mood, overall progress, and pain allow for comparison of the relationship of pain to the total clinical picture, thereby rounding out the clinician's understanding of the patient's syndrome.
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Categorical rating scales . Ad hoc categorical rating scales may be devised that comprise three to five categories for the ranking of pain severity.
The Psychiatry Consultant as Pain Physician
The Psychiatrist's Role
Physicians and patients alike seek knowledge, order, and relief when dealing with pain's chameleon-like manifestations; some of the common reasons pain patients or treating physicians seek consultation and treatment from psychiatrists include:
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To separate functional from non-functional factors. Unfortunately, the request to separate psyche from soma is often vexing. Through such consultations some physicians wish to absolve themselves of further responsibility
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To resolve inconsistencies between symptoms and physical findings (or the lack thereof): “No anatomic lesion could account for this.” The referring physician wonders if a psychiatric disorder or central nervous system (CNS) pain is present or if he or she is missing something
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To assess the patient for depression, anxiety, or some other co-morbid neuropsychiatric disorder and its relation to the experience of pain
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To address a patient's or physician's fear or misunderstanding of opioids (e.g., use of high-dose analgesics, maintenance treatment, or toxicity)
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To determine if the use of psychopharmacologic agents might help alleviate pain and suffering
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To satisfy the referring physician's personal desire to punish a “hateful” patient, one who will not take yes or no for an answer and who interferes with normal medical decision-making.
The psychiatrist begins with a clarification of the reason for the consultation, creates some initial hypotheses, and examines the patient. If possible, the psychiatric consultant should be brought into the case early on and introduced as a member of the medical team. The referring physician should take care to ensure that the patient does not interpret the referral as a sign that he or she is not believed, and the physician should state that a psychiatrist is routinely asked to evaluate patients with longstanding pain. When the referring physician is comfortable using the services of a psychiatrist, the patient typically accepts the examination without protest. When the psychiatrist is called in at the end of a long and frustrating stand-off, the patient typically balks.
Gathering Important Preliminary Information
The psychiatric consultant's job begins by answering five questions: (1) Is the pain intractable because of nociceptive stimuli (e.g., from the skin, bones, muscles, or blood vessels)? (2) Is the pain maintained by non-nociceptive mechanisms (i.e., have the spinal cord, brainstem, limbic system, and cortex been recruited as reverberating pain circuits)? (3) Is the complaint of pain primary, as occurs in disorders such as major depression or delusional disorder? (4) Is there a more efficacious pharmacologic treatment? (5) Have pain behavior and disability become more important than the pain itself? Answering these questions allows the mechanism(s) of the pain and suffering to be pursued. Table 18-2 is a useful guideline to organize the questions, to test hypotheses, and to determine the diagnosis.
TABLE 18-2
Questions to Ask When Pain Persists
| PAIN SYNDROMES: WHAT IS THE PROBLEM? | SELECTED DIAGNOSTIC CONSIDERATIONS | CONSIDER: |
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| Is there an ongoing physical disease? (e.g., infection, cancer) |
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| Is there a problem with the use and response to opioids? (e.g., misuse, lack of efficacy) |
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| Is it a pain behavior syndrome? | Somatic symptom disorder; rule out depression, substance use disorder, physical/sexual abuse, missed physical disorder |
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Malingering or factitious disorders with physical symptoms are rare, much more likely to be something else |
| Is an unusual problem responsible for pain? | Muscle trigger points absent, deep sleep | Myofascial pain often comorbid with other pain syndrome |
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MRI, magnetic resonance imaging; ESR, erythrocyte sedimentation rate; SSRI, selective serotonin re-uptake inhibitor.
Physical Examination
A clinician's physical examination of the pain patient includes examination of the painful area, muscles, and sensation to pinprick and light touch ( Table 18-3 ). The examination is essential to the psychiatric evaluation for pain and serves three purposes. First, examination of the patient allows for better history-taking, therapeutic alliances, and integration of data; it also helps to eliminate the physical–mental dichotomy, which, left unspoken, often contributes to the patient's defensiveness. Second, the psychiatrist can search for signs of different types of pain and distinguish them from symptoms of a conversion disorder. Third, inconsistent findings suggestive of somatic symptom disorder may be uncovered.
