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The investigators recently showed that visuomotor integration was significantly altered in schizophrenic patients during: (i) a grip force task (Teremetz et al., 2014), and (ii) a saccadic paradigm (oculomotor task)(Amado et al., 2008). Given this findings, the investigators propose a combined study of oculomotor and grip force control to better characterize the sensorimotor integration deficit. This approach may allow for identification of behavioural biomarkers of vulnerability to develop schizophrenia.
Full description
1 - Scientific background and rational Use of sensory cues is essential for execution and correction of voluntary movements. The motor areas and their regulation is of special interest in patients with schizophrenia as there is clear evidence of motor abnormalities independent of the effects of antipsychotic medication, even before the onset of the disorder. Sensorimotor abnormalities have been proposed as a valid endophenotype in schizophrenia. Our global objective is to study and provide vulnerability markers for schizophrenia.
2 - Description of the project methodology There is strong evidence for schizophrenia being a neuro-developmental disorder (Rapoport et al., 2005). It has been shown, for many years, that patients with schizophrenia exhibit abnormal patterns of sensorimotor integration (Manschreck et al., 1982), which is the capacity to integrate different sensory stimuli into appropriate motor actions. It is clinically relevant, in terms of early diagnosis and prevention, whether deficient sensorimotor integration is present in the prodromal phase of schizophrenia, and whether this constitutes a vulnerability marker for the disease.
Our global objective is to study the interactions and related substratum of oculomotor movements during force control task.
The secondary objectives:
(i) To show that increased motor noise is indeed present in schizophrenia. (ii) To show by TMS that cortical excitability in the primary motor cortex (M1) is task-modulated and decreased in schizophrenia.
(iii) Assess the role of deficient cortical inhibition in these behavioral deficits To this end, three different groups of subjects will be studied: schizophrenic patients, non-affected siblings, ultra high risk patients, non-treated schizophrenic patients and healthy control subjects.
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Inclusion criteria
All groups:
Group of patient suffering from schizophrenia:
Group of UHR patient:
Exclusion criteria
• All groups:
IQ<70,
Contraindications for TMS protocol: no previous history of neurosurgery or seizures or 1st degree relative with history of seizures, heart disease, drug abuse or addiction in the last 12 months, medications that lower seizure threshold including clozapine, bupropion, méthadone or theophylline.
Metallic implant in head (except dental fillings)
Pacemaker, or other electronic implanted devices
Central neurological disease: parkinsonism, x
Severe heart attack
Instable clinical state (e.g. stroke)
Previous history of drug abuse lasting more than 5 years or during the last year
Life event with a moderate to severe impact
Caffeine intake in the last two hours preceding visuomotor assessment
• Groups of Siblings and Healthy controls:
No previous history of psychiatric disease, psychotic spectrum disorder (according to DIGS 3.0)
No previous history of antipsychotic medication (entire life)
• Groups of UHR patient:
Chlorpromazine dose >100mg over more than 12 weeks
No previous history of autism spectrum disorder, bipolar disorder or diagnozed schizophrenia (according to DSM-IV-TR criteria), isolated anxiety disorders (e.g. social phobia, agoraphobia)
Primary purpose
Allocation
Interventional model
Masking
105 participants in 4 patient groups
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Central trial contact
Isabelle Amado, Dr; Marie GODARD
Data sourced from clinicaltrials.gov
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