Neuropsychiatry of Psychosis Secondary to Traumatic Brain Injury

Perhaps the most difficult differential diagnostic problem is discriminating patients with PSTBI from those with schizophrenia. As the aforementioned review of the literature suggests, there is much overlap in presentation. In addition, it is likely that many patients diagnosed with schizophrenia have sustained recent head injuries that are undocumented or actually meet the criteria for PSTBI (Burg et al., 1996; Fujii and Ahmed, 1996).

To address the complex relationship between TBI and psychosis, Fujii and Ahmed (2002b) developed a classification scheme for PSTBI that was adapted from Lishman's (1998) description of the possible relationships between TBI and psychotic disorder. This conceptual framework is based on the assumption that psychosis is a neurobehavioral cognitive syndrome that results with sufficient damage to frontal and temporal structures and the dysregulation of the dopamine(Drug information on dopamine) system (Fujii and Ahmed, 2002b). Tenets of this framework are presented in the Table and discussed below.

In the first category, the development of psychosis is directly caused by the TBI. In these cases, there is no family history of schizophrenia and no or low genetic risk for psychosis.

In the second category, TBI contributes to the development of psychosis. One way this can occur is the development of a seizure disorder that, in turn, generates the development of a psychosis. As mentioned previously, the relationship between seizure disorder and psychotic disorder is well-established, and seizure disorder is a common sequelae of TBI.

Traumatic brain injury may also contribute to the development of a psychosis by increasing biological vulnerability or risk. Vulnerability can be increased by damage to frontal and temporal structures or dysregulation of the dopamine system. These structures have been implicated in schizophrenia and many disorders associated with secondary psychosis. Damage to these structures may render the person vulnerable to developing a psychosis with additional damage or changes to these areas. In addition to direct structural damage, the sequelae of TBI--for example cognitive deficits, behavioral dyscontrol and emotional problems--can contribute to risk by increasing the individual's psychological vulnerability in dealing with stress. A reduction in coping skills would render one vulnerable to stress that is associated with increases in the release of dopamine (Roth et al., 1988). Reduced coping abilities may also foster behaviors that would increase the risk for psychosis such as substance abuse and damage from future TBI.

Traumatic brain injury can also contribute to the development of a psychosis by triggering a psychotic episode in patients who have biological risk such as those with a genetic vulnerability for schizophrenia or those with a pre-existing seizure disorder. In these cases, the person already has significant vulnerability to develop a psychosis due to frontal systems and temporal abnormalities. Traumatic brain injury is the factor that raises them above the threshold for psychosis. For these patients, the development of psychosis may have been inevitable with additional damage or changes. Furthermore, it is possible that they may never develop a psychosis if good health is maintained.

The proposed subcategories for how TBI contributes to the development of a psychosis are not mutually exclusive. Thus, these subcategories should be conceptualized as illustrations of different ways that TBI can contribute to meeting the threshold for psychosis.

In the final category, the episode of TBI and the onset of psychosis are coincidental. The TBI may, however, exacerbate cognitive deficits or the severity and treatability of the psychotic condition. In these cases, there is likely a high genetic loading for schizophrenia. Traumatic brain injury may also be very mild without loss of consciousness, or it may be sustained after the onset of psychotic symptoms.