Chronic Pain, Psychopathology, and DSM-5 Somatic Symptom Disorder

Abstract

Unlike acute pain that warns us of injury or disease, chronic or persistent pain serves no adaptive purpose. Though there is no agreed on definition of chronic pain, it is commonly referred to as pain that is without biological value, lasting longer than the typical healing time, not responsive to treatments based on specific remedies, and of a duration greater than 6 months. Chronic pain that is severe and intractable has detrimental consequences, including psychological distress, job loss, social isolation, and, not surprisingly, it is highly comorbid with depression and anxiety. Historically, pain without an apparent anatomical or neurophysiological origin was labelled as psychopathological. This approach is damaging to the patient and provider alike. It pollutes the therapeutic relationship by introducing an element of mutual distrust as well as implicit, if not explicit, blame. It is demoralizing to the patient who feels at fault, disbelieved, and alone. Moreover, many medically unexplained pains are now understood to involve an interplay between peripheral and central neurophysiological mechanisms that have gone awry. The new Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, somatic symptom disorder overpsychologizes people with chronic pain; it has low sensitivity and specificity, and it contributes to misdiagnosis, as well as unnecessary stigma. Adjustment disorder remains the most appropriate, accurate, and acceptable diagnosis for people who are overly concerned about their pain.

Pain has survival value. It serves as a warning that all is not well, frequently signalling injury or disease. It encourages us to seek medical help, contributes to the healing process by promoting rest and recovery, and lets us know, by its absence, when to resume activities. Pain reminds us of past harmful events and situations, it teaches us what to avoid in the future, and motivates us to act to terminate it. People born without the capacity to feel pain often do not live beyond childhood because they fail to appreciate the implications of injury and disease.¹ These protective functions concern acute pain, a relatively short, time-limited experience that abates when the injury heals or the disease is cured.

However, there is another kind of pain—chronic pain or persistent pain—that serves no adaptive purpose. When chronic pain is severe and intractable, it lodges itself in the core of the person and causes distress and suffering. Chronic pain ruins marriages and families. It leads to job loss and other financial problems, social isolation, worry, anxiety, depression, and, at times, suicide. The IASP defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage.”2, p 210 In contrast, we do not have a generally agreed on definition of chronic pain. Chronic pain was traditionally defined by the length of time that pain persists,³ but a time-based approach ignores many other important features. Recent conceptualizations have introduced a more nuanced approach.² The IASP currently defines chronic pain variously as “pain without apparent biological value,” pain “that has persisted beyond the normal tissue healing time . . . as determined by common medical experience,” and (or) as “a persistent pain that is not amenable, as a rule, to treatments based upon specific remedies.”2, p xii But even these refinements do not capture all the varieties of persistent pain, and an acceptable definition continues to elude us. For example, some chronic pain conditions, such as rheumatoid arthritis, will likely never heal, and others, such as migraine headaches, remit (that is, heal) and then recur.² Notwithstanding the challenges associated with defining chronic pain and the problems with a solely time-based definition, for research purposes, chronic nonmalignant pain is typically defined as pain that persists for longer than 6 months.^4–6

From a neurobiological perspective, pain involves nociceptive, inflammatory, and (or) neuropathic components.⁷ Pain arising from nociceptive afferent input is the first stage of an “early-warning physiological protective system”7, p 3742 designed to minimize contact with tissue-damaging and other noxious stimuli. It involves activation of high-threshold receptors (nociceptors) on sensory neurons located in skin, muscle, and viscera. Pain due to inflammatory inputs is usually caused by tissue-damaging stimuli, such as injury, trauma, and surgery. Tissue damage activates a cascade of neuromolecular immune responses that results in swelling and tenderness, which as noted above, encourages rest and promotes recovery. Nociceptive and inflammatory pains are adaptive and protective; they typically comprise what is referred to as acute pain in that they are time-limited and resolve when the noxious stimulus has been removed or healing occurs.

Highlights

• About 1 in 5 Canadian adults suffers with chronic pain of at least moderate intensity.

• Many strange and unusual pain symptoms once thought to be caused by psychopathology can now be explained by peripheral and central neurophysiological mechanisms that have gone awry.

• DSM-5 SSD with predominant pain replaces DSM-IV-TR pain disorder, but, because the diagnostic criteria for SSD are overly inclusive, many medical patients with significant symptoms of emotional distress will receive an inappropriate psychiatric diagnosis.

