Neurological deficits are associated with increased brain calcinosis, hypoperfusion, and hypometabolism in idiopathic basal ganglia calcification.
Identifieur interne : 002819 ( PubMed/Curation ); précédent : 002818; suivant : 002820Neurological deficits are associated with increased brain calcinosis, hypoperfusion, and hypometabolism in idiopathic basal ganglia calcification.
Auteurs : Misuzu Saiki [Japon] ; Shinji Saiki ; Koichiro Sakai ; Ichiro Matsunari ; Kotaro Higashi ; Ken-Ya Murata ; Nobutaka Hattori ; Genjiro HiroseSource :
- Movement disorders : official journal of the Movement Disorder Society [ 0885-3185 ] ; 2007.
English descriptors
- KwdEn :
- Aged, 80 and over, Basal Ganglia Diseases (pathology), Basal Ganglia Diseases (physiopathology), Calcinosis (physiopathology), Family Health, Female, Humans, Male, Metabolism, Inborn Errors (physiopathology), Middle Aged, Positron-Emission Tomography (methods), Tomography, Emission-Computed, Single-Photon (methods), Tomography, X-Ray Computed (methods).
- 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.
DOI: 10.1002/mds.21438
PubMed: 17357130
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pubmed:17357130Le document en format XML
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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="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 Ya" sort="Murata, Ken Ya" 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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<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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<Abstract><AbstractText>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.</AbstractText>
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