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Featured researches published by Julie Nordgaard.


Schizophrenia Bulletin | 2014

Self-disorders and the Schizophrenia Spectrum: A Study of 100 First Hospital Admissions

Julie Nordgaard; Josef Parnas

Introduction: Self-disorders (SD) have been described as a core feature of schizophrenia both in classical and recent psychopathological literature. However, the specificity of SD for the schizophrenia spectrum disorders has never been demonstrated in a diagnostically heterogeneous sample, nor has the concurrent validity of SD been examined. Aim: (1) To examine the specificity of Examination of Anomalous Self-Experiences (EASE) measured SD to the schizophrenia spectrum disorder in first contact inpatients, (2) to explore the internal consistency and factorial structure of the EASE, (3) to assess the concurrent validity of SD by exploring correlations between SD and the canonical psychopathological dimensions of schizophrenia, (4) to explore relations of SD to intelligence, sociodemographic, and extrinsic illness characteristics. Methods: A total of 100 consecutive first admission patients underwent a comprehensive psychopathological examination and an assessment of SD with the EASE scale. The diagnostic distribution of the EASE scores was tested with ANOVA, whereas the relations between the EASE scores and other symptomatic dimensions of schizophrenia were tested with Spearman’s rho. A potential factorial structure and the internal consistency of the EASE scale were also examined. Results: SD aggregated significantly in the schizophrenia spectrum disorders, with no differences between schizophrenia and schizotypal disorders. EASE scores correlated moderately with canonical psychopathological dimensions of schizophrenia. Factor analysis of the EASE disclosed only one factor and the internal consistency of the EASE was excellent. Conclusions: SD aggregate selectively in the schizophrenia spectrum disorders, with similar levels in schizophrenia and schizotypy. The study lends validity to the view of SD as an experiential vulnerability phenotype of the schizophrenia spectrum disorders.


European Archives of Psychiatry and Clinical Neuroscience | 2013

The psychiatric interview: validity, structure, and subjectivity

Julie Nordgaard; Louis A. Sass; Josef Parnas

There is a glaring gap in the psychiatric literature concerning the nature of psychiatric symptoms and signs, and a corresponding lack of epistemological discussion of psycho-diagnostic interviewing. Contemporary clinical neuroscience heavily relies on the use of fully structured interviews that are historically rooted in logical positivism and behaviorism. These theoretical approaches marked decisively the so-called “operational revolution in psychiatry” leading to the creation of DSM-III. This paper attempts to examine the theoretical assumptions that underlie the use of a fully structured psychiatric interview. We address the ontological status of pathological experience, the notions of symptom, sign, prototype and Gestalt, and the necessary second-person processes which are involved in converting the patient’s experience (originally lived in the first-person perspective) into an “objective” (third person), actionable format, used for classification, treatment, and research. Our central thesis is that psychiatry targets the phenomena of consciousness, which, unlike somatic symptoms and signs, cannot be grasped on the analogy with material thing-like objects. We claim that in order to perform faithful distinctions in this particular domain, we need a more adequate approach, that is, an approach that is guided by phenomenologically informed considerations. Our theoretical discussion draws upon clinical examples derived from structured and semi-structured interviews. We conclude that fully structured interview is neither theoretically adequate nor practically valid in obtaining psycho-diagnostic information. Failure to address these basic issues may have contributed to the current state of malaise in the study of psychopathology.


World Psychiatry | 2012

Assessing the diagnostic validity of a structured psychiatric interview in a first‐admission hospital sample

Julie Nordgaard; Rasmus Revsbech; Ditte Sæbye; Josef Parnas

The use of structured psychiatric interviews performed by non-clinicians is frequent for research purposes and is becoming increasingly common in clini-cal practice. The validity of such interviews has rarely been evaluated empirically. In this study of a sample of 100 diagnostically heterogeneous, first-admitted inpatients, the results of an assessment with the Structured Clinical Interview for DSM-IV (SCID), yielding a DSM-IV diagnosis and performed by a trained non-clinician, were compared with a consensus lifetime best diagnostic estimate (DSM-IV) by two experienced research clinicians, based on multiple sources of information, which included videotaped comprehensive semi-structured narrative interviews. The overall kappa agreement was 0.18. The sensitivity and specificity for the diagnosis of schizophrenia by SCID were 19% and 100%, respectively. It is concluded that structured interviews performed by non-clinicians are not recommendable for clinical work and should only be used in research with certain precautions. It is suggested that a revival of systematic theoretical and practical training in psychopathology is an obvious way forward in order to improve the validity and therapeutic utility of psychiatric diagnosis.


