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Artykuły w czasopismach na temat „Brain calcifications”

Autor: Grafiati

Data publikacji: 3 czerwca 2025

Data aktualizacji: 31 lipca 2025

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PEG, Sounga Bandzouzi. "Primary Brain Calcification in a Case and Review of the Literature." Neurology & Neurotherapy Open Access Journal 4, no. 2 (2019): 1–4. http://dx.doi.org/10.23880/nnoaj-16000137.

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Primary brain calcifications are most often described in a family context (PFBC). It is a rare neurodegenerative disease characterized by calcifications of the basal ganglia and other brain regions. the diagnostic criteria for this disease are defined by: bilateral calcifications of the nuclei of the base; progressive neurological disorders; the absence of abnormalities suggestive of another metabolic or mitochondrial disorder, the absence of an infectio us, traumatic or toxic cause and an evocative family context. His pathophysiology is unclear. We report an observation of sporadic primary ce

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Nicolas, Gaël, Monica Sanchez-Contreras, Eliana Marisa Ramos, et al. "Brain calcifications and PCDH12 variants." Neurology Genetics 3, no. 4 (2017): e166. http://dx.doi.org/10.1212/nxg.0000000000000166.

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Objective:To assess the potential connection between PCDH12 and brain calcifications in a patient carrying a homozygous nonsense variant in PCDH12 and in adult patients with brain calcifications.Methods:We performed a CT scan in 1 child with a homozygous PCDH12 nonsense variant. We screened DNA samples from 53 patients with primary familial brain calcification (PFBC) and 26 patients with brain calcification of unknown cause (BCUC).Results:We identified brain calcifications in subcortical and perithalamic regions in the patient with a homozygous PCDH12 nonsense variant. The calcification patter

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Golüke, Nienke M. S., Enrico Meijer, Emiel A. van Maren, et al. "Amount and Distribution of Intracranial Calcification in Symptomatic and Asymptomatic Primary Familial Brain Calcification." Neurology: Clinical Practice 13, no. 4 (2023): e200163. http://dx.doi.org/10.1212/cpj.0000000000200163.

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Background and ObjectivesIn clinical practice, it can be difficult to differentiate between intracranial calcifications related to primary familial brain calcification (PFBC) or aging. Also, little is known about the consequences of the amount of intracranial calcifications in patients with PFBC. Therefore, we aimed to compare the amount and distribution of intracranial calcifications in persons with PFBC with controls and between asymptomatic and symptomatic PFBC cases.MethodsThis was a case-control study including patients with PFBC and controls. Controls received a CT of the brain because o

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Monfrini, Edoardo, Federica Arienti, Paola Rinchetti, Francesco Lotti, and Giulietta M. Riboldi. "Brain Calcifications: Genetic, Molecular, and Clinical Aspects." International Journal of Molecular Sciences 24, no. 10 (2023): 8995. http://dx.doi.org/10.3390/ijms24108995.

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Many conditions can present with accumulation of calcium in the brain and manifest with a variety of neurological symptoms. Brain calcifications can be primary (idiopathic or genetic) or secondary to various pathological conditions (e.g., calcium–phosphate metabolism derangement, autoimmune disorders and infections, among others). A set of causative genes associated with primary familial brain calcification (PFBC) has now been identified, and include genes such as SLC20A2, PDGFB, PDGFRB, XPR1, MYORG, and JAM2. However, many more genes are known to be linked with complex syndromes characterized

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Badiu, Corin. "Brain Calcifications." Acta Endocrinologica (Bucharest) 2, no. 1 (2006): 109. http://dx.doi.org/10.4183/aeb.2006.109.

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Goo, Hyung mo, Sang-Youl Yoon, and Seong-Hyun Park. "Fahr disease presenting with multiple cerebral calcifications." Journal of the Korean Society of Stereotactic and Functional Neurosurgery 19, no. 1 (2023): 22–25. http://dx.doi.org/10.52662/jksfn.2023.00038.