In contrast, pain of neuropathic origin, which arises from direct lesion or damage to somatosensory system, is considered pathological.⁸ Neuropathic pain involves profound alterations in the normal peripheral and central neural processing of afferent input. As a consequence of injury or disease, nociceptive neurons change their response properties; they may display spontaneous activity, an increase in responsiveness, and a reduction in activation threshold to normal and subthreshold inputs (Table 1).^9,10 Pain of neuropathic origin is often described as burning, aching, and electric shock-like in quality. It is typically more severe and less responsive to conventional treatments than are nociceptive and inflammatory pain. Pathological pain with similar features also occurs in people who have not sustained an injury or who have no discernable disease, such as in fibromyalgia, irritable bowel syndrome, and tension headaches.^8,10 Regardless of the presence or absence of an identifiable etiological trigger, when neuroplasticity goes awry in certain at-risk people, the pain becomes the disease.^7,11,12

Table 1.

Mechanisms of dorsal horn neuronal central sensitization and other physiological findings associated with pathological pain states showing possible associated experiences and (or) symptoms that in the past were medically unexplained and contributed to the misdiagnosis of chronic pain patients as having mental illness (for example, hysteria, hypochondriasis, malingering, pain-prone, psychogenic pain disorder, somatization)

Physiological mechanism	Experience (symptom)
Development of and (or) increase in spontaneous neural activity9	Stimulus-independent pain (spontaneous pain)
Reduction in neural threshold for activation9	Pain in response to a stimulus that does not normally produce pain (allodynia)
Increased neural response to repeated, fixed-intensity, C-fibre strength stimulus72	Increased pain from a stimulus that normally provokes pain (hyperalgesia)
Enlargement of neuronal receptive fields9	Spread of pain to adjacent, undamaged tissue (secondary hyperalgesia)
Injury-induced unmasking of previously ineffective synaptic connections37	Spread of pain to distant body regions (remote hyperalgesia)
Cross-system, viscero–visceral interactions within the central nervous system40	Spread of pain to distant body regions (remote hyperalgesia)
Ipsilateral injury-induced, contralateral peripheral neurite loss49	Mirror-image pain (allochiria)

Recent epidemiologic studies reveal surprisingly high prevalence estimates for chronic pain. Using the World Mental Health version of the World Health Organization CIDI, the 12-month prevalence of chronic pain was found to be about 37% in developed countries and 41% in developing countries.¹³ When only moderate-to-severe pain is considered, lifetime prevalence rates drop to about 25% of the general population.¹⁴ These data are consistent with 3 Canadian surveys showing a prevalence rate for chronic noncancer pain between 19% and 29%, with most respondents reporting pain of moderate to severe intensity.^5,15,16 Chronic pain prevalence increases with age, is greater among females than males, and among people with lower, compared with higher, socioeconomic status.^5,13,17,18 Common causes of chronic noncancer pain include traumatic injury, surgery, and arthritis.^5,17,19 The most frequent body locations for chronic pain include the low back, knee joints, head, and neck.^5,6

Comorbidity Between Chronic Pain and the Mood and Anxiety Disorders

Chronic pain is highly comorbid with anxiety and depression. Space limitations preclude a thorough review. Two recent, large-scale, population-based surveys examined the comorbidity between chronic neck and (or) back pain and the DSM-IV mood and anxiety disorders.^20,21 Both surveys used the third version of the CIDI to assess mood and anxiety disorders as well as interviews to determine the 12-month prevalence of comorbid neck and (or) back pain. Von Korff et al²¹ surveyed 5692 community-dwelling people in the United States. Demyttenaere et al²⁰ conducted a cross-national survey of 85 088 community-dwelling people in 18 countries around the world. The ORs (adjusted for age, sex, race and [or] ethnicity, and education) associated with having comorbid neck and (or) back pain and any anxiety disorder or major depression relative to neck and (or) back pain alone (that is, the added risk of having a mental disorder in people with neck and [or] back pain) for the 2 studies were remarkably similar.

