The Missing P in Psychiatric Training: Title and subTitle BreakWhy It Is Important to Teach Pain to PsychiatristsThe Missing P in Psychiatric Training

Chronic pain is a public health problem of pandemic proportions that affects more than 70 million Americans^{1 - 2} and remains the most common concern brought to the attention of health care professionals.³ Its annual cost to American society is staggering and is estimated to be approximately $100 billion owing to medical costs and loss of earnings and productivity.⁴ Current demographic trends⁵ and the tremendous shortage of pain experts⁶ forecast the need for even greater attention to pain from the medical establishment because of a substantial rise in the overall proportion of geriatric patients, who are naturally at a heightened risk for the development of pain-related conditions.⁷ Specifically, 50% of community-dwelling elderly people and as many as 80% of nursing home residents experience chronic pain.⁸ The number of Americans older than 65 years has increased steadily owing to the rise in life expectancy from 4% at the beginning of the 20th century to 12% now and is projected to surpass 20% within the next 25 years.⁹ Pain is exceedingly prevalent in psychiatric samples¹⁰ ; because more people will be experiencing pain, so will psychiatric patients.¹¹

One of the most daunting challenges faced by psychiatric professionals is how to distinguish and approach physical and emotional symptoms arising in the context of pain experienced by their patients. We respond to this question by proposing to integrate fundamental tenets of pain medicine within the core psychiatric residency training curriculum.¹² Besides altered pain function,^{13 - 14} psychiatric patients can be noncompliant with pain treatment and may additionally develop comorbid addiction to opioid analgesics.¹⁵ On the other hand, chronic pain is frequently associated with anxiety and depressive symptoms¹⁶ as well as with degenerative cortical changes^{17 - 18} that may further deteriorate affective states and cognition.^{18 - 19}

Sensory areas are recruited by both acute and chronic pain, but the latter is a more complex phenomenon engaging a broader stress-related neural network with emotional, motivational, and cognitive components²⁰ that converge on the mesocorticolimbic dopaminergic and endogenous opioid circuits, which are involved in reward/salience/motivational mechanisms.²¹ With this premise of neurobiological overlap between the processing of pain and of other stressful and emotionally salient signals, our article considers the aspects of pain that are related to stress, reward, and motivational regulation and are pertinent to psychiatric morbidity. First, we compare clinical data on physical and emotional types of pain, and this comparison is used as the basis for the assumption of an overlap between these frequently related entities. Second, we address the mechanisms involved in the mediation of pain as they relate to normal processing of emotions, reward, and motivation. Next, we provide clinical and scientific contexts for the association between key psychiatric syndromes and pain conditions. Finally, we propose psychiatrists' training in pain medicine and discuss the importance of this endeavor.

In addition to the epidemiologic association between pain and psychiatric disorders,¹⁰ clinical and even diagnostic features of pain syndromes point to neuropsychiatric origin. The definition of pain by the International Association for the Study of Pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue damage”^{22 (p210)} recognizes its multifaceted nature with causes that extend well beyond direct physical harm. This is expressed in the Diagnostic and Statistical Manual of Mental Disorders (Fourth Edition) (DSM-IV) as the Axis I diagnostic category of pain disorder, which is encoded in 3 of the 5 diagnostic criteria: “A. Pain . . . is of sufficient severity to warrant clinical attention; B. Pain causes clinically significant distress or impairment in social, occupational, or other important areas of functioning; and C. Psychological factors are judged to have an important role in the onset, severity, exacerbation, or maintenance of pain.”^{23 (pp461-462)} Pain arising from physical sources is classified among the DSM-IV Axis III disorders, solely reserved for medical conditions.²³ In reality the distinction between Axis I and Axis III pain disorders is not that obvious, and both pain categories share clinical characteristics, symptom severity, and functional impairment.²⁴ Such blurring of diagnostic boundaries is rooted in the lay language, in which the term pain is used interchangeably in both physical and emotional situations.²⁵