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Fahr disease, also known as idiopathic basal ganglion calcification, is a rare and genetically heterogeneous neurological disorder. Herein, we report a rare case of Fahr disease presenting with multiple cerebral calcifications. A 63-year-old woman presented with dizziness to a local clinic. Brain computed tomography performed on admission revealed multiple high-intensity lesions in both basal ganglia, both cerebellar hemispheres, and the left frontal lobe. In contrast, brain magnetic resonance imaging (MRI) showed no prominent lesions on T2- and T1-weighted images, and there was no contrast en

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Som, Panchali, Rajarshi Roy, Sumit Datta, Asis Kumar Ghosal, Anubha Saha, and Subhajit Halder. "Physiological Intracranial Calcification in Eastern Indian Population-A CT Scan Study." National Journal of Clinical Anatomy 06, no. 01 (2017): 059–70. http://dx.doi.org/10.1055/s-0039-1700723.

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Abstract Background and Aims:Knowledge of physiological calcification in brain parenchyma is essential to avoid misinterpretation during radiological evaluation. The calcifications are commonly seen in pineal gland, falx cerebri, tentorium cerebelli and choroid plexus. Objective:To determine the incidence of physiological intracranial calcification and its relationship to age and sex in eastern Indian population. Materials and Method: A cross sectional descriptive study of CT scan brain was performed in age group between 20-80 yrs in eastern India. The study was conducted on 64 Slice MDCT PHIL

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Garaba, Alexandru, Pier Paolo Panciani, Aida Da’ana, et al. "Unveiling the Hidden Burden: A Systematic Review on the Prevalence and Clinical Implications of Calcified Brain Metastases." Biomolecules 14, no. 12 (2024): 1585. https://doi.org/10.3390/biom14121585.

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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. Brain metastases are the most common neoplastic lesions in adults, with their incidence increasing due to improved diagnostic tools and overall oncologic patient survival. Calcifications within brain metastases are

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Cen, Zhidong, You Chen, Si Chen, et al. "Biallelic loss-of-function mutations in JAM2 cause primary familial brain calcification." Brain 143, no. 2 (2019): 491–502. http://dx.doi.org/10.1093/brain/awz392.

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Abstract Primary familial brain calcification is a monogenic disease characterized by bilateral calcifications in the basal ganglia and other brain regions, and commonly presents motor, psychiatric, and cognitive symptoms. Currently, four autosomal dominant (SLC20A2, PDGFRB, PDGFB, XPR1) and one autosomal recessive (MYORG) causative genes have been identified. Compared with patients with autosomal dominant primary familial brain calcification, patients with the recessive form of the disease present with more severe clinical and imaging phenotypes, and deserve more clinical and research attenti

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Sridhar, Sucheta, Yingyue Zhou, Adiljan Ibrahim, et al. "Targeting TREM2 signaling shows limited impact on cerebrovascular calcification." Life Science Alliance 8, no. 1 (2024): e202402796. http://dx.doi.org/10.26508/lsa.202402796.

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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 thePdgfbret/retmouse 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 adminis

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Mu, Weiyi, Laura Tochen, Caroline Bertsch, Harvey S. Singer, and Kristin W. Barañano. "Intracranial calcifications and dystonia associated with a novel deletion of chromosome 8p11.2 encompassing SLC20A2 and THAP1." BMJ Case Reports 12, no. 5 (2019): e228782. http://dx.doi.org/10.1136/bcr-2018-228782.

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Several genes located within the chromosome 8p11.21 region are associated with movement disorders including SLC20A2 and THAP1. SLC20A2 is one of four genes associated with primary familial brain calcification, a syndrome that also includes movement disorders, cognitive decline and psychiatric issues. THAP1 is associated with dystonia type 6, a dominantly inherited dystonia with variable expression. In addition, several reports in the French-Canadian population have described microdeletions within the 8p11.2 region presenting with dystonia-plus syndromes including brain calcifications. This cas

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Mathijssen, Gini, Evelien van Valen, Pim A. de Jong, et al. "The Association between Intracranial Calcifications and Symptoms in Patients with Primary Familial Brain Calcification." Journal of Clinical Medicine 13, no. 3 (2024): 828. http://dx.doi.org/10.3390/jcm13030828.

