Electrophysiological studies of early stage corticobasal degeneration
Identifieur interne : 007F28 ( Main/Merge ); précédent : 007F27; suivant : 007F29Electrophysiological studies of early stage corticobasal degeneration
Auteurs : C. S. Lu [Taïwan] ; A. Ikeda [Japon] ; K. Terada [Japon] ; T. Mima [Japon] ; T. Nagamine [Japon] ; H. Fukuyama [Japon] ; N. Kohara [Japon] ; Y. Kojima [Japon] ; Y. Yonekura [Japon] ; R. S. Chen [Taïwan] ; C. H. Tsai [Taïwan] ; N. S. Chu [Taïwan] ; J. Kimura [Japon] ; Shibasaki [Japon]Source :
- Movement Disorders [ 0885-3185 ] ; 1998-01.
English descriptors
- KwdEn :
- Action myoclonus, Aged, Basal Ganglia Diseases (physiopathology), Basal Ganglia Diseases (radionuclide imaging), Corticobasal degeneration, Electromyography, Evoked Potentials, Motor, Evoked Potentials, Somatosensory, Female, Humans, MEP, Male, Middle Aged, Motor Cortex (physiopathology), Motor Cortex (radionuclide imaging), Movement Disorders (physiopathology), Movement Disorders (radionuclide imaging), Neurodegenerative Diseases (physiopathology), Neurodegenerative Diseases (radionuclide imaging), SPECT, Tomography, Emission-Computed, Single-Photon, electrophysiology.
- MESH :
- physiopathology : Basal Ganglia Diseases, Motor Cortex, Movement Disorders, Neurodegenerative Diseases.
- radionuclide imaging : Basal Ganglia Diseases, Motor Cortex, Movement Disorders, Neurodegenerative Diseases.
- Aged, Electromyography, Evoked Potentials, Motor, Evoked Potentials, Somatosensory, Female, Humans, Male, Middle Aged, Tomography, Emission-Computed, Single-Photon.
Abstract
We conducted electrophysiological studies in two Asian patients with probable corticobasal degeneration (CBD). The duration of illness from onset was 16 and 20 months, respectively. The clinical manifestations were markedly asymmetric and characterized by cortical sensory loss, apraxia, action myoclonus, action tremor, and akinetic‐rigid parkinsonism. Neither patient responded to levodopa therapy. Simple photon‐emission computed tomography (SPECT) study showed significantly decreased regional cerebral blood flow in the frontoparietal areas and thalamus opposite to the predominantly affected limb. A series of electrophysiological studies failed to identify giant somatosensory evoked potentials (SEPs), enhanced long latency electromyography (EMG) reflex, and cortical spikes preceding myoclonic jerk. However, the earliest cortical component of the median nerve SEP was exclusively enlarged in one patient and preserved with depression of the subsequent components in the other patient. Significantly shorter postmotor‐evoked potential (MEP) silent period was found after the transcranial magnetic stimulation of the motor cortex in both patients. CBD is a unique clinical entity characterized by action myoclonus probably the result of the pathologic hyperexcitability of the motor cortex, based on a loss of inhibitory input form the sensory cortex.
Url:
DOI: 10.1002/mds.870130126
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Terada</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Mima, T" sort="Mima, T" uniqKey="Mima T" first="T." last="Mima">T. 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Kohara</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Kojima, Y" sort="Kojima, Y" uniqKey="Kojima Y" first="Y." last="Kojima">Y. Kojima</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Yonekura, Y" sort="Yonekura, Y" uniqKey="Yonekura Y" first="Y." last="Yonekura">Y. Yonekura</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>High Energy Medical Research Center, Fukui Medical School, Fukui</wicri:regionArea><wicri:noRegion>Fukui</wicri:noRegion></affiliation></author><author><name sortKey="Chen, R S" sort="Chen, R S" uniqKey="Chen R" first="R. S." last="Chen">R. S. Chen</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Tsai, C H" sort="Tsai, C H" uniqKey="Tsai C" first="C. H." last="Tsai">C. H. Tsai</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Chu, N S" sort="Chu, N S" uniqKey="Chu N" first="N. S." last="Chu">N. S. Chu</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Kimura, J" sort="Kimura, J" uniqKey="Kimura J" first="J." last="Kimura">J. Kimura</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Shibasaki" sort="Shibasaki" uniqKey="Shibasaki" last="Shibasaki">Shibasaki</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1998-01">1998-01</date><biblScope unit="vol">13</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="140">140</biblScope><biblScope