The role of negative symptoms in the context of cognitive remediation for schizophrenia

BackgroundRecent theories suggest that poor working memory (WM) may be the cognitive underpinning of negative symptoms in people with schizophrenia. In this study, we first explore the effect of cognitive remediation (CR) on two clusters of negative symptoms (i.e. expressive and social amotivation), and then assess the relevance of WM gains as a possible mediator of symptom improvement.MethodData were accessed for 309 people with schizophrenia from the NIMH Database of Cognitive Training and Remediation Studies and a separate study. Approximately half the participants received CR and the rest were allocated to a control condition. All participants were assessed before and after therapy and at follow-up. Expressive negative symptoms and social amotivation symptoms scores were calculated from the Positive and Negative Syndrome Scale. WM was assessed with digit span and letter-number span tests.ResultsParticipants who received CR had a significant improvement in WM scores (d = 0.27) compared with those in the control condition. Improvements in social amotivation levels approached statistical significance (d = −0.19), but change in expressive negative symptoms did not differ between groups. WM change did not mediate the effect of CR on social amotivation.ConclusionsThe results suggest that a course of CR may benefit behavioural negative symptoms. Despite hypotheses linking memory problems with negative symptoms, the current findings do not support the role of this cognitive domain as a significant mediator. The results indicate that WM improves independently from negative symptoms reduction.

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Inflammation and JNK's Role in Niacin-GPR109A Diminished Flushed Effect in Microglial and Neuronal Cells With Relevance to Schizophrenia

Frontiers in Psychiatry ◽

10.3389/fpsyt.2021.771144 ◽

2021 ◽

Vol 12 ◽

Author(s):

Sabrina H. Ansarey

Keyword(s):

Inflammatory Mediators ◽

Neuronal Death ◽

Microglial Activation ◽

Negative Symptoms ◽

Genome Wide Association Study ◽

Genetic Mutation ◽

Genome Wide ◽

Ultra High Risk ◽

Altered Proteins

Schizophrenia is a neuropsychiatric illness with no single definitive aetiology, making its treatment difficult. Antipsychotics are not fully effective because they treat psychosis rather than the cognitive or negative symptoms. Antipsychotics fail to alleviate symptoms when patients enter the chronic stage of illness. Topical application of niacin showed diminished skin flush in the majority of patients with schizophrenia compared to the general population who showed flushing. The niacin skin flush test is useful for identifying patients with schizophrenia at their ultra-high-risk stage, and understanding this pathology may introduce an effective treatment. This review aims to understand the pathology behind the diminished skin flush response, while linking it back to neurons and microglia. First, it suggests that there are altered proteins in the GPR109A-COX-prostaglandin pathway, inflammatory imbalance, and kinase signalling pathway, c-Jun N-terminal kinase (JNK), which are associated with diminished flush. Second, genes from the GPR109A-COX-prostaglandin pathway were matched against the 128-loci genome wide association study (GWAS) for schizophrenia using GeneCards, suggesting that G-coupled receptor-109A (GPR109A) may have a genetic mutation, resulting in diminished flush. This review also suggests that there may be increased pro-inflammatory mediators in the GPR109A-COX-prostaglandin pathway, which contributes to the diminished flush pathology. Increased levels of pro-inflammatory markers may induce microglial-activated neuronal death. Lastly, this review explores the role of JNK on pro-inflammatory mediators, proteins in the GPR109A-COX-prostaglandin pathway, microglial activation, and neuronal death. Inhibiting JNK may reverse the changes observed in the diminished flush response, which might make it a good therapeutic target.

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The role of premorbid adjustment in schizophrenia: Focus on cognitive remediation outcome

Neuropsychological Rehabilitation ◽

10.1080/09602011.2018.1433048 ◽

2018 ◽

Vol 29 (10) ◽

pp. 1611-1624 ◽

Cited By ~ 2

Author(s):

Mariachiara Buonocore ◽

Francesca Bosinelli ◽

Margherita Bechi ◽

Marco Spangaro ◽

Marco Piantanida ◽

...

Keyword(s):

Cognitive Remediation ◽

Premorbid Adjustment

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Cognitive Remediation Therapy in Chronic Schizophrenia

Advances in Psychology, Mental Health, and Behavioral Studies - Chronic Mental Illness and the Changing Scope of Intervention Strategies, Diagnosis, and Treatment ◽

10.4018/978-1-5225-0519-8.ch016 ◽

2017 ◽

pp. 292-307

Author(s):

Susmita Halder ◽

Akash Mahato

Keyword(s):

Cognitive Deficits ◽

Social Skills Training ◽

Intervention Program ◽

Cognitive Remediation ◽

Chronic Schizophrenia ◽

Skills Training ◽

Psychotic Symptoms ◽

Behavioral Management ◽

Supportive Psychotherapy

Cognitive impairments are now recognized as one of the most ubiquitous features of schizophrenia. Cognitive deficits appear to play a large role in how patients with schizophrenia function in their everyday lives. The role of cognitive deficits in schizophrenia may be gauged by the fact that even when patients with schizophrenia are relatively free of psychotic symptoms, many still have extraordinary difficulty with communication, motivation, self-care, and establishing and maintaining relationships with others. Patients with schizophrenia are often additionally treated with supportive psychotherapy, behavioral management, or social skills training as required. However, the efficacy of these adjunct therapies could be limited in presence of marked cognitive deficits. Thus it becomes crucial to have specific intervention for the underlying cognitive deficits that appear detrimental to improvement of functioning of patients with schizophrenia. The present chapter focuses on cognitive training based intervention program for schizophrenia patients and its efficacy.