Acute pain signals real or perceived tissue damage from environmental threats.²⁶ Although not clinically similar, cancer pain is also etiologically linked to direct tissue damage due to malignant neoplasms or to surgical, chemotherapy, or radiotherapy treatments.^{27 - 28} Chronic nonmalignant pain is not a unitary sensation evoked by a local injury, inflammation, or other tissue abnormality but is a complex state modulated by genetic, cognitive, and emotional variables.^{29 - 30} Most cases of chronic nonmalignant pain are neuropathic; that is, caused by damage to the peripheral or central nervous system.²⁰ Whatever the cause may be, chronic pain is now considered a disease of the central nervous system.³¹ Such centralization is conceptualized to be a stand-alone neuropsychopathologic entity occurring at the level of the spinal cord pathways and the supraspinal integrative circuits, respectively manifested as spontaneous pain or in exaggerated responses to painful (hyperalgesia) and nonpainful (allodynia) stimuli in combination with negative affective states and a persistent drive to eliminate pain via behavioral or pharmacologic measures.^{20 ,31} The apparent link between pain and emotions/motivations underscores the importance of dynamic interactions between neurobiological and psychological factors for understanding the experience of chronic pain (Figure 1).

Figure 2 schematically displays a compilation of the interactions between sensory and emotional systems with ensuing affective states and symptoms. Evidence of such interaction is provided by functional magnetic resonance imaging in humans showing that grief-related emotional pain activates classic pain circuitry (eg, periaqueductal gray matter, insular cortex, and anterior cingulate cortex),³³ whereas clinical or experimental pain engages emotion/reward/motivational circuits (eg, nucleus accumbens [NAC] and ventral tegmentum [VT]^{32 ,34 - 35} ). Furthermore, induction of acute emotional or physical pain in patients with the respective chronic conditions (eg, complicated grief and back pain) via exposure to reminders of the deceased³³ or thermal pain³⁶ robustly engages the key reward and reinforcement structure, namely the NAC. These findings suggest that in some conditions emotional and physical pain may become a reinforcing stimulus and thus may contribute to the unremitting course of illness. In more general terms, critical for the survival of the organisms, the pain system is embedded within extensive emotion/reward/motivation circuitry, representing a neural network responsible for the continued existence of individuals and species via pursuit of food, water, and sex as well as via learning, decision making, and adaptation to stress. Considering the survival significance of social affiliations, their pleasurable acquisitions and painful losses may have evolutionarily used the same motivational systems,³⁷ an idea consistent with the reward-aversion continuum hypothesis promulgated by Baruch de Spinoza.³⁸ A practical offshoot of the continuum idea is that pain is a functional probe of the brain reward and motivational systems.³² This is an important contribution, given the paucity of reliable probes and the pivotal role played by reward and motivation in the course of psychiatric illnesses.

Evidence that emotional brain circuitry abnormalities arise in psychiatrically healthy people exposed to persistent pain¹⁹ supports a compelling argument that propensity for the pain condition is worsened by neuropsychopathologic features affecting the same neural structures. A model partially suited to explain this link is the diathesis-stress theory postulating preexisting, sometimes subclinical, traits that manifest in the form of overt psychopathologic abnormalities in the context of prolonged pain-induced stress.^{16 ,39 - 40}

The list of psychiatric conditions associated with heightened pain prevalence in at least 1 extant epidemiologic survey would stretch the entire DSM-IV diagnostic range from “Disorders Usually First Diagnosed in Infancy, Childhood, or Adolescence” to “Other Conditions That May Be a Focus of Clinical Attention.” For illustrative purposes, we address 4 key syndromes: major depressive disorder (MDD), borderline personality disorder (BPD), addictions, and posttraumatic stress disorder (PTSD).

Elicitation of depressed vs happy affective states in laboratory settings respectively worsens and improves the experience of pain in healthy individuals and in patients with chronic pain.^{41 - 42} A substantial proportion of patients with MDD have chronic pain,⁴³ the intensity of which increases with the severity of depressive symptoms.⁴⁴ On the other hand, sustained pain leads to increased negative affective states^{45 - 46} and eventually to high MDD prevalence in patients with chronic pain.⁴⁷ Compared with pain alone or MDD with other medical conditions, patients with pain and comorbid MDD experience a greater severity of depressive symptoms and substantially poorer treatment outcomes.⁴⁸

To evaluate the role of pain in the neuropathologic mechanism of MDD, painful heat stimuli were applied to the dorsal forearm in depressed patients during functional magnetic resonance imaging.¹³ Among other functional alterations, depressed patients had proportionally (to depressive symptoms) heightened right amygdala activity when they anticipated and experienced painful stimuli.¹³ Other lines of evidence supporting recursive, partly shared neural systems by MDD and pain processing include (1) serotonergic and noradrenergic pathways' involvement in mood regulation and in the control of ascending pain stimuli, explaining the analgesic action of dual serotonergic/noradrenergic reuptake inhibitors and tricyclic antidepressants⁴⁹ ; (2) other shared treatment modalities (eg, transcranial magnetic or vagus nerve stimulation); and (3) abnormalities of the analgesic opioidergic system in patients with MDD and the involvement of this neurotransmitter in emotional regulation.⁵⁰ These findings support the idea that MDD and pain can trigger and perpetuate each other owing to overlapping neural and emotional alterations. Therefore, assessment of pain function may provide important diagnostic and therapeutic leads in MDD, which is projected to become the second most common cause of disability after heart disease.⁵¹