unit="page" to="146">146</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">50D8C2B0832A6AB1C96F96850090CDFCF8700710</idno><idno type="DOI">10.1002/mds.870130126</idno><idno type="ArticleID">MDS870130126</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Action myoclonus</term><term>Aged</term><term>Basal Ganglia Diseases (physiopathology)</term><term>Basal Ganglia Diseases (radionuclide imaging)</term><term>Corticobasal degeneration</term><term>Electromyography</term><term>Evoked Potentials, Motor</term><term>Evoked Potentials, Somatosensory</term><term>Female</term><term>Humans</term><term>MEP</term><term>Male</term><term>Middle Aged</term><term>Motor Cortex (physiopathology)</term><term>Motor Cortex (radionuclide imaging)</term><term>Movement Disorders (physiopathology)</term><term>Movement Disorders (radionuclide imaging)</term><term>Neurodegenerative Diseases (physiopathology)</term><term>Neurodegenerative Diseases (radionuclide imaging)</term><term>SPECT</term><term>Tomography, Emission-Computed, Single-Photon</term><term>electrophysiology</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Basal Ganglia Diseases</term><term>Motor Cortex</term><term>Movement Disorders</term><term>Neurodegenerative Diseases</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Basal Ganglia Diseases</term><term>Motor Cortex</term><term>Movement Disorders</term><term>Neurodegenerative Diseases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Electromyography</term><term>Evoked Potentials, Motor</term><term>Evoked Potentials, Somatosensory</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Tomography, Emission-Computed, Single-Photon</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We conducted electrophysiological studies in two Asian patients with probable corticobasal degeneration (CBD). The duration of illness from onset was 16 and 20 months, respectively. The clinical manifestations were markedly asymmetric and characterized by cortical sensory loss, apraxia, action myoclonus, action tremor, and akinetic‐rigid parkinsonism. Neither patient responded to levodopa therapy. Simple photon‐emission computed tomography (SPECT) study showed significantly decreased regional cerebral blood flow in the frontoparietal areas and thalamus opposite to the predominantly affected limb. A series of electrophysiological studies failed to identify giant somatosensory evoked potentials (SEPs), enhanced long latency electromyography (EMG) reflex, and cortical spikes preceding myoclonic jerk. However, the earliest cortical component of the median nerve SEP was exclusively enlarged in one patient and preserved with depression of the subsequent components in the other patient. Significantly shorter postmotor‐evoked potential (MEP) silent period was found after the transcranial magnetic stimulation of the motor cortex in both patients. CBD is a unique clinical entity characterized by action myoclonus probably the result of the pathologic hyperexcitability of the motor cortex, based on a loss of inhibitory input form the sensory cortex.</div></front></TEI><double doi="10.1002/mds.870130126"><ISTEX><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title xml:lang="en">Electrophysiological studies of early stage corticobasal degeneration</title><author><name sortKey="Lu, C S" sort="Lu, C S" uniqKey="Lu C" first="C. S." last="Lu">C. S. Lu</name></author><author><name sortKey="Ikeda, A" sort="Ikeda, A" uniqKey="Ikeda A" first="A." last="Ikeda">A. Ikeda</name></author><author><name sortKey="Terada, K" sort="Terada, K" uniqKey="Terada K" first="K." last="Terada">K. Terada</name></author><author><name sortKey="Mima, T" sort="Mima, T" uniqKey="Mima T" first="T." last="Mima">T. Mima</name></author><author><name sortKey="Nagamine, T" sort="Nagamine, T" uniqKey="Nagamine T" first="T." last="Nagamine">T. Nagamine</name></author><author><name sortKey="Fukuyama, H" sort="Fukuyama, H" uniqKey="Fukuyama H" first="H." last="Fukuyama">H. Fukuyama</name></author><author><name sortKey="Kohara, N" sort="Kohara, N" uniqKey="Kohara N" first="N." last="Kohara">N. Kohara</name></author><author><name sortKey="Kojima, Y" sort="Kojima, Y" uniqKey="Kojima Y" first="Y." last="Kojima">Y. Kojima</name></author><author><name sortKey="Yonekura, Y" sort="Yonekura, Y" uniqKey="Yonekura Y" first="Y." last="Yonekura">Y. Yonekura</name></author><author><name sortKey="Chen, R S" sort="Chen, R S" uniqKey="Chen R" first="R. S." last="Chen">R. S. Chen</name></author><author><name sortKey="Tsai, C H" sort="Tsai, C H" uniqKey="Tsai