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(1) Background: Primary Familial Brain Calcification (PFBC) is a neurodegenerative disease characterized by bilateral calcifications of the basal ganglia and other intracranial areas. Many patients experience symptoms of motor dysfunction and cognitive disorders. The aim of this study was to investigate the association between the amount and location of intracranial calcifications with these symptoms. (2) Methods: Patients with suspected PFBC referred to our outpatient clinic underwent a clinical work-up. Intracranial calcifications were visualized on Computed Tomography (CT), and a Total Calc

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Bhatt, Bhupendra Prasad. "Evaluation of intracranial physiological calcifications in Computed Tomography." Radiography Open 9, no. 1 in progress (2023): 50–59. http://dx.doi.org/10.7577/radopen.5205.

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Introduction: Intracranial physiological calcifications are not related to any pathological conditions, rather they are due to the normal deposition of calcium or iron in the different parts of the brain. Computed Tomography (CT) scan is superior to all other modalities in terms of sensitivity in the detection of intracranial physiological calcifications. The objective of the study was to evaluate the frequency and location of intracranial physiological calcifications and also study them according to age and gender. Methods: A prospective cross-sectional study with a purposive sampling t

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Oliveira, E., I. Coelho, P. Manuel, and F. Girão. "Bilateral brain calcifications." European Journal of Internal Medicine 24 (October 2013): e189-e190. http://dx.doi.org/10.1016/j.ejim.2013.08.487.

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Sun, Ming-Tsung, Sung-Sen Yang, Chun-Jung Juan, and Shih-Hua Lin. "Symmetrical Brain Calcifications." American Journal of Medicine 123, no. 2 (2010): 131–33. http://dx.doi.org/10.1016/j.amjmed.2009.12.002.

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Gilani, Ahmed, Laura A. Adang, Adeline Vanderver, Abigail Collins, and BK Kleinschmidt-DeMasters. "Neuropathological Findings in a Case of IFIH1-Related Aicardi–Goutières Syndrome." Pediatric and Developmental Pathology 22, no. 6 (2019): 566–70. http://dx.doi.org/10.1177/1093526619837797.

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Aicardi–Goutières syndrome (AGS) is a rare syndrome characterized by calcification, diffuse demyelination, and variable degree of brain atrophy. The syndrome is genetically heterogeneous with mutations in 7 genes, including TREX1, RNASEH2A, RNASEH2B, RNASEH2C, SAMHD1, ADAR1, and IFIH1 (interferon-induced helicase c domain-containing protein 1) associated with the syndrome, so far. These mutations lead to the overproduction of α-interferon within the central nervous system. Mutations in IFIH1 have been recently described in a subset of AGS, with only 1 previous report of neuropathological findi

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Westenberger, Ana, Alexander Balck, and Christine Klein. "Primary familial brain calcifications." Current Opinion in Neurology 32, no. 4 (2019): 571–78. http://dx.doi.org/10.1097/wco.0000000000000712.

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Aldo, Bertoli, Valentini Alessia, Mauriello Alessandro, and Tarantino Umberto. "Hypoparathyroidism, Brain Calcifications and Seizures." International Journal of Medical and Pharmaceutical Case Reports 9, no. 3 (2017): 1–5. https://doi.org/10.9734/IJMPCR/2017/33721.

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<strong>Background:</strong> The most common cause of hypoparathyroidism is iatrogenic in the context of surgical procedures to the neck and commonly the thyroid gland. Hypoparathyroidism is characterized by hypocalcaemia, hyperphosphatemia and low or inappropriately normal levels of parathyroid hormone (PTH) and may be associated with multiorgan complications and variable clinical presentation. Seizures may be the only presenting symptom and may result in antiepileptic therapy. Knowledge of all possible consequences of hypoparathyroidism is essential for correct patient management. <strong>Ca

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Shen, Jack, Amelle Shillington, Alberto J. Espay, and Emily J. Hill. "Familial Brain Calcifications With Leukoencephalopathy." Neurology Genetics 8, no. 4 (2022): e200001. http://dx.doi.org/10.1212/nxg.0000000000200001.

