Why has it taken so long for biological psychiatry to develop clinical tests and what to do about it?

Kapur, Shitij; Phillips, Anthony G.; Insel, Thomas R.

doi:10.1038/mp.2012.105

Cited by 891 publications

(797 citation statements)

References 53 publications

Supporting

Mentioning

754

Contrasting

Unclassified

Order By: Relevance

“…The use of different tasks, the technical aspects of image acquisition and analysis, lack of a gold standard, underpowered studies, and extreme comparisons, as well as antipsychotic treatment effects may partly explain the current contradictory findings [46]. Therefore, further confirmation of the current results needs the evaluation of larger sample sizes of drugnaive first-episode schizophrenia patients (FESPs) as well as the examination of medication effects.…”

Section: Anti-correlation With the Task Positive Networkmentioning

confidence: 97%

A Review of the Functional and Anatomical Default Mode Network in Schizophrenia

et al. 2016

View full text Add to dashboard Cite

Schizophrenia is a severe mental disorder characterized by impaired perception, delusions, thought disorder, abnormal emotion regulation, altered motor function, and impaired drive. The default mode network (DMN), since it was first proposed in 2001, has become a central research theme in neuropsychiatric disorders, including schizophrenia. In this review, first we define the DMN and describe its functional activity, functional and anatomical connectivity, heritability, and inverse correlation with the task positive network. Second, we review empirical studies of the anatomical and functional DMN, and anti-correlation between DMN and the task positive network in schizophrenia. Finally, we review preliminary evidence about the relationship between antipsychotic medications and regulation of the DMN, review the role of DMN as a treatment biomarker for this disease, and consider the DMN effects of individualized therapies for schizophrenia.

show abstract

Section: Anti-correlation With the Task Positive Networkmentioning

confidence: 97%

A Review of the Functional and Anatomical Default Mode Network in Schizophrenia

et al. 2016

View full text Add to dashboard Cite

show abstract

“…Although the sample size of the current study is comparatively large, it is likely that significantly larger studies will be required to define clinically meaningful biological or neurocognitive markers of treatment response. It will be important going forward for clinical studies of ketamine or other mechanistically novel rapid-acting antidepressants to utilize standardized neurocognitive assessments to avoid the problem of 'approximate replication' (Kapur et al, 2012). For example, the study by Shiroma et al (2014) found that impaired attention, but not impaired processing speed per se, was associated with improved antidepressant response to ketamine.…”

Section: Discussionmentioning

confidence: 99%

“…Prior studies have found associations between clinical and demographic factors and therapeutic response to conventional antidepressants (Perlis, 2013), however, a quantitative laboratory-based behavioral or biological predictor of treatment response has remained elusive (Kapur et al, 2012;Simon and Perlis, 2010;Trivedi, 2013). Prior research involving ketamine for unipolar or bipolar depression has suggested candidate clinical or demographic variables associated with therapeutic response, including a family history of alcoholism and a higher body mass index (BMI) (Niciu et al, 2014).…”

Section: Discussionmentioning

confidence: 99%

Neurocognitive Effects of Ketamine and Association with Antidepressant Response in Individuals with Treatment-Resistant Depression: A Randomized Controlled Trial

Murrough

Burdick

Levitch

et al. 2014

Neuropsychopharmacol

116

View full text Add to dashboard Cite

The glutamate N-methyl-D-aspartate (NMDA) receptor antagonist ketamine displays rapid antidepressant effects in patients with treatment-resistant depression (TRD); however, the potential for adverse neurocognitive effects in this population has not received adequate study. The current study was designed to investigate the delayed neurocognitive impact of ketamine in TRD and examine baseline antidepressant response predictors in the context of a randomized controlled trial. In the current study, 62 patients (mean age ¼ 46.2 ± 12.2) with TRD free of concomitant antidepressant medication underwent neurocognitive assessments using components of the MATRICS Consensus Cognitive Battery (MCCB) before and after a single intravenous infusion of ketamine (0.5 mg/kg) or midazolam (0.045 mg/kg). Participants were randomized to ketamine or midazolam in a 2:1 fashion under double-blind conditions and underwent depression symptom assessments at 24, 48, 72 h, and 7 days post treatment using the Montgomery-Asberg Depression Rating Scale (MADRS). Post-treatment neurocognitive assessment was conducted once at 7 days. Neurocognitive performance improved following the treatment regardless of treatment condition. There was no differential effect of treatment on neurocognitive performance and no association with antidepressant response. Slower processing speed at baseline uniquely predicted greater improvement in depression at 24 h following ketamine (t ¼ 2.3, p ¼ 0.027), while controlling for age, depression severity, and performance on other neurocognitive domains. In the current study, we found that ketamine was devoid of adverse neurocognitive effects at 7 days post treatment and that slower baseline processing speed was associated with greater antidepressant response. Future studies are required to further define the neurocognitive profile of ketamine in clinical samples and to identify clinically useful response moderators.

