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Friedreich's ataxia is a genetic disease and is associated with a mutation of the 9th chromosome, as a result of which there is a deficiency or deficiency of the frataxin protein. This protein is responsible for the transport of iron from the mitochondria. Violation of its function leads to the accumulation of a large amount of iron inside the mitochondria and an increase in free radicals inside the cell. The latter have a damaging effect on the cell. In this case, the most active cells of Ondansetron pills suffer: neurons (nerve cells), myocardiocytes (cardiac muscle cells), insulin-synthesizing β - pancreatic cells, retinal receptor cells (rods and cones) and bone tissue cells. The defeat of these cells leads to the development of symptoms characteristic of Friedreich's ataxia from the peripheral and central nervous system, diabetes mellitus, cardiomyopathy, visual impairment, bone deformities.
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Friedreich's ataxia was described in 1860 by a German physician, whose name the disease still bears. Friedreich's ataxia belongs to the group of ataxias, which also includes cerebellar ataxia, Pierre-Marie's ataxia, Louis-Bar syndrome, cortical and vestibular ataxia. In this group, Friedreich's ataxia is the most common disease. Its prevalence worldwide is 2-7 cases per 100 thousand population. Friedreich's ataxia is inherited in an autosomal recessive manner. The carrier of Zofran mutation that causes it, according to some sources, is 1 out of 120 people. But Fredreich's ataxia develops only if a person inherits a distorted gene from both his father and mother. At the same time, his parents are only carriers of a genetic disorder and do not themselves suffer from Fredreich's ataxia. Symptoms of Friedreich's ataxia.
As a rule, Friedreich's ataxia begins to appear in the first two decades of life. In much rarer cases, signs of the disease appear in the third or fourth decade.
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Physiotherapy exercises are of great importance for patients with Friedreich's ataxia. Constant physical therapy exercises aimed at training coordination and muscle strength make it possible to maintain motor activity and stop the resulting pain. Since Friedreich's ataxia is accompanied by a violation of energy metabolism, patients with this disease need to limit the intake of carbohydrates with food, the excess of which can provoke an aggravation of metabolic disorders.
The disease is characterized by a syndrome of damage to the posterior and lateral funiculi of the spinal cord, more often in the lumbosacral segments, the death of cells of Clark's pillars and dorsal spinocerebellar tracts. In the later stages, degeneration of the nuclei of the cranial nerves, the dentate nucleus, and the cerebellar peduncle is characteristic, and the cells of the cerebral hemispheres suffer somewhat less frequently.