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Identifying the Disconnect: Examining the Role of Connectedness in Cognitive Remediation for Children

International Journal of School and Cognitive Psychology ◽

10.4172/2469-9837.s2-014 ◽

2015 ◽

Vol 01 (s2) ◽

Author(s):

McBride Y ◽

Frates EP

Keyword(s):

Cognitive Remediation

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New dopaminergic and non-dopaminergic theories in schizophrenia and their therapeutic impact

Acta Neuropsychiatrica ◽

10.1017/s0924270800036826 ◽

1997 ◽

Vol 9 (2) ◽

pp. 64-67

Author(s):

R.S. Kahn

Keyword(s):

Cognitive Deficits ◽

Negative Symptoms ◽

Dopamine Neurons ◽

Psychotic Symptoms ◽

Positive Symptoms ◽

The Core ◽

Schizophrenic Patients ◽

Core Symptoms ◽

Influential Theory

The dopamine (DA) hypothesis of schizophrenia, postulating that schizophrenia is characterized by increased dopamine function, has been the most influential theory on the pathogenesis of schizophrenia. It has recently been revised based on the appreciation that the core symptoms of schizophrenia may not be the positive (psychotic) symptoms, but rather the negative symptoms and the cognitive deficits found in schizophrenic patients. This revision has prompted the hypothesis that schizophrenia is characterized by both decreased prefrontal dopamine activity (causing deficit symptoms) and increased dopamine activity in mesolimbic dopamine neurons (causing positive symptoms).Notwithstanding this revision of a role for dopamine in schizophrenia, it has become increasingly evident that dysfunction of other monoaminergic systems may be as important in contributing to the pathophysiology of schizophrenia. Specifically, the putative role of serotonin (5-hydroxytryptamine, 5-HT) in schizophrenia is gaining considerable attention. Several observations, such as the ability of the 5-HT antagonist, ritanserin, to alleviate schizophrenic symptoms and, when added to haloperidol (Haldol®), to decrease its extrapyramidal side-effects (EPS), have stimulated studies into a role of 5-HT in schizophrenia. The finding that clozapine (Leponex®), clinically superior to conventional neuroleptics, is a weak DA2 antagonist but a potent 5-HT1c and 5-HT2 antagonist has further stimulated 5-HT-related research in schizophrenia.

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The role of dysfunctional attitudes in models of negative symptoms and functioning in schizophrenia

Schizophrenia Research ◽

10.1016/j.schres.2014.05.025 ◽

2014 ◽

Vol 157 (1-3) ◽

pp. 182-189 ◽

Cited By ~ 32

Author(s):

Thomas Quinlan ◽

Scott Roesch ◽

Eric Granholm

Keyword(s):

Negative Symptoms ◽

Dysfunctional Attitudes

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Epidemiology and pathobiology of bipolar disorder, and their exploration within a complete catchment area population

Acta Neuropsychiatrica ◽

10.1017/s0924270800035444 ◽

2000 ◽

Vol 12 (3) ◽

pp. 73-76 ◽

Cited By ~ 3

Author(s):

P.J. Scully ◽

J.M. Owens ◽

A. Kinsella ◽

J.L. Waddington

Keyword(s):

Bipolar Disorder ◽

Life Events ◽

Catchment Area ◽

Negative Symptoms ◽

Age At Onset ◽

Later Life ◽

Positive Symptoms ◽

Left Hand ◽

Duration Of Illness

ABSTRACTEpidemiological and pathobiological findings in bipolar disorder [BP] have often been limited by selection bias and lack of epidemiological representativeness. In a rural, circumscribed catchment area, ‘all’ patients with BP were identified and assessed. On preliminary analysis, morbid risk [MR] for BP over the area as a whole was 5.0 ± 0.6/1000. The distribution of MR for BP over geographical subregions showed no significant deviation from a statistical model for random occurrences in space by place at birth, in contrast to schizophrenia [SZ], and varied only modestly among males by place at onset. These results imply different etiological factors acting in BP in comparison with SZ, particularly with regard to the role of early versus later life events. In preliminary analyses of psychotic and cognitive features, current severity of positive symptoms was predicted in BP only by increasing dominance of the left hand; negative symptoms by duration of illness and current anticholinergic exposure; poorer general and frontal cognitive function by older age at onset of illness, increasing duration of illness, and current anticholinergic exposure. The finding on handedness suggests disturbance of cerebral asymmetry associated with positive symptoms in BP, while both negative symptoms and cognitive impairment may involve progressive processes. Further analysis of this epidemiologically complete population, including systematic comparisons of BP with schizoaffective disorder and SZ, continues.

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