Scamvougeras and Castle argue that appeals to dualism are frequently deployed to dismiss psychological explanations in favour of framing functional neurological disorder (FND) as a "brain disorder." Yet participants on all sides of this debate often conflate "dualism" with Cartesian substance dualism. Contemporary philosophy of mind, by contrast, accommodates multi-level, non-reductive accounts that are fully compatible with the brain as the organ of the mind. Positions such as property dualism and non-reductive physicalism demonstrate that recognising psychological mechanisms does not entail commitment to a non-physical substance, nor denial of the dependence of mental processes on brain function. A more pressing question, therefore, is why psychological explanations are resisted at all, given that scientific psychology, as opposed to folk psychology, does not necessarily equate the psychological with conscious will or personal control. We may be better off by ditching debates about dualism and focusing instead on the integration of neurobiological and psychological accounts within evidence-based models of FND, with each explanatory level evaluated on its merits.
This commentary responds to an article by Anton Scamvougeras and David Castle arguing that contemporary accounts of Functional Neurological Disorder (FND) overemphasise neurobiology and that the disorder should be understood primarily as a psychiatric condition. There are areas of agreement, including the need for a biopsychosocial model and acknowledgement that some academic and public discourse about FND has minimised psychological factors. However, proposed distinctions between neurological and psychiatric disorders based on the presence or absence of pathology are conceptually unstable. Many neurological conditions, such as Parkinson's disease and epilepsy, are intrinsically neuropsychiatric, while others, including migraine and Tourette syndrome, lack pathology on standard investigations. FND also raises another fundamental question: whether a neurologist's role is to seek pathological disease or to diagnose and manage neurological symptoms. Claims that current literature promotes a purely biological model are overstated. The proposal that the psychiatric level is the best way in which to understand FND promotes the idea that psychiatric factors are universally explanatory. Instead, the evidence supports a multi-level understanding of the aetiology and mechanisms of FND symptoms, including how they arise from altered brain networks. A non-dualistic framework, as seen, for example, in chronic nociplastic pain, allows a psychiatric perspective to sit alongside a neurobiological one, without one having to dominate the other.
Psychological and psychiatric explanations for Functional Neurological Disorders (FND) are routinely dismissed as embodying "dualism" or "mind-body dualism", strongly implying that any notion of psychogenicity should be rejected outright. This reflects a widespread misunderstanding. DSM5 nomenclature and recent mainstream literature emphasise neurobiological causation - framing FND as a "multi-network brain disorder" or "dysregulation of neural circuitry" - while downplaying psychological formulations, despite high rates of psychiatric symptomatology and the fact that the majority of clinicians worldwide continue to prefer psychogenic models and treatment with psychotherapy. The charge of dualism is misplaced: while Cartesian substance dualism has been correctly rejected by modern neuroscience, the term is now commonly misused to criticise any distinction between neurological and psychiatric causation. We argue that neuropsychiatric conditions exist on a clinically useful continuum from predominantly neurological to predominantly psychiatric/psychological disorders, while fully accepting that all are ultimately brain-based. Psychiatric symptomatology, clinician perspectives, and response to psychological approaches place FND firmly on the psychiatric/psychological side of this continuum. Framing FND as driven by psychological/psychiatric engines offers far greater clinical utility and therapeutic direction than reductionistic neurobiological models. We conclude that psychological/psychiatric conceptualisations remain the most valid and effective framework for understanding and managing FND.
INTRODUCTION:Catatonia is a neuropsychiatric syndrome associated with cognitive impairments, yet the neurocognitive performance of catatonia relative to other psychiatric disorders is poorly understood. This study characterised neurocognitive profiles in patients with a history of catatonia compared to schizophrenia spectrum (SSD), bipolar disorder (BD), and major depressive disorder (MDD) across a comprehensive battery of neuropsychological tests. METHODS:Sixty-seven adults who underwent neuropsychological assessment were classified into catatonia (n = 10), SSD (n = 23), BD (n = 19), and MDD (n = 15) groups. Composite z-scores were generated across six domains: language, visuospatial skills, memory, attention, processing speed, and executive functioning. RESULTS:Global neurocognitive functioning was similar, and approximated population norms, in BD and MDD, but significantly lower in catatonia (z = -1.63) and SSD (z = -1.14) groups. Significant differences emerged in overall neurocognitive scores (ηp2 = .47) and memory, attention, processing speed, executive functioning (ηp² = 0.30-0.41), but not language. Post hoc tests showed MDD and BD outperformed SSD and catatonia groups, with no differences within these pairs. Neurobehavioural examinations distinguished catatonia from SSD by increased affective blunting, withdrawal, psychomotor slowing, and slow mentation. CONCLUSIONS:Catatonia is associated with substantial neurocognitive impairment, most similar to SSD, but with distinct neurobehavioural features. Routine screening and targeted neurocognitive assessment may enhance diagnosis and understanding of catatonia.
Introduction: A vast body of cognitive research in psychosis has focused on auditory hallucinations, though more recent studies are turning towards other sensory modalities. This study aimed to compare the cognitive profile of persons experiencing uni- or multisensory versus multimodal hallucinations. Methods: Participants with primary diagnosis of a psychotic disorder were subdivided into those experiencing uni- or multisensory (UMS; n = 31) versus multimodal (MM; n = 28) hallucinations relative to non-clinical controls (NC; n = 32). Cognitive assessment comprised the MATRICS Consensus Cognitive Battery, supplemented by a Colour Word Interference Test. Analyses of variance (ANOVAs) and correlation analyses were performed. Results: The UMS and MM groups performed significantly worse than the NC group on some cognitive domains (i.e. speed of processing, attention/vigilance, working memory, verbal learning), but not others (i.e. reasoning and problem-solving, social cognition). For visual learning, the MM group performed significantly worse than the NC group only, whereas for inhibition, the UMS group performed significantly worse than the NC group only. Conclusion: A novel cognitive profile associated with multimodal hallucinations was documented. Dissociation between performance of the two clinical groups on visual learning and inhibition suggests these cognitive domains may be of relevance to hallucinations, pending further investigations.
