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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

Jurnalul Român <strong>de</strong> Psih<strong>of</strong>armacologie<br />

Romanian Journal <strong>of</strong> Psychopharmacology<br />

Vol. 6, Nr. 1, 2<br />

PENTRU EVALUAREA RISCULUI SUICIDAR ÎN SCHIZOFRENIE<br />

D. Marinescu, T. Udriştoiu, I. Udriştoiu<br />

Universitatea <strong>de</strong> Medicină şi Farmacie Craiova<br />

Rezumat<br />

Rata comportamentului suicidar în schiz<strong>of</strong>renie rămâne înaltă, 20-40% pentru<br />

tentativele suicidare (Meltzer, Okaili, 1995) şi 18% pentru suicidul finalizat<br />

(Baldwin, 2001), ceea ce a impus re-evaluarea simptomatologiei <strong>de</strong>presive din<br />

schiz<strong>of</strong>renie. Leff (1990) consi<strong>de</strong>ră că <strong>de</strong>presia din schiz<strong>of</strong>renie este <strong>de</strong> tip secundar<br />

şi <strong>de</strong>scrie 3 submo<strong>de</strong>le psihopatologice: a) <strong>de</strong>presia ca simptom reactiv la<br />

ameliorarea simptomelor psihotice pozitive (conştientizarea bolii şi, implicit, a<br />

gravităţii acesteia); b) <strong>de</strong>presia secundară pier<strong>de</strong>rii capacităţii <strong>de</strong> comunicare,<br />

direct proporţională cu retracţia autistă şi pier<strong>de</strong>rea in<strong>de</strong>pen<strong>de</strong>nţei eului; c)<br />

<strong>de</strong>presia ca simptom psihotic activ şi in<strong>de</strong>pen<strong>de</strong>nt, evoluând şi după episodul acut.<br />

Din punctul nostru <strong>de</strong> ve<strong>de</strong>re, mo<strong>de</strong>lul explicativ <strong>de</strong> inspiraţie psihopatologică nu<br />

<strong>of</strong>eră suficiente explicaţii în ceea ce priveşte comportamentul <strong>de</strong> tip suicidar.<br />

Elementele <strong>de</strong> neurobiologie pot explica parţial comportamentul suicidar pe baza<br />

nivelelor <strong>de</strong> vulnerabilitate primară (anomalii biochimice şi genetice), secundară<br />

(legată <strong>de</strong> boală şi tratament) şi cognitivă. Corelaţiile neurobiologice posibile între<br />

clinica sindromului <strong>de</strong>presiv din schiz<strong>of</strong>renie, comportamentul suicidar şi mo<strong>de</strong>lul<br />

neurobiologic pot permite strategii terapeutice diferenţiate.<br />

Cuvinte cheie: schiz<strong>of</strong>renie, suicid.<br />

FOR THE EVALUATION OF THE SUICIDAL RISK IN SCHIZOPHRENIA<br />

Abstract<br />

The suici<strong>de</strong> rate in schizophrenia remains at high rates: 20-40% for the estimated<br />

attempts (Meltzer, Okaili, 1995) and 18% for the finalized suici<strong>de</strong> (Baldwin, 2001),<br />

which has <strong>de</strong>termined the re-evaluation <strong>of</strong> the <strong>de</strong>pressive symptoms in schizophrenia.<br />

Leff (1990) consi<strong>de</strong>rs the <strong>de</strong>pression in schizophrenia as secondary and <strong>de</strong>scribes 3<br />

psychopathological submo<strong>de</strong>ls: a) <strong>de</strong>pression as reactive to the improvement <strong>of</strong><br />

positive symptoms (awareness <strong>of</strong> disor<strong>de</strong>r and <strong>of</strong> its gravity); b) <strong>de</strong>pression as<br />

secondary to the loss <strong>of</strong> communication skills, proportional with the autistic<br />

retraction and loss <strong>of</strong> self; c) <strong>de</strong>pression as active and in<strong>de</strong>pen<strong>de</strong>nt psychotic<br />

symptom, ongoing beyond the acute episo<strong>de</strong>.<br />

In our point <strong>of</strong> view, the psychopathological mo<strong>de</strong>l does not contribute completely to<br />

the un<strong>de</strong>rstanding <strong>of</strong> suicidary behaviour. The neurobiological perspective may<br />

partially explain the suicidal behaviour based on the levels <strong>of</strong> primary (biochemical<br />

and genetic abnormalities), secondary (due to the disor<strong>de</strong>r itself and to the<br />

treatment) and cognitive vulnerability. The possible neurobiological correlations<br />

between the <strong>de</strong>pressive syndrome in schizophrenia, the suicidal behaviour and the<br />

neurobiological mo<strong>de</strong>l may trigger differentiated therapeutic strategies.<br />

Key words: schizophrenia, suici<strong>de</strong>.<br />

21

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