Early Intervention in Psychiatry | 2016

Premorbid self‐disorders and lifetime diagnosis in the schizophrenia spectrum: a prospective high‐risk study

Josef Parnas; John Carter; Julie Nordgaard

The notion of a disordered self as a core disturbance of schizophrenia was proposed in many foundational texts. Recent studies, spurred by the development of the Examination of Anomalous Self‐Experience (EASE), seem to indicate that self‐disorders are a specific manifestation of schizophrenia vulnerability. Follow‐up studies of help‐seeking, prodromal and first‐admission patients have demonstrated the utility of self‐disorders for predicting later schizophrenia‐spectrum disturbance. We wished to extend these findings by gauging the predictive value of self‐disorders in a premorbid, non‐clinical population at high risk for schizophrenia.


Acta Psychiatrica Scandinavica | 2013

A haunting that never stops: psychiatry's problem of description

Julie Nordgaard; Josef Parnas

One hundred years ago, Karl Jaspers published his ‘Allgemeine Psychopathologie’ (1), a book, which in its seventh edition from 1959, provided the most comprehensive analysis of psychiatry’s theoretical foundations, concepts, and methods needed to investigate consciousness, particularities of psychiatric interviewing, classificatory principles, and many other issues, deemed relevant for clinical psychiatry. Today’s psychiatry is very far from Jaspers’ emphasis on adequate concepts and methods for exploring the patient’s perspective and his correlated insistence on the interdisciplinary nature of psychiatric enterprise, bordering not only biology but also psychology, sociology, philosophy, and other disciplines. Since the late 1960s, psychiatry, conforming itself to the scientific ideals of behaviorism, underwent a radical remake, the so-called operational revolution. The operational revolution resulted in criteria-based diagnostic categories and ‘operational definitions’ of such criteria. The body of the then-accumulated clinical knowledge and sophisticated descriptions was simplified and shortened into diagnostic manuals, available to lay public because written in lay-language and free of theoretical burden. These manuals became the main teaching source for psychiatrists, a situation that progressively has led to a ‘death’ of psychiatric description and tended to dehumanize the clinical encounter (2). The structured diagnostic interviews and checklists have emerged as adequate methodology to cut through the complexities of subjectivity and communication. The structured interviews, modelled upon the behaviorist stimulus–response paradigm, consist of preformulated questions (paraphrasing the corresponding diagnostic criteria), presented in a fixed, predetermined order. They are believed to eventuate in a faithful and valid reproduction of the patient’s inner world and point of view. At the heydays of operationalism, it was widely predicted that enhanced reliability would lead to rapid breakthroughs in the etiological knowledge, ‘carving nature at its joints’ (3). Unfortunately, a ‘gaping disconnect’ is today widely recognized between the impressive progress in genetics and neurosciences and ‘its almost complete failure’ to elucidate the causes and guide the diagnosis and treatment of psychiatric disorders (4). Psychiatry increasingly worries about its own status as a clinical profession (5), partly due to vigorous attacks from a reborn antipsychiatry, this time originating from within the academia. The research stagnation has generated diverse criticisms of psychiatric classifications, together with proposals to focus elsewhere, for example, on domains of psychopathology (e.g. depression, reality distortion), proxy-variables (e.g. endo-phenotypes), or behavioral constructs with known neural bases (e.g. the RDoC: negative/positive valence systems, arousal/regulatory systems) (see 6). We suggest a somewhat different approach to psychiatry’s current impasse (7). A cardinal problem, in our view, is that our very conception of psychiatry’s object of study has been vastly oversimplified, and that this oversimplification has been reinforced by reliance on methodologies that are unable, because unsuited, to capture the distinctions in experience and expression that constitute the essentials of the ‘psychiatric object’. It is worthwhile to recall that the ‘operational’ criteria are not, in fact, operational in their original sense of specifying action rules, linking psychiatric concepts with their counterparts in reality (operations, as in: ‘X is harder than Y because X can make a scratch on Y, but not vice versa’). What the adjective ‘operational’ actually amounts to, despite its air of scientific precision, is no more than simplified, lay-language, common-sense descriptions of symptoms and signs, which are, moreover, occasionally phenomenologically incorrect (8). A general account of consciousness, its form of being, its structure, its aspects or phenomena (symptoms, signs, existential patterns), and a discussion of how to adequately address and translate the patient’s experience, lived in the first person perspective, into a third-person, sharable-objective format for use in diagnosis and treatment, can nowhere be found in the today’s literature (7). This is in a stark contrast with contemporary neuroscience, cognitive science, developmental psychology,