show abstract

“…Em 2002, em uma contribuição para a preparação da quinta edição do DSM (lançado em 2013), um grupo de psiquiatras biológicos proeminentes observou que a psiquiatria não tinha até o momento "conseguido identificar um único marcador neurobiológico fenotípico ou gene que fosse útil para fazer um diagnóstico de um transtorno psiquiátrico ou para prever a resposta ao tratamento psicofarmacológico" (CHARNEY et al, 2002, p. 33). Mais de uma década depois, a situação demonstra não ter mudado (SERPA JR., 1998;CHARNEY et al, 2002;HYMAN, 2008;WALSH et al, 2011;MAYBERG, 2014;INSEL et al, 2010;INSEL, 2013;KAPUR;PHILLIPS;INSEL, 2012;CRAFA, 2014;ROSE, 2013b;GABRIELI;GHOSH;WHITFIELD-GABRIELI, 2015;ROSE;ABI-RACHED, 2013).…”

unclassified

“…Daí, a iniciativa do National Institute for Mental Health (NIMH) norte-americano, lançada em 2011, de afastar-se das categorias do DSM e desenvolver o Projeto Research Domain Criteria (RDOC), destinado a transformar o diagnóstico psiquiátrico através da convergência da genética, neuroimagem e ciências cognitivas (INSEL et al, 2010;INSEL, 2013;KAPUR;PHILLIPS;INSEL, 2012). O RDOC representa uma nova perspectiva na busca de marcadores neurobiológicos, mas não um novo ponto de partida radical.…”

unclassified

Psiquiatria Biológica e Psicofarmacologia: a formação de uma rede tecnocientífica

Aguiar

Ortega

2017

Physis

View full text Add to dashboard Cite

Resumo: A Psiquiatria Biológica emerge nos anos de 1980, nos Estados Unidos, com a publicação do DSM-III (Diagnostic and Statistical Manual of Mental Disorders). Este manual tem a proposta de ser a-teórico e apresentar descrições objetivas dos, então, chamados "distúrbios mentais" a partir de um critério classificatório que não inclui discussões acerca da etiologia destes "distúrbios". Isto implica que, apesar da denominação biológica conferida a esta vertente psiquiátrica, não houve nenhuma descoberta acerca da etiologia biológica destes distúrbios que justificasse sua denominação e seu estrondoso sucesso mundial. Neste artigo, pretendemos analisar as modificações ocorridas na psiquiatria norte-americana a partir da introdução do DSM-III, dos primeiros medicamentos psicotrópicos e o subsequente papel desempenhado pela indústria farmacêutica neste processo. Desse modo, o que está em análise neste artigo é que, ao se apropriar dos medicamentos psicotrópicos como primeira opção terapêutica, a Psiquiatria Biológica cria uma aliança com a indústria farmacêutica que a insere numa rede tecnocientífica que dificulta saber os limites entre Psiquiatria Biológica, Psicofarmacologia e Indústria farmacêutica.

show abstract

Why has it taken so long for biological psychiatry to develop clinical tests and what to do about it?

Cited by 891 publications

References 53 publications

A Review of the Functional and Anatomical Default Mode Network in Schizophrenia

A Review of the Functional and Anatomical Default Mode Network in Schizophrenia

Neurocognitive Effects of Ketamine and Association with Antidepressant Response in Individuals with Treatment-Resistant Depression: A Randomized Controlled Trial

Psiquiatria Biológica e Psicofarmacologia: a formação de uma rede tecnocientífica

Contact Info

Product

Resources

About