328. DELAYED ONSET POST-STROKE MANIA, A CASE REPORT AND LITERATURE REVIEW

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Abstract Background Post-stroke depression is one of the common comorbidities following cerebrovascular events. However, secondary mania occurs in a smaller proportion of stroke patients, typically affecting 1-2% within two years of an ischemic event. The pathophysiology underlying post-stroke mania, especially in cases of delayed onset, remains poorly understood and needs further investigation. Aims & Objectives This study focuses on a rare case of delayed onset mania following a stroke. We aim to highlight the challenges in differentiating post-stroke mania from other causes of secondary mania and to discuss how treatment strategies differ from primary mania. Method We reported a case of a 79 year-old man with a history of right middle cerebral artery cortical infarction 16 years ago, with several transient ischemic attacks and paroxysmal atrial fibrillation diagnosed under anticoagulant therapy. Over the past two years, he experienced personality changes, including rigid thinking and disinhibited behaviours. He presented with manic symptoms such as expansive and irritable mood, increased self-esteem, excessive talkativeness and goal directed behaviours for the first episode in his lifetime for 2 months. A review of the current literature helped identify potential risk factors contributing to post-stroke mania and provided insight into treatment approaches. Results Post-stroke mania often had the similarities of the right hemispheric ischemic lesions with risk factors of cardiovascular disease. The late age of onset, presence of neurologic deficits, and poor response to treatment distinguish this case from primary mania. Valproic acid and benzodiazepines are commonly used for treatment in post-stroke mania. Discussion & Conclusions Our findings of secondary mania associated with right-sided stroke are consistent with previous studies. The delayed onset of manic symptoms may be attributed to the progression of the silent cerebral infarctions in cortical and subcortical white matter regions, leading to hypoactivation and dysfunction of brain networks. This process may be further exacerbated by poor cardiovascular conditions over time. Further research is needed to explore the mechanisms behind delayed onset mania and refine treatment strategies for these complex neuropsychiatric presentations.

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