Movement Disorders (revue)

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Limb‐kinetic apraxia in corticobasal degeneration: Clinical and kinematic features

Identifieur interne : 004051 ( Main/Exploration ); précédent : 004050; suivant : 004052

Limb‐kinetic apraxia in corticobasal degeneration: Clinical and kinematic features

Auteurs : Ram N C. Leiguarda [Argentine] ; Marcelo Merello [Argentine] ; María Inés Nouzeilles [Argentine] ; Jorge Balej [Argentine] ; Alberto Rivero [Argentine] ; Martín Nogués [Argentine]

Source :

RBID : ISTEX:AF9AEC18BFEDE3B317641409AA4901B36789A7EB

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English descriptors

Abstract

Current concepts regarding the organisation of the motor system indicate the existence of a frontoparietal circuit involved in prehension and manipulation, whose damage may result in a motor behavioural disorder strongly resembling the one originally described as limb‐kinetic apraxia. To determine the specific clinical and kinematic features of this distinctive praxic disorder, 5 patients with corticobasal degeneration (apraxic group), 5 with Parkinson's disease (nonapraxic group), and 10 control subjects were studied by a comprehensive apraxic battery, three‐dimensional motion analysis of manipulative movements and motor evoked potentials. A mathematical model [quality of movement coefficient (QMC)] was applied to quantify differential kinematic characteristics between elementary motor deficits and the praxic disorder. Transcranial magnetic stimulation was used to evaluate corticomotoneural projections and cortical inhibition. All five patients in the apraxic group exhibited a unilateral praxic deficit characterised by derangement of fractionated and segmental finger movements. QMC was significantly greater in apraxic than in nonapraxic patients (P < 0.02), revealing a chaotic movement with marked interfinger uncoordination. Conventional transcranial magnetic stimulation parameters were within normal limits in both groups of patients; however, the silent period was significantly shorter in the apraxic limb when compared with control subjects (P < 0.001). Limb‐kinetic apraxia is a distinctive disorder affecting the performance of finger and hand postures and movements over and above a corticospinal or basal ganglion deficit. Disruption of the frontoparietal circuit devoted to grasping and manipulation, together with defective cortical inhibition, which would also interfere with the selection and control of hand muscle activity, are the most likely underlying physiopathological mechanisms of limb‐kinetic apraxia in patients with corticobasal degeneration.

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DOI: 10.1002/mds.10303


Affiliations:


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Le document en format XML

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<term>Aged</term>
<term>Apraxia</term>
<term>Apraxia, Ideomotor (diagnosis)</term>
<term>Apraxia, Ideomotor (physiopathology)</term>
<term>Atrophy</term>
<term>Basal ganglion</term>
<term>Biomechanical Phenomena</term>
<term>Cerebral cortex</term>
<term>Complication</term>
<term>Degeneration</term>
<term>Diagnosis, Differential</term>
<term>Elderly</term>
<term>Female</term>
<term>Frontal Lobe (blood supply)</term>
<term>Frontal Lobe (pathology)</term>
<term>Frontal Lobe (physiopathology)</term>
<term>Gripping</term>
<term>Humans</term>
<term>Imaging, Three-Dimensional</term>
<term>Kinematics</term>
<term>Limb</term>
<term>Magnetic Resonance Imaging</term>
<term>Magnetic stimulus</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Neurodegenerative Diseases (diagnosis)</term>
<term>Neurodegenerative Diseases (physiopathology)</term>
<term>Neurologic Examination</term>
<term>Parietal Lobe (blood supply)</term>
<term>Parietal Lobe (pathology)</term>
<term>Parietal Lobe (physiopathology)</term>
<term>Parkinson Disease (diagnosis)</term>
<term>Parkinson Disease (physiopathology)</term>
<term>Pathogenesis</term>
<term>Psychomotor Performance (physiology)</term>
<term>Regional Blood Flow (physiology)</term>
<term>Tomography, Emission-Computed, Single-Photon</term>
<term>Transcranial route</term>
<term>frontoparietal circuit</term>
<term>grasping and manipulation</term>
<term>limb‐kinetic apraxia</term>
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<term>Frontal Lobe</term>
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<term>Parietal Lobe</term>
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<term>Atrophy</term>
<term>Biomechanical Phenomena</term>
<term>Diagnosis, Differential</term>
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<term>Imaging, Three-Dimensional</term>
<term>Magnetic Resonance Imaging</term>
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<term>Middle Aged</term>
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<term>Cinématique</term>
<term>Complication</term>
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<term>Dégénérescence</term>
<term>Membre</term>
<term>Noyau gris central</term>
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<term>Personne âgée</term>
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<term>Stimulus magnétique</term>
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<front>
<div type="abstract" xml:lang="en">Current concepts regarding the organisation of the motor system indicate the existence of a frontoparietal circuit involved in prehension and manipulation, whose damage may result in a motor behavioural disorder strongly resembling the one originally described as limb‐kinetic apraxia. To determine the specific clinical and kinematic features of this distinctive praxic disorder, 5 patients with corticobasal degeneration (apraxic group), 5 with Parkinson's disease (nonapraxic group), and 10 control subjects were studied by a comprehensive apraxic battery, three‐dimensional motion analysis of manipulative movements and motor evoked potentials. A mathematical model [quality of movement coefficient (QMC)] was applied to quantify differential kinematic characteristics between elementary motor deficits and the praxic disorder. Transcranial magnetic stimulation was used to evaluate corticomotoneural projections and cortical inhibition. All five patients in the apraxic group exhibited a unilateral praxic deficit characterised by derangement of fractionated and segmental finger movements. QMC was significantly greater in apraxic than in nonapraxic patients (P < 0.02), revealing a chaotic movement with marked interfinger uncoordination. Conventional transcranial magnetic stimulation parameters were within normal limits in both groups of patients; however, the silent period was significantly shorter in the apraxic limb when compared with control subjects (P < 0.001). Limb‐kinetic apraxia is a distinctive disorder affecting the performance of finger and hand postures and movements over and above a corticospinal or basal ganglion deficit. Disruption of the frontoparietal circuit devoted to grasping and manipulation, together with defective cortical inhibition, which would also interfere with the selection and control of hand muscle activity, are the most likely underlying physiopathological mechanisms of limb‐kinetic apraxia in patients with corticobasal degeneration.</div>
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<name sortKey="Leiguarda, Ram N C" sort="Leiguarda, Ram N C" uniqKey="Leiguarda R" first="Ram N C." last="Leiguarda">Ram N C. Leiguarda</name>
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<name sortKey="Balej, Jorge" sort="Balej, Jorge" uniqKey="Balej J" first="Jorge" last="Balej">Jorge Balej</name>
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