Psychosis Secondary to Traumatic Brain Injury: Critical Literature Review and Illustrative Case Study

Abstract

Psychosis secondary to traumatic brain injury (PSTBI) is rare yet a serious sequela of traumatic brain injury (TBI).
We provide a critical literature review on PSTBI, outlining clinical features and approach to the diagnosis and treatment. Finally, we illustrate a case description, to discuss its conceptual framework. Conceptualizing PSTBI as a neurobiological syndrome has clinical relevance, insofar as, it facilitates a rational scheme, by which specific diagnostic dilemmas should be tackled in the workup, to provide a tailored treatment. Additionally, it may shed light on the understanding of psychotic disorders by integrating data on primary and secondary psychosis. TBI can contribute to the emergence of psychotic symptoms in various manners. It may precipitate psychosis in susceptible individuals, occur in a direct relationship to post‐traumatic epilepsy, or develop directly due to brain injury. It is this last clinical entity that we focus on in this article. Its neurobiological underpinnings comprise the following mechanisms: damage to frontal and temporal lobes (primary injury); structural and/or functional dysconnectivity in sensory‐ and other information‐ ‐processing networks, such as the Default‐Mode network, which stem from diffuse axonal injury (DAI) (primary injury); neuroinflammation and neurodegeneration (secondary injury).

The clinical presentation may take two forms: delusional disorder or schizophrenia‐like psychosis. Both subtypes
are often preceded by a prodromal phase superimposed on other sequelae, namely affective instability, social and occupational functional decline. In comparison to primary schizophrenia, PSTBI has a lower genetic load, fewer negative symptoms, more neurocognitive symptoms, which may be intertwined with frontal‐subcortical system dysfunction/ frontal syndromes and are more likely to present findings on neuroimaging and electroencephalographic studies. PSTBI has a bimodal distribution of onset. Latencies of under a year (early‐onset) have been associated with DAI and delusional disorder subtype. Schizophrenia‐like psychosis subtype usually develops after a latency of 1‐5 years (late‐onset), and has been more associated with epilepsy, focal brain lesions and a chronic course.

Antipsychotics should be used cautiously considering the increased sensitivity to the sedating, anticholinergic, and seizure threshold‐lowering side effects. Late‐onset PSTBI might benefit from anticonvulsants, by virtue of its anti‐ ‐kindling properties. Additionally, further pharmacological approaches may be used to address cognitive, emotional, and behavioural issues.