Frontiers in Human Neuroscience | 2017

Genetics of Schizophrenia: Overview of Methods, Findings and Limitations

Mads Gram Henriksen; Julie Nordgaard; Lennart Jansson

Genetics constitute a crucial risk factor to schizophrenia. In the last decade, molecular genetic research has produced novel findings, infusing optimism about discovering the biological roots of schizophrenia. However, the complexity of the object of inquiry makes it almost impossible for non-specialists in genetics (e.g., many clinicians and researchers) to get a proper understanding and appreciation of the genetic findings and their limitations. This study aims at facilitating such an understanding by providing a brief overview of some of the central methods and findings in schizophrenia genetics, from its historical origins to its current status, and also by addressing some limitations and challenges that confront this field of research. In short, the genetic architecture of schizophrenia has proven to be highly complex, heterogeneous and polygenic. The disease risk is constituted by numerous common genetic variants of only very small individual effect and by rare, highly penetrant genetic variants of larger effects. In spite of recent advances in molecular genetics, our knowledge of the etiopathogenesis of schizophrenia and the genotype-environment interactions remain limited.


Cephalalgia | 2014

Phosphodiesterases 3 and 5 express activity in the trigeminal ganglion and co-localize with calcitonin gene-related peptide

Julie Nordgaard; Lars Schack Kruse; Morten Møller; Christina Kruuse

Background Understanding of the neuropathology leading to migraine pain has centered on either a vascular or neuronal origin. Sildenafil, a specific inhibitor of phosphodiesterase 5 (PDE5), induces migraine-like headache in a human headache model without concomitant artery dilation. The presence and activity of PDE3 and PDE5 is known in cerebral arteries. However, the presence in the neuronal part of the trigeminovascular pathway, i.e. the trigeminal ganglion and the possible co-localization with calcitonin gene-related peptide (CGRP), is not known. Methods Rat trigeminal ganglia were isolated and immunohistochemistry and in situ hybridization was applied. Evaluations of cyclic adenosine monophosphate (cAMP) and cyclic guanosine monophosphate (cGMP) hydrolysis were performed using scintillation proximity assays. Results PDE3 and PDE5 were present and active in the trigeminal ganglia. A subset of PDE3- and PDE5-positive neurons contained CGRP. In contrast to cGMP, both sildenafil and cilostazol influenced cAMP hydrolysis. Interpretation Sildenafil may exert its effect on the neuronal part of the migraine pain pathway. In addition to the effects on cGMP signaling, sildenafil may indirectly affect cAMP signaling in the trigeminal ganglion. This result may suggest a common cAMP-related pathway for sildenafil, cilostazol, and CGRP in eliciting migraine pain.


Archive | 2016

Self-Disorders in Schizophrenia

Mads Gram Henriksen; Julie Nordgaard

The notion of disordered self as the core, trait-phenotypic disturbance of schizophrenia was ventilated in nearly all foundational texts on schizophrenia, and it is strongly supported by recent empirical studies. In this chapter, we introduce the reader to a variety of clinical manifestations of self-disorders in single, comprehensive case story, which we subsequently analyze in the light of contemporary phenomenological research. We also briefly address the psychopathological core that appears to underlie the various manifestations of self-disorders. Moreover, we provide a dense overview of the results from empirical studies, and we discuss the adequate way of assessing self-disorders in the psychiatric interview. We conclude that self-disorders are crucial elements in the psychopathology of schizophrenia and that they may aid the understanding of our patients and their experiential life, play a significant role in diagnostic and differential diagnostic procedures, and offer vital resources for a more phenomenologically informed psychotherapy for schizophrenia.


