There is substantial psychological and neuro-behavioral evidence available to support the fact that traumatic brain injury (TBI) is a risk factor for subsequent psychiatric disorders. In the Journal of Brain Injury (van Reekum R, 1996). The study revealed high rates for post-TBI patients of major depression, bipolar affective disorder, generalized anxiety disorder, borderline and avoidant personality disorders. A large epidemiological study in Australia, following 7,485 patients, showed that reassessment 22 years later indicated that a history of TBI was a risk factor for continued psychiatric problems of increased depression and anxiety and suicidal ideation and that these problems go on for several decades subsequent to the TBI (Anstey KJ, 2004). There is also a connection between mild traumatic brain injury and psychiatric conditions (Mooney G, 2001). Those patients who had some form of preexisting psychiatric difficulty prior to the trauma made a much poorer recovery than those without preexisting psychiatric difficulties.
Unfortunately, the long term outcome of brain injury patients suggest that TBI may cause decades-lasting vulnerability to psychiatric illness in some individuals. Traumatic brain injury seems to make patients particularly susceptible to depressive episodes, delusional disorder, and personality disturbances. A 30 year follow-up study undertaken in Finland (Koponen S, 2002), said that between 48% and 61% of those patients developed psychiatric difficulties after TBI, including major depression, alcohol abuse with dependance, panic disorder, phobias, or psychiatric disorders. On noting that major depression is a frequent psychiatric complication among patients with TBI, a recent study found major depressive disorder observed in 33% of the patients during the first year following a TBI. These patients were more likely to have a personal history of mood and anxiety disorders than patients who did not have major depression. (Jorge RE, 2004). They found that these symptoms were associated with executive dysfunction and prominent anxiety symptoms. As to the biology of the changes phenomena, they found that the changes produced by TBI lead to deactivation of lateral and dorsal prefontal cortices and increased activation of ventral limbic and paralimbic structures including the amygdala.
The National Institute on Disability and Rehabilitation research did a multicenter investigation on depression after traumatic brain injury (Seel RT, 2003). To determine the frequency of depression after TBI and the factors contributing to develop this mood disorder. They found that patients with TBI are at "great risk" for developing depressive symptoms. They noted that unemployment and poverty may be substantial risk factors for development of depressive symptoms. They noted that certain factors were significantly related to the depression - time after injury, injury severity, and post injury marital status. Therefore, the degree of initial injury, be it mild, moderate, or severe, can all lead to crippling depression.
The increased probability of decades of psychiatric difficulty following TBI may explain, in part, a recent multicenter analysis of re-hospitalizations of patients five years after brain injury (Marwitz JH, 2001). The study of 895 rehabilitation patients followed 1 to 5 years following TBI, they found that there remained a relatively high rate of hospitalization in the long term after TBI. The incidents of readmissions for seizures and psychiatric difficulties was substantially increased. They noted that the costs of these re-hospitalizations over the long term should be considered when evaluating long term consequences of injury.