The clinical and prognostic value of motor abnormalities in psychosis, and the importance of instrumental assessment

Harten, Peter N. van; Walther, Sebastian; Kent, Jerillyn S.; Sponheim, Scott R.; Mittal, Vijay A.

doi:10.1016/j.neubiorev.2017.06.007

Cited by 80 publications

(82 citation statements)

References 104 publications

(164 reference statements)

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“…Next, a GO stimulus appeared for a duration of 500-850 ms (length of time varied by participant). Fz and Cz electrodes were examined for the N2 component because inhibition-related N2 has historically been characterized as a frontocentral component (Hughes et al, 2012;Kok et al, 2004;Ramautar et al, 2006;van Boxtel et al, 2001). If no response or an incorrect response occurred during Go trials, then the crosshairs turned red for the 200 ms after the GO stimulus disappeared.…”

Section: Lateralized Readiness Potential Analysismentioning

confidence: 99%

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Abnormal neural functions associated with motor inhibition deficits in schizophrenia and bipolar disorder

Voorhis

Kent

Kang

et al. 2019

Human Brain Mapping

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Deficits in response inhibition have been observed in schizophrenia and bipolar disorder; however, the neural origins of the abnormalities and their relevance to genetic liability for psychosis are unknown. We used a stop‐signal task to examine motor inhibition and associated neural processes in schizophrenia patients (n = 57), bipolar disorder patients (n = 21), first‐degree biological relatives of patients with schizophrenia (n = 34), and healthy controls (n = 56). Schizophrenia patients demonstrated motor control deficits reflected in longer stop‐signal reaction times and elongated reaction times. With the possibility of needing to inhibit a button press, both schizophrenia and bipolar disorder patients showed diminished reductions of the P300 brain response and only the healthy controls demonstrated adjustments in response execution time, as measured by response‐locked lateralized readiness potentials. Schizotypal traits in the biological relatives were associated with less P300 modulation consistent with the motor‐related anomalies being associated with subtle schizophrenia‐spectrum symptomatology in family members. The two patient groups had elongated response selection processes as manifest in the delayed onset of the stimulus‐locked lateralized readiness potential. The bipolar disorder group was unique in showing significantly diminished neural responses to the stop‐signal to inhibit a response. Antipsychotic medication dosage was related to worse motor inhibition, thus motor inhibition deficits in schizophrenia may be partially explained by the effect of pharmacological agents. Failed modulation of brain processes in relation to response inhibition probability and the lengthening of motor response selection appear to be transdiagnostic abnormalities spanning schizophrenia and bipolar disorder.

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Section: Lateralized Readiness Potential Analysismentioning

confidence: 99%

“…Finally, the N2 component precedes the P300 and has been found to be particularly important to stop-signal processing (van Boxtel, van der Molen, Jennings, & Brunia, 2001). N2s during failures of inhibition are later and larger than during successful inhibition of responses Ramautar et al, 2004).…”

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confidence: 94%

Abnormal neural functions associated with motor inhibition deficits in schizophrenia and bipolar disorder

Voorhis

Kent

Kang

et al. 2019

Human Brain Mapping

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“…Motor abnormalities are increasingly being recognized as markers for the risk of psychosis or course of schizophrenia [105, 106], as they occur in healthy first-degree relatives of patients with schizophrenia [107] and in subjects at a clinically high risk of developing psychoses [108, 109]. They predict poor cognitive outcomes in first-episode patients [110].…”

Section: Mapping Symptoms Onto Brain Systems: Empirical Evidence For mentioning

confidence: 99%

Systems Neuroscience of Psychosis: Mapping Schizophrenia Symptoms onto Brain Systems

et al. 2017

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Schizophrenia research has been in a deadlock for many decades. Despite important advances in clinical treatment, there are still major concerns regarding long-term psychosocial reintegration and disease management, biological heterogeneity, unsatisfactory predictors of individual course and treatment strategies, and a confusing variety of controversial theories about its etiology and pathophysiological mechanisms. In the present perspective on schizophrenia research, we first discuss a methodological pitfall in contemporary schizophrenia research inherent in the attempt to link mental phenomena with the brain: we claim that the time-honored phenomenological method of defining mental symptoms should not be contaminated with the naturalistic approach of modern neuroscience. We then describe our Systems Neuroscience of Psychosis (SyNoPsis) project, which aims to overcome this intrinsic problem of psychiatric research. Considering schizophrenia primarily as a disorder of interindividual communication, we developed a neurobiologically informed semiotics of psychotic disorders, as well as an operational clinical rating scale. The novel psychopathology allows disentangling the clinical manifestations of schizophrenia into behavioral domains matching the functions of three well-described higher-order corticobasal brain systems involved in interindividual human communication, namely, the limbic, associative, and motor loops, including their corticocortical sensorimotor connections. The results of several empirical studies support the hypothesis that the proposed three-dimensional symptom structure, segregated into the affective, the language, and the motor domain, can be specifically mapped onto structural and functional abnormalities of the respective brain systems. New pathophysiological hypotheses derived from this brain system-oriented approach have helped to develop and improve novel treatment strategies with noninvasive brain stimulation and practicable clinical parameters. In clinical practice, the novel psychopathology allows confining the communication deficits of the individual patient, shifting attention from the symptoms to the intact resources. We have studied this approach and observed important advantages for therapeutic alliances, personalized treatment, and de-escalation strategies. Future studies will further conjoin clinical definitions of psychotic symptoms with brain structures and functions, and disentangle structural and functional deficit patterns within these systems to identify neurobiologically distinct subsyndromes. Neurobiologically homogeneous patient groups may provide new momentum for treatment research. Finally, lessons learned from schizophrenia research may contribute to developing a comprehensive perspective on human experience and behavior that integrates methodologically distinct, but internally consistent, insights from humanities and neuroscience.

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“…Dyskinesia is also present in antipsychotic-naive patients with psychotic disorders 2. It has been suggested that ‘spontaneous dyskinesia’ in antipsychotic-naive patients should be considered as a symptom of psychotic disorders 3. Since there is no test, in patients using antipsychotics, to differentiate between drug-induced and ‘spontaneous’ dyskinesia, studies for TD will include both.…”

Section: Limitationsmentioning

confidence: 99%

There has been very little progress in treating or preventing antipsychotic-induced tardive dyskinesia

Harten

2018

Evid Based Mental Health

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The clinical and prognostic value of motor abnormalities in psychosis, and the importance of instrumental assessment

Cited by 80 publications

References 104 publications

Abnormal neural functions associated with motor inhibition deficits in schizophrenia and bipolar disorder

Abnormal neural functions associated with motor inhibition deficits in schizophrenia and bipolar disorder

Systems Neuroscience of Psychosis: Mapping Schizophrenia Symptoms onto Brain Systems

There has been very little progress in treating or preventing antipsychotic-induced tardive dyskinesia

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