Structural alterations of the motor cortex and higher order cortical areas suggest early neurodevelopmental origin of catatonia in schizophrenia

Walther, Sebastian; Nadesalingam, Niluja; Nuoffer, Melanie G; Kyrou, Alexandra; Wüthrich, Florian; Lefebvre, Stéphanie

doi:10.1016/j.schres.2022.10.004

Cited by 9 publications

(7 citation statements)

References 45 publications

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“…Aberrant gait might be a result of the well-known motor system dysfunction in schizophrenia. Motor abnormalities have been linked to abnormal brain structure 44,45 and connectivity 46 within the motor network, including the cerebellum 47 . Aberrant functional connectivity in the motor system in schizophrenia 46,48 correlated with behavioural motor abnormalities, suggesting that the motor system in schizophrenia might be out of balance 46,48,49 .…”

Section: Discussionmentioning

confidence: 99%

Psychomotor slowing alters gait velocity, cadence, and stride length and indicates negative symptom severity in psychosis

et al. 2022

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Schizophrenia is a severe mental disorder, in which 50% of the patients present with motor abnormalities such as psychomotor slowing. Slow spontaneous gait has been reported in schizophrenia. However, comprehensive objective instrumental assessments of multiple gait conditions are missing. Finally, the specific gait patterns of subjects with psychomotor slowing are still unknown. Therefore, this study aimed to objectively assess multiple gait parameters at different walking conditions in patients with schizophrenia with and without psychomotor slowing. Also, we hypothesised gait impairments to correlate with expert ratings of hypokinetic movement disorders and negative symptoms. We collected gait data (GAITRite®) in 70 patients with psychomotor slowing (SRRS (Salpetriere retardation rating scale) ≥15), 22 non-psychomotor slowed patients (SRRS < 15), and 42 healthy controls. Participants performed four walking conditions (self-selected speed, maximum speed, head reclined, and eyes closed) and six gait parameters were extracted (velocity, cadence, stride length, functional ambulation profile (FAP), and variance of stride length and time). Patients with psychomotor slowing presented slower velocity, lower cadence, and shorter stride length in all walking conditions compared to healthy controls, with the non-slowed patients in an intermediate position (all F > 16.18, all p < 0.001). Secondly, slower velocity was associated with more severe hypokinetic movement disorders and negative symptoms. In conclusion, gait impairments exist in a spectrum with healthy controls on one end and patients with psychomotor slowing on the other end. Patients with psychomotor slowing are specifically impaired when an adaptation of gait patterns is required, contributing to the deleterious effects of sedentary behaviours.

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Section: Discussionmentioning

confidence: 99%

Psychomotor slowing alters gait velocity, cadence, and stride length and indicates negative symptom severity in psychosis

et al. 2022

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“…A proportion of this sample was included in reports on grey matter structure in catatonia or structural brain correlates of formal thought disorder. 60 , 61 …”

Section: Methodsmentioning

confidence: 99%

The pathobiology of psychomotor slowing in psychosis: altered cortical excitability and connectivity

