Comprehensive neuropsychiatric assessments of patients experiencing neurocognitive and neurobehavioral symp-tomatology and/or functional disability subsequent to brain injuries due to trauma as well as anoxia, hypoxia, and electrocution are essential and should assist the clini-cian in choosing optimal combinations of pharmacother-apy; individual, group, and family psychotherpharmacother-apy; and rehabilitation, occupational, and resocialization interven-tions. Such assessments should elicit and integrate clinical data from each of the three major biopsychosocial domains as they apply to patients with TBIs.
Optimal outcomes from neuropsychiatric treatment de-pend on careful elicitation of medical, neurological, psychi-atric, and substance abuse histories, with special emphasis on premorbid functioning, details of the acute traumatic event, delineation of the nature and time course of development of posttraumatic neurocognitive and neurobehavioral prob-lems, and precise descriptions of the patient’s current psychi-atric and behavioral symptomatology and functional disabil-ities. In addition to psychotherapeutic, behavioral, and rehabilitative interventions, psychotropic drug treatment is often beneficial if the clinician is aware that the patient may have residual symptoms due to brain trauma and prescribes lower-than-usual doses of psychotropic medications.
The more the neurophysiological effects of various kinds of brain injuries and diseases of the brain are understood, the more commonalities in their underlying pathophysiological mechanisms may be identified. Perhaps individuals who ex-perience poor outcomes from TBI and/or later develop MS, schizophrenia, or dementia, are particularly vulnerable to free radicals, the excitotoxic cascade, calcium toxicity, N-methyl-D-aspartate activation, cytokines, and other neu-rocellular apoptotic processes. As future research defines the mechanisms of cellular damage and destruction after brain trauma, it may be discovered that many are identical to those found in a variety of primary neuropsychiatric diseases. Illuminating these shared pathophysiological mechanisms may then focus attention on promising treat-ments that might be effective in traumatic brain injury as well as other neuropsychiatric and neurodegenerative dis-ease states.
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