Endogenous and reactive cyclicity in bipolar disorder

Ciclicità endogena e reattiva nel disturbo bipolare

A. Koukopoulos1, G. Serra2, F. Zazzara3, G. Sani1 2, A.E. Koukopoulos1 2

1 Centro Lucio Bini Roma; 2 Azienda Ospedaliera Sant'Andrea, Dipartimento di Psichiatria, 3 Policlinico Umberto I, Sapienza Università di Roma



The goal of this paper is to examine the triggering factors associated with the emergence of manic episodes and see whether the cyclicity of BPI patients is driven exclusively by endogenous factors or it is determined also by exogenous triggering factors. After a historical overview of the evolution of the concept of cyclicity and its fundamental significance in manicdepressive illness, we look at the intimate relationship between mania and depression and we discuss the hypothesis of the primacy of mania.


We reviewed the clinical charts of 100 consecutive index manias that were examined at the Centro Lucio Bini in Rome. The diagnosis was based on the DSM-IV diagnostic criteria for manic episode. We focus the search on the presence of factors recognized in literature as able to trigger a mania 1. We also examined the premorbid temperament of these patients applying Akiskal and Mallya’s criteria.


We found that 80 manias occurred in association with one or more triggering factors and only in 20 manias we did not find any evident triggering factor. Thirty manias were trigged by antidepressant treatments, 18 by drug abuse, 17 by withdrawal of antimanic treatments, 4 by very distressing life events, 3 by cortisone treatment, 3 by sleep deprivation, 2 by child-birth, one by jet-lag, one by excessive thyroxine dose, and one by cranial injury. As far as the temperament of these patients is concerned we found that 69 were hyperthymic, 12 cyclothymic, 8 dysthymic, and 4 irritable.


External factors may act on a particulary excitable temperament and trigger a manic episode. Temperament is an endogenous factor, but exogenous factors may determine the cyclic course of BPI disorder. We finally present a possible neurobiological explanation supporting the view that treatment with antidepressant drugs, by increasing dopaminergic transmission in the mesolimbic system, may trigger acute mania and destabilise long-term course.

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