Emotional dysregulation, affective lability, and impulsive behavior in patients with BPD are associated with increased pain thresholds⁵² that predict the dissociative symptoms and negative affect.⁵³ Compared with healthy individuals, patients with BPD demonstrated enhanced opioid neurotransmission during molecular imaging with positron emission tomography⁵⁴ as well as greater pain-induced functional magnetic resonance imaging signal changes in the prefrontal cortex but less activity in the amygdala and anterior cingulate.⁵² These regions interface emotion, pain, and stress regulation and are where the endogenous opioid system plays critical modulatory roles.⁴⁵ Impulsivity, a trait characterizing not only patients with BPD but also those at risk for addictive disorders, was also associated with greater endogenous opioid function in similar brain regions of healthy people.⁵⁵

Numerous epidemiologic surveys have documented that some addictions (eg, nicotine and alcohol) are particularly prevalent among patients with pain, who may also receive treatment with opioid analgesics and develop tolerance of and dependence on those drugs.^{16 ,56 - 57} The mechanisms of this link are likely multifactorial and involve both psychosocial and neurobiological causes. Among neurobiological factors, the brain reward and motivational system probably plays an important role. The mesoaccumbens dopamine pathway, extending from the VT of the midbrain to the forebrain regions such as the NAC, is the crucial component of this system.^{58 - 59} Physiological significance of increases in the NAC's dopamine level, a common result of the effects of natural rewards as well as drugs of abuse,^{58 ,60 - 61} is a subject of complementary hypotheses^{21 ,62 - 63} including the subjective pleasure or “high” (reward) sought by drug users as well as motivation, appraisal of stimuli salience, stress, learning, and decision making.^{64 - 66}

Both acute pain^{35 ,67} and euphorogenic drugs^{58 ,60 - 61} activate dopamine transmission in the brain reward circuitry, including the NAC, whereas prolonged periods of pain^{68 - 70} or of drug consumption^{71 - 72} produce the opposite effect, accompanied by reduced motivation toward normally pleasurable stimuli.^{59 ,73 - 76} These findings can be interpreted in the context of the incentive motivation theory,³⁴ viewing the brain reward function as composed of core motivational and emotional processes. Pain- or drug-induced effects in the mesolimbic dopaminergic circuitry are salient and motivate behavior, so persistent exposure to this type of stimuli dysregulates the system, possibly increasing the incentive salience assigned to pain- or drug-related cues.^{34 ,36} Such incentive sensitization, construed by some as an animal homologue of human craving,³⁴ may be responsible for the continued use of substances with short-lived antinociceptive effects (eg, nicotine in tobacco) in addition to compulsive seeking of opioid drugs driven by the desire to ameliorate inadequately treated pain (ie, pseudoaddiction⁷⁷ ) or to avoid a feared opioid withdrawal (ie, therapeutic dependence⁷⁸ ).

A closely related concept, derived from studies in primates, is the aberrant theory that the learning of new rewarding or aversive experiences is encoded via interactions between tonic (baseline) and phasic spikes in dopaminergic neurons; phasic firing predicts unanticipated stimuli.⁶³ Therefore, neural adaptations to excessive dopaminergic bombardment in response to pain may lead to low signal-to-noise detection capability for natural rewards^{74 - 76} along with profound overlearning of the motivational significance of cues that either predict painful episodes or are associated with painful experience.⁶³

These ideas provide rich opportunities for neuropsychiatric physicians and researchers to decipher seemingly elusive interactions between pain and analgesia regarding addiction to opioid analgesics.^{79 - 81} Three potential classes of interaction may coexist between pain and opioids, including competition, independence (ie, additive effects), and synergism. Competition (Figure 3A) may be the most notable interaction because opioid analgesics, when administered at an adequate dose, restore the homeostatic equilibrium⁶² by eliminating pain while pain offsets opioids' reinforcing properties.^{79 ,82} Dependence, including tolerance and withdrawal, may sometimes occur^{83 - 84} during opioid pharmacotherapy, but it qualitatively differs from addiction by lacking the compulsive nature and loss of control.^{62 ,85}

