RESUMEN
The current understanding of major depressive disorder (MDD) and bipolar disorder (BD) is plagued by a cacophony of controversies as evidenced by competing schools to understand MDD/BD. The DSM/ICD taxonomies have cemented their status as the gold standard for diagnosing MDD/BD. The aim of this review is to discuss the false dogmas that reign in current MDD/BD research with respect to the new, data-driven, machine learning method to model psychiatric illness, namely nomothetic network psychiatry (NNP). This review discusses many false dogmas including: MDD/BD are mind-brain disorders that are best conceptualized using a bio-psycho-social model or mind-brain interactions; mood disorders due to medical disease are attributable to psychosocial stress or chemical imbalances; DSM/ICD are the gold standards to make the MDD/BD diagnosis; severity of illness should be measured using rating scales; clinical remission should be defined using threshold values on rating scale scores; existing diagnostic BD boundaries are too restrictive; and mood disorder spectra are the rule. In contrast, our NNP models show that MDD/BD are not mind-brain or psycho-social but systemic medical disorders; the DSM/ICD taxonomies are counterproductive; a shared core, namely the reoccurrence of illness (ROI), underpins the intertwined recurrence of depressive and manic episodes and suicidal behaviors; mood disorders should be ROI-defined; ROI mediates the effects of nitro-oxidative stress pathways and early lifetime trauma on the phenome of mood disorders; severity of illness and treatment response should be delineated using the NNP-derived causome, pathway, ROI and integrated phenome scores; and MDD and BD are the same illness.
RESUMEN
Psychiatry remains in a permanent state of crisis, which fragmented psychiatry from the field of medicine. The crisis in psychiatry is evidenced by the many different competing approaches to psychiatric illness including psychodynamic, biological, molecular, pan-omics, precision, cognitive and phenomenological psychiatry, folk psychology, mind-brain dualism, descriptive psychopathology, and postpsychiatry. The current "gold standard" Diagnostic and Statistical Manual of Mental Disorders/International Classification of Diseases taxonomies of mood disorders and schizophrenia are unreliable and preclude to employ a deductive reasoning approach. Therefore, it is not surprising that mood disorders and schizophrenia research was unable to revise the conventional classifications and did not provide more adequate therapeutic approaches. The aim of this paper is to explain the new nomothetic network psychiatry (NNP) approach, which uses machine learning methods to build data-driven causal models of mental illness by assembling risk-resilience, adverse outcome pathways (AOP), cognitome, brainome, staging, symptomatome, and phenomenome latent scores in a causal model. The latter may be trained, tested and validated with Partial Least Squares analysis. This approach not only allows to compute pathway-phenotypes or biosignatures, but also to construct reliable and replicable nomothetic networks, which are, therefore, generalizable as disease models. After integrating the validated feature vectors into a well-fitting nomothetic network, clustering analysis may be applied on the latent variable scores of the R/R, AOP, cognitome, brainome, and phenome latent vectors. This pattern recognition method may expose new (transdiagnostic) classes of patients which if cross-validated in independent samples may constitute new (transdiagnostic) nosological categories.
RESUMEN
BACKGROUND: Over the past decade, resting-state functional magnetic resonance imaging (rs-fMRI) has concentrated on brain networks such as the default mode network (DMN), the salience network (SN), and the central executive network (CEN), allowing for a better understanding of cognitive deficits observed in mental disorders, as well as other characteristic psychopathological phenomena such as thought and behavior disorganization. AIM: To investigate differential patterns of effective connectivity across distributed brain networks involved in schizophrenia (SCH) and mood disorders. METHODS: The sample comprised 58 patients with either paranoid syndrome in the context of SCH (n = 26) or depressive syndrome (Ds) (n = 32), in the context of major depressive disorder or bipolar disorder. The methods used include rs-fMRI and subsequent dynamic causal modeling to determine the direction and strength of connections to and from various nodes in the DMN, SN and CEN. RESULTS: A significant excitatory connection from the dorsal anterior cingulate cortex to the anterior insula (aI) was observed in the SCH patient group, whereas inhibitory connections from the precuneus to the ventrolateral prefrontal cortex and from the aI to the precuneus were observed in the Ds group. CONCLUSION: The results delineate specific patterns associated with SCH and Ds and offer a better explanation of the underlying mechanisms of these disorders, and inform differential diagnosis and precise treatment targeting.
