[MRI morphometry of neuroplastic changes in the brain after conservative treatment of traumatic brachial plexopathy]. / Magnitno-rezonansnaia morfometriia neiroplasticheskikh izmenenii golovnogo mozga pri konservativnoi terapii travmaticheskoi plechevoi pleksopatii.

AIM: To identify neuroplastic changes in the brain structures during treatment of traumatic axonotomy of the brachial plexus (the pathology of peripheral nervous system). MATERIAL AND METHODS: MRI morphometry of white and grey matter was studied in 62 patients with traumatic axonotomy of the brachial plexus. RESULTS: There were correlations between the thickness of sensorimotor cortex, morphometric parameters (volume, diffusion, fractional anisotropy) of subcortical formations (corticospinal tracts, the forceps minor), severity of neurological deficit and dynamics of clinical course depending on the therapeutic strategy. CONCLUSION: The results expand the current view on central mechanisms of posttraumatic axon regeneration on the model of traumatic brachial plexopathy and establish a neuromodulative effect of neuromidin and noofen. Some morphometric parameters may be used as the markers of reactive neuroplastic processes in the central nervous system.

Metastases development following local tumour treatment.

Transplantable mouse methylcholanthrene- induced fibrosarcoma (CMC4 tumour growing in CBA/HZgr mice), characterized by lung metastases developing shortly after local tumour cell transplantation, was used as an experimental model to investigate the problem of tumour metastases after local tumour treatment. Surgery and/or irradiation were performed on locally growing tumour of particular size. Further, heavily irradiated, viable but not dividing tumour cells, imitating the situation in treated tumour-bearing organism, were injected intraperitoneally in a parallel group of treated tumour-bearing mice. The animals were killed 35 days after tumour transplantation and the number and volume of lung metastases were determined. Depending on the treatment performed, when the tumour mass was reduced or even eliminated, the number of lung metastases and their volume were significantly lower than in control mice, but the addition of tumour mass (injection of heavily irradiated tumour cells) resulted in a significant increase in lung metastases parameters, pointing to a possible role of the host's immune reaction against the tumour. Further, the release of a simple molecule, such as nitric oxide, from tumour mass seems to be detrimental for the survival of tumour cells and subsequently their metastases through the induction of angiogenesis and possible suppression of immune reaction. Thus, complex mechanisms could be involved when a locally growing tumour is exposed to a particular therapeutic approach.