To our knowledge, no studies to date have directly investigated whether undertreated or overtreated pain has competitive, independent, or synergistic effects on the development of addiction. Opioid analgesics and pain share the ability to affect extracellular dopamine concentrations in the NAC. Opioids robustly activate dopaminergic neurotransmission via inhibition of the γ-aminobutyric acid (GABA) neurons⁸⁶ and by direct action at the mesocorticolimbic dopamine system (eg, VT and NAC).^{87 - 88} Pain likewise produces dopamine releases in the NAC with the involvement of GABA-ergic mechanisms.⁸⁹ Chronic pain perpetuation and development of addiction may result from dysregulation of these systems. For instance, activation of mesolimbic dopaminergic pathways involved in motivational processing^{32 ,35} by inadequately treated or untreated pain (Figure 3B) leads to heightened incentive salience attribution to pain and pain-related stimuli.⁶³ Opioid analgesics providing quick pain relief (ie, negative reinforcement) can thus become a sensitized motivational target capturing greater attentional resources and resulting in drug craving, clinically manifested in the expenditure of greater behavioral effort relative to normal reinforcers to seek and obtain opioids.^{82 ,90} Although this state is viewed as a pseudoaddiction rather than a genuine one,⁷⁷ the latter's features may predominate with time, causing opioid overuse in the form of attempts to self-medicate perceivably intolerable pain and pain-related anxiety.⁶² Such an outcome is relatively uncommon, and its likelihood is increased with a history of drug abuse, treatment noncompliance, and disability litigation.^{91 - 92}

Changes in the mesolimbic dopaminergic circuitry induced by opioids, taken at doses exceeding the homeostatic need for pain alleviation (Figure 3C), may be responsible for transforming regular motivational drives into heightened incentive salience assigned to opioids or opioid-related cues (ie, drug craving).³⁴ An additional critical aspect of opioid overuse in the context of an ongoing pain condition is the amplification of hyperkatifeia or negative affective states and of physical pain itself,^{62 ,93 - 94} which together with pain-driven opioid intake may be a variant of cross-sensitization.^{95 - 96} Cross-sensitization typically refers to a situation in which prior exposure to one stimulus (eg, addictive drug) increases the subsequent response to itself and to a different stimulus (eg, stress).

A common outcome in patients with pain could be generation of the “spiraling distress cycle,”⁷² in which opioid overuse provoked by heightened pain salience produces additional deterioration in the pain^{93 - 94} and emotional⁶² problems, leading to further opioid consumption that may eventually produce a transition from excessive opioid use to the bona fide addiction. Given such an autonomous, self-sustaining feedforward loop, it is plausible that pain combined with excessive opioids brings about synergistic processes favoring addictive phenomena. In sum, safe and effective care for patients with chronic pain requires a thorough understanding of the complex interplay among pain-, analgesia-, and addiction-related factors.

Anxiety syndromes are also commonly comorbid with chronic pain.⁹⁷ A conditioned fear and anxiety syndrome, PTSD, could be yet another example of reward/motivational circuitry involvement in the association between chronic pain and psychiatric disorders. Several lines of evidence implicate pain in the course of PTSD. Neuroanatomically, in addition to their involvement in pain processing,^{32 ,35} dopamine terminal fields including the NAC, amygdala, and medial prefrontal cortex play key roles in stress, aversive responses, and PTSD.^{65 ,98} From the pathophysiological perspective, peritraumatic pain is recognized among the independent risk factors for PTSD,⁹⁹ whereas timely morphine analgesia reduces the severity and even prevents the appearance of PTSD symptoms.¹⁰⁰

Several mechanisms may contribute to PTSD-pain comorbidity, which carries a substantially poorer prognosis than each condition in isolation.^{101 - 102} Pain, paired with emotional trauma and its recollections, can become a conditioned stimulus evoking fear and anxiety responses that in turn augment subjective pain perception and its neural correlates,^{103 - 104} leading to additional deterioration and avoidance of pain- and trauma-related situations.^{105 - 107} Such a “mutual maintenance” cycle may be evident in PTSD symptoms caused by surgical pain awareness despite seemingly adequate general anesthesia¹⁰⁸ or in a PTSD incidence surge in accident survivors who continue to experience pain after their injury.¹⁰⁹

