508 - LATE ONSET BIPOLAR DISORDER: CASE REPORT AND LITERATURE REVIEW

Abstract

Background:Late-onset bipolar disorder (LOBD) remains an incompletely understood nosological entity, in reason ofits complexity and the paucity of research in this issue. It is not yet clear whether LOBD is a "phenocopy"of the classic early-onset bipolar disorder (EOBD), sharing symptoms but having a different aetiology, orwhether both have a common underlying vulnerability that interacts with age-specific triggering factors.Some authors have proposed that LOBD is a heterogeneous entity, comprising secondary mania(including organic brain disease), bipolarity in the context of dementia-like processes (BD type VI), andLOBD as expression of a lower vulnerability to bipolarity.Case Report:Female patient with previous medical history of hypertension and dyslipidaemia, and psychiatric historyof recurrent severe depressive episodes since early age, with melancholic and psychotic features, had afirst hypomanic episode at 76 years-old, under treatment with tricyclic antidepressant andelectroconvulsive therapy. Meanwhile, she suffered a traumatic brain injury (TBI) complicated withsubdural and subarachnoid hematoma, as well as intraventricular haemorrhage, which is an indirect signof diffuse axonal injury (DAI). Later, at 79 years-old, she presented a mixed episode characterized byracing thoughts, flight of ideas, non-systematized persecutory and ruin delusions, hyposomnia, andultradian alternation between dysphoric and depressive mood, psychomotor agitation and retardation,emotional lability, hypersyntonic contact and hostility. Medical conditions that could account forsecondary mania were ruled out. This clinical picture subsided within few weeks under treatment witholanzapine and electroconvulsive therapy. After recovery memory deficits were noticed.Concluding remarks:This case illustrates a "latent" BD, in a patient with previous recurrent depressive disorder, manifestingthe first episode of mania in late life. Several triggering factors may have contributed to this longitudinalevolution, lowering the threshold to manifest mania, namely cerebrovascular risk factors, a possibleunderlying degenerative process and DAI secondary to TBI, which through structural dysconnectivityalso contributes to cognitive dysfunction. The deleterious effect of recurrent and severe depressiveepisodes on cognition is well documented. The question of whether some forms of LOBD couldconstitute a special risk factor for developing dementia deserves further investigation.