MovDisordV3, Main, Curation, bibRecord, 002D23

Neurological deficits are associated with increased brain calcinosis, hypoperfusion, and hypometabolism in idiopathic basal ganglia calcification

Identifieur interne : 002D23 ( Main/Curation ); précédent : 002D22; suivant : 002D24

Neurological deficits are associated with increased brain calcinosis, hypoperfusion, and hypometabolism in idiopathic basal ganglia calcification

Auteurs : Misuzu Saiki [Japon] ; Shinji Saiki [Japon] ; Koichiro Sakai [Japon] ; Ichiro Matsunari [Japon] ; Kotaro Higashi [Japon] ; Ken-Ya Murata [Japon] ; Nobutaka Hattori [Japon] ; Genjiro Hirose [Japon]

Source :

Movement Disorders [ 0885-3185 ] ; 2007-05-15.

RBID : ISTEX:9211FFEC371EA7FFE035DB61C907AC299E609E5E

Descripteurs français

Pascal (Inist)
- Calcification, Calcinose, Encéphale, Idiopathique, Noyau gris central, Photon, Positon, Système nerveux pathologie, Tomographie émission positon, Tomoscintigraphie émission monophotonique.

English descriptors

KwdEn :
- Aged, 80 and over, Basal Ganglia Diseases (pathology), Basal Ganglia Diseases (physiopathology), Basal ganglion, Calcification, Calcinosis, Calcinosis (physiopathology), Encephalon, Family Health, Female, Humans, Idiopathic, Male, Metabolism, Inborn Errors (physiopathology), Middle Aged, Nervous system diseases, Photon, Positron, Positron emission tomography, Positron-Emission Tomography (methods), Single photon emission tomography, Tomography, Emission-Computed, Single-Photon (methods), Tomography, X-Ray Computed (methods), [18F]FDG‐PET, [99mTc]HMPAO‐SPECT, idiopathic basal ganglia calcification (IBGC).
MESH :
- methods : Positron-Emission Tomography, Tomography, Emission-Computed, Single-Photon, Tomography, X-Ray Computed.
- pathology : Basal Ganglia Diseases.
- physiopathology : Basal Ganglia Diseases, Calcinosis, Metabolism, Inborn Errors.
- Aged, 80 and over, Family Health, Female, Humans, Male, Middle Aged.

Abstract

We report two familial cases of idiopathic basal ganglia calcification. A 60‐year‐old proband with choreoathetosis, dysarthria, and cognitive decline showed more extensive brain calcinosis, hypoperfusion, and hypometabolism than did his asymptomatic 82‐year‐old mother. The mother had no frontal lobe calcinosis but basal ganglia and dentate nucleus depositions were detectable. Perfusion neuroimaging, however, was normal in the asymptomatic mother and abnormal in the clinically impaired proband. The presence of calcinosis cannot be used as an index of neurological impairment but the extent of calcinosis and reduction in perfusion and metabolism may be useful for separating symptomatic from asymptomatic subjects with IBGC. These findings suggest that an interruption of neuronal circuitry may cause neurological deficits. The degree of neurological deficits may correlate with the severity of calcinosis and the reduction of perfusion and metabolism. © 2007 Movement Disorder Society

Url:

https://api.istex.fr/document/9211FFEC371EA7FFE035DB61C907AC299E609E5E/fulltext/pdf

DOI: 10.1002/mds.21438

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ISTEX:9211FFEC371EA7FFE035DB61C907AC299E609E5E

