Neuropathology of primary restless leg syndrome: Absence of specific τ‐ and α‐synuclein pathology
Identifieur interne : 001F75 ( Main/Exploration ); précédent : 001F74; suivant : 001F76Neuropathology of primary restless leg syndrome: Absence of specific τ‐ and α‐synuclein pathology
Auteurs : Sean J. Pittock [États-Unis] ; Timothy Parrett [États-Unis] ; Charles H. Adler [États-Unis] ; Joseph E. Parisi [États-Unis] ; Dennis W. Dickson [États-Unis] ; J. Eric Ahlskog [États-Unis]Source :
- Movement Disorders [ 0885-3185 ] ; 2004-06.
English descriptors
- Teeft :
- Arthritis rheum, Basal ganglia, Braak, Braak braak stage, Brosis, Cardiac valvular, Chronic ischemic changes, Coronary artery disease, Dopamine, Dopaminergic, Early seropositive, Electrophysiological pattern, Entorhinal cortex, Eric ahlskog, Etat crible, Family history, Ibzm spect, Legs syndrome, Legs syndrome study group, Lewy bodies, Many years, Mayo, Mayo clinic, Medical center, Minocycline, Movement disorder society, Movement disorders, Myocardial infarction, Ndings, Neuroanatomical substrate, Neurology, Neurology mayo clinic, Neuropathological, Neuropathology, Neuropathy, Pergolide, Periodic limb movements, Peripheral neuropathy, Preganglionic nerves, Rare complication, Renal failure, Restless legs, Restless legs syndrome, Semin arthritis rheum, Severe arteriosclerosis, Spinal, Spinal cord, Spinal cord lesions, Spinal levels, Spinal stenosis, Substantia nigra, Syndrome, Synuclein, Synuclein immunohistochemistry, Vascular disease, Wiley interscience.
Abstract
The neuroanatomical substrate for restless legs syndrome (RLS) is unknown. We identified 4 patients with idiopathic RLS who came to post‐mortem examination, where brain and spinal cord tissue were available for neuropathological assessment. Lewy bodies were not identified and α‐synuclein immunohistochemistry was uniformly negative. Neurofibrillary tangle pathology was variable and nonspecific. These findings suggest that τ‐ or α‐synuclein brain pathology is not a component of primary RLS. Although chronic ischemic changes were found in all 4 cases, these were probably incidental. The absence of diagnostic microscopic brain or spinal cord pathology suggests that the pathologic substrate may be neurochemical or receptor based. © 2004 Movement Disorder Society
Url:
DOI: 10.1002/mds.20042
Affiliations:
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Eric Ahlskog</name><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><wicri:regionArea>Department of Neurology Mayo Clinic, Rochester, Minnesota</wicri:regionArea><placeName><region type="state">Minnesota</region></placeName></affiliation><affiliation wicri:level="1"><country wicri:rule="url">États-Unis</country></affiliation><affiliation wicri:level="2"><country xml:lang="fr">États-Unis</country><placeName><region type="state">Minnesota</region></placeName><wicri:cityArea>Correspondence address: Department of Neurology, Mayo Clinic, 200 First Street S.W., Rochester</wicri:cityArea></affiliation></author></analytic><monogr></monogr><series><title level="j" type="main">Movement Disorders</title><title level="j" type="alt">MOVEMENT DISORDERS</title><idno type="ISSN">0885-3185</idno><idno type="eISSN">1531-8257</idno><imprint><biblScope unit="vol">19</biblScope><biblScope unit="issue">6</biblScope><biblScope unit="page" from="695">695</biblScope><biblScope unit="page" to="699">699</biblScope><biblScope unit="page-count">4</biblScope><publisher>Wiley Subscription Services, Inc., A Wiley Company</publisher><pubPlace>Hoboken</pubPlace><date type="published" when="2004-06">2004-06</date></imprint><idno type="ISSN">0885-3185</idno></series></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0885-3185</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="Teeft" xml:lang="en"><term>Arthritis