Depressive syndrome in schizophrenia

Planansky, Karel; Johnston, Roy

doi:10.1111/j.1600-0447.1978.tb06887.x

Cited by 45 publications

(13 citation statements)

References 8 publications

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“…Schizophrenia is characterised by diverse psychopathology with symptoms that are commonly divided into five dimensions: positive symptoms, negative symptoms, cognitive symptoms, aggressive symptoms and affective symptoms 3. Depressive symptoms (seen as one end on the spectrum of affective symptoms) frequently accompany schizophrenia, may be part of the prodromal symptomology, following an acute episode, or occur between psychotic episodes 4. Although not as dramatic as positive and aggressive symptoms, it should be noted that the depressive symptoms of schizophrenia have been reported to be associated with various less favourable outcomes in schizophrenia 5–7.…”

Section: Introductionmentioning

confidence: 99%

Increased plasma leptin as a novel predictor for psychopathological depressive symptoms in chronic schizophrenia

Jiao

Xing

et al. 2018

Gen Psych

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BackgroundDepressive symptoms are often seen in schizophrenia. The overlap in presentation makes it difficult to distinguish depressive symptoms from the negative symptoms of schizophrenia. The adipokine leptin was found to be altered in both depression and schizophrenia. There are few studies focusing on the prediction of leptin in diagnosis and evaluation of depressive symptoms in schizophrenia.ObjectiveAimsTo assess the plasma leptin level in patients with schizophrenia and its relationships with depressive symptoms.MethodsCross-sectional studies were applied to (1) compare the levels of plasma leptin between schizophrenia (n=74) and healthy controls (n=50); and (2) investigate the relationship between plasma leptin levels and depressive subscores.Results(1) Plasma leptin levels were significantly higher in patients with schizophrenia than in healthy controls. (2) Correlation analysis revealed a significant negative association between leptin levels and the depressed factor scores on the Positive and Negative Syndrome Scale (PANSS). (3) Stepwise multiple regression analyses identified leptin as an influencing factor for depressed factor score on PANSS.ConclusionLeptin may serve as a predictor for the depressive symptoms of chronic schizophrenia.

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Section: Introductionmentioning

confidence: 99%

Increased plasma leptin as a novel predictor for psychopathological depressive symptoms in chronic schizophrenia

Jiao

Xing

et al. 2018

Gen Psych

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“… 4 – 8 Depressive symptoms have long been regarded as integral to the psychopathology associated with schizophrenia. 9 The presence of depressive symptoms in patients with schizophrenia reduces patients’ ability to function, increases the burden imposed by the underlying psychotic illness, and worsens outcomes and prognosis. 5 , 10 – 14…”

Section: Introductionmentioning

confidence: 99%

Lurasidone for the treatment of depressive symptoms in schizophrenia: analysis of 4 pooled, 6-week, placebo-controlled studies

et al. 2014

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ObjectiveDepressive symptoms are common in schizophrenia and can worsen outcomes and increase suicide risk. Lurasidone is an atypical antipsychotic agent indicated for the treatment of schizophrenia and for the treatment of major depressive episodes associated with bipolar I disorder. This post hoc analysis evaluated the effect of lurasidone on depressive symptoms in patients with schizophrenia.MethodsPatient-level data were pooled from 4 similarly designed, double-blind, placebo-controlled, 6-week registration studies of lurasidone (40–160 mg/d) in adult patients with an acute exacerbation of schizophrenia. Changes in depressive symptoms, measured by the Montgomery–Åsberg Depression Rating Scale (MADRS), were analyzed for the overall sample and for subgroups of patients stratified by baseline MADRS scores.ResultsMADRS assessments at baseline and endpoint (day 42 or last observation carried forward [LOCF]) were available for 1330 patients. Patients receiving lurasidone experienced significantly greater decreases in MADRS score (–2.8, least-squares [LS] mean change, LOCF) compared with patients receiving placebo (–1.4, P < .001, effect size 0.24). Analysis of change in MADRS score (LOCF) by baseline symptom severity (MADRS score of ≥12, ≥14, ≥16, ≥18) showed significantly greater improvement for lurasidone-treated patients across all severity groups; effect sizes ranged from 0.25 to 0.34. Among patients with a baseline MADRS score of ≥12, depressive symptom remission (defined as MADRS score <10 at LOCF endpoint) was attained by 45.0% of lurasidone-treated patients and 36.3% of patients receiving placebo (P < .05).ConclusionsIn a pooled analysis of short-term, placebo-controlled studies, lurasidone significantly improved depressive symptoms in patients with schizophrenia.

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“…Although no related studies of RDC (Spitzer et al 1978) and DSM-III (APA, 1980) schizophrenics have been reported, since a depression occurring after the psychosis (though not before or during) is believed to be compatible with a diagnosis of schizophrenia, this depression is likely to occur, perhaps with similarly high frequency, in these schizophrenics. Although commonly noted in acute and good prognosis schizophrenics (McGlashan & Carpenter, 1976 a), moreover, high percentages reported in chronic patients (20-70 %; Floru et al 1975;Kayton et al 1976;Planansky & Johnston, 1978;Roy, 1980), Langfeldt nuclears (67%; Singh & Kay, 1979), and asocial schizophrenics (group mean; Klein & Rosen, 1973), plus lack of correlation with the Phillips and Strauss -Carpenter scales (McGlashan & Carpenter, 19766), further imply that this depression occurs independently of prognostic criteria or long-term outcome.…”

Section: Pharmacogenetic Depression and Pharmacogenetic Pseudoparkinsmentioning

confidence: 99%

Genetic factors in the response to neuroleptics in schizophrenia: a psychopharmacogenetic study

et al. 1981

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SynopsisA psychopharmacogenetic strategy was used to investigate a genetic heterogeneity model of schizophrenia. This model consisted of various genetic subtypes represented by patients classified hypothetically according to the types and genealogical (Mendelian) patterns of illnesses in first-degree relatives. The effect of neuroleptics on these subtypes (drug x genetic subtype interactions) were tested for evidence of post-treatment responses which discriminated between them. The findings revealed that schizophrenics who had depressed relatives tended to exhibit (1) depression and more severe pseudoparkinsonism irrespective of types of neuroleptics, and (2) greater remission of paranoid-hostility symptoms when treated with neuroleptics of the aliphatic-piperadine type. Schizophrenics who had schizophrenic relatives failed to show these responses.Interpretation of these findings emphasized the recognition of these responses as arising from neuroleptic-induced alterations of defective neurologic-neurochemical systems underlying this subtype and as ‘pharmacogenetic criteria’ by which it can be discriminated.

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Depressive syndrome in schizophrenia

Cited by 45 publications

References 8 publications

Increased plasma leptin as a novel predictor for psychopathological depressive symptoms in chronic schizophrenia

Increased plasma leptin as a novel predictor for psychopathological depressive symptoms in chronic schizophrenia

Lurasidone for the treatment of depressive symptoms in schizophrenia: analysis of 4 pooled, 6-week, placebo-controlled studies

Genetic factors in the response to neuroleptics in schizophrenia: a psychopharmacogenetic study

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