Le document en format XML

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<front><div type="abstract" xml:lang="en">We report two familial cases of idiopathic basal ganglia calcification. A 60‐year‐old proband with choreoathetosis, dysarthria, and cognitive decline showed more extensive brain calcinosis, hypoperfusion, and hypometabolism than did his asymptomatic 82‐year‐old mother. The mother had no frontal lobe calcinosis but basal ganglia and dentate nucleus depositions were detectable. Perfusion neuroimaging, however, was normal in the asymptomatic mother and abnormal in the clinically impaired proband. The presence of calcinosis cannot be used as an index of neurological impairment but the extent of calcinosis and reduction in perfusion and metabolism may be useful for separating symptomatic from asymptomatic subjects with IBGC. These findings suggest that an interruption of neuronal circuitry may cause neurological deficits. The degree of neurological deficits may correlate with the severity of calcinosis and the reduction of perfusion and metabolism. © 2007 Movement Disorder Society</div>
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<author><name sortKey="Higashi, Kotaro" sort="Higashi, Kotaro" uniqKey="Higashi K" first="Kotaro" last="Higashi">Kotaro Higashi</name>
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<author><name sortKey="Murata, Ken Ya" sort="Murata, Ken Ya" uniqKey="Murata K" first="Ken-Ya" last="Murata">Ken-Ya Murata</name>
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</author>
<author><name sortKey="Hattori, Nobutaka" sort="Hattori, Nobutaka" uniqKey="Hattori N" first="Nobutaka" last="Hattori">Nobutaka Hattori</name>
<affiliation wicri:level="3"><inist:fA14 i1="04"><s1>Department of Neurology, Juntendo University School of Medicine</s1>
<s2>Tokyo</s2>
<s3>JPN</s3>
<sZ>7 aut.</sZ>
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<country>Japon</country>
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<author><name sortKey="Hirose, Genjiro" sort="Hirose, Genjiro" uniqKey="Hirose G" first="Genjiro" last="Hirose">Genjiro Hirose</name>
<affiliation wicri:level="1"><inist:fA14 i1="01"><s1>Department of Neurology, Kanazawa Medical University</s1>
<s2>Ishikawa</s2>
<s3>JPN</s3>
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<series><title level="j" type="main">Movement disorders</title>
<title level="j" type="abbreviated">Mov. disord.</title>
<idno type="ISSN">0885-3185</idno>
<imprint><date when="2007">2007</date>
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<profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Basal ganglion</term>
<term>Calcification</term>
<term>Calcinosis</term>
<term>Encephalon</term>
<term>Idiopathic</term>
<term>Nervous system diseases</term>
<term>Photon</term>
<term>Positron</term>
<term>Positron emission tomography</term>
<term>Single photon emission tomography</term>
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<keywords scheme="Pascal" xml:lang="fr"><term>Système nerveux pathologie</term>
<term>Encéphale</term>
<term>Calcinose</term>
<term>Idiopathique</term>
<term>Noyau gris central</term>
<term>Calcification</term>
<term>Tomoscintigraphie émission monophotonique</term>
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<front><div type="abstract" xml:lang="en">We report two familial cases of idiopathic basal ganglia calcification. A 60-year-old proband with choreoathetosis, dysarthria, and cognitive decline showed more extensive brain calcinosis, hypoperfusion, and hypometabolism than did his asymptomatic 82-year-old mother. The mother had no frontal lobe calcinosis but basal ganglia and dentate nucleus depositions were detectable. Perfusion neuroimaging, however, was normal in the asymptomatic mother and abnormal in the clinically impaired proband. The presence of calcinosis cannot be used as an index of neurological impairment but the extent of calcinosis and reduction in perfusion and metabolism may be useful for separating symptomatic from asymptomatic subjects with IBGC. These findings suggest that an interruption of neuronal circuitry may cause neurological deficits. The degree of neurological deficits may correlate with the severity of calcinosis and the reduction of perfusion and metabolism.</div>
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<author><name sortKey="Saiki, Misuzu" sort="Saiki, Misuzu" uniqKey="Saiki M" first="Misuzu" last="Saiki">Misuzu Saiki</name>
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<author><name sortKey="Saiki, Shinji" sort="Saiki, Shinji" uniqKey="Saiki S" first="Shinji" last="Saiki">Shinji Saiki</name>
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<author><name sortKey="Sakai, Koichiro" sort="Sakai, Koichiro" uniqKey="Sakai K" first="Koichiro" last="Sakai">Koichiro Sakai</name>
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<author><name sortKey="Matsunari, Ichiro" sort="Matsunari, Ichiro" uniqKey="Matsunari I" first="Ichiro" last="Matsunari">Ichiro Matsunari</name>
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<author><name sortKey="Higashi, Kotaro" sort="Higashi, Kotaro" uniqKey="Higashi K" first="Kotaro" last="Higashi">Kotaro Higashi</name>
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<author><name sortKey="Murata, Ken A" sort="Murata, Ken A" uniqKey="Murata K" first="Ken-Ya" last="Murata">Ken-Ya Murata</name>
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<author><name sortKey="Hattori, Nobutaka" sort="Hattori, Nobutaka" uniqKey="Hattori N" first="Nobutaka" last="Hattori">Nobutaka Hattori</name>
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<author><name sortKey="Hirose, Genjiro" sort="Hirose, Genjiro" uniqKey="Hirose G" first="Genjiro" last="Hirose">Genjiro Hirose</name>
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<author><name sortKey="Saiki, Shinji" sort="Saiki, Shinji" uniqKey="Saiki S" first="Shinji" last="Saiki">Shinji Saiki</name>
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<author><name sortKey="Sakai, Koichiro" sort="Sakai, Koichiro" uniqKey="Sakai K" first="Koichiro" last="Sakai">Koichiro Sakai</name>
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<author><name sortKey="Matsunari, Ichiro" sort="Matsunari, Ichiro" uniqKey="Matsunari I" first="Ichiro" last="Matsunari">Ichiro Matsunari</name>
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<author><name sortKey="Hattori, Nobutaka" sort="Hattori, Nobutaka" uniqKey="Hattori N" first="Nobutaka" last="Hattori">Nobutaka Hattori</name>
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<author><name sortKey="Hirose, Genjiro" sort="Hirose, Genjiro" uniqKey="Hirose G" first="Genjiro" last="Hirose">Genjiro Hirose</name>
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<term>Basal Ganglia Diseases (pathology)</term>
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<term>Calcinosis (physiopathology)</term>
<term>Family Health</term>
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<front><div type="abstract" xml:lang="en">We report two familial cases of idiopathic basal ganglia calcification. A 60‐year‐old proband with choreoathetosis, dysarthria, and cognitive decline showed more extensive brain calcinosis, hypoperfusion, and hypometabolism than did his asymptomatic 82‐year‐old mother. The mother had no frontal lobe calcinosis but basal ganglia and dentate nucleus depositions were detectable. Perfusion neuroimaging, however, was normal in the asymptomatic mother and abnormal in the clinically impaired proband. The presence of calcinosis cannot be used as an index of neurological impairment but the extent of calcinosis and reduction in perfusion and metabolism may be useful for separating symptomatic from asymptomatic subjects with IBGC. These findings suggest that an interruption of neuronal circuitry may cause neurological deficits. The degree of neurological deficits may correlate with the severity of calcinosis and the reduction of perfusion and metabolism. © 2007 Movement Disorder Society</div>
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	Movement Disorders (revue)
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Movement Disorders (revue)

Neurological deficits are associated with increased brain calcinosis, hypoperfusion, and hypometabolism in idiopathic basal ganglia calcification

Neurological deficits are associated with increased brain calcinosis, hypoperfusion, and hypometabolism in idiopathic basal ganglia calcification

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