Depression

In the US-based study,²¹ the 12-month prevalence of comorbid chronic pain and any mood disorder was 17.5% (SE [standard error] 1.1), with major depression comprising the most frequent comorbid mood disorder (12.6%, SE 0.07). ORs for any mood disorder ranged from 2.5 to 3.2, with an OR of 2.5 for major depression. In the cross-national study,²⁰ the 12-month prevalence of comorbid chronic pain and major depression ranged from 2.5% to 15.7%, with ORs greater than zero in 16 out of 18 of the countries and a pooled OR of 2.3 (95% CI 2.1 to 2.5). The STOP-PAIN Project evaluated the burden of chronic pain in 728 people waiting for treatment at 1 of 8 university-based multidisciplinary pain treatment facilities in Canada.²² Eighty-two per cent endorsed symptoms of depression (as measured by the Beck Depression Inventory), with about 56% reporting moderate to extremely severe levels and 34.6% reporting suicidal ideation.

Anxiety

ORs ranged from 1.5 (95% CI 0.9 to 2.4) for agoraphobia to 2.6 (95% CI 2.1 to 3.3) for PTSD, with a pooled OR of 2.3 (95% CI 1.9 to 2.7) for any anxiety disorder in the US-based study²¹ and pooled across countries from 1.9 (95% CI 1.7 to 2.2) for social phobia to 2.7 (95% CI 2.4 to 3.1) for generalized anxiety disorder with a pooled OR of 2.2 (95% CI 2.1 to 2.4) for any anxiety disorder for the cross-national study.²⁰ It is notable that, with the exception of agoraphobia without panic disorder,²¹ all of the anxiety disorders in both surveys were significantly more likely to occur in people with neck and (or) back pain than in people without. Moreover, the highest ORs were found for generalized anxiety disorder (OR 2.6; 95% CI 2.0 to 3.5²¹ and OR 2.7; 95% CI 2.4 to 3.1²⁰) and PTSD (OR 2.614; 95% CI 2.2 to 3.0²⁰ and OR 2.6; 95% CI 2.1 to 3.3²¹). The substantial overlap in comorbidity and symptomatology between the anxiety disorders and chronic pain has been documented both when examining the presence of anxiety disorders in people with chronic pain and the presence of chronic pain in people with anxiety (mainly PTSD).^23–25 Interested readers are referred to recent reviews describing the theoretical models and mechanisms proposed to underlie the high comorbidity between chronic pain and the anxiety disorders.^23–25

Chronic Pain and Psychopathology

There are many pains whose cause is not known. If a diligent search has been made in the periphery and no cause is found, we have seen that clinicians act as though there was only one alternative. They blame faulty thinking, which for many classically-thinking doctors is the same thing as saying that there is no cause and even no disease. They ignore a century’s work on disorders of the spinal cord and brainstem and target the mind. . . . These are the doctors who repeat again and again to a Second World War amputee in pain that there is nothing wrong with him and that it is all in his head.26, p 107

Pains that do not conform to present-day anatomical and neurophysiological knowledge are often attributed to psychopathology. This view of medically unexplained pain persists, notwithstanding evidence to the contrary. Psychological dysfunction has been proposed to cause phantom limb pain,²⁷ dyspareunia,²⁸ orofacial pain,^29,30 fibromyalgia,³¹ pelvic pain,³² and a host of others, including abdominal pain, chest pain, and headache.³³ However, the complexity of the pain transmission circuitry means that many pains that are currently poorly understood will ultimately be explained without resorting to a psychopathological etiology.¹⁰ Pain that is nonanatomical in distribution, spread of pain to noninjured territory, pain that is said to be out of proportion to the degree of injury, and pain in the absence of injury have all, at one time or another, been used as evidence to support the idea that psychological disturbance underlies the pain. Notably, each of these features once thought to be caused by psychopathology can now be explained by peripheral and central neurophysiological mechanisms that have gone awry (Table 1).^29,34

Spontaneous pain, pain from a stimulus, such as gentle touch, that does not normally provoke pain (allodynia), and increased pain from a stimulus that normally provokes pain (hyperalgesia) are perceptual correlates of well-documented mechanisms of central sensitization that develop after injury to the peripheral or CNS.^9,10,35 There is also a less-well-known body of literature on the expression of novel receptive fields^36,37 and the expansion of existing receptive fields^38,39 in response to alterations in the flow of afferent input. Further, previously undocumented cross-system, viscero–visceral interactions within the CNS have recently been described among women with chronic pelvic pain.⁴⁰ This literature provides a neurophysiological basis for clinical observations in humans that pain may occur in the absence a known trigger, spread to distant, previously nonpainful, and otherwise healthy body regions,^9,40 as well as a rationale for why a local intervention applied to one body region may relieve pain at another.^40,41

