Motor Impairment and Developmental Psychotic Risk: Connecting the Dots and Narrowing the Pathophysiological Gap

Abstract

The motor system in its manifold articulations is receiving increasing clinical and research attention. This is because motor impairments constitute a central, expressive component of the mental state examination and a key transdiagnostic feature indexing disease severity. Furthermore, within the schizophrenia spectrum, the integration of neurophysiological, developmental, and phenomenological perspectives suggests that motor impairment is not simply a generic, extrinsic proxy of an altered neurodevelopment, but might be more intimately related to psychotic risk. Therefore, an increased understanding, conceptualization, and knowledge of such motor system and its anomalies could empower contemporary risk prediction and diagnostic procedures.

Along the fringes of Agency: neurodevelopmental account of the obsessive mind

“…A pathogenetic cascade partly echoing the putative one of obsessive mind has been proposed for the neurodevelopment of the psychotic mind (ie, from early childhood alterations of CD signals to distal psychotic symptoms as passivity delusions and auditory verbal hallucinations, through intermediate phenomena represented by an altered implicit SoA and anomalous self-experiences). 32,49,50 In this perspective, the hypothesis of a neurodevelopmentally determined dimensional gradient of altered sensorimotor prediction may offer a pathophysiological bridge between OCD and schizophrenia spectrum disorder, that 1) are epidemiologically associated above chance, [51][52][53] 2) present a partial polygenic overlap, 54 and 3) are clinically overlapping in terms of obsessive-compulsive features in the schizophrenia spectrum and increased schizotypy in OCD, [55][56][57][58] supporting the hypothesis of a schizo-obsessive spectrum. 59 Subjective effects of altered sensorimotor predictions, indeed, cannot be considered all-or-none phenomena 60 : the failure of sensorimotor prediction that conditions the development of both altered SoA and SoO may represent a substrate for the progressive build-out of the psychotic mind; on the contrary, milder alterations of sensorimotor predictions (and related attenuation of SoA associated with preserved SoO) may represent an enabling condition for the development of the obsessive mind.…”

Reduced readiness potential and post-movement beta synchronization reflect self-disorders in early course schizophrenia

“…Specifically, RP and ERS abnormalities may be associated with the motor neurological soft signs often seen in the prodromal stages of SCZ spectrum disorders 74 , 75 , and that were recently linked to a higher risk of a chronic course of illness after a first psychotic episode 76 . Interestingly, Poletti et al recently argued that CD mechanisms are likely to develop in early childhood and that abnormalities in this neurophysiological domain may represent an early trace (and, putatively, a core pathophysiological mechanism) of SCZ 25 . In this perspective, the clinical relevance of RP and ERS in the prodromal stages of psychosis should be further investigated by future studies.…”

“…For instance, EC/CD are affected in the oculomotor system 23 , during talking and inner speech in SCZ patients 24 . These mechanisms could provide a unique translational bridge to explore underlying neurophysiology on one side, and subtle motor abnormalities observed in patients on the other 25 .…”

Neurocognition and Social Cognition Predicting 1-Year Outcomes in First-Episode Psychosis

“…As for factors combining processing speed and negative symptoms, antipsychotic medication may slow down cognitive processes and increase the manifestation of negative symptoms. Also, extrapyramidal symptoms and other motor impairments could have a role in the relationship between cognition and negative symptoms, both as the side effects of antipsychotics and as primary traits in psychotic disorders (64,65). Both a toxic effect of antipsychotic treatment on cognition (66) and a protective effect on it (48,67) have been suggested, but cognitive deficits are also evident in drug-naïve schizophrenia patients (68).…”