Psychopathology | 2015

Self-Disorders, Neurocognition and Rationality in Schizophrenia: A Preliminary Study

Julie Nordgaard; Rasmus Revsbech; Mads Gram Henriksen

Background/Aims: Although the very idea that the generative disorder in schizophrenia is a disturbance of the self is as old as the schizophrenia concept itself, empirical studies have only recently emerged, documenting that anomalous self-experiences (i.e. self-disorders, SDs) aggregate in schizophrenia spectrum disorders but not in other mental disorders. The aim of this study is to explore potential associations between SDs, neurocognitive performance, rationality and IQ in patients with schizophrenia. Methods: The sample comprises 31 patients diagnosed with schizophrenia (DSM-IV). All patients underwent comprehensive evaluation. SDs were assessed with the Examination of Anomalous Self-Experience scale. Neurocognitive performance was measured with 4 PC-implemented subtests from the Cambridge Neuropsychological Test Automated Battery. Rationality was measured using syllogism tests. The IQ was indexed by a summary score of 4 IST-2000-R computerized subtests. Results: No correlation was found between SDs and neurocognitive performance or between SDs and IQ. SDs were found to correlate with rationality. Neurocognitive performance correlated with rationality, and both correlated with IQ, respectively. Conclusions: The lack of correlation between SDs and neurocognitive performance is consistent with the results from the only previous study exploring this issue, suggesting that SDs depict something essential to schizophrenia, whereas neurocognitive impairment does not. The correlation between SDs and rationality indicates that the syllogism tests reflect something central for schizophrenia, but the result needs further corroboration from larger, empirical studies.


Psychopathology | 2017

Panic, Self-Disorder, and EASE Research: Methodological Considerations

Josef Parnas; Julie Nordgaard; Mads Gram Henriksen

cusing also on schizotypal traits, would be necessary. For example, one study demonstrated that healthy subjects with few schizotypal traits (not warranting a clinical diagnosis) score higher on self-disorders than healthy subjects completely free of schizotypal features [9] . In the study by Madeira et al. [1] , diagnoses were allocated by treating clinicians, using the MINI, and the patients were not diagnosed by a thorough in-depth psychopathological research assessment. In fact, European clinicians practically never use the diagnosis of schizotypal disorder with the few exceptions of university clinics with a long track record of research on schizophrenia spectrum disorders [10] . The use of the MINI is not a safeguard – on the contrary, as is explicitly stated in the MINI 5.0.0 manual (July 1, 2006): “This program is not designed or intended to be used in the place of a full medical and psychiatric evaluation by a qualified licensed physician-psychiatrist.” Moreover, the MINI does not address personality disorders, including DSM schizotypal disorder. Thus, with respect to the sample, we are left with a group of chronic patients, whose diagnostic profile is basically unclear and who were certainly not screened for schizotypal features. If we look at the self-disorders scored in this sample, it is peculiar that none of the patients was found to be psychotic or schizotypic, given the fact that all experiential schizotypal items are present in the EASE and several patients had first-rank symptoms (EASE item 1.7.3) or delusional Isplit (EASE item 2.7.4). Madeira et al. [1] report high levels of EASE-measured self-disorders in a sample of chronic, treatmentresistant, panic disorder (PD) patients without a comorbid diagnosis ( n = 47) and compared to populationdrawn controls ( n = 47). They motivate their study by considering self-disorders as a potentially “transdiagnostic” phenotype and seem basically to show that their patient group exhibits self-disorder scores on a similar level as that reported in schizophrenia spectrum patients [2–6] . Our commentary is prompted by a concern about the potential confusion the study [1] may bring about in this research field. Instead of perceiving self-disorders as a transdiagnostic feature, as the authors seem to do, it is perhaps more appropriate to consider anxiety and panic as transdiagnostic features. DSM-5 explicitly states: “Panic disorder infrequently occurs in clinical settings in the absence of other psychopathology” [7] . Several studies have shown that PD patients show comorbidity in 80% of cases and that the PD diagnosis massively increases the odds ratio (OR = 35.66) for comorbid psychosis [8] . In other words, the sample in Madeira et al. [1] is peculiar with regard to the total absence of comorbidity. Another crucial issue concerns the diagnostic assessment of this sample. If the motivation of the study was to explore the presence of self-disorders beyond the schizophrenia spectrum, then a systematic and comprehensive, in-depth psychopathological research assessment of the study population, foReceived: March 9, 2017 Accepted after revision: March 16, 2017 Published online: April 11, 2017

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Josef Parnas

University of Copenhagen

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Ditte Sæbye

University of Copenhagen

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Helene Stephensen

Copenhagen University Hospital

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Kasper Jessen

University of Copenhagen

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