In addition, increased central opiodergic tone^{110 - 111} along with robust elevations in endogenous opioid concentrations in the cerebral spinal fluid¹¹² and plasma¹¹³ are relatively consistent clinical findings in PTSD. Therefore, as in long-term users of opioid analgesics (Figure 3C), exaggerated central nervous system opioidergic activity in PTSD could contribute to the sensitized pain phenomenon potentially mediated via amplification of the excitatory (eg, glutamatergic) neurotransmission.¹¹⁴ The proposed mechanism of excessive pain occurrence could have treatment implications because it implies prophylactic use of opioid receptor antagonists. On the basis of the hypothesis that opioidergic mechanisms are involved in the pathophysiological features and symptoms of PTSD,^{110 ,115} opioid antagonists have been evaluated for potential efficacy in several clinical trials.^{111 ,116 - 117} On the whole, they were safe and well tolerated and resulted in significant improvements in various PTSD symptoms such as emotional numbing, startle response, nightmares, flashbacks, intrusive thoughts, and comorbid alcoholism.^{111 ,116 ,118}

Pain themes in psychiatry, such as those noted previously, are only marginally addressed by the respective training and certification requirements set forth by the Accreditation Council for Graduate Medical Education¹¹⁹ and the American Board of Psychiatry and Neurology.¹²⁰ The former includes intractable pain among “Medical Knowledge” items but not among “Patient Care” competencies, whereas the latter only lists pain medicine in the section called “Psychiatric Subspecialties and Other Areas of Psychiatric Endeavors.” Psychiatrists appear to be inadequately trained in pain medicine and to consequently perceive their work with patients who have chronic pain as ungratifying,^{121 - 122} so the current psychiatric training requirements may be suboptimal for the physicians who are uniquely poised to evaluate and treat patients experiencing pain while sharing responsibility with their medical colleagues for the treatment of mental health issues.

Empirical data on the potential benefits of increased pain training for psychiatric residents are missing. Educators may be concerned that training add-ons would encroach on the established rigorous curriculum of the essential clinical skills and knowledge base in psychiatry.¹²¹ In our opinion, far from being adverse for psychiatric education, participation in pain training may be beneficial for psychiatric residents, their patients, and the medical field as a whole.

A pain curriculum could build on residents' proficiency in neurobiology and on the existing guidelines of the International Association for the Study of Pain.¹²³ Because the training could be operationalized in countless ways, a consensus concerning the adoption of various training components should be developed by a committee composed of psychiatric residency training directors and/or through the American Psychiatric Association Task Force. The following is a brief outline of possible components that might be considered by these committees.

The main objective of the first postgraduate year is to shape the physician identity of new medical school graduates. Recent graduates spend at least 4 months in primary care clinical settings, so part of their caseload requirements may include treatment and follow-up of patients with chronic pain. This clinical experience can be reinforced via didactics and direct patient care during the 2 months' mandatory neurology rotation. The second postgraduate year, focused on physicians' identities as psychiatrists, may include assessments of patients with dually diagnosed pain and psychiatric disorders in conjunction with psychotherapeutic¹²⁴ and psychopharmacologic⁴⁹ strategies in the treatment of patients with chronic pain. The third postgraduate year would provide an opportunity to refine the previously acquired skills in more specialized settings, including an inpatient detoxification unit and outpatient addiction clinic. A consultation-liaison rotation in the fourth postgraduate year could emphasize the integrative nature of pain treatment within the entire medical field and the distinctive roles played by psychiatrists in handling challenges inherent in the provision of care to a sometimes noncompliant and treatment-resistant patient population. Those who are interested in more advanced postresidency training can pursue the fellowship in pain medicine approved by the Accreditation Council for Graduate Medical Education, which is open to physicians from various disciplines.¹²⁵

Rather than viewing psychosocial and biological interventions as distinct therapeutic modalities, psychiatrists are trained to conceptualize patients' care on the psychosocial-biological continuum and to shift across various parts of this spectrum. Thus, wide-ranging involvement of psychiatrists will invigorate essential elements of the evaluation and treatment armamentarium that may be underused by their colleagues. This is a timely effort because most pain syndromes are only partially responsive to opioids,^{28 ,126} so innovative approaches are essential.

Psychiatrists are understandably suited to recognize and treat subtle psychological processes including expression of feelings via somatic pain concerns, defense mechanisms (eg, denial and repression vs lying and malingering), and conscious and unconscious motivations,¹²⁷ such as self-reported pain with adequate analgesia owing to unwarranted anxiety about an impending opioid dose reduction (ie, pseudo-opioid resistance¹²⁸ ) or drug craving vs pseudoaddiction⁷⁷ or therapeutic dependence.⁷⁸ An additional pertinent function is motivational enhancement¹²⁹ fostering compliance and active participation in pain treatment plans.

