Somatoform diagnoses encompass disorders of somatization, conversion, pain, body dysmorphic disorder, and hypochondriasis, according to Diagnostic and Statistical Manual of Mental Disorders-IV (DSM-IV) criteria (American Psychiatric Association). Each is characterized by symptoms affecting voluntary motor or sensory function, having a resemblance to neurologic or medical diseases, concomitant involvement of psychologic factors, and unintentional, unfeigned symptoms. In contrast to most acute pain syndromes, chronic pain states often lack a clear pathoanatomic or pathophysiologic correlate. Our limited understanding of pain mechanisms tends to invite the clinician to suggest psychogenic origins or motives when an immediate organic cause is not confirmed. A dualistic model of chronic pain, perceived as either wholly organic or psychogenic, is not supported by prevailing basic or clinical understanding of pain pathophysiology. Thus diagnostic constructs including conversion disorder are less commonly applied now.
The biopsychosocial model of pain is the most widely utilized heuristic means to characterize the experience of chronic pain. Viewed as a complex interplay of biologic, psychologic, and social factors, this model embraces concepts of both disease and illness. Disease is defined as an objective biologic event involving the disruption of specific bodily organ systems, whereas illness refers to the subjective experience or self-attribution that a disease is present. Accordingly, the biopsychosocial model distinguishes between nociception and pain. Nociception is defined as the stimulation of nerves that relay information about potential tissue damage to the brain. Conversely, pain is the subjective perception resulting from transduction, transmission, and modulation of sensory information. This model incorporates concepts of suffering, including fear and apprehension about the future, triggered by nociception and pain behaviors that provide a means to communicate pain and distress.
PSYCHOLOGIC FORMULATIONS OF PAIN BEHAVIOR AND “CONVERSION” DISORDERS
Pain behaviors serve not only to gain attention, or avoid undesirable consequences, but may also be considered as pain-reducing strategies or as protective strategies to diminish exacerbation of pain. So-called “abnormal illness behavior” describes patients who present with symptom complaints in the absence of physical pathology or who present with exaggerated illness behavior. It is considered a social mechanism that exempts a patient from certain responsibilities, concurrently establishing an obligation to seek treatment and cooperate in the healing process. In other words, pain behavior may offer a more socially legitimate way to express distress or anxiety. In contrast, psychoanalytic explanations of conversion emphasize unconscious drives, including sexuality, aggression, or dependency, and the internalized prohibition against their expression. Other psychoanalytic explanations focus on the need to suffer or identification with a lost object.
Other theories emphasize the role of fear-avoidance beliefs and catastrophizing (tendency to engage in negative thinking and worry about pain) as the catalysts of persistent pain and disability. Catastrophizing is a strong risk factor for increased pain, increased illness behavior, and the development of both physical and psychologic disability. Fear-avoidance beliefs stem from a conviction that pain is synonymous with harm and that any painprovoking activity should thus be avoided; such beliefs are likely to be predictive of pain chronicity and disability.
The neuromatrix model of pain proposes that pain experience results from the integration of outputs from perceptual, behavioral, and homeostatic systems in response to injury and chronic stress. It is considered the output of the diffuse brain neural networks rather than a direct response to sensory information. Neuroimaging studies are beginning to delineate the neural processes implicated in the somatoform disorders. The cortical correlates of the touch and pain pathways include the primary and secondary somatosensory cortex (S1, S2), insula, and anterior cingulate cortex (ACC). However, additional cortical regions associated with attention, such as posterior parietal cortex (PPC), prefrontal cortex, and the temporoparietal junction, can also impact on or be influenced by somatosensory processing.

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