TABLE 18-3
General Physical Examination of Pain by the Psychiatrist
| PHYSICAL FINDING | PURPOSE OF EXAMINATION |
|---|---|
| Motor deficits | Does the patient give-way when checking strength? Does the person try? Is there a pseudoparesis, astasia-abasia or involuntary movements suggesting a somatoform disorder? |
| Trigger points in head, neck, shoulder, and back muscles | Are any of the common myofascial trigger points present, suggesting myofascial pain? Presence of evoked pain (such as allodynia, hyperpathia, or anesthesia) suggests neuropathic pain |
| Evanescent, changeable pain, weakness, and numbness | Does the psychological complaint pre-empt the physical? |
| Abnormal sensory findings | Detection of lateral anesthesia to pinprick ending sharply at the midline Presence of topographic confusion Presence of non-dermatomal distribution of pain and sensation suggests either a somatoform or CNS pain disorder Presence of abnormal sensation suggests neuropathy or CNS pain |
| Sympathetic or vascular dysfunction | Detection of swelling, skin discoloration, or changes in sweating or temperature suggests a vascular or sympathetic element to the pain |
| Uncooperativeness, erratic responses to the physical examination | Detection of an interpersonal aspect to the pain, causing abnormal pain behavior, as in somatoform disease |
Psychiatric Examination
Interviewing the patient with chronic pain demands close attention to both what was said and what was not said, as well as to mindfulness of the patient's style of discourse. Because patients with an extensive history of pain often delight in regaling the examiner with their odysseys through clinics, spas, and hospitals, it is helpful to ask them to write detailed accounts of their pain from its onset to the present. A detailed history of when and how the pain began, inquiring about the various treatments received, and the patient's relationships with other physicians are also important in the evaluation of the pain patient. Throughout the history, look for fluctuations in the course of the pain. Why did it improve? Did the medication help, or was it some other factor that proved palliative? In addition, one should explore the patient's past and present mental state and consider the family history and cultural beliefs. Open-ended questions may include: Have you ever suffered like this before? What do you do think about in the early morning hours when you cannot sleep? What do others think is the nature of the problem? The psychiatrist also plays an important role in the treatment of the pain by his or her ability to recognize co-morbid psychiatric conditions that may present with pain.
Depression
Major depressive illness can be diagnosed in approximately 25% of patients who suffer from chronic pain. Recurrent affective illness, a family history of depression, and psychiatric co-morbidity (with anxiety and substance use) are often present. More often than not, depression pre-dates the pain; overall, 60% to 100% of pain patients have depressive symptoms. Although some depressive syndromes are secondary to pain itself (e.g., adjustment disorder with affective symptoms), many patients have major depression masked by denial or by medications that promote sleepiness. Denial of affect, particularly anger, is observed in many chronic pain patients referred for consultation. Diagnosing an affective illness when abnormal mood is minimized by the patient may be difficult, but the following tactics can be used to help find out affective disorders.
Ask questions about neurovegetative symptoms. Examples of questions to be posed include: How often do you wake from sleep at night? How long does it take you to return to sleep? Do you have early-morning awakening? When was the last time you really enjoyed yourself? Does food taste the same as it always has? Do you enjoy eating? What do you do for fun? Can you still smile? Do you have an interest in people, such as your grandchildren or friends? Do you have difficulty with decision-making? What do you do when you are angry? Do you sometimes feel you would rather be dead?
Evaluate the person's limbic (i.e., genuine and uncensored) response to emotionally charged stimuli. Look for denial of any strong emotion, particularly anger or sadness, and note if the patient answers affective questions with affective responses or only with avoidance and denial. Denial, displacement, or suppression of emotions suggests psychopathology. One could ask questions, such as, “Can you laugh at a joke at your own expense? Can you acknowledge anger at yourself and others?” The Minnesota Multiphasic Personality Inventory (MMPI) may be of particular use in refining the differential diagnosis when denial or repression is suspected. Covert hostility is typically elevated, which adds some validity to the label of denier. The so-called “conversion V” is present in many patients, and it occurs more often among those in denial. Patients with other chronic illnesses are more likely to have an “inverted V” configuration.
Anxiety Disorders
In the pain patient, denial of fear, worry, or nervousness is a more ominous sign than is the mere expression of modulated fear or worry about pain. Given that it is normal to worry about a painful threat to the body and the mind, pathologic denial of any affect may be suggestive of psychosis, hypochondriasis, conversion, factitious disorder, or personality disorder. Questions, such as the following, may help glean important information: “Does the pain make you panic? Do you feel your heart beating fast, have an overwhelming feeling of dread or doom, or experience a sense of sudden high anxiety that overwhelms you?”
Anxiety disorders occur in approximately 30% of patients with intractable pain (usually in the form of generalized anxiety or panic disorder). More than 50% of patients with anxiety disorders also have a current or past history of major depression or another psychiatric disorder. Alcohol and substance use disorders are the most common co-morbid diagnoses; consequently, recognition and treatment of co-morbid depression and substance use is critical to long-term treatment outcome.