C" first="C. H." last="Tsai">C. H. Tsai</name></author><author><name sortKey="Chu, N S" sort="Chu, N S" uniqKey="Chu N" first="N. S." last="Chu">N. S. Chu</name></author><author><name sortKey="Kimura, J" sort="Kimura, J" uniqKey="Kimura J" first="J." last="Kimura">J. Kimura</name></author><author><name sortKey="Shibasaki" sort="Shibasaki" uniqKey="Shibasaki" last="Shibasaki">Shibasaki</name></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:50D8C2B0832A6AB1C96F96850090CDFCF8700710</idno><date when="1998" year="1998">1998</date><idno type="doi">10.1002/mds.870130126</idno><idno type="url">https://api.istex.fr/document/50D8C2B0832A6AB1C96F96850090CDFCF8700710/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001865</idno><idno type="wicri:Area/Istex/Curation">001865</idno><idno type="wicri:Area/Istex/Checkpoint">003751</idno><idno type="wicri:doubleKey">0885-3185:1998:Lu C:electrophysiological:studies:of</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a" type="main" xml:lang="en">Electrophysiological studies of early stage corticobasal degeneration</title><author><name sortKey="Lu, C S" sort="Lu, C S" uniqKey="Lu C" first="C. S." last="Lu">C. S. Lu</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Ikeda, A" sort="Ikeda, A" uniqKey="Ikeda A" first="A." last="Ikeda">A. Ikeda</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Terada, K" sort="Terada, K" uniqKey="Terada K" first="K." last="Terada">K. Terada</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Mima, T" sort="Mima, T" uniqKey="Mima T" first="T." last="Mima">T. Mima</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Nagamine, T" sort="Nagamine, T" uniqKey="Nagamine T" first="T." last="Nagamine">T. Nagamine</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Fukuyama, H" sort="Fukuyama, H" uniqKey="Fukuyama H" first="H." last="Fukuyama">H. Fukuyama</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Kohara, N" sort="Kohara, N" uniqKey="Kohara N" first="N." last="Kohara">N. Kohara</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Kojima, Y" sort="Kojima, Y" uniqKey="Kojima Y" first="Y." last="Kojima">Y. Kojima</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Yonekura, Y" sort="Yonekura, Y" uniqKey="Yonekura Y" first="Y." last="Yonekura">Y. Yonekura</name><affiliation wicri:level="1"><country xml:lang="fr">Japon</country><wicri:regionArea>High Energy Medical Research Center, Fukui Medical School, Fukui</wicri:regionArea><wicri:noRegion>Fukui</wicri:noRegion></affiliation></author><author><name sortKey="Chen, R S" sort="Chen, R S" uniqKey="Chen R" first="R. S." last="Chen">R. S. Chen</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Tsai, C H" sort="Tsai, C H" uniqKey="Tsai C" first="C. H." last="Tsai">C. H. Tsai</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Chu, N S" sort="Chu, N S" uniqKey="Chu N" first="N. S." last="Chu">N. S. Chu</name><affiliation wicri:level="1"><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Kimura, J" sort="Kimura, J" uniqKey="Kimura J" first="J." last="Kimura">J. Kimura</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Departments of Neurology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author><author><name sortKey="Shibasaki" sort="Shibasaki" uniqKey="Shibasaki" last="Shibasaki">Shibasaki</name><affiliation wicri:level="4"><country xml:lang="fr">Japon</country><wicri:regionArea>Departments of Brain Pathophysiology, Kyoto University, Faculty of Medicine, Shogoin, Sakyo‐ku, Kyoto</wicri:regionArea><orgName type="university">Université de Kyoto</orgName><placeName><settlement type="city">Kyoto</settlement><region type="prefecture">Région du Kansai</region></placeName></affiliation></author></analytic><monogr></monogr><series><title level="j">Movement Disorders</title><title level="j" type="sub">Official Journal of the Movement Disorder Society</title><title level="j" type="abbrev">Mov. Disord.