Schizoaffective disorder: diagnostic issues and future recommendations

Malhi, Gin S; Green, Melissa; Fagiolini, Andrea; Peselow, Eric D.; Kumari, Veena

doi:10.1111/j.1399-5618.2007.00564.x

Cited by 142 publications

(103 citation statements)

References 130 publications

(142 reference statements)

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“…Schizophrenia has been documented in all ethnic groups investigated to date (22). Schizoaffective disorder (SZA) is a related, common disorder that lies on a continuum between SZ and bipolar I disorder (BP1) with regard to its clinical features and possibly also in relation to etiology (7,32).…”

Section: Clinical Featuresmentioning

confidence: 99%

Genetic Association Studies of Antioxidant Pathway Genes and Schizophrenia

Chowdari

Bamne²,

Nimgaonkar³

2011

Antioxidants & Redox Signaling

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The endogenous production of highly reactive oxidation species is an inherent by-product of cellular energy metabolism. Cellular antioxidant defense systems (AODS) comprising various antioxidants counter these damaging effects. Several lines of evidence, including postmortem studies, suggest increased oxidative stress in patients with schizophrenia. Some genetic association studies and gene-expression studies suggest that patients also may have altered ability to mount antioxidative mechanisms. As the genetic associations may provide etiologic evidence in support of the oxidative-stress hypothesis of schizophrenia, a focused review has been conducted. We also suggest avenues for further research. Antioxid. Redox Signal. 15, 2037Signal. 15, -2045

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Section: Clinical Featuresmentioning

confidence: 99%

Genetic Association Studies of Antioxidant Pathway Genes and Schizophrenia

Chowdari

Bamne²,

Nimgaonkar³

2011

Antioxidants & Redox Signaling

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“…[8][9][10] Among the many issues that represent points of controversy is the level and pattern of neurocognitive deficit associated with each disorder. 11 Mixed findings are reported in the limited research that has been conducted with adult samples, 12 and the issue has not been carefully examined in children and adolescents.…”

Section: Introductionmentioning

confidence: 99%

Neurocognition in Early-Onset Schizophrenia and Schizoaffective Disorders

Hooper¹,

Giuliano²,

Youngstrom³

et al. 2010

Journal of the American Academy of Child & Adolescent Psych

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Objective-We examined the neuropsychological functioning of youth enrolled in the NIMH funded trial, Treatment of Early-Onset Schizophrenia Spectrum Disorders (TEOSS). We compared the baseline neuropsychological functioning of youth with schizophrenia (SZ, n = 79) to those with schizoaffective disorder (SA, n = 40), and examined the relationship of different variables of illness severity and adaptive behavior to neuropsychological functioning. ©2010 American Academy of Child and Adolescent PsychiatryCorrespondence to Dr. Stephen R. Hooper, Center for Development and Learning, CB# 7255, The Carolina Institute for Developmental Disabilities, University of North Carolina School of Medicine, Chapel Hill, NC 27599-7255; Stephen. hooper@cdl.unc.edu. The opinions and assertions contained in this report are the private views of the authors and are not to be construed as official or as reflecting the views of the Department of Health and Human Services, the National Institutes of Health, or the National Institute of Mental Health. Disclosure: Dr. Hooper receives or has received research support or served as a speaker/consultant for Eli Lilly and Sanofi-Aventis. Dr. Youngstrom has previously served on the Data Safety and Monitoring Board for Eli Lilly and consulted in the past with Otsuka. Dr. Sikich has a current financial interest and receives research funding or participates in clinical trials with Janssen, Pfizer, Bristol Myers-Squibb, Neuropharm, Curemark, and Seaside Pharmaceuticals. She also received software for a computer intervention in schizophrenia from Posit Science. In the past, Dr. Sikich received research funding from Eli Lilly, Janssen, Pfizer, Otsuka, and Astra Zeneca, and has served as a consultant for Sanofi Aventis and ABT Associates. Dr. Frazier receives or has received research support and acted as a consultant for Bristol-Myers Squibb Company, Eli Lilly, GlaxoSmithKline, Johnson & Johnson, Neuropharm, Otsuka America Pharmaceutical, and Pfizer. Dr. Findling receives or has received research support, acted as a consultant, and/or served on a speaker's bureau for Abbott, Addrenex, AstraZeneca, Biovail, Bristol-Myers Squibb, Forest, GlaxoSmithKline, Johnson & Johnson, KemPharm, Eli Lilly, Lundbeck, Neuropharm, Novartis, Organon, Otsuka, Pfizer, Sanofi-Aventis, Sepracore, Shire, Solvay, Supernus Pharmaceuticals, Validus, and Wyeth. Dr. McClellan has had past research support from Pfizer. Dr. Hamer has served as a consultant or advisor for Acadia, Cenerx, Corcept, Epix, Johnson & Johnson, NeuroPharmaBoost, Pepper-Hamil-ton, PureTechVentures, SanofiAventis, and Takeda. He has served on the advisory board for Enabled MD, Novartis, and Wyeth. He has served on a Data Safety Monitoring Board (DSMB) for Allergan, Eli Lilly & Company, Pfizer, Schwartz, and Solvey. He has served on a Mock Advisory Panel for Alpharma. He has served as a statistician on a University of North Carolina contract for a clinical trial with AstraZeneca. He has taught several seminars for SAS Institute. He has served as an expert...

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“…But simply refining the definition of schizophrenia, both internally with respect to subtypes so as to diminish heterogeneity, and externally so as to demarcate its boundaries with adjacent constructs, is not enough. Schizoaffective disorder (SAD) is a good example of a nebulous diagnosis that can be used to fill in the gaps as the dominant diagnosis of schizophrenia expands and contracts (Malhi et al, 2008). Indeed, in DSM-5, SAD has once again been modified so as to increase its specificity and limit its misuse (Malhi, 2013), but as long as it shares a boundary with schizophrenia it will continue to obfuscate diagnosis.…”

mentioning

confidence: 99%