Recent data linking the immune system and the CNS have provided an explanation for another medically unexplained pain problem. Mirror-image pain or allochiria has puzzled clinicians and basic scientists ever since it was first documented in the late-1800s.⁴² Injury to one side of the body is experienced as pain at the site of injury as well as at the contralateral, mirror-image point.^43,44 Recent animal studies show induction of a sciatic inflammatory neuritis by peri-sciatic microinjection of immune system activators results in both an ipsilateral hyperalgesia and hyperalgesia at the mirror-image point on the opposite side in the territory of the contralateral healthy sciatic nerve.⁴⁵ Moreover, both the ipsilateral and contralateral hyperalgesia are prevented or reversed by intrathecal injection of various proinflammatory cytokine antagonists.⁴⁶

Mirror-image pain is likely not a unitary phenomenon and other nonimmune mechanisms may also be involved.⁴⁷ For example, recent human^48,49 and animal evidence⁵⁰ point to a potential combination of central and peripheral contributions to mirror-image pain as nerve injury to 1 side of the body has been shown to result in a 50% reduction in the innervation of the territory of the same nerve on the opposite side of the body in uninjured skin.⁵⁰ Interestingly, while documented contralateral neurite loss can occur in the absence of contralateral pain or hyperalgesia, pain intensity at the site of the injury correlates significantly with the extent of contralateral neurite loss.⁴⁹ This raises the intriguing possibility that the intensity of pain at the site of an injury may be facilitated by contralateral neurite loss induced by the ipsilateral injury⁵⁰—a situation that most clinicians would never have imagined possible. More recently, tactile allochiria (for example, touch applied to a finger on the right hand was experienced only as pain in the corresponding left finger) occurred in patients with complex regional pain syndrome—type I who also showed evidence of possible parietal lobe dysfunction.⁴⁸

Taken together, these novel mechanisms explain some of the most puzzling pain symptoms. But there remain many other pains that defy present-day understanding. This should keep us mindful that emotional distress and psychological disturbance in our patients are not the cause of the pain. Attributing pain to a psychological disturbance is damaging to the patient and provider alike. It pollutes the therapeutic relationship by introducing an element of mutual distrust as well as implicit, if not explicit, blame. It is demoralizing to the patient who feels at fault, disbelieved, and alone.

Diagnostic and Statistical Manual of Mental Disorders, Fifth Edition, and Chronic Pain

The golden rule: an underlying medical illness or medication side effect has to be ruled out before ever deciding that someone’s symptoms are caused by mental disorder. . . . There are serious risks attached to over-psychologizing somatic symptoms and mislabeling the normal reactions to being sick − especially when the judgments are based on vague wording that can’t possibly lead to reliable diagnosis. DSM-5 as it now stands will add to the suffering of those already burdened with all the cares of having a medical illness.51, p 484

The hard-fought gains to have pain disorder expunged from the DSM-IV⁵² have come at the expense of an overly inclusive and unreliable new DSM-5⁵³ disorder termed SSD. Nevertheless, that DSM-5 does not include a pain-specific disorder (for example, psychogenic pain disorder,⁵⁴ somatoform pain disorder,⁵⁵ and pain disorder⁵²), as in past editions of the DSM, is a welcomed advance (see Merskey^56,57 for reviews on the history of DSM pain and somatoform diagnoses).

SSD is a single diagnostic entity that replaces 3 of the DSM-IV⁵² somatoform disorders (somatization disorder, pain disorder, and undifferentiated somatoform disorder, and in some cases hypochondriasis). Table 2 lists the diagnostic criteria for SSD, which include 1 or more physical symptoms lasting 6 months or longer that are associated with excessive thoughts, feelings, or behaviours. Three specifiers describe the nature (with predominant pain), duration (persistent, if longer than 6 months), and severity (mild, moderate, or severe) of the symptoms. Brief SSD is diagnosed under other specified somatic symptom and related disorder when the duration of symptoms is less than 6 months. The SSD specifier, persistent, indicating a duration greater than 6 months appears to be redundant and unnecessary, as SSD is diagnosed only at 6 months and brief SSD is diagnosed when the symptoms have persisted for less than 6 months.

Table 2.

