Brain calcinosis syndrome (BCS) usually is defined as bilateral calcium accumulation in the brain parenchyma, primarily in the basal ganglia. More than 50 reported clinical conditions have been associated with BCS. We reviewed clinical, radiological, and genetic features of heredofamilial BCS accompanying all conditions associated with calcium accumulation in the brain reported in English between 1962 and 2003 in MEDLINE. The location, extent, and degree of calcification in the brain show diversity not only among the various disorders but also among patients sharing the same condition. The pathogenesis of BCS is uncertain. More complicated mechanisms may be Involved when brain calcinosis is present but calcium, phosphorus, and parathyroid hormone metabolism abnormalities are absent. We review conditions associated with heredofamilial BCS in which brain calcinosis is nearly uniformly present because such information may be Important to the clinician pursuing an investigative strategy.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.4065/80.5.641 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Unveiling the Hidden Burden: A Systematic Review on the Prevalence and Clinical Implications of Calcified Brain Metastases.
Biomolecules
December 2024
Department of Surgical Specialties, Radiological Sciences and Public Health, University of Brescia, 25123 Brescia, Italy.
Background: Brain calcifications, found in various conditions, may be incidental or crucial for diagnosis. They occur in physiological changes, infections, genetic diseases, neurodegenerative conditions, vascular syndromes, metabolic disorders, endocrine disorders, and primary tumors like oligodendroglioma. While often incidental, their presence can be vital for accurate diagnosis.
View Article and Find Full Text PDFExtended endoscopic endonasal trans-tubercular approach and radical resection of a giant calcified craniopharyngioma with pituitary stalk preservation - Technical nuances and steps.
J Clin Neurosci
December 2024
Head Neck Surgical Oncology, Tata Memorial Centre, Mumbai, India.
This case highlights the surgical steps and nuances in preserving the pituitary stalk to ensure good endocrinological outcomes during endoscopic craniopharyngioma resection.
View Article and Find Full Text PDFMedial intracranial carotid artery calcifications and hematoma expansion in deep intracerebral hemorrhage.
Ann Clin Transl Neurol
December 2024
Department of Continuity of Care and Frailty, Neurology Unit, ASST-Spedali Civili, Brescia, Italy.
Background: Medial intracranial carotid artery calcifications (ICAC) are associated with impaired vascular physiology, increased arterial stiffness and pulse pressure. Their presence might therefore be associated with increased risk of intracerebral hemorrhage (ICH) expansion, according to the avalanche model. We explored the association between ICAC presence and pattern and hematoma expansion (HE).
View Article and Find Full Text PDFMechanism and significance of diffusion restriction followed by calcification in high-grade glioma treated with bevacizumab.
Sci Rep
November 2024
Division of Neurosurgery, Department of Brain and Neurosciences, Faculty of Medicine, Tottori University, 36-1, Nishi-cho, Yonago, 683-8504, Tottori, Japan.
In this study, we focused on calcification and diffusion restriction, which sometimes appear around the resection cavity or periventricular white matter in patients with high-grade glioma (HGG) treated with bevacizumab (BVZ), as candidate imaging biomarkers for BVZ treatment efficacy. We investigated the timing of the appearance of diffusion restriction and calcification using magnetic resonance imaging and computed tomography in 35 patients with newly diagnosed or recurrent HGG treated with BVZ. In 17 (48.
View Article and Find Full Text PDFTargeting TREM2 signaling shows limited impact on cerebrovascular calcification.
Life Sci Alliance
January 2025
Department of Neurosurgery, Clinical Neuroscience Center, University Hospital Zurich, University of Zurich, Zurich, Switzerland
Brain calcification, the ectopic mineral deposits of calcium phosphate, is a frequent radiological finding and a diagnostic criterion for primary familial brain calcification. We previously showed that microglia curtail the growth of small vessel calcification via the triggering receptor expressed in myeloid 2 (TREM2) in the mouse model of primary familial brain calcification. Because boosting TREM2 function using activating antibodies has been shown to be beneficial in other disease conditions by aiding in microglial clearance of diverse pathologies, we investigated whether administration of a TREM2-activating antibody could mitigate vascular calcification in mice.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!