Strong Inference, Theory Testing, and the Neuroanatomy of Schizophrenia

Carpenter, William T.; Boyer, Robert; Kirkpatrick, Brian; Tamminga, Carol A.; Wood, Frank

doi:10.1001/archpsyc.1993.01820220081009

Cited by 142 publications

(63 citation statements)

References 75 publications

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“…The study of etiology and pathophysiology at the syndrome level fails to address heterogeneity. It is increasingly imperative to develop information on the molecular basis of each aspect of the disease to perform definitive studies about the illness and generate models that are more informative (Carpenter et al, 1993).…”

Section: Nine Items Impeding Drug Discovery In 2007 and Recommendatiomentioning

confidence: 99%

The Evolution of Drug Development in Schizophrenia: Past Issues and Future Opportunities

Carpenter

Koenig

2007

Neuropsychopharmacol

185

128

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Section: Nine Items Impeding Drug Discovery In 2007 and Recommendatiomentioning

confidence: 99%

The Evolution of Drug Development in Schizophrenia: Past Issues and Future Opportunities

Carpenter

Koenig

2007

Neuropsychopharmacol

185

128

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“…BDV infection also is specifically associated with hippocampal damage in that, with or without inflammation, infection leads to a marked loss of hippocampal neurons (Narayan et al, 1983;Carbone et al, 1991Carbone et al, , 1996. The prefrontal system is regarded to be central in the pathophysiology of the schizophrenia deficit syndrome (Weinberger, 1987;Carpenter et al, 1993). This system could be affected by BDV.…”

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confidence: 99%

Borna disease virus antibodies and the deficit syndrome of schizophrenia

Waltrip

Boyer

Carpenter

et al. 1997

Schizophrenia Research

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We detected anti-Borua disease virus (BDV) antibodies at a 14.4% rate in patients with schizophrenia. The hypothesis of a higher rate of BDV seropositivity in deficit syndrome was borne out in a subset of 64 patients categorized according to the Schedule for the Deficit Syndrome with 5/15 seropositive deficit and 4/49 seropositive nondeficit (p <0.05). This suggests that the antibodies and possibly a BDV-like virus are pathogenetically linked to this form of schizophrenia.

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“…Failure to address pseudospcificity in clinical trials testing efficacy for negative symptoms or cognition [7][8][9] ; and c. Failure to move knowledge forward with strong inference research. 10 Here too relying on publications and meeting presentations in the 1980s and 1990s was modest in effect. For example, a recent meta-analyses of negative symptom clinical trials revealed most did not even deal with the primary/secondary distinction in discussion and almost none used a study design that would permit an efficacy interpretation.…”

Section: W T Carpentermentioning

confidence: 99%

Fifty Years: Do Over or Move Forward

Carpenter

2017

Schizophrenia Bulletin

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The following text reflects remarks presented at the 2016 SIRS meeting where four of us from the durable goods department were asked to comment on what we would do if starting our careers today. For reasons best understood in the framework of ego psychology I opted to indicate how I would change what I have done before speculating on beginning a career now envisioning the next 50 years.My best contributions to knowledge and understanding regarding schizophrenia have been in the context of bright and fun colleagues who think deeply and critically. My most regrettable self-identified flaw is the failure to be bold in pressing the field to change rapidly in areas that related to our data and my understanding of collective knowledge. Several examples will illustrate before commenting on the future I would like to have.1. Stop DSM-III from moving schizophrenia to a reality distortion disorder. In the late 1960s it was clear that the diagnosis of schizophrenia needed to be harmonized internationally and a (the) critical problem was perceived as a broad definition applied in the United States that ignore the central features of true or nuclear schizophrenia. These features were not the weakening of the well-springs of volition that Kraepelin defined, together with the dissociative pathology described by Bleuler, as the two central clinical features. Rather, psychopathology proposed by Schneider as indicating the presence of schizophrenia and by Langsfeldt to distinguish true from pseudo schizophrenia was viewed as critical. DSM-III gave unique status to first rank symptoms (FRS) with the presence of a single FRS being sufficient to meet the criteria for a diagnosis of schizophrenia.In the early 1970's, together with John Strauss and John Bartko, we conducted the only empirical test of the central hypotheses related to Langfeldt and Schneider criteria. 1,2 We found them in psychotic conditions other than schizophrenia and within schizophrenia these symptoms lacked prognostic significance. Schneider and Langfeldt positive schizophrenia did not differ from schizophrenia without these reality distortion symptoms. Heterogeneity of the syndrome was not reduced. My mistake was to only make these data known to the DSM-III leaders and publish results, trusting the normal processes to be effective. The result was a unique role in DSM for FRSs that was not changed until DSM-5 in 2013. Negative symptoms were omitted from the criteria DSM-III and the concept shifted to a reality distortion syndrome (ego boundary disturbances if you prefer the concepts of 50 years ago) contributing to the greatly diminished current attention to thought disorder. We also provided data on the clinical features most discriminating in differential diagnosis of schizophrenia and published in Science without any effect on the DSM-III criteria. 3At the SIRS conference I noted the effectiveness of a forceful personality and believe that if I had been more like Fuller Torrey I would have found a way for science rather than pre-conceptions to define core path...

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Strong Inference, Theory Testing, and the Neuroanatomy of Schizophrenia

Cited by 142 publications

References 75 publications

The Evolution of Drug Development in Schizophrenia: Past Issues and Future Opportunities

The Evolution of Drug Development in Schizophrenia: Past Issues and Future Opportunities

Borna disease virus antibodies and the deficit syndrome of schizophrenia

Fifty Years: Do Over or Move Forward

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