DSM-5 diagnostic criteria for somatic symptom disorder

A.	One or more somatic symptoms that are distressing or result in significant disruption of daily life.
B.	Excessive thoughts, feelings, or behavio[u]rs related to the somatic symptoms or associated health concerns as manifested by at least one of the following: Disproportionate and persistent thoughts about the seriousness of one’s symptoms. Persistently high level of anxiety about health or symptoms. Excessive time and energy devoted to these symptoms or health concerns.
C.	Although any one somatic symptom may not be continuously present, the state of being symptomatic is persistent (typically more than 6 months).
	Specify if:
	With predominant pain (previously pain disorder): This specifier is for individuals whose somatic symptoms predominantly involve pain.
	Specify if:
	Persistent: A persistent course is characterized by severe symptoms, marked by impairment, and long duration (more than 6 months).
	Specify current severity:
	Mild: Only one of the symptoms specified in Criterion B is fulfilled.
	Moderate: Two or more of the symptoms specified in Criterion B are fulfilled.
	Severe: Two or more of the symptoms specified in Criterion B are fulfilled, plus there are multiple somatic complaints (or one very severe symptom).

Reproduced, with permission, from the American Psychiatric Association.53, p 311

DSM-IV pain disorder was rightly criticized on 2 counts: The questionable importance of medically unexplained pain^58,59 in pain disorder associated with psychological factors; and, the lack of a definition of psychological factors or a description of when they are of sufficient importance or magnitude to play a role in the pain experience in the presence of a general medical condition made it a diagnosis of exclusion.^59,60 The DSM-5 SSD represents an advance over DSM-IV pain disorder with the removal of the requirement that the symptoms be medically unexplained and the addition of subjective distress as diagnostic of SSD, but it has ignored the sage advice that this is a diagnosis that should rarely be made.⁵⁶

Notwithstanding these improvements, 2 major criticisms have been levelled against the DSM-5: diagnostic inflation and inadequate field testing.⁶¹ Both appear to apply to the new diagnostic category of SSD. The main criticism of SSD is the high probability of misdiagnosing a medical illness, including chronic pain conditions, as a mental illness.^61–63 Further, the conditions that qualify for a diagnosis of SSD are extremely variable. They include a highly mixed group of patients with medically unexplained symptoms, medical patients with significant symptoms of emotional distress, patients with typical chronic pain conditions (for example, low-back pain, fibromyalgia, rheumatoid arthritis) and patients with health-related anxiety.⁶⁴ According to Frances,⁶² 15% of cancer patients, 15% of patients with heart disease, and 25% of patients with irritable bowel syndrome and chronic widespread pain would qualify for a diagnosis of SSD. Moreover, the false-positive rate in the general population would approach 7%.

DSM-5 field testing in the United States and Canada showed a test–retest kappa coefficient of 0.61 (95% CI 0.40 to 0.77) for complex SSD (revised), as well as a prevalence for complex SSD (revised) of 0.08 (95% CI 0.06 to 0.11) and a corresponding DSM-IV prevalence of 0.1 for somatoform disorder (excluding conversion and body dysmorphic disorders).⁶⁵ However, note that in the absence of more data on the validity of SSD, even a moderately high reliability coefficient is not very meaningful. It is also not clear how the diagnostic criteria for complex SSD (revised), as described in the field testing,^65,66 map onto those that now appear in the DSM-5 under SSD. Moreover, there is no mention of whether any of the patients in the field trial sample actually had chronic pain conditions (compared with other body system symptoms). Further, although a stated aim of SSD was to simplify and clarify the diagnostic procedure for use in primary care, field testing did not include primary care settings or physicians.⁶⁵ Finally, sample size was inadequate. Considering that field testing usually produces higher reliability estimates than exist in clinical practice,⁶¹ the data on reliability seem unrealistically high for what is an extremely broad range of patients who qualify for a diagnosis of SSD. A subsequent field trial in routine mental health clinical practice settings reported the DSM-5 approach to diagnosis was feasible, useful, and acceptable to clinicians and patients but the sample size diagnosed with SSD was extremely small.⁶⁷

