Neurological deficits are associated with increased brain calcinosis, hypoperfusion, and hypometabolism in idiopathic basal ganglia calcification.
Mov Disord
; 22(7): 1027-30, 2007 May 15.
Article
en En
| MEDLINE
| ID: mdl-17357130
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.
Buscar en Google
Colección:
01-internacional
Base de datos:
MEDLINE
Asunto principal:
Enfermedades de los Ganglios Basales
/
Calcinosis
/
Errores Innatos del Metabolismo
Tipo de estudio:
Risk_factors_studies
Límite:
Aged80
/
Female
/
Humans
/
Male
/
Middle aged
Idioma:
En
Revista:
Mov Disord
Asunto de la revista:
NEUROLOGIA
Año:
2007
Tipo del documento:
Article
País de afiliación:
Japón