Faculty Bibliography

PRIMARY OBJECTIVE: To determine the association of report of any history of head injury with loss of consciousness or confusion and a lifetime diagnosis of psychiatric disorder in a general population. RESEARCH DESIGN: A probability sample of adults from the New Haven portion of the NIMH Epidemiologic Catchment Area programme were administered standardized and validated structured interviews. The main outcome measures were lifetime prevalence of psychiatric disorders and suicide attempt in individuals with and without a history of traumatic brain injury. MAIN OUTCOMES AND RESULTS: Among 5034 individuals interviewed, 361 admitted to a history of severe brain trauma with loss of consciousness or confusion (weighted rate of 8.5/100). When controlling for sociodemographic factors, quality of life indicators and alcohol use, risk was increased for major depression, dysthymia, panic disorder, OCD, phobic disorder and drug abuse/dependence. In addition, lifetime risk of suicide attempt was greater in those who had suffered head injury. CONCLUSION: Individuals with a history of traumatic brain injury have significantly higher occurrence for psychiatric disorders and suicide attempts in comparison with those without head injury and have a poorer quality of life. Future studies should examine the nature of this relationship, focusing on the severity of the brain injury and the temporal contiguity of the brain injury and psychiatric disorder

Traumatic brain injury (TBI) may produce a variety of neuropsychiatric problems, including impaired cognition, depression, mania, affective lability, irritability, anxiety, and psychosis. Despite the common occurrence of these symptoms following TBI, there are relatively few studies that provide clear guidance regarding management. Many symptoms (eg, irritability, affective lability, fatigue, sleep disturbance, and impaired cognition) are primarily consequences of brain injury rather than symptoms of a comorbid psychiatric disorder such as major depression. Although it is difficult to study the complicated treatments needed for such symptom complexes, we are able to recommend an approach to the evaluation and treatment of neuropsychiatric problems following traumatic brain injury. A thorough assessment of the patient is a prerequisite to the prescription of any treatment. This assessment should include a thorough developmental, psychiatric, and medication history; a detailed mental status examination; a complete neurologic examination; and quantification of neuropsychiatric symptoms using standardized and accepted inventories (eg, Neurobehavioral Rating Scale, Neuropsychiatric Inventory ). All symptoms must be evaluated in the context of the patient's premorbid history and current treatment because neuropsychiatric symptoms may be influenced by either factor or by both factors. Psychotherapy is an important component of the treatment of neuropsychiatric problems following TBI. Additionally, patients should be encouraged to become involved with local TBI support groups. When medications are prescribed, it is essential to use cautious dosing (low and slow) and empiric trials with continuous reassessment of symptoms using standardized scales and monitoring for drug-drug interactions. In general, medications with significant sedative, antidopaminergic, and anticholinergic properties should be avoided, and benzodiazepines should be used sparingly, if at all. Although patients with TBI may be particularly susceptible to adverse effects of psychopharmacologic medications, at times dosages similar to those used for the non-brain-injured psychiatric patient may be needed. When a single medication does not provide adequate relief of symptoms or cannot be tolerated at therapeutic doses, an alternative strategy is to augment the effect of one medication by using a second low-dose agent with a different mechanism of action.

Many neuropsychiatric disorders affect memory. Brain regions important in the neuroanatomic substrate of memory include the hippocampus, and sections of the frontal, temporal, and parietal cortices and the thalamus. Acetylcholine and many other neurotransmitters and neuromodulators including dopamine, glutamate, GABA, the catecholamines, and estrogen modulate cognitive function. Treatment approaches to memory loss typically use Alzheimer's dementia as the template, and are discussed in this report