Cause Of Basal Ganglia Calcification Research Articles

Hypoparathyroidism presenting with seizures and intracranial calcifications in a child

Introduction The most common potentially treatable cause of basal ganglia calcification is hypoparathyroidism. Case report We present a case of incidentally detected basal ganglia calcification due to hypoparathyroidism in a child presenting with seizures and discuss the clinical features, imaging findings, and management of hypoparathyroidism. Conclusion Prompt detection and treatment of hypoparathyroidism can prevent intracranial calcification and the risk of intracerebral haemorrhages in patients with intracranial calcification.

A rare cause of basal ganglia calcification: Down syndrome

Down syndrome, the most common chromosomal abnormality, may be associated with various neurologic complications such as mental retardation, epilepsy, and basal ganglia calcification. Basal ganglia calcification is a rare complication which can be determined in children with Down syndrome. Herein, we have reported a case of Down syndrome in a 6-year-old boy presented with epilepsy, and basal ganglia calcification. In conclusion, patients with Down syndrome should be suspected for the presence of other neurologic disorders.

Intramuscular Hemangioma of the Temporalis Muscle With Incidental Finding of Bilateral Symmetric Calcification of the Basal Ganglia: A Case Report

We report an 11-year-old boy whose brain computed tomography findings incidentally revealed bilateral basal ganglia calcification. He was symptom-free and had no abnormal neurological findings. He was diagnosed with Fahr's disease based on radiological findings and after excluding other etiologies such as infection, metabolic disorders, congenital malformation and malignancies. Most of the reported cases display an autosomal dominant mode of inheritance. Although Fahr's disease is a rare cause of basal ganglia calcification in children, this disease should be considered in children with a family history of neuropsychiatric disorders.

The genetic causes of basal ganglia calcification, dementia, and bone cysts: DAP12 and TREM2

The genetic causes of basal ganglia calcification, dementia, and bone cysts: <i>DAP12</i> and <i>TREM2</i>

The genetic causes of basal ganglia calcification, dementia, and bone cysts

Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy (PLOSL), or Nasu-Hakola disease, is a presenile dementia associated with loss of myelin, basal ganglia calcification, and bone cysts. It is caused by recessively inherited mutations in two genes encoding subunits of a cell membrane-associated receptor complex: TREM2 and DAP12. The clinical course of PLOSL has not been characterized in a series of patients with TREM2 mutations. The authors compare neurologic and neuroradiologic follow-up data of six patients carrying TREM2 mutations with PLOSL due to defective DAP12 genes. The authors review the known mutations in these two genes. Mutations in DAP12 and TREM2 result in a uniform disease phenotype. In Finnish and Japanese patients with PLOSL, DAP12 mutations predominate, whereas TREM2 is mutated more frequently elsewhere. Polycystic lipomembranous osteodysplasia with sclerosing leukoencephalopathy should be considered in adult patients under age 50 years with dementia and basal ganglia calcification. Radiographs of ankles and wrists, and DNA test in uncertain cases, confirm the diagnosis.

Basal ganglia calcification as a late radiation effect.

Basal ganglia calcification following radiation therapy has rarely been documented in the literature. A case of diffuse bilateral basal ganglia calcification developing 6 years after irridiation of a hypothalamic glioma is presented. Review of previous reports and other causes of basal ganglia calcification are discussed.