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ObjectiveTo describe a family with primary familial brain calcifications (PFBCs) and leukoencephalopathy associated with a novel variant in PDGFB.MethodsWe present 3 generations of a family with PFBC associated with a previously unreported variant in PDGFB.ResultsA 24-year-old woman with migraine, bipolar disorder, and functional neurologic disorder was found to have bilateral calcifications of the basal ganglia and frontally predominant periventricular white matter disease. Her father had mild cognitive impairment and action tremor of the hands with basal ganglia and cerebellar calcifications

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Snyder-Keller, Abigail, Valerie J. Bolivar, Steven Zink, and Laura D. Kramer. "Brain Iron Accumulation and the Formation of Calcifications After Developmental Zika Virus Infection." Journal of Neuropathology & Experimental Neurology 79, no. 7 (2020): 767–76. http://dx.doi.org/10.1093/jnen/nlaa043.

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Abstract Intracranial calcifications (ICC) are the most common neuropathological finding in the brains of children exposed in utero to the Zika virus (ZIKV). Using a mouse model of developmental ZIKV infection, we reported widespread calcifications in the brains of susceptible mice that correlated in multiple ways with the behavioral deficits observed. Here, we examined the time course of ICC development and the role of iron deposition in this process, in 3 genetically distinct inbred strains of mice. Brain iron deposits were evident by Perls’ staining at 2 weeks post infection, becoming incre

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Chelban, Viorica, Miryam Carecchio, Gillian Rea, et al. "MYORG-related disease is associated with central pontine calcifications and atypical parkinsonism." Neurology Genetics 6, no. 2 (2020): e399. http://dx.doi.org/10.1212/nxg.0000000000000399.

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ObjectiveTo identify the phenotypic, neuroimaging, and genotype-phenotype expression of MYORG mutations.MethodsUsing next-generation sequencing, we screened 86 patients with primary familial brain calcification (PFBC) from 60 families with autosomal recessive or absent family history that were negative for mutations in SLC20A2, PDGFRB, PDGBB, and XPR1. In-depth phenotyping and neuroimaging investigations were performed in all cases reported here.ResultsWe identified 12 distinct deleterious MYORG variants in 7 of the 60 families with PFBC. Overall, biallelic MYORG mutations accounted for 11.6%

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Schievink, Wouter I., Lindsey Ross, Ravi S. Prasad, and M. Marcel Maya. "Vanishing calcification associated with a spontaneous ventral spinal cerebrospinal fluid leak." Cephalalgia 36, no. 14 (2016): 1366–69. http://dx.doi.org/10.1177/0333102416628468.

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Background Some patients with spontaneous intracranial hypotension have a ventral spinal cerebrospinal fluid (CSF) leak and these CSF leaks may be associated with calcified disk herniations. Identifying these calcifications is helpful in directing treatment. We report here the unusual case of a patient with a ventral CSF leak in whom the associated calcification absorbed over a five-month period. Case report A 42-year-old woman developed orthostatic headaches and bilateral abducens nerve palsies. Magnetic resonance imaging of her brain showed typical findings of spontaneous intracranial hypote

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Bertoli, Aldo, Alessia Valentini, Alessandro Mauriello, and Umberto Tarantino. "Hypoparathyroidism, Brain Calcifications and Seizures." International Journal of Medical and Pharmaceutical Case Reports 9, no. 3 (2017): 1–5. http://dx.doi.org/10.9734/ijmpcr/2017/33721.

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Hastrup, Jørgen, and Edith Reske-Nielsen. "SYMMETRICAL BRAIN CALCIFICATIONS IN INFANTS." Acta Neurologica Scandinavica 41, S13 (2009): 637–44. http://dx.doi.org/10.1111/j.1600-0404.1965.tb01940.x.

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Kobayashi, Yuya, Jun Tsuyuzaki, and Yoichi Koizumi. "Pseudohypoparathyroidism Causing Multiple Brain Calcifications." Internal Medicine 57, no. 1 (2018): 153–54. http://dx.doi.org/10.2169/internalmedicine.8926-17.

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Bustos, Javier A., Hector H. Garcia, and Edinson Montoya. "Residual Brain Calcifications in Neurocysticercosis." American Journal of Tropical Medicine and Hygiene 78, no. 3 (2008): 363. http://dx.doi.org/10.4269/ajtmh.2008.78.363.

