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Descriptive Psychopathology: The Signs and Symptoms of ...

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75 Chapter 3: <strong>The</strong> brain <strong>and</strong> psychopathologythe body: impaired immunity, atherosclerosis, obesity, bone demineralization,<strong>and</strong> atrophy <strong>of</strong> nerve cells in brain. <strong>The</strong>se are reported in persons with manicdepressiveillness <strong>and</strong> in patients with chronic anxiety disorders. 111<strong>The</strong> serotonin–noradrenergic–glucocorticoid system supports the stress response.112 Under normal physiological conditions this assemblage protects thebrain’s adaptive systems against extreme fluctuation in sensory input. Impairmentin this system, however, triggers brain changes associated with chronic anhedonia(e.g. the “concentration camp syndrome”) <strong>and</strong> other depressive-like syndromes. 113Under conditions <strong>of</strong> sustained or intense stress, neurochemical utilization eventuallyexceeds synthesis <strong>and</strong> reduction in amine function occurs. This reduction ismediated by the nature <strong>of</strong> the stressor (e.g. uncontrollable or not), experientialfactors (e.g. prior exposure to acute stressors), or variables specific to the individual(e.g. age). Because <strong>of</strong> the reduced amine concentrations the individual is lessprepared to respond to the dem<strong>and</strong>s <strong>of</strong> future stress. <strong>The</strong> more persistent thereduction in amine function, the greater the likelihood <strong>of</strong> structural pathology. 114Repeated stress in animal models elicits structural remodeling in brain regionsinvolved in memory <strong>and</strong> emotions (e.g. hippocampus, amygdala, <strong>and</strong> prefrontalcortex) that is associated with impairments in memory, <strong>and</strong> the inappropriateexpression <strong>of</strong> anxiety <strong>and</strong> aggressiveness. 115 Studies <strong>of</strong> humans experiencingprolonged <strong>and</strong> intense stress <strong>and</strong> the emotional response to the stress report suchpathology. 116<strong>The</strong> neurology <strong>of</strong> manic-depressive illnessManic-depression is a disease with substantial heritability that affects the limbicsystem <strong>and</strong> frontal circuitry. <strong>The</strong> ventral emotion generation system is directlyaffected, eliciting characteristic problems in behavior (see Chapter 8) <strong>and</strong> cognition,neuroendocrine <strong>and</strong> ultradian <strong>and</strong> circadian rhythm perturbations, <strong>and</strong>brain metabolic <strong>and</strong> structural abnormalities. 117Cognitive deficits are seen in acute mania <strong>and</strong> melancholia. For many sufferers,the problems remain even when symptoms resolve. While such patients donot exhibit overall decline in intellectual functioning, they do experience adysexecutive syndrome.Manic <strong>and</strong> hypomanic patients have problems in sustained attention, exhibitingdeficits in both acquisition <strong>and</strong> retention <strong>of</strong> verbal <strong>and</strong> non-verbal memory. 118Compared to patients with schizophrenia, manic-depressive patients have fargreater visuospatial problems. 119Being euthymic does not guarantee good functioning. Of asymptomaticmanic-depressive patients who are not demented, 30–50% nevertheless functionpoorly <strong>and</strong> have substantial impairment in several cognitive domains, includingverbal memory <strong>and</strong> learning, oral fluency, visual organization <strong>and</strong> reasoning, <strong>and</strong>

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