Limb-kinetic apraxia in corticobasal degeneration: clinical and kinematic features.
Identifieur interne : 003743 ( PubMed/Checkpoint ); précédent : 003742; suivant : 003744Limb-kinetic apraxia in corticobasal degeneration: clinical and kinematic features.
Auteurs : Ram N C. Leiguarda [Argentine] ; Marcelo Merello ; María Inés Nouzeilles ; Jorge Balej ; Alberto Rivero ; Martín NoguésSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2003.
English descriptors
- KwdEn :
- Aged, Apraxia, Ideomotor (diagnosis), Apraxia, Ideomotor (physiopathology), Atrophy, Biomechanical Phenomena, Diagnosis, Differential, Female, Frontal Lobe (blood supply), Frontal Lobe (pathology), Frontal Lobe (physiopathology), Humans, Imaging, Three-Dimensional, Magnetic Resonance Imaging, Male, Middle Aged, Neurodegenerative Diseases (diagnosis), Neurodegenerative Diseases (physiopathology), Neurologic Examination, Parietal Lobe (blood supply), Parietal Lobe (pathology), Parietal Lobe (physiopathology), Parkinson Disease (diagnosis), Parkinson Disease (physiopathology), Psychomotor Performance (physiology), Regional Blood Flow (physiology), Tomography, Emission-Computed, Single-Photon.
- MESH :
- blood supply : Frontal Lobe, Parietal Lobe.
- diagnosis : Apraxia, Ideomotor, Neurodegenerative Diseases, Parkinson Disease.
- pathology : Frontal Lobe, Parietal Lobe.
- physiology : Psychomotor Performance, Regional Blood Flow.
- physiopathology : Apraxia, Ideomotor, Frontal Lobe, Neurodegenerative Diseases, Parietal Lobe, Parkinson Disease.
- Aged, Atrophy, Biomechanical Phenomena, Diagnosis, Differential, Female, Humans, Imaging, Three-Dimensional, Magnetic Resonance Imaging, Male, Middle Aged, Neurologic Examination, Tomography, Emission-Computed, Single-Photon.
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.
DOI: 10.1002/mds.10303
PubMed: 12518300
Affiliations:
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<author><name sortKey="Nouzeilles, Maria Ines" sort="Nouzeilles, Maria Ines" uniqKey="Nouzeilles M" first="María Inés" last="Nouzeilles">María Inés Nouzeilles</name>
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<term>Atrophy</term>
<term>Biomechanical Phenomena</term>
<term>Diagnosis, Differential</term>
<term>Female</term>
<term>Frontal Lobe (blood supply)</term>
<term>Frontal Lobe (pathology)</term>
<term>Frontal Lobe (physiopathology)</term>
<term>Humans</term>
<term>Imaging, Three-Dimensional</term>
<term>Magnetic Resonance Imaging</term>
<term>Male</term>
<term>Middle Aged</term>
<term>Neurodegenerative Diseases (diagnosis)</term>
<term>Neurodegenerative Diseases (physiopathology)</term>
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<term>Parietal Lobe (pathology)</term>
<term>Parietal Lobe (physiopathology)</term>
<term>Parkinson Disease (diagnosis)</term>
<term>Parkinson Disease (physiopathology)</term>
<term>Psychomotor Performance (physiology)</term>
<term>Regional Blood Flow (physiology)</term>
<term>Tomography, Emission-Computed, Single-Photon</term>
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<term>Parietal Lobe</term>
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<term>Parkinson Disease</term>
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<term>Magnetic Resonance Imaging</term>
<term>Male</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>
</front>
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<ArticleTitle>Limb-kinetic apraxia in corticobasal degeneration: clinical and kinematic features.</ArticleTitle>
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<Abstract><AbstractText>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.</AbstractText>
<CopyrightInformation>Copyright 2002 Movement Disorder Society</CopyrightInformation>
</Abstract>
<AuthorList CompleteYN="Y"><Author ValidYN="Y"><LastName>Leiguarda</LastName>
<ForeName>Ramón C</ForeName>
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<name sortKey="Nogues, Martin" sort="Nogues, Martin" uniqKey="Nogues M" first="Martín" last="Nogués">Martín Nogués</name>
<name sortKey="Nouzeilles, Maria Ines" sort="Nouzeilles, Maria Ines" uniqKey="Nouzeilles M" first="María Inés" last="Nouzeilles">María Inés Nouzeilles</name>
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<country name="Argentine"><noRegion><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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