Frances and Chapman⁵¹ list 10 negative consequences of the new DSM-5 SSD diagnostic category, including the following that relate specifically to chronic pain conditions: stigma; overlooked diagnoses owing to a failure to investigate new or worsening somatic symptoms; increased risk of a parent, with a child who has a chronic illness, being diagnosed with SSD, leading to inappropriate claims of parental overinvolvement or of encouraging the child’s sick role behaviour; increased risk of receiving inappropriate psychotropic medications; and falling prey to the gender trap⁶⁸ by further marginalizing women in the health care system as they present with physical symptoms such as persistent pain more frequently than do men. This is supported by a comparison of DSM-5 SSD and DSM-IV somatoform disorders assessed in the same group of patients showing that a significantly greater proportion of women than men received the former but not the latter diagnosis.⁶⁹

Several authors have proposed modified diagnostic criteria to reduce the likelihood of diagnostic inflation and the misdiagnosis of medical illness as mental illness.^62,64,70 Table 3 contains a set of revised diagnostic criteria recommended by Frances.⁷¹ These criteria were developed to establish an appropriate balance between sensitivity and specificity, and to reduce the likelihood of false-positive diagnoses. However, given the problems with current diagnostic criteria for SSD, noted above, alternative diagnoses have been suggested as appropriate for people with chronic pain; including, psychological factors affecting other medical conditions⁷⁰ and adjustment disorder.^70,71 The distinction between SSD and psychological factors affecting other medical conditions is not clear-cut, especially for people with chronic pain conditions, as both involve a diagnosable medical condition. For SSD, the emphasis is said to be on “maladaptive thoughts, feelings and behavior,” whereas for psychological factors affecting other medical conditions the emphasis in on “the exacerbation of the medical condition.”53, p 324 This distinction seems arbitrary for people with chronic pain, as pain is known to produce worry and worry is known to exacerbate pain. Until the criteria for SSD are appropriately revised, adjustment disorder is a “safer and more accurate” diagnosis when one is needed for someone who is “medically ill or otherwise troubled by puzzling symptoms”71, p 531 Chronic pain is highly comorbid with anxiety and depression

Table 3.

Recommended⁷¹ revised DSM-5 diagnostic criteria for somatic symptom disorder

Criteria A, B, C, D, E, F, and G must all be fulfilled to make the diagnosis:
D.	One or more prominent physical symptoms.
E.	Excessive and maladaptive thoughts, feelings, and behavio[u]rs related to the physical symptoms. All three [3] of the following must be present: clearly disproportionate and intrusive worries about the seriousness of the symptoms, extreme anxiety about the symptoms, and excessive time and energy devoted to the symptoms or health concerns.
F.	The concerns have persisted at a clearly problematic and maladaptive level for at least 6 months.
G.	The excessive concerns about physical symptoms are pervasive and cause significant disruption and impairment in daily life.
H.	If a diagnosed medical condition is present, the thoughts, feelings, and behavio[u]rs are grossly in excess of what would be expected, given the nature of the medical condition.
I.	If no medical diagnosis has been made, a thorough medical workup has been performed to rule out possible causes and is repeated at suitable intervals to uncover medical conditions that may declare themselves with the passage of time.
J.	The physical symptom or concern it is not better accounted for by another mental disorder (e.g. [for example], anxiety, depressive, or psychotic disorder).

Reproduced, with permission, from Frances.⁷¹

Summary and Conclusions

Acute pain is protective in the short term when it signals tissue damage or disease via nociceptive and inflammatory inputs, but chronic pathological pain has no adaptive value. Chronic pain is highly prevalent worldwide and highly comorbid with anxiety and depression. It is associated with substantial financial, occupational, psychological, and social burden. Pain that is not readily explained medically has frequently been attributed to psychopathology, largely because of puzzling and bizarre symptoms, but recent basic science findings have provided a neurophysiological basis for many of these symptoms. These advances in our understanding of pain mechanisms have had parallel effects in psychiatry where, for the first time in more than 30 years, the most recent edition of the DSM no longer includes a pain-specific mental disorder. DSM-5 SSD with predominant pain replaces DSMIV pain disorder but it is not recommended for people with chronic pain, because it lacks validity, and is overly inclusive and stigmatizing. Instead, adjustment disorder remains the most appropriate, accurate, and acceptable diagnosis for people who are overly concerned about their pain.

Abbreviations

CIDI

Composite International Diagnostic Interview

CNS

central nervous system

DSM

Diagnostic and Statistical Manual of Mental Disorders

IASP

International Association for the Study of Pain

OR

odds ratio

PTSD

posttraumatic stress disorder

SSD

somatic symptom disorder