A variety of agents, including TCAs, selective serotonin re-uptake inhibitors (SSRIs), serotonin norepinephrine re-uptake inhibitors (SNRIs), mirtazapine, and clonazepam, alone or in combination, improve panic, anxiety, and depression as well as neuropathic pain, muscle tension, and sleep. Anxiety that results from disruptions of bodily integrity, sense of self, or attachment to caregivers occurs in one-third to one-half of chronic pain patients. This type of narcissistic injury can block efforts at physical and emotional rehabilitation and requires a pragmatic treatment approach. Anger is often linked to anxiety, although it is typically denied and expressed in terms of somatic symptoms. One can provoke affect quickly by holding up a clenched fist and asking the patient what he or she would do with it. The response will often be telling regarding denied anger. SSRIs are helpful with anger, anxiety, and mood disorders. Existential anxiety may increase when cancer is first diagnosed, when death nears, or when pain engenders feelings of helplessness. Spending time with the person, telling the truth, accepting the situation, and re-connecting with family members (parents and children) often decreases existential anxiety.
Somatic Symptom Disorders
Somatic symptom disorder occurs in 5% to 15% of treated chronic pain patients, and somatizers account for 36% of all cases of psychiatric disability, as well as 48% of all sick-leave occasions.
Among those with a history of somatic complaints, pain in the head or neck, epigastrium, and limbs predominates. Visceral pain from the esophagus, abdomen, and pelvis associated with psychiatric co-morbidity, especially somatoform disorders, can be challenging to diagnose. Missed ovarian cancers, central pain following inflammatory disorders, and referred pain are often over-looked because of the non-specific presentations of visceral pain. Moreover, in one study, 64% of women with chronic pelvic pain reported a history of sexual abuse. Those that experience somatoform disorders often have painful physical complaints and excessive anxiety about their physical illness. Most of their pain complaints to physicians do not have a well-defined cause, and a psychiatric diagnosis is often particularly difficult to establish ( Table 18-4 ).
TABLE 18-4
Somatoform and Related Disorders
| DISORDERS | DIAGNOSTIC TIPS |
|---|---|
| Somatic symptom disorder | Physical symptoms that suggest physical illness or injury—symptoms that cannot be explained fully by a general medical condition, or by the direct effect of a substance, and are not attributable to another mental disorder Central and visceral pain, especially pelvic pain, can mimic somatic symptom disorder(s) Pain may improve with psychopharmacologic medications or psychological interventions without clear psychiatric diagnosis |
| Conversion disorder | Identifiable physical illness and conversion symptoms often co-occur An undiagnosed medical condition may underlie the psychiatric diagnosis Deciding if psychological factors are causative or a response is often impossible in chronic pain patients Culturally determined stress responses, numbness, total body pain, weakness, astasia-abasia, fainting, voices, and non-epileptiform seizure activity are transient and not included as conversion disorders |
| Hypochondriasis | Transient hypochondriasis is particularly common in the elderly Psychosis and depression may be concealed because of the patient's fears |
| Malingering/factitious disorder | Pseudomalingering with dissociative features (Ganser syndrome) presents with malingering, but also underlies real psychiatric illness. Some classify it as a conversion, dissociative, or factitious disorder |
Functional Neurologic Symptom Disorder
Functional neurologic symptom disorders (FND) may be manifest as a pain syndrome with a significant loss or alteration in physical functioning that mimics a physical disorder. Conversion symptoms may include paresthesias, numbness, dysphonia, dizziness, seizures, globus hystericus, limb weakness, sexual dysfunction, or pain. If pain or sexual symptoms are the sole complaints, the diagnosis is pain disorder or sexual pain disorder rather than FND. Pain, numbness, and weakness often form a conversion triad in the pain clinic.
Psychological factors are judged to be etiologic for the pain when a temporal relationship between the symptoms and a psychosocial stressor exists—the person must not be intentionally producing their symptom. A mechanism of primary or secondary gain needs to be evident before the diagnosis can be confirmed. La belle indifference and histrionic personality traits have little value in making or excluding the diagnosis of conversion. A conversion V on the MMPI denotes the hypochondriacal traits and relative absence of depression that accompany conversion. Evoked responses, electromyogram (EMG), electroencephalogram (EEG), MRI, PET scans, and repeated physical examinations are useful for identification of patients who had been diagnosed erroneously as “hysterical.”