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de la Plaza Llamas, Roberto, José Manuel Ramia Ángel, Vladimir Arteaga Peralta, Jaime Hernández Cristóbal, and Aylhin Joana López Marcano. "Brain Calcifications and Primary Hyperparathyroidism." Cirugía Española (English Edition) 94, no. 1 (2016): e5-e7. http://dx.doi.org/10.1016/j.cireng.2015.12.001.

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Gusbi, Osama, and Gary L. Bernardini. "Brain Calcifications in Systemic Sclerosis." Archives of Neurology 59, no. 10 (2002): 1642. http://dx.doi.org/10.1001/archneur.59.10.1642.

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Oster, S., E. Reske-Nielsen, and I. Bruun. "Lafora's disease and brain calcifications." Acta Neuropathologica 76, no. 5 (1988): 532–38. http://dx.doi.org/10.1007/bf00686395.

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Ghose, Tumpa Indrani, Sayedul Ashraf Kushal, Md Mohidul Islam, Yahia Md Amin, Zunayed Al Azdi, and Saiful Islam Saif. "Fahr’s Disease Presenting with Seizures and Behavioral Disturbance in a 14-Year-Old Adolescent." Journal of Bangladesh College of Physicians and Surgeons 43, no. 2 (2025): 183–85. https://doi.org/10.3329/jbcps.v43i2.80669.

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Fahr's disease is a rare neurodegenerative disorder characterized by abnormal brain calcifications, typically presented in middle age. This case report describes an unusual presentation in a 14-year-old boy, highlighting the importance of considering Fahr's disease in pediatric patients. The patient had a 5-year history of seizures, cognitive decline, and behavioral disturbances, along with obesity, short stature, low intelligence, and a clumsy gait. Imaging revealed extensive symmetrical calcifications in the basal ganglia, dentate nucleus, and cerebral white matter, confirming Fahr's disease

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Lorente-Poch, Leyre, Sílvia Rifà-Terricabras, Juan José Sancho, Danilo Torselli-Valladares, Sofia González-Ortiz, and Antonio Sitges-Serra. "Prevalence of basal ganglia and carotid artery calcifications in patients with permanent hypoparathyroidism after total thyroidectomy." Endocrine Connections 9, no. 10 (2020): 955–62. http://dx.doi.org/10.1530/ec-20-0387.

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Objective: Permanent hypoparathyroidism is an uncommon disease resulting most frequently from neck surgery. It has been associated with visceral calcifications but few studies have specifically this in patients with post-surgical hypoparathyroidism. The aim of the present study was to assess the prevalence of basal ganglia and carotid artery calcifications in patients with long-term post-thyroidectomy hypoparathyroidism compared with a control population. Design: Case–control study. Methods: A cross-sectional review comparing 29 consecutive patients with permanent postoperative hypoparathyroid

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Magistrelli, Luca, Roberta Croce, Fabiola De Marchi, et al. "Expanding the genetic spectrum of primary familial brain calcification due to SLC2OA2 mutations: a case series." neurogenetics 22, no. 1 (2021): 65–70. http://dx.doi.org/10.1007/s10048-021-00634-9.

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AbstractPrimary familial brain calcification (PFBC) is a neurological condition characterized by the presence of intracranial calcifications, mainly involving basal ganglia, thalamus, and dentate nuclei. So far, six genes have been linked to this condition: SLC20A2, PDGFRB, PDGFB, and XPR1 inherited as autosomal-dominant trait, while MYORG and JAM2 present a recessive pattern of inheritance. Patients mainly present with movement disorders, psychiatric disturbances, and cognitive decline or are completely asymptomatic and calcifications may represent an occasional finding. Here we present three

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Ziani, G., EL Azouzi R., N. Doghmi, and M. Cherti. "INTERRELATION BETWEENCARDIAC CONDUCTION ANOMALIES AND RADIOLOGICALFEATURES OF FAHRS SYNDROME: AFACT OR COINCIDENCE? CASE REPORT AND REVIEW OF THE LITTERATURE." International Journal of Advanced Research 12, no. 04 (2024): 135–41. http://dx.doi.org/10.21474/ijar01/18531.