Although numerous cognitive and behavioral strategies (eg, cognitive restructuring, stress management, and systemic desensitization) are reportedly helpful for chronic pain,¹²⁴ the National Institutes of Health Technology Panel assigned the highest score to the effectiveness of muscle relaxation.¹³⁰ Psychiatrists can become strong advocates for the use of cognitive and behavioral techniques in the field of pain as they routinely apply them to the care of psychiatric patients. Moreover, being experts in psychopharmacology, psychiatrists can promulgate opioid drugs (eg, buprenorphine hydrochloride) with safety profiles superior to those of conventional agents and with lesser addiction potential¹³¹ as well as viable nonaddictive analgesic alternatives to opioids such as antidepressants, anticonvulsants, and neuroleptics.⁴⁹ Also, psychiatrists can diagnose and treat suicidal tendencies¹ as well as mood, anxiety, psychotic, and personality disorders exerting pivotal effects on pain intensity and treatment outcomes.¹⁶

Psychiatrists' dialectical perspective on pain alleviation while preventing, diagnosing, and treating addiction to prescription opioid painkillers is addressed previously. Additional contributions from the field of addiction may involve empirically driven treatment-matching algorithms allowing the provision of individualized-level care with regard to patients' medical status, employment/support, drug addiction, family situation, and psychiatric condition. The patient placement criteria by the American Society of Addiction Medicine¹³² may be adapted to patients with pain¹³³ because they provide multidimensional assessment of illness severity and level of function as well as treatment assignment based on need for service and level of care determination.

In summary, it may be of broad public health interest to engage psychiatrists in the care of patients with chronic pain. Such a goal will not only generate additional clinical expertise to evaluate and treat a large spectrum of pain-related problems but it will also help expand the field of psychiatry to include pain as an entity rooted in numerous other specialties (eg, neurology, medicine, surgery, and anesthesiology) and will thus advance integration of psychiatry into mainstream medical care and underscore the significance of attending in concert to both mental and physical problems.

Chronic pain is a major problem affecting the modern world. The coalescence of epidemiologic and clinical data suggests that psychiatric patients have a predilection for the development of various pain conditions, whereas neuropsychiatric characteristics form an integral component of chronic pain disorders. This is at least partially due to functionally impaired neural substrates that overlap pain, emotion, reward, and motivation processing. Although psychiatry is only one of many appropriate settings where patients with pain can be treated, this approach has several advantages. First, psychiatry is comprehensively focused on etiopathophysiological mind-body interactions with direct relevance to pain syndromes. Second, neurobiological research in animal models and more recently in humans confirms a substantial degree of overlap between pain regions and brain areas implicated in the main psychiatric symptoms. Third, the relationship and comorbidity between persistent pain and psychiatric disorders has been extensively documented.

If the interactions between pain and psychiatric illnesses can be further elucidated, they might be used to screen patients at risk for the development or worsening of psychopathologic characteristics (ie, primary prevention). Psychiatric patients may also need to be targeted for early intervention, even in the presence of mild pain problems (ie, secondary prevention). Finally, pain medicine training could underscore the importance of neurobiological training in psychiatry education as well as the introduction of other essential medical topics into the psychiatric curriculum that are now timely (eg, metabolic disorders¹⁴ ). Filling in the missing P and thereby elevating psychiatrists' new role in patient care, teaching, and research in the field of pain medicine may be a substantial clinical contribution in a domain that currently offers relatively little in terms of effective therapeutic interventions.

Correspondence: David Borsook, MD, PhD, Department of Psychiatry, McLean Hospital, 115 Mill St, Belmont, MA 02478 (dborsook@partners.org).

Submitted for Publication: February 12, 2010; final revision received August 5, 2010; accepted August 11, 2010.

Financial Disclosure: Dr Zubieta is a consultant for Merck and Eli Lilly.

Funding/Support: This work was supported by grants DA017959 (Dr Elman); R01 DA 016423, R01 DA 022520, and R01 AT 001415 (Dr Zubieta); and K24NS064050 (Dr Borsook) from the National Institutes of Health.

Additional Contributions: We thank Lauren Nutile and Jeanette Cohan for their assistance with the preparation of the manuscript.