Progressive delayed‐onset dystonia after cerebral anoxic insult in adults
Identifieur interne : 004322 ( Main/Exploration ); précédent : 004321; suivant : 004323Progressive delayed‐onset dystonia after cerebral anoxic insult in adults
Auteurs : Mikko Kuoppam Ki [Royaume-Uni] ; Kailash P. Bhatia [Royaume-Uni] ; Niall Quinn [Royaume-Uni]Source :
- Movement Disorders [ 0885-3185 ] ; 2002-11.
Descripteurs français
- Pascal (Inist)
- Wicri :
English descriptors
- KwdEn :
- Adult, Basal Ganglia Diseases (diagnosis), Basal Ganglia Diseases (etiology), Cardiocirculatory arrest, Case study, Complication, Disease Progression, Dystonia, Dystonic Disorders (diagnosis), Dystonic Disorders (etiology), Female, Follow-Up Studies, Globus Pallidus (pathology), Heart Arrest (complications), Human, Humans, Hypoxia, Hypoxia, Brain (complications), Hypoxia, Brain (diagnosis), Internal Capsule (pathology), Late, Magnetic Resonance Imaging, Neurologic Examination, Oxygen, Pallidum, Parkinsonism, Progressive, anoxia, apoptosis, dystonia, globus pallidus, parkinsonism.
- MESH :
- complications : Heart Arrest, Hypoxia, Brain.
- diagnosis : Basal Ganglia Diseases, Dystonic Disorders, Hypoxia, Brain.
- etiology : Basal Ganglia Diseases, Dystonic Disorders.
- pathology : Globus Pallidus, Internal Capsule.
- Adult, Disease Progression, Female, Follow-Up Studies, Humans, Magnetic Resonance Imaging, Neurologic Examination.
Abstract
The basal ganglia, especially the globi pallidi (GP), are highly vulnerable to generalized cerebral anoxia/hypoxia. We report on 2 new cases with delayed‐onset generalized dystonia due to cerebral anoxia. The onset of dystonia in both of our patients was delayed by about 2 months. In both cases, the unusual feature was the progressive worsening and the spread of dystonia over many years after delayed onset. Dystonia progressed for 16 years in Case 1 and for 4 years in Case 2. Furthermore, initial magnetic resonance imaging (MRI) scan of Case 1 showed mild changes of the internal capsule sparing the basal ganglia. Years later, in line with clinical progression, the follow‐up MRI scan showed isolated bilateral lesions involving the entire GP. MRI scans in Case 2 showed bilateral lesions of caudate and lentiform nuclei. There may be several mechanisms underlying delayed and progressive symptoms after time‐limited brain anoxia. We hypothesize that anoxia‐induced excitotoxicity resulting in mitochondrial dysfunction and subsequent apoptosis may explain, at least partly, the delayed‐onset and progressive extrapyramidal syndromes seen in these patients. © 2002 Movement Disorder Society
Url:
DOI: 10.1002/mds.10260
Affiliations:
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Le document en format XML
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Bhatia</name><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</region></placeName></affiliation></author><author><name sortKey="Quinn, Niall" sort="Quinn, Niall" uniqKey="Quinn N" first="Niall" last="Quinn">Niall Quinn</name><affiliation wicri:level="3"><country xml:lang="fr">Royaume-Uni</country><wicri:regionArea>Sobell Department of Motor Neuroscience and Movement Disorders, Institute of Neurology, Queen Square, London</wicri:regionArea><placeName><settlement type="city">Londres</settlement><region type="country">Angleterre</region><region type="région" nuts="1">Grand Londres</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>New York</pubPlace><date type="published" when="2002-11">2002-11</date><biblScope unit="vol">17</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="1345">1345</biblScope><biblScope unit="page" to="1349">1349</biblScope></imprint><idno type="ISSN">0885-3185</idno></series><idno type="istex">32C0C5260E90F89AD0864857CF73A4C826180616</idno><idno type="DOI">10.1002/mds.10260</idno><idno type="ArticleID">MDS10260</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Adult</term><term>Basal Ganglia Diseases (diagnosis)</term><term>Basal Ganglia Diseases (etiology)</term><term>Cardiocirculatory arrest</term><term>Case study</term><term>Complication</term><term>Disease Progression</term><term>Dystonia</term><term>Dystonic Disorders (diagnosis)</term><term>Dystonic Disorders (etiology)</term><term>Female</term><term>Follow-Up Studies</term><term>Globus Pallidus (pathology)</term><term>Heart Arrest (complications)</term><term>Human</term><term>Humans</term><term>Hypoxia</term><term>Hypoxia, Brain (complications)</term><term>Hypoxia, Brain (diagnosis)</term><term>Internal Capsule (pathology)</term><term>Late</term><term>Magnetic Resonance Imaging</term><term>Neurologic Examination</term><term>Oxygen</term><term>Pallidum</term><term>Parkinsonism</term><term>Progressive</term><term>anoxia</term><term>apoptosis</term><term>dystonia</term><term>globus pallidus</term><term>parkinsonism</term></keywords><keywords scheme="MESH" qualifier="complications" xml:lang="en"><term>Heart Arrest</term><term>Hypoxia, Brain</term></keywords><keywords scheme="MESH" qualifier="diagnosis" xml:lang="en"><term>Basal Ganglia Diseases</term><term>Dystonic Disorders</term><term>Hypoxia, Brain</term></keywords><keywords scheme="MESH" qualifier="etiology" xml:lang="en"><term>Basal Ganglia Diseases</term><term>Dystonic Disorders</term></keywords><keywords scheme="MESH" qualifier="pathology" xml:lang="en"><term>Globus Pallidus</term><term>Internal Capsule</term></keywords><keywords scheme="MESH" xml:lang="en"><term>Adult</term><term>Disease Progression</term><term>Female</term><term>Follow-Up Studies</term><term>Humans</term><term>Magnetic Resonance Imaging</term><term>Neurologic Examination</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Arrêt cardiocirculatoire</term><term>Complication</term><term>Dystonie</term><term>Etude cas</term><term>Homme</term><term>Hypoxie</term><term>Oxygène</term><term>Pallidum</term><term>Parkinsonisme</term><term>Progressif</term><term>Tardif</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Homme</term><term>Oxygène</term></keywords></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The basal ganglia, especially the globi pallidi (GP), are highly vulnerable to generalized cerebral anoxia/hypoxia. We report on 2 new cases with delayed‐onset generalized dystonia due to cerebral anoxia. The onset of dystonia in both of our patients was delayed by about 2 months. In both cases, the unusual feature was the progressive worsening and the spread of dystonia over many years after delayed onset. Dystonia progressed for 16 years in Case 1 and for 4 years in Case 2. Furthermore, initial magnetic resonance imaging (MRI) scan of Case 1 showed mild changes of the internal capsule sparing the basal ganglia. Years later, in line with clinical progression, the follow‐up MRI scan showed isolated bilateral lesions involving the entire GP. MRI scans in Case 2 showed bilateral lesions of caudate and lentiform nuclei. There may be several mechanisms underlying delayed and progressive symptoms after time‐limited brain anoxia. We hypothesize that anoxia‐induced excitotoxicity resulting in mitochondrial dysfunction and subsequent apoptosis may explain, at least partly, the delayed‐onset and progressive extrapyramidal syndromes seen in these patients. © 2002 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>Royaume-Uni</li></country><region><li>Angleterre</li><li>Grand Londres</li></region><settlement><li>Londres</li></settlement></list><tree><country name="Royaume-Uni"><region name="Angleterre"><name sortKey="Kuoppam Ki, Mikko" sort="Kuoppam Ki, Mikko" uniqKey="Kuoppam Ki M" first="Mikko" last="Kuoppam Ki">Mikko Kuoppam Ki</name></region><name sortKey="Bhatia, Kailash P" sort="Bhatia, Kailash P" uniqKey="Bhatia K" first="Kailash P." last="Bhatia">Kailash P. Bhatia</name><name sortKey="Quinn, Niall" sort="Quinn, Niall" uniqKey="Quinn N" first="Niall" last="Quinn">Niall Quinn</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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