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Introduction:Fahrs syndrome is a rare, slowly progressive, neurodegenerativedisorder, characterized by extensive, bilateral, and symmetrical basal ganglia calcification. It isassociatedwithneuropsychiatric manifestations and gradually progressive cognitive impairment. Fahrs syndrome is the secondaryform of brain calcification thatiscaused by variousmetabolic, infectious, or degenerativediseases. Case report:An old manwasadmittedto ourdepartmentwithrecurrentepisodes of syncope. An electrocardiogramrevealedcomplete AV block.Laboratoryresultsdisclosedhypocalcemia, pseudo hypoparathyroidism, and h

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Kazemian, M., B. Emadi, and S. H. Fakhraee. "A Newborn Infant with Brain Calcifications." NeoReviews 17, no. 8 (2016): e499-e501. http://dx.doi.org/10.1542/neo.17-8-e499.

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Shapiro, Steven D., James Goldman, Susan Morgello, et al. "Pathological correlates of brain arterial calcifications." Cardiovascular Pathology 38 (January 2019): 7–13. http://dx.doi.org/10.1016/j.carpath.2018.09.003.

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Sarac Sivrikoz, T., R. Has, I. Kalelioglu, B. Tatli, G. Turkyilmaz, and A. Yuksel. "P30.10: Prenatal brain calcifications: congenital toxoplasmosis." Ultrasound in Obstetrics & Gynecology 48, S1 (2016): 269. http://dx.doi.org/10.1002/uog.16802.

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Morris, Meaghan, Regina Kwon, and Liam Chen. "Pediatric Idiopathic Basal Ganglia Calcification and Spherocytosis With Chromosome 8p11 Deletion." Journal of Neuropathology & Experimental Neurology 79, no. 2 (2020): 238–41. http://dx.doi.org/10.1093/jnen/nlz133.

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Abstract Idiopathic basal ganglia calcification (IBGC), also known as Fahr disease, is a rare neurodegenerative disorder characterized by the accumulation of extensive parenchymal and vascular calcifications in the basal ganglia, with variable calcifications elsewhere in the brain. Typically, IBGC presents with neurologic and psychiatric symptoms in middle-aged adults. Recent genetic studies have identified alterations in 4 genes causing IBGC, including alterations in SLC20A2 on chromosome 8p11.2. Currently, there are no clinical descriptions of patients with IBGC occurring within the context

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Yakoob, Zarah, and C. Smit. "Maxillofacial Radiology 197." South African Dental Journal 77, no. 02 (2022): 107–8. http://dx.doi.org/10.17159/2519-0105/2022/v77no2a10.

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Large field of view cone beam computed tomography (CBCT) images allows the visualisation of anatomical structures outside of the teeth and jaws. These areas include the cranial vault and paranasal sinuses. Occasionally pathology, anatomical variation and various other incidental findings can be seen.1 As the use of CBCT has become more common amongst general dentists and specialists, awareness and understanding of incidental findings are of great importance, for the patient as well as medico-legal reasons. Calcifications that are found as incidental findings on CBCT scans within the brain can

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Jacob, Anu, and George Sarin Zacharia. "A case of familial intracranial calcification – Fahr’s disease." Muller Journal of Medical Sciences and Research 16, no. 1 (2025): 89–91. https://doi.org/10.4103/mjmsr.mjmsr_20_25.

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ABSTRACT Fahr’s disease, an uncommon disorder characterized by bilateral intracranial brain parenchymal calcification, presents with diverse neurological manifestations. It is often an autosomal dominantly inherited disorder with incomplete penetrance. The most frequently implicated are mutations involving SLC20A2 on chromosome 8p, while others involve genes XPR1, PDGFRB, PDGFB, and IBGC1. Neuroimaging typically reveals symmetrical dense calcifications, predominantly affecting the basal ganglia but may extend to other brain regions. Diagnosis relies on classical imaging findings, exclusion of

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Hajar, Dr Khaoulani, Dr Chaimae Jeddi, Amenzouy Amenzouy, et al. "Fahr Syndrome and Psychosis: Clinical Case." SAS Journal of Surgery 10, no. 10 (2024): 1141–42. http://dx.doi.org/10.36347/sasjs.2024.v10i10.010.