Factitious Disorder With Physical Symptoms
Factitious disorder with physical symptoms involves the intentional production or feigning of physical symptoms. Onset is usually in early adulthood with successive hospitalizations forming the life-long pattern. The cause is a psychological need to assume the sick role, and as such, the intentional production of painful symptoms distinguishes factitious disorder from somatic symptom disorders, in which intention to produce symptoms is absent. Renal colic, orofacial pain, and abdominal pain are three of the common presenting complaints in factitious disorder; of these, abdominal pain and an abdomen with scars herald the diagnosis most often. Despite the seeming irrationality of the behavior, those with factitious disorder are not psychotic.
Pain may be described as occurring anywhere in the body, and the patient often uses elaborate technical detail to intrigue the listener with pseudologia fantastica . Opioid medication-seeking behavior, multiple hospitalizations under different names in different cities, inconclusive invasive investigations and surgery, lack of available family, and a suave truculence are characteristic of this disorder. An assiduous inquiry into the exact circumstances of the previous admission and discharge leads to a sudden outraged discharge against medical advice. There is typically no effective treatment. If the patient were willing to receive care; however, psychotherapy would be the treatment of choice, coupled with addiction recovery services if there is an underlying substance use disorder.
Malingering
In malingering, the patient feigns a complaint, although no pain is felt, because of an external incentive, such as obtaining money, drug, or the avoidance of work. The conscious manipulation by malingerers precludes much diagnostic help from amytal interviews or hypnosis because of the willful withholding of information by the patient. The patient typically refuses psychological tests; this raises suspicion even before a diagnosis is made. Even when agreeable to testing, the MMPI can be skewed to normality by some patients, although differences (>7) between obvious and subtle scale scores and high L, F, K scale scores (T >70) may be suggestive nonetheless. The mnemonic for suspicion of the diagnosis is WASTE ( W ithholding of information; A ntisocial personality; S omatic examination inconclusive and changeable; T reatment erratic with non-compliance and vagueness; E xternal incentives exist, such as occur in a medicolegal context). The psychiatrist's familiarity with the neurologic examination is always useful, but it is of critical importance for the diagnosis of malingering when nonanatomic findings arise. Once a non-functional etiology has been excluded, careful scrutiny of old records and calls to previous physicians may unearth evidence of similar behavior in the past. Similar to lying, malingering tends to be a character trait used in times of stress from early adolescence through the senium. Once revealed, psychotherapy can be offered; unfortunately, non-compliance is typical and prognosis guarded.
Dissociative States
Dissociation is caused by psychological trauma, and it involves a disturbance or alteration in the normally integrative functions of identity, memory, or consciousness. Pelvic pain, sexual pain disorders, headache, and abdominal pain are the most common pain complaints in developmentally traumatized individuals. Walker and associates reported that in 22 women with chronic pelvic pain, 18 experienced childhood abuse. Of the 21 women selected as controls (i.e., without pelvic pain), nine had childhood abuse ( P <0.0005). Dissociation, somatic distress, and general disability were more frequent in the group with pain. Denial makes the diagnosis of dissociative disorders in pain patients a longitudinal process, because truth is shared slowly with the physician only when the patient can tolerate it. Signs of an underlying dissociative disorder are periods of amnesia, nightmares, and panic, as well as anxious intolerance of close personal relationships.
General Principles of Pain Therapy
Pain Is Not Psychological by Default
The patient should not have his or her pain called “psychological” or “supratentorial” merely because it is not understood or because it is unresponsive to treatment. The physician should assure the patient that there is no question about the degree of suffering involved. Furthermore, psychological factors may play a role, but this by no means diminishes either the quality or the quantity of pain the patient endures. Education about the close relation of “psyche and soma” in CNS is often useful to establish an effective doctor–patient relationship.
Longstanding pain is difficult to assess largely because what we learn about pain is based on our concept of acute pain. The patient with acute pain moans, writhes, sweats, begs for help, and gives every appearance of being in great distress. Those nearby someone in acute pain typically feel an urge to help. When pain persists over days and weeks, the individual adapts to it, often without realizing it. The patient becomes able to sit in the physician's examining room and complains of agonizing pain while giving little or no evidence of actually being in agony. This adaptation means that the pain has become bearable, although there seems to be no change in intensity. This may be accounted for by several explanations: the sensation may become intermittent; the CNS inhibits the pain; or the patient becomes more capable of using distraction. It is ironic that the capacity to adapt to severe pain is often the patient's undoing because it causes the examiner to doubt the patient's veracity. The pain patient now is in the position of having to prove that he or she is in pain. The patient may feel himself or herself to be “on trial.” To counter this end, the physician must know the pathophysiology of pain and employ the full range of neurologic, pharmacologic, and psychological therapies available.
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