Lefebvre,

Gehrig,

Nadesalingam

et al. 2023

Brain

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Psychomotor slowing is a frequent symptom of schizophrenia. Short-interval intracortical inhibition assessed by transcranial magnetic stimulation demonstrated inhibitory dysfunction in schizophrenia. The inhibitory deficit results from additional noise during information processing in the motor system in psychosis. Here, we tested whether cortical inhibitory dysfunction was linked to psychomotor slowing and motor network alterations. In this cross-sectional study, we included 60 patients with schizophrenia and psychomotor slowing determined by the Salpetriere Retardation Rating Scale, 23 patients without slowing and 40 healthy controls, we acquired single and double-pulse transcranial magnetic stimulation effects from the left primary motor cortex, resting-state functional connectivity, and diffusion imaging on the same day. Groups were compared on resting motor threshold, amplitude of the motor evoked potentials, as well as short-interval intracortical inhibition. Regression analyses calculated the association between motor evoked potential amplitudes or cortical inhibition with seed-based resting-state functional connectivity from the left primary motor cortex and fractional anisotropy at whole brain level and within major motor tracts. In patients with schizophrenia and psychomotor slowing, we observed lower amplitudes of motor evoked potentials, while the short-interval intracortical inhibition/motor evoked potentials amplitude ratio was higher than in healthy controls, suggesting lower cortical inhibition in these patients. Patients without slowing also had lower amplitudes of motor evoked potentials. Across the combined patient sample, cortical inhibition deficits were linked to more motor coordination impairments. In patients with schizophrenia and psychomotor slowing, lower amplitudes of motor evoked potentials were associated with lower fractional anisotropy in motor tracts. Moreover, resting-state functional connectivity between the primary motor cortex, the anterior cingulate cortex and the cerebellum increased with lower cortical inhibition. In contrast, in healthy controls and patients without slowing, stronger cortical inhibition was linked to lower resting-state functional connectivity between the left primary motor cortex and premotor or parietal cortices. Psychomotor slowing in psychosis is linked to less cortical inhibition and aberrant functional connectivity of the primary motor cortex. Higher neural noise in the motor system may drive psychomotor slowing and thus may become a treatment target.

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“…Structural magnetic resonance imaging studies have revealed that catatonia was associated with widespread reductions in gray-matter volume, including in the orbitofrontal, cingulate, and visual cortices and the insula when compared with healthy individuals. Patients with catatonia demonstrated hypergyrification in the motor, premotor, and somatosensory cortices compared with controls; however, no differences in cortical thickness were observed between patients with catatonia and controls[ 29 ]. In addition, patients with catatonia were found to have significantly smaller volumes in the anterior inferior hypothalamus, the cortical nucleus of the amygdala, and the hippocampal fimbria[ 30 ].…”

Section: Research Developments In the Field Of Catatoniamentioning

confidence: 99%

First 150 years of catatonia: Looking back at its complicated history and forward to the road ahead

Csihi,

Ungvari,

Caroff

et al. 2024

World J Psychiatry

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Karl Ludwig Kahlbaum (1828-1899) was the first to conceptualize and describe the main clinical features of a novel psychiatric illness, which he termed catatonia in his groundbreaking monograph published 150 years ago. Although Kahlbaum postulated catatonia as a separate disease entity characterized by psychomotor symptoms and a cyclical course, a close examination of his 26 cases reveals that most of them presented with motor symptom complexes or syndromes associated with various psychiatric and medical conditions. In his classification system, Kraepelin categorized catatonic motor symptoms that occur in combination with psychotic symptoms and typically have a poor prognosis within his dementia praecox (schizophrenia) disease entity. Because of the substantial influence of Kraepelin’s classification, catatonia was predominantly perceived as a component of schizophrenia for most of the 20th century. However, with the advent of the psychopharmacotherapy era starting from the early 1950s, interest in catatonia in both clinical practice and research subsided until the early 2000s. The past two decades have witnessed a resurgence of interest in catatonia. The Diagnostic and Statistical Manual of Mental Disorders Fifth Edition, marked a paradigmatic shift by acknowledging that catatonia can occur secondary to various psychiatric and medical conditions. The introduction of an independent diagnostic category termed “Catatonia Not Otherwise Specified” significantly stimulated research in this field. The authors briefly review the history and findings of recent catatonia research and highlight promising directions for future exploration.

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Structural alterations of the motor cortex and higher order cortical areas suggest early neurodevelopmental origin of catatonia in schizophrenia

Cited by 9 publications

References 45 publications

Psychomotor slowing alters gait velocity, cadence, and stride length and indicates negative symptom severity in psychosis

Psychomotor slowing alters gait velocity, cadence, and stride length and indicates negative symptom severity in psychosis

The pathobiology of psychomotor slowing in psychosis: altered cortical excitability and connectivity

First 150 years of catatonia: Looking back at its complicated history and forward to the road ahead

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