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Fahr syndrome is a rare neurodegenerative disease characterized by bilateral, symmetrical calcification of the basal ganglia and gray matter. We present the case of a 27-year-old woman who presented to the emergency department with febrile consciousness disturbance. Brain CT revealed extensive, bilateral, symmetrical calcifications of the basal ganglia and cerebellum. A rare syndrome, Fahr syndrome should be kept in mind and appropriate symptomatic treatment should be applied in order to stop progression and improve symptoms and clinical signs.

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Sumnu, Abdullah, Zeki Aydin, Meltem Gursu, et al. "A Case of Primary Hypoparathyroidism Presenting with Acute Kidney Injury Secondary to Rhabdomyolysis." Case Reports in Nephrology 2016 (2016): 1–4. http://dx.doi.org/10.1155/2016/3240131.

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Hypoparathyroidism is the most common cause of symmetric calcification of the basal ganglia. Herein, a case of primary hypoparathyroidism with severe tetany, rhabdomyolysis, and acute kidney injury is presented. A 26-year-old male was admitted to the emergency clinic with leg pain and cramps, nausea, vomiting, and decreased amount of urine. He had been treated for epilepsy for the last 10 years. He was admitted to the emergency department for leg pain, cramping in the hands and legs, and agitation multiple times within the last six months. He was prescribed antidepressant and antipsychotic med

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Oliveira, Matheus Fernandes de, Edison Barros e. Silva, and João Ricardo Mendes de Oliveira. "Prevalence of brain calcifications in a Brazilian cohort: A retrospective study in radiology services." Dementia & Neuropsychologia 7, no. 2 (2013): 210–15. http://dx.doi.org/10.1590/s1980-57642013dn70200012.

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ABSTRACT Brain calcifications may be present in a wide range of neuropsychiatric, infectious traumatic, neoplastic and endocrine conditions, associated with motor and cognitive symptoms. They are often considered "physiologic" or pathologic. Objective: To determine the prevalence of brain calcifications in a Brazilian cohort. Methods: 1898 consecutive patients underwent skull CTs, comprising 836 men and 1062 women. Results: Among all 1898 patients, 333 (197 women and 136 men) presented with brain calcifications, representing an overall prevalence of 17.54%. The prevalence in the female group w

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Kolotilov, Nikolay. "Pineal gland calcifications in patients with benign and malignant tumors of the larynx, pharynx, paranasal sinuses and auditory nerve." Radiation Diagnostics, Radiation Therapy, no. 2 (2020): 18–27. http://dx.doi.org/10.37336/2707-0700-2020-2-2.

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Calcifications of the brain – pineal gland, choroid plexuses of the lateral ventricles – are a long-known phenomenon. Calcification in such functionally important organs as the pineal gland and choroid plexuses of the lateral ventricles cannot be physiological (it is enough to recall the formation of stones in the gallbladder, kidneys, prostate gland, calcinosis of the heart valves and coronary vessels) or relatively neutral process in the body and not affect the activity of these organs. The purpose of the investigation is to study the nosological predisposition of calcifications and the inci

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Dhungel, Omkar, Apeksha Aryal, Sulochana Joshi, Bastabika Neupane, and Nidesh Sapkota. "Psychosis possibly associated with Fahr’s disease: A case report from the Himalayan country." Journal of Psychiatrists' Association of Nepal 14, no. 1 (2025): 59–61. https://doi.org/10.3126/jpan.v14i1.80943.

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Fahr’s disease (FD) is a progressive and degenerative familial autosomal dominant, rare neurological disorder, characterized by bilateral calcifications in the brain. FD may have neurological manifestations corresponding to the area of the brain involved. Significant proportions have neuro-psychiatric symptoms and psychosis is one. There is no specific treatment for FD but the neuropsychiatric manifestations can be managed. We present a case of a 30-year-old male with a 12-year history of psychosis, an episode of mania with psychotic symptoms, and an unsteady gait for 3 years. Baseline investi

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Shin, Ji-Yong, and Sa-Yoon Kang. "Bilateral striopallidodentate calcinosis in a patient with myasthenia gravis." Journal of Medicine and Life Science 12, no. 2 (2015): 37–38. http://dx.doi.org/10.22730/jmls.2015.12.2.37.

