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Ideomotor apraxia, a disorder that affects patients with stroke and a variety of other brain lesions, features disturbed timing, sequence, and spatial organization of skilled movements. This study will look at how different areas of the human brain control fine hand movements.
Thirty-five participants 21 years and older will be enrolled in this study-25 healthy, right-handed people, and 10 stroke patients. They will undergo two outpatient sessions, each lasting up to 3 hours. The first visit for the stroke patients will occur between 2 weeks and 3 months after the stroke; the second visit will be at least 6 months after the stroke.
Participants will have a physical exam, give a medical history, and complete a questionnaire. Then they will undergo magnetic resonance imaging (MRI) scans. They will lie in the MRI scanner and will be asked to do a number of skilled hand movements using the right hand (such as pretending to use a hammer or waving goodbye) in response to directions that will appear on a screen mounted over their head. Their movements will be recorded on videotape during the procedures.
OBJECTIVE: The present study focuses on evaluating neural activation patterns underlying praxis movements in normal controls and in patients with ideomotor apraxia using event-related functional magnetic resonance imaging (fMRI). Ideomotor apraxia is a disorder affecting patients with stroke and a variety of other brain lesions. The disorder involves disturbed timing, sequence, and spatial organization of skilled movements, during the execution and probably also preparatory phases. As a consequence, patients suffer from incorrect temporal and spatial components to movements as evidenced during pantomime of transitive (object/tool related) and intransitive (independent of object/tool use) gestures. Thus far, damage to posterior parietal regions and parietofrontal circuits has been implicated in significantly contributing to this disorder. However, little is known about the mechanism of cortical reorganization following damage, notably during recovery process. We hypothesize that recruitment of parallel and contralateral motor pathways compensates for reduced communication within parietofrontal circuits which prevents accurate motor performance.
STUDY POPULATION: We will study two groups of participants: one group of patients with ideomotor apraxia and one group of healthy subjects.
DESIGN: We will measure fMRI activation on transitive and intransitive gestures in 10 patients with ideomotor apraxia during subacute and chronic stage compared to 25 normal controls. The design of the behavioral paradigm incorporates a distinct period of planning prior to each movement.
OUTCOME MEASURES: The design of this study allows evaluating any differences in the planning and execution phases between patients and controls. Further analysis will examine patterns of functional connectivity between activated brain areas, notably their altered interactions in ideomotor apraxia. Of special interest is the putative engagement of perilesional or even remote brain areas in a neuronal network during attempted recovery from motor deficit.
It is expected from the study that a better understanding of cortical plasticity compensating for motor deficits in ideomotor apraxia can be therapeutically exploited, notably in the rehabilitation process.
National Institutes of Health Clinical Center, 9000 Rockville Pike
National Institutes of Health Clinical Center (CC)
Published on BioPortfolio: 2014-08-27T03:55:07-0400
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A group of cognitive disorders characterized by the inability to perform previously learned skills that cannot be attributed to deficits of motor or sensory function. The two major subtypes of this condition are ideomotor (see APRAXIA, IDEOMOTOR) and ideational apraxia, which refers to loss of the ability to mentally formulate the processes involved with performing an action. For example, dressing apraxia may result from an inability to mentally formulate the act of placing clothes on the body. Apraxias are generally associated with lesions of the dominant PARIETAL LOBE and supramarginal gyrus. (From Adams et al., Principles of Neurology, 6th ed, pp56-7)
A form of apraxia characterized by an acquired inability to carry out a complex motor activity despite the ability to mentally formulate the action. This condition has been attributed to a disruption of connections between the dominant parietal cortex and supplementary and premotor cortical regions in both hemispheres. (From Adams et al., Principles of Neurology, 6th ed, p57)
Impaired ambulation not attributed to sensory impairment or motor weakness. FRONTAL LOBE disorders; BASAL GANGLIA DISEASES (e.g., PARKINSONIAN DISORDERS); DEMENTIA, MULTI-INFARCT; ALZHEIMER DISEASE; and other conditions may be associated with gait apraxia.
Functional neuroanatomical region of the inferior frontal gyrus consisting of pars opercularis and pars triangularis. It is important in SPEECH and LANGUAGE production. Injuries to Broca area are associated with BROCA APHASIA and APRAXIA.
An apraxia characterized by the affected limb having involuntary, autonomous, and purposeful behaviors that are perceived as being controlled by an external force. Often the affected limb interferes with the actions of the normal limb. Symptoms develop from lesions in the CORPUS CALLOSUM or medial frontal cortex, stroke, infarction, and neurodegenerative diseases (e.g., CREUTZFELDT-JAKOB SYNDROME, corticobasal degeneration).
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