rheum</term><term>Basal ganglia</term><term>Braak</term><term>Braak braak stage</term><term>Brosis</term><term>Cardiac valvular</term><term>Chronic ischemic changes</term><term>Coronary artery disease</term><term>Dopamine</term><term>Dopaminergic</term><term>Early seropositive</term><term>Electrophysiological pattern</term><term>Entorhinal cortex</term><term>Eric ahlskog</term><term>Etat crible</term><term>Family history</term><term>Ibzm spect</term><term>Legs syndrome</term><term>Legs syndrome study group</term><term>Lewy bodies</term><term>Many years</term><term>Mayo</term><term>Mayo clinic</term><term>Medical center</term><term>Minocycline</term><term>Movement disorder society</term><term>Movement disorders</term><term>Myocardial infarction</term><term>Ndings</term><term>Neuroanatomical substrate</term><term>Neurology</term><term>Neurology mayo clinic</term><term>Neuropathological</term><term>Neuropathology</term><term>Neuropathy</term><term>Pergolide</term><term>Periodic limb movements</term><term>Peripheral neuropathy</term><term>Preganglionic nerves</term><term>Rare complication</term><term>Renal failure</term><term>Restless legs</term><term>Restless legs syndrome</term><term>Semin arthritis rheum</term><term>Severe arteriosclerosis</term><term>Spinal</term><term>Spinal cord</term><term>Spinal cord lesions</term><term>Spinal levels</term><term>Spinal stenosis</term><term>Substantia nigra</term><term>Syndrome</term><term>Synuclein</term><term>Synuclein immunohistochemistry</term><term>Vascular disease</term><term>Wiley interscience</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The neuroanatomical substrate for restless legs syndrome (RLS) is unknown. We identified 4 patients with idiopathic RLS who came to post‐mortem examination, where brain and spinal cord tissue were available for neuropathological assessment. Lewy bodies were not identified and α‐synuclein immunohistochemistry was uniformly negative. Neurofibrillary tangle pathology was variable and nonspecific. These findings suggest that τ‐ or α‐synuclein brain pathology is not a component of primary RLS. Although chronic ischemic changes were found in all 4 cases, these were probably incidental. The absence of diagnostic microscopic brain or spinal cord pathology suggests that the pathologic substrate may be neurochemical or receptor based. © 2004 Movement Disorder Society</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Arizona</li><li>Floride</li><li>Minnesota</li></region></list><tree><country name="États-Unis"><region name="Minnesota"><name sortKey="Pittock, Sean J" sort="Pittock, Sean J" uniqKey="Pittock S" first="Sean J." last="Pittock">Sean J. Pittock</name></region><name sortKey="Adler, Charles H" sort="Adler, Charles H" uniqKey="Adler C" first="Charles H." last="Adler">Charles H. Adler</name><name sortKey="Ahlskog, J Eric" sort="Ahlskog, J Eric" uniqKey="Ahlskog J" first="J. Eric" last="Ahlskog">J. Eric Ahlskog</name><name sortKey="Ahlskog, J Eric" sort="Ahlskog, J Eric" uniqKey="Ahlskog J" first="J. Eric" last="Ahlskog">J. Eric Ahlskog</name><name sortKey="Ahlskog, J Eric" sort="Ahlskog, J Eric" uniqKey="Ahlskog J" first="J. Eric" last="Ahlskog">J. Eric Ahlskog</name><name sortKey="Dickson, Dennis W" sort="Dickson, Dennis W" uniqKey="Dickson D" first="Dennis W." last="Dickson">Dennis W. Dickson</name><name sortKey="Parisi, Joseph E" sort="Parisi, Joseph E" uniqKey="Parisi J" first="Joseph E." last="Parisi">Joseph E. Parisi</name><name sortKey="Parrett, Timothy" sort="Parrett, Timothy" uniqKey="Parrett T" first="Timothy" last="Parrett">Timothy Parrett</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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