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Bilateral symmetric calcification involing striatum, pallidum with or without deposit in dentate nucleus is reported fromasymptomatic individuals to a variety of neurological conditions. Clinically it may present with an array of movement disorders,dementia, cerebellar impairment and speech disorder. We report a myasthenia gravis patient with dysarthria which did notrespond to pyridostigmin. Brain MRI showed bilateral striopallidodentate calcinosis (BSPDC). To our knowledge, there is noreported case having anti-acetylcholine receptor antibody and massive intracranial calcifications. This case

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Nwankwo, Nnenna, Brianna Pierce, Natalie Smith, and Jamie Fraser. "Blood-brain barrier dysfunction in leukoencephalopathy, brain calcifications, and cysts." Molecular Genetics and Metabolism 141, no. 4 (2024): 108194. http://dx.doi.org/10.1016/j.ymgme.2024.108194.

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Del Brutto, Oscar H. "Parenchymal brain calcified cysticercus and progression of hippocampal atrophy." Revista Ecuatoriana de Neurologia 33, no. 2 (2024): 92–93. http://dx.doi.org/10.46997/revecuatneurol33200092.

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A seizure-free 74-year-old woman had a single calcified cysticercus (Figure 1), and normal hippocampi (Figure 2, upper panel). Neuroimaging exams were practiced for a study aimed to assess the association between neurocysticercosis and hippocampal atrophy (HA).1 Seven years later, a control MRI showed bilateral HA (Figure 2, lower panel). The patient remained seizure-free during the observation period. The association between calcified cysticercus and HA in seizure-free individuals has been recognized.2 It has been postulated that repetitive episodes of inflammation from antigens released to t

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Ayrignac, Xavier, Gaël Nicolas, Clarisse Carra-Dallière, Didier Hannequin, and Pierre Labauge. "Brain Calcifications in Adult-Onset Genetic Leukoencephalopathies." JAMA Neurology 74, no. 8 (2017): 1000. http://dx.doi.org/10.1001/jamaneurol.2017.1062.

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Fatema, Kaniz, Shriear Tanbeen, Md Sahidul Hoque Ashek, et al. "An Elderly Lady with Tetany and Brain Calcification." Bangladesh Critical Care Journal 12, no. 2 (2024): 160–62. http://dx.doi.org/10.3329/bccj.v12i2.76462.

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We present the case of a 59-year-old Bangladeshi lady who presented in Intensive Care Unit with tetany and altered level of consciousness. Tetany resolved after giving IV calcium injection. Initial laboratory investigations showed hypocalcemia. Non-contrast CT brain showed irregular bilateral symmetrical calcifications in basal ganglia, thalami, cerebellum and corona radiata. Subsequent laboratory test revealed low parathyroid hormone level. So, she was diagnosed as Fahr’s syndrome due to secondary hypoparathyroidism. This is a rare neurological disorder characterized by metabolic, biochemical

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Bouktib, Y., K. Elhadri, B. Boutakioute, M. Ouali El Idrissi, and N. CherifIdrissi El Ganouni. "Fahr's Syndrome- An Interesting Case Presentation." Scholars Journal of Medical Case Reports 10, no. 6 (2021): 621–23. http://dx.doi.org/10.36347/sjmcr.2021.v09i06.002.

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Idiopathic basal ganglia calcification (IBGC), commonly referred to as Fahr’s disease, is a rare neurological disorder characterized by the abnormal, symmetrical, and bilateral calcification of the basal ganglia and other brain regions. Patients typically present in their forties and fifties with various neurologic and/or psychiatric symptoms, including movement disorders, Parkinsonism, psychosis, and depression. The pathophysiology of this disease is not completely understood; however, several gene mutations have been identified in the pathogenesis of Fahr’s disease. These mutations display a

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