Elsevier

Brain and Cognition

Volume 45, Issue 3, April 2001, Pages 325-341
Brain and Cognition

Regular Article
Bimanual Coordination in Chronic Schizophrenia

https://doi.org/10.1006/brcg.2000.1261Get rights and content

Abstract

Anomalies of movement are observed both clinically and experimentally in schizophrenia. While the basal ganglia have been implicated in its pathogenesis, the nature of such involvement is equivocal. The basal ganglia may be involved in bimanual coordination through their input to the supplementary motor area (SMA). While a neglected area of study in schizophrenia, a bimanual movement task may provide a means of assessing the functional integrity of the motor circuit. Twelve patients with chronic schizophrenia and 12 matched control participants performed a bimanual movement task on a set of vertically mounted cranks at different speeds (1 and 2 Hz) and phase relationships. Participants performed in-phase movements (hands separated by 0°) and out-of-phase movements (hands separated by 180°) at both speeds with an external cue on or off. All participants performed the in-phase movements well, irrespective of speed or cueing conditions. Patients with schizophrenia were unable to perform the out-of-phase movements, particularly at the faster speed, reverting instead to the in-phase movement. There was no effect of external cueing on any of the movement conditions. These results suggest a specific problem of bimanual coordination indicative of SMA dysfunction per se and/or faulty callosal integration. A disturbance in the ability to switch attention during the out-of-phase task may also be involved.

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    • Alteration of rhythmic unimanual tapping and anti-phase bimanual coordination in Alzheimer's disease: A sign of inter-hemispheric disconnection?

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      Specific changes in anti-phase coordination are found in schizophrenia (Bellgrove et al., 2001), Huntington’s disease (Johnson et al., 2000) and PD (Almeida & Brown, 2013; Almeida, Wishart, & Lee, 2002; Johnson et al., 1998; Ponsen et al., 2006; Verheul & Geuze, 2004; Wu, Wang, Hallett, Li, & Chan, 2010). Even if bilateral dysfunction of the SMA and its input regions (e.g., basal ganglia) cannot be excluded (Johnson et al., 2000; Potgieser, de Jong, Wagemakers, Hoving, & Groen, 2014), specific alteration of anti-phase coordination in these patient populations has been explained by faulty IHT via the CC (Almeida & Brown, 2013; Bellgrove et al., 2001; Bonzano et al., 2008; Caeyenberghs et al., 2011; Larson et al., 2002; Potgieser et al., 2014; Wu et al., 2010). Another important finding is that difficulty in producing anti-phase coordination worsens when visual information is withdrawn, i.e., when study subjects are asked to continue producing coordination without external stimulation.

    • Interactions between brain structure and behavior: The corpus callosum and bimanual coordination

      2014, Neuroscience and Biobehavioral Reviews
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      A large number of pathologies are characterized by white matter alterations, including the CC, such as multiple sclerosis (MS) (Audoin et al., 2007; Bonzano et al., 2008; Brown et al., 2010; Evangelou et al., 2000; Llufriu et al., 2012; Pelletier et al., 1993; e.g., Ranjeva et al., 2003; Scherer et al., 1997), traumatic brain injury (TBI) (for reviews see Bigler and Maxwell, 2011; Hulkower et al., 2013; Levin et al., 2000), schizophrenia (for reviews see Innocenti et al., 2003; Samartzis et al., 2014), cerebral microangiopathy (CMA) (Meguro et al., 2000) and developmental disorders like preterm birth, fetal alcohol syndrome, dyslexia, attention-deficit hyperactivity disorder and Tourette's (for a review on developmental disorders see Paul, 2011). In almost all of these pathologies, deficits in bimanual coordination have indeed been established and were interpreted as a possible result of CC deterioration/malformation (Bellgrove et al., 2001; Klimkeit et al., 2004; Margolis et al., 2006; Roebuck-Spencer et al., 2004; Schneider et al., 2008; Willford et al., 2010). A more ‘definite’ link between bimanual coordination deficits and CC alterations has, however, only been established in patients with MS, TBI and CMA.

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    We gratefully acknowledge the assistance of the staff and patients of the Adult Mental Health Rehabilitation Unit at Sunshine Hospital and the Park St. Community Care Unit, Parkville.

    Address correspondence and reprint requests to Mark A. Bellgrove, Department of Psychology, Monash University, Clayton VIC 3168, Australia. Fax: +61-9905 3948.

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