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The basal ganglia is a collective group of structures in the brain. These include the striatum, (composed of the putamen and caudate nucleus), globus pallidus, substantia nigra, and the subthalamic nucleus. Along with other structures, the basal ganglia are part of a neural circuit that is integral to voluntary motor function. [1]
Wilson's disease (also called hepatolenticular degeneration) is a genetic disorder characterized by the excess build-up of copper in the body. Symptoms are typically related to the brain and liver .
Corticobasal degeneration (CBD) is a rare neurodegenerative disease involving the cerebral cortex and the basal ganglia. [1] CBD symptoms typically begin in people from 50 to 70 years of age, and typical survival before death is eight years.
Primary familial brain calcification [1] (PFBC), also known as familial idiopathic basal ganglia calcification (FIBGC) and Fahr's disease, [1] is a rare, [2] genetically dominant or recessive, inherited neurological disorder characterized by abnormal deposits of calcium in areas of the brain that control movement.
The basal ganglia (BG) or basal nuclei are a group of subcortical nuclei found in the brains of vertebrates. In humans and other primates , differences exist, primarily in the division of the globus pallidus into external and internal regions, and in the division of the striatum .
Cerebral calcifications: Calcifications on CT (computed tomography) are seen as areas of abnormal signal, typically bilateral and located in the basal ganglia, but sometimes also extending into the white matter.
Calcification [55–95%] of the cerebral cortex (especially depths of sulci, basal ganglia, cerebellum, thalamus; also of the arteries, arterioles, and capillaries). Vascular changes - String vessels, especially in areas of Metachromatic leukodystrophy, calcification in leptomeningeal vessels, accelerated atherosclerosis and arteriolosclerosis.
Neuroferritinopathy is classified as a late-onset basal ganglia disease and is a dominantly inherited neurodegenerative disease. [3] Four different alleles are responsible for neuroferritinopathy. Three arise from nucleotide insertions in the ferritin light chain (FTL) polypeptide gene while the fourth arises from a missense mutation in the FTL ...