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Aim: to analyze modern professional literature and summarize data on treatment methods for peripheral nerve injuries, taking into account the mechanisms of positive effects. The article presents an overview of possible methods for treatment of peripheral nerve injuries, fundamental classifications of peripheral nerve injuries, their differences are considered, pathophysiological mechanisms and the probability of spontaneous recovery depending on the degree of injury, general principles and conditions for successful regeneration of the peripheral nerve. Options, combinations, advantages and disadvantages of such surgical methods for peripheral nerve injury treatment as neurorrhaphy, autotransplantation and allotransplantation are described in detail, such terms as “small”, “large” and “critical” gaps between the nerve stumps are specified. Classifications and characteristics of conduits are described, types of synthetic conduits are considered. The use of drugs, Schwann cells, growth and neurotrophic factors, neural, embryonic and mesenchymal stem cells of various origins, exosomes of mesenchymal stem cells in the so-called “stem cell-free therapy” in treating this pathology is mentioned. Genetically modified mesenchymal stem cells, optokinetics are also noted, such physical methods for peripheral nerve injury treatment as short-term low-frequency electrical stimulation of the nerve, magnetic stimulation, low-intensity ultrasound, photobiomodulation therapy, photochemical bonding are discussed, indicating some mechanisms of their positive effects. Conclusions. Improving the quality of life and reducing the degree of disability in patients with injuries of the main nerve trunks depends on the combined use of a number of surgical, bioengineering and regenerative technologies. These involve the restoration of the anatomical continuity of the nerve, including through the use of natural or artificial elements, cellular technologies and the management of regenerative processes. Therefore, every time, a surgeon is facing a major challenge to create a combination of various means from the indicated basic components for the treatment of nerve damage in managing a particular patient. However, such a treatment approach requires proper competences of surgeons as well as specific material and technical bases in order to bring down the level of social tension in patients with injuries of the main nerve trunks.

The scientific review based on an analysis of the literature examines key points in the etiology, pathomorphology and clinical picture of basal ganglia calcification. It also involves the so-called physiological calcification of the central nervous system. Juvenile and senile forms of a disease and frequency of occurrence of this nosological form are described. The historical information and modes of inheritance are briefly provided. The article considers the numerous synonyms of this disease and the causes of secondary calcification of the brain (Fahr’s syndrome). Four genes are described associated with primary calcification of the basal ganglia: SLC20A2 and XPR1 coding transmembrane conveyors of inorganic phosphate; PDGFB and PDGFRB which are involved in integrity of a blood-brain barrier and survival of pericytes. Pathogenetic mechanisms of clinical displays of a disease are presented. The article displays the features of macro- and microscopic changes in the brain with this nosology. The characteristic signs of the initial and advanced forms of the disease are described in detail, taking into account the age of the debut of calcification of the basal ganglia. The main and auxiliary instrumental methods for diagnosing this disease are also considered, the results of positron emission tomography and magnetic resonance spectroscopy are described, which confirm the pathophysiological mechanism of neurological manifestations of the disease associated with the disorganization of the front-striatal pathways in the area of ​​calcified basal ganglia. A number of additional general clinical laboratory and functional studies are listed to confirm or exclude the diagnosis of primary family idiopathic ferrocalcinosis (Fahr’s diseases). The main directions in the treatment of the described pathology are given.

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