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Jurnalul Român de Psihofarmacologie Romanian Journal of Psychopharmacology Vol. 6, Nr. 1, 2 10. Francis-Turner L and Valouskova V, 1996 – Nerve growth factor and nootropic drug Cerebrolysin but not fibroblast growth factor can reduce spatial memory impairment elicited by fimbria-fornix transection: short-term study. Neurosci Lett., 202, 193-6. 11. Panisset M, Gauthier S, Moessler H and Windisch M, 2002 – Cerebrolysin in Alzheimer's disease: a randomized, double-blind placebo-controlled trial with a neurotrophic agent. J Neural Transm. 109, 1089-104. 12. Bae CY, Cho CY, Cho K, Hoon Oh B, Choi KG, Lee HS, Jung SP, KimDH, Lee S, Choi GD, Cho H and Lee H, 2000 – A double-blind, placebo-controlled, multicenter study of Cerebrolysin for Alzheimer's disease. J Am Geriatr Soc. 48, 1566-71. 20
Jurnalul Român de Psihofarmacologie Romanian Journal of Psychopharmacology Vol. 6, Nr. 1, 2 PENTRU EVALUAREA RISCULUI SUICIDAR ÎN SCHIZOFRENIE D. Marinescu, T. Udriştoiu, I. Udriştoiu Universitatea de Medicină şi Farmacie Craiova Rezumat Rata comportamentului suicidar în schizofrenie rămâne înaltă, 20-40% pentru tentativele suicidare (Meltzer, Okaili, 1995) şi 18% pentru suicidul finalizat (Baldwin, 2001), ceea ce a impus re-evaluarea simptomatologiei depresive din schizofrenie. Leff (1990) consideră că depresia din schizofrenie este de tip secundar şi descrie 3 submodele psihopatologice: a) depresia ca simptom reactiv la ameliorarea simptomelor psihotice pozitive (conştientizarea bolii şi, implicit, a gravităţii acesteia); b) depresia secundară pierderii capacităţii de comunicare, direct proporţională cu retracţia autistă şi pierderea independenţei eului; c) depresia ca simptom psihotic activ şi independent, evoluând şi după episodul acut. Din punctul nostru de vedere, modelul explicativ de inspiraţie psihopatologică nu oferă suficiente explicaţii în ceea ce priveşte comportamentul de tip suicidar. Elementele de neurobiologie pot explica parţial comportamentul suicidar pe baza nivelelor de vulnerabilitate primară (anomalii biochimice şi genetice), secundară (legată de boală şi tratament) şi cognitivă. Corelaţiile neurobiologice posibile între clinica sindromului depresiv din schizofrenie, comportamentul suicidar şi modelul neurobiologic pot permite strategii terapeutice diferenţiate. Cuvinte cheie: schizofrenie, suicid. FOR THE EVALUATION OF THE SUICIDAL RISK IN SCHIZOPHRENIA Abstract The suicide rate in schizophrenia remains at high rates: 20-40% for the estimated attempts (Meltzer, Okaili, 1995) and 18% for the finalized suicide (Baldwin, 2001), which has determined the re-evaluation of the depressive symptoms in schizophrenia. Leff (1990) considers the depression in schizophrenia as secondary and describes 3 psychopathological submodels: a) depression as reactive to the improvement of positive symptoms (awareness of disorder and of its gravity); b) depression as secondary to the loss of communication skills, proportional with the autistic retraction and loss of self; c) depression as active and independent psychotic symptom, ongoing beyond the acute episode. In our point of view, the psychopathological model does not contribute completely to the understanding of suicidary behaviour. The neurobiological perspective may partially explain the suicidal behaviour based on the levels of primary (biochemical and genetic abnormalities), secondary (due to the disorder itself and to the treatment) and cognitive vulnerability. The possible neurobiological correlations between the depressive syndrome in schizophrenia, the suicidal behaviour and the neurobiological model may trigger differentiated therapeutic strategies. Key words: schizophrenia, suicide. 21
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