</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="1998-01">1998-01</date><biblScope unit="vol">13</biblScope><biblScope unit="issue">1</biblScope><biblScope unit="page" from="140">140</biblScope><biblScope unit="page" to="146">146</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">50D8C2B0832A6AB1C96F96850090CDFCF8700710</idno><idno type="DOI">10.1002/mds.870130126</idno><idno type="ArticleID">MDS870130126</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Action myoclonus</term><term>Corticobasal degeneration</term><term>MEP</term><term>SPECT</term><term>electrophysiology</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We conducted electrophysiological studies in two Asian patients with probable corticobasal degeneration (CBD). The duration of illness from onset was 16 and 20 months, respectively. The clinical manifestations were markedly asymmetric and characterized by cortical sensory loss, apraxia, action myoclonus, action tremor, and akinetic‐rigid parkinsonism. Neither patient responded to levodopa therapy. Simple photon‐emission computed tomography (SPECT) study showed significantly decreased regional cerebral blood flow in the frontoparietal areas and thalamus opposite to the predominantly affected limb. A series of electrophysiological studies failed to identify giant somatosensory evoked potentials (SEPs), enhanced long latency electromyography (EMG) reflex, and cortical spikes preceding myoclonic jerk. However, the earliest cortical component of the median nerve SEP was exclusively enlarged in one patient and preserved with depression of the subsequent components in the other patient. Significantly shorter postmotor‐evoked potential (MEP) silent period was found after the transcranial magnetic stimulation of the motor cortex in both patients. CBD is a unique clinical entity characterized by action myoclonus probably the result of the pathologic hyperexcitability of the motor cortex, based on a loss of inhibitory input form the sensory cortex.</div></front></TEI></ISTEX><PubMed><TEI><teiHeader><fileDesc><titleStmt><title xml:lang="en">Electrophysiological studies of early stage corticobasal degeneration.</title><author><name sortKey="Lu, C S" sort="Lu, C S" uniqKey="Lu C" first="C S" last="Lu">C S Lu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Ikeda, A" sort="Ikeda, A" uniqKey="Ikeda A" first="A" last="Ikeda">A. Ikeda</name></author><author><name sortKey="Terada, K" sort="Terada, K" uniqKey="Terada K" first="K" last="Terada">K. Terada</name></author><author><name sortKey="Mima, T" sort="Mima, T" uniqKey="Mima T" first="T" last="Mima">T. Mima</name></author><author><name sortKey="Nagamine, T" sort="Nagamine, T" uniqKey="Nagamine T" first="T" last="Nagamine">T. Nagamine</name></author><author><name sortKey="Fukuyama, H" sort="Fukuyama, H" uniqKey="Fukuyama H" first="H" last="Fukuyama">H. Fukuyama</name></author><author><name sortKey="Kohara, N" sort="Kohara, N" uniqKey="Kohara N" first="N" last="Kohara">N. Kohara</name></author><author><name sortKey="Kojima, Y" sort="Kojima, Y" uniqKey="Kojima Y" first="Y" last="Kojima">Y. Kojima</name></author><author><name sortKey="Yonekura, Y" sort="Yonekura, Y" uniqKey="Yonekura Y" first="Y" last="Yonekura">Y. Yonekura</name></author><author><name sortKey="Chen, R S" sort="Chen, R S" uniqKey="Chen R" first="R S" last="Chen">R S Chen</name></author><author><name sortKey="Tsai, C H" sort="Tsai, C H" uniqKey="Tsai C" first="C H" last="Tsai">C H Tsai</name></author><author><name sortKey="Chu, N S" sort="Chu, N S" uniqKey="Chu N" first="N S" last="Chu">N S Chu</name></author><author><name sortKey="Kimura, J" sort="Kimura, J" uniqKey="Kimura J" first="J" last="Kimura">J. Kimura</name></author><author><name sortKey="Shibasaki, H" sort="Shibasaki, H" uniqKey="Shibasaki H" first="H" last="Shibasaki">H. Shibasaki</name></author></titleStmt><publicationStmt><idno type="wicri:source">PubMed</idno><date when="1998">1998</date><idno type="RBID">pubmed:9452339</idno><idno type="pmid">9452339</idno><idno type="doi">10.1002/mds.870130126</idno><idno type="wicri:Area/PubMed/Corpus">004504</idno><idno type="wicri:Area/PubMed/Curation">004504</idno><idno type="wicri:Area/PubMed/Checkpoint">004445</idno><idno type="wicri:Area/Ncbi/Merge">004E81</idno><idno type="wicri:Area/Ncbi/Curation">004E81</idno><idno type="wicri:Area/Ncbi/Checkpoint">004E81</idno><idno type="wicri:doubleKey">0885-3185:1998:Lu C:electrophysiological:studies:of</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en">Electrophysiological studies of early stage corticobasal degeneration.</title><author><name sortKey="Lu, C S" sort="Lu, C S" uniqKey="Lu C" first="C S" last="Lu">C S Lu</name><affiliation wicri:level="1"><nlm:affiliation>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei, Taiwan.