Dr hab. Łukasz Gawęda, wspólnie z zespołem z Centre for Youth Mental Health, The University of Melbourne, Australia (Prof. Barnaby Nelson) opublikował współautorską pracę („The neurophenomenology of early psychosis: An integrative empirical study”) na temat neuropoznawczego modelu zaburzeń poczucia Ja (self-disturbances) w stanach klinicznego ryzyka psychozy. W pracy wykazano związku trudności różnicowania wyobrażeń od rzeczywistości z zaburzeniami poczucia Ja u pacjentów doświadczających subklinicznych objawów psychotycznych. Praca stanowi element szerszego projektu realizowanego we współpracy międzynarodowej przez Prof. Nelsona, którego celem jest poszukiwanie neuropoznawczych i neurofizjologicznych wskaźników zaburzeń poczucia Ja we wczesnych etapach rozwoju zaburzeń psychotycznych i ich stanów ryzyka.
Zapraszamy do lektury:
https://www.sciencedirect.com/science/article/pii/S1053810019302284
Abstract:
Background: The integration of various domains or levels of analysis (clinical, neurobiological, genetic, etc.) has been a challenge in schizophrenia research. A promising approach is to use the core phenomenological features of the disorder as an organising principle for other levels of analysis. Minimal self-disturbance (fragility in implicit first-person perspective, presence and agency) is emerging as a strong candidate to play this role. This approach was adopted in a previously described theoretical neurophenomenological model that proposed that source monitoring deficits and aberrant salience may be neurocognitive/neurobiological processes that correlate with minimal self-disturbance on the phenomenological level, together playing an aetiological role in the onset of schizophrenia spectrum disorders. The current paper presents full cross-sectional data from the first empirical test of this model.
Methods: Fifty ultra-high risk for psychosis patients, 39 first episode psychosis patients and 34 healthy controls were assessed with a variety of clinical measures, including the Examination of Anomalous Self-Experience (EASE), and neurocognitive and neurophysiological (EEG) measures of source monitoring deficits and aberrant salience.
Results: Linear regression indicated that source monitoring (composite score across neurocognitive and neurophysiological measures), with study group as an interaction term, explained 39.8% of the variance in EASE scores (R2 = 0.41, F(3,85) = 14.78, p < 0.001), whereas aberrant salience (composite score) explained only 6% of the variance in EASE scores (R2 = 0.06, F(3,85) = 1.44, p = 0.93). Aberrant salience measures were more strongly related to general psychopathology measures, particularly to positive psychotic symptoms, than to EASE scores.
Discussion: A neurophenomenological model of minimal self-disturbance in schizophrenia spectrum disorders may need to be expanded from source monitoring deficits to encompass other relevant constructs such as temporal processing, intermodal/multisensory integration, and hierarchical predictive processing. The cross-sectional data reported here will be expanded with longitudinal analysis in subsequent reports. These data and other related recent research show an emerging picture of neuro-features of core phenomenological aspects of schizophrenia spectrum disorders beyond surface-level psychotic symptoms.