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Post-Traumatic Bipolar Disorder: A Case Report

Aug 2026 · Scholars Journal of Medical Case Reports · Vol 14, pp. 1796-1799 · 0 citations

TL;DR

This case underscores the pathophysiological role of ventromedial limbic networks in the genesis of secondary bipolar phenotypes and highlights the clinical necessity of maintaining aggressive, multimodal psychopharmacological adherence to mitigate high-risk behavioral decompensation.

Abstract

Background: Traumatic brain injury (TBI) is increasingly recognized as a profound risk factor for neuropsychiatric sequelae, including secondary mood disorders. Post-traumatic bipolar disorder (PTBD) represents a complex phenotype characterized by unique structural pathology, high rates of treatment non-adherence, comorbid substance use disorders, and distinct management challenges. Case Presentation: We report the case of Mr. B.K., a 34-year-old unemployed male with a history of a severe TBI in 2015 requiring neurosurgical evacuation of an extradural hematoma. Two weeks post-intensive care unit discharge, he developed his first characterized manic episode. Over the subsequent decade, he experienced multiple recurrent manic episodes with psychotic features, consistently precipitated by poor treatment adherence. His most recent admission was triggered by severe psychomotor agitation, verbal and physical hetero-aggressiveness, grandiose delusions, disinhibited pedophilic impulses, and an addictive spiral involving cannabis, alcohol, tobacco, and alprazolam misuse. Structural brain magnetic resonance imaging (MRI) revealed extensive sequelae of cerebral contusions, focal necrosis/gliosis within the basomedial temporal cortex, and decreased fractional anisotropy in the uncinate fasciculus. The patient was successfully stabilized on a combination of quetiapine (600 mg/day) and sodium valproate (1000 mg/day), leading to full resolution of behavioral, delusional, and deviant sexual symptoms over a six-week period. Conclusion: This case underscores the pathophysiological role of ventromedial limbic networks in the genesis of secondary bipolar phenotypes and highlights the clinical necessity of maintaining aggressive, multimodal psychopharmacological adherence to mitigate high-risk behavioral decompensation.

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