</nlm:affiliation><country xml:lang="fr">Taïwan</country><wicri:regionArea>Department of Neurology, Chang Gung Medical College and Memorial Hospital, Taipei</wicri:regionArea><wicri:noRegion>Taipei</wicri:noRegion></affiliation></author><author><name sortKey="Ikeda, A" sort="Ikeda, A" uniqKey="Ikeda A" first="A" last="Ikeda">A. Ikeda</name></author><author><name sortKey="Terada, K" sort="Terada, K" uniqKey="Terada K" first="K" last="Terada">K. Terada</name></author><author><name sortKey="Mima, T" sort="Mima, T" uniqKey="Mima T" first="T" last="Mima">T. Mima</name></author><author><name sortKey="Nagamine, T" sort="Nagamine, T" uniqKey="Nagamine T" first="T" last="Nagamine">T. Nagamine</name></author><author><name sortKey="Fukuyama, H" sort="Fukuyama, H" uniqKey="Fukuyama H" first="H" last="Fukuyama">H. Fukuyama</name></author><author><name sortKey="Kohara, N" sort="Kohara, N" uniqKey="Kohara N" first="N" last="Kohara">N. Kohara</name></author><author><name sortKey="Kojima, Y" sort="Kojima, Y" uniqKey="Kojima Y" first="Y" last="Kojima">Y. Kojima</name></author><author><name sortKey="Yonekura, Y" sort="Yonekura, Y" uniqKey="Yonekura Y" first="Y" last="Yonekura">Y. Yonekura</name></author><author><name sortKey="Chen, R S" sort="Chen, R S" uniqKey="Chen R" first="R S" last="Chen">R S Chen</name></author><author><name sortKey="Tsai, C H" sort="Tsai, C H" uniqKey="Tsai C" first="C H" last="Tsai">C H Tsai</name></author><author><name sortKey="Chu, N S" sort="Chu, N S" uniqKey="Chu N" first="N S" last="Chu">N S Chu</name></author><author><name sortKey="Kimura, J" sort="Kimura, J" uniqKey="Kimura J" first="J" last="Kimura">J. Kimura</name></author><author><name sortKey="Shibasaki, H" sort="Shibasaki, H" uniqKey="Shibasaki H" first="H" last="Shibasaki">H. Shibasaki</name></author></analytic><series><title level="j">Movement disorders : official journal of the Movement Disorder Society</title><idno type="ISSN">0885-3185</idno><imprint><date when="1998" type="published">1998</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Aged</term><term>Basal Ganglia Diseases (physiopathology)</term><term>Basal Ganglia Diseases (radionuclide imaging)</term><term>Electromyography</term><term>Evoked Potentials, Motor</term><term>Evoked Potentials, Somatosensory</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Motor Cortex (physiopathology)</term><term>Motor Cortex (radionuclide imaging)</term><term>Movement Disorders (physiopathology)</term><term>Movement Disorders (radionuclide imaging)</term><term>Neurodegenerative Diseases (physiopathology)</term><term>Neurodegenerative Diseases (radionuclide imaging)</term><term>Tomography, Emission-Computed, Single-Photon</term></keywords><keywords scheme="MESH" qualifier="physiopathology" xml:lang="en"><term>Basal Ganglia Diseases</term><term>Motor Cortex</term><term>Movement Disorders</term><term>Neurodegenerative Diseases</term></keywords><keywords scheme="MESH" qualifier="radionuclide imaging" xml:lang="en"><term>Basal Ganglia Diseases</term><term>Motor Cortex</term><term>Movement Disorders</term><term>Neurodegenerative Diseases</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Aged</term><term>Electromyography</term><term>Evoked Potentials, Motor</term><term>Evoked Potentials, Somatosensory</term><term>Female</term><term>Humans</term><term>Male</term><term>Middle Aged</term><term>Tomography, Emission-Computed, Single-Photon</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">We conducted electrophysiological studies in two Asian patients with probable corticobasal degeneration (CBD). The duration of illness from onset was 16 and 20 months, respectively. The clinical manifestations were markedly asymmetric and characterized by cortical sensory loss, apraxia, action myoclonus, action tremor, and akinetic-rigid parkinsonism. Neither patient responded to levodopa therapy. Simple photon-emission computed tomography (SPECT) study showed significantly decreased regional cerebral blood flow in the frontoparietal areas and thalamus opposite to the predominantly affected limb. A series of electrophysiological studies failed to identify giant somatosensory evoked potentials (SEPs), enhanced long latency electromyography (EMG) reflex, and cortical spikes preceding myoclonic jerk. However, the earliest cortical component of the median nerve SEP was exclusively enlarged in one patient and preserved with depression of the subsequent components in the other patient. Significantly shorter postmotor-evoked potential (MEP) silent period was found after the transcranial magnetic stimulation of the motor cortex in both patients. CBD is a unique clinical entity characterized by action myoclonus probably the result of the pathologic hyperexcitability of the motor cortex, based on a loss of inhibitory input from the sensory cortex.</div></front></TEI></PubMed></double></record>Pour manipuler ce document sous Unix (Dilib)
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