Late-onset bipolar disorder (LOBD) remains an incompletely understood nosological entity, in reason of its 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, or whether 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), and LOBD as expression of a lower vulnerability to bipolarity.

Female patient with previous medical history of hypertension and dyslipidaemia, and psychiatric history of recurrent severe depressive episodes since early age, with melancholic and psychotic features, had a first hypomanic episode at 76 years-old, under treatment with tricyclic antidepressant and electroconvulsive therapy. Meanwhile, she suffered a traumatic brain injury (TBI) complicated with subdural and subarachnoid hematoma, as well as intraventricular haemorrhage, which is an indirect sign of diffuse axonal injury (DAI). Later, at 79 years-old, she presented a mixed episode characterized by racing thoughts, flight of ideas, non-systematized persecutory and ruin delusions, hyposomnia, and ultradian alternation between dysphoric and depressive mood, psychomotor agitation and retardation, emotional lability, hypersyntonic contact and hostility. Medical conditions that could account for secondary mania were ruled out. This clinical picture subsided within few weeks under treatment with olanzapine and electroconvulsive therapy. After recovery memory deficits were noticed.

This case illustrates a “latent” BD, in a patient with previous recurrent depressive disorder, manifesting the first episode of mania in late life. Several triggering factors may have contributed to this longitudinal evolution, lowering the threshold to manifest mania, namely cerebrovascular risk factors, a possible underlying degenerative process and DAI secondary to TBI, which through structural dysconnectivity also contributes to cognitive dysfunction. The deleterious effect of recurrent and severe depressive episodes on cognition is well documented. The question of whether some forms of LOBD could constitute a special risk factor for developing dementia deserves further investigation.