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Descriptive Psychopathology: The Signs and Symptoms of ...

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266 Section 3: Examination domainsChronic pain can be understood as an expression <strong>of</strong> neuronal plasticity at thelevels <strong>of</strong> the nociceptor neurons, spinal cord, <strong>and</strong> brain. Faced with repeated stimulifrom an injury, the brain compensates by adjusting its responses to it. At somepoint the adjustment is sustained even if the injury resolves. 61 <strong>The</strong> patient is nothistrionic or malingering, rather a form <strong>of</strong> long-term learning has taken place.<strong>The</strong> underlying process in plasticity initially involves nociceptor <strong>and</strong> spinal cordmicroglia sensitization. This is reported in inflammatory disease, diabetes <strong>and</strong>injury. 62 Long-term potentiation <strong>of</strong> dorsal horn neurons occurs, <strong>and</strong> underliessuch experiences as tactile allodynia <strong>and</strong> sensory hyperalgesia. 63 “On” <strong>and</strong> “<strong>of</strong>f”cells in the rostral ventromedial medulla that modulate the transmission <strong>of</strong> painbecome “stuck” in the “on” position leading to further sensitization. 64 Pain-specificthalamic nuclei then become sensitized, effecting the cortical perception <strong>of</strong> pain. 65Anterior cingulate cortex metabolism increases in response to painful stimulation<strong>and</strong> thalamic input. 66 <strong>The</strong> somatosensory cortex reorganizes to accommodate theincreased input, highlighting the sensitization <strong>of</strong> involved body areas. 67 Thus, whatappears to be chronic pain <strong>of</strong> psychological origin is more likely the result <strong>of</strong>CNS sensitization leading to hypersensitivity. A co-occurring intense emotionalstate as part <strong>of</strong> a mood or anxiety disorder exacerbates pain hypersensitivity,but the resolution <strong>of</strong> the emotional state may not resolve the chronic pain.Perceptual disturbances associated with migraineAlthough migraine is classified as a headache disorder, it is a complex syndromethat also includes perceptual, autonomic <strong>and</strong> other neurologic disturbances. <strong>The</strong>perceptual features <strong>of</strong> migraine may be misunderstood as conversion disorder orhysteria, malingering, or as part <strong>of</strong> borderline personality disorder resulting inthe sufferer being denied appropriate treatment. Patients with cluster headacheare so fearful <strong>of</strong> future attacks that they may threaten suicide to avoid the painfulexperiences. This risk is high when headache control is poor <strong>and</strong> the threatmisinterpreted as manipulative. Patients with migraine are also most likely toexperience severe but treatable headache after ECT.<strong>The</strong> psychopathology <strong>of</strong> migraine is similar to that <strong>of</strong> seizure disorder, <strong>and</strong> thetwo conditions co-occur in patients <strong>and</strong> their first-degree relatives. 68 In migrainethe visual phenomena are commonly experienced in the peripheral visual field,while in seizure disorder perceptual symptoms are experienced centrally. 69 Sixtypercent <strong>of</strong> migraineurs report a prodrome <strong>of</strong> several minutes, hours or days thatinclude non-melancholic depression, irritability, fatigue, drowsiness, sluggishness,photo- <strong>and</strong> phono phobia, hyperosmia, neck stiffness, feeling cold, feelingthirsty, a change in appetite, <strong>and</strong> abdominal distress.About 20% <strong>of</strong> migraine sufferers report an aura <strong>of</strong> minutes to an hour thatimmediately precedes the headache. Auras include visual phenomena such as

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