Morphological Changes in the Peripheral Nerves in Trauma, Mercury Intoxication, Hypothyroidism, and Their Correction

Abstract

Traumatic peripheral nerve injury (PNI) significantly impacts patients' quality of life, and its treatment necessitates a multidisciplinary approach. Additionally, different non-traumatic factors such as environmental toxicants and endocrine disorders can significantly affect the regenerative capacity of damaged nerves.The aim of this study was to assess the morphological changes in the recovery of the damaged peripheral nerve, considering the impact of environmental heavy metal intoxication (mercury) and hypothyroidism, including their treatment.The study involved a total of 90 white rats divided into three groups, each group further subdivided into subgroups (a and b). All rats underwent surgical cutting of the sciatic nerve. Subgroup Ia underwent sciatic nerve injury alone, while subgroups IIa and IIIa were additionally subjected to experimental mercurialism and hypothyroidism, respectively. Subgroups Ib, IIb, and IIIb received treatments with Cerebrolysin, Thiotriazoline, and L-Thyroxine+Miacalcic, respectively, in addition to the traumatic nerve injury and experimental influences. The damaged nerves were then examined using both light and electron microscopy assessments.The findings of the study suggest that there are general patterns of de -and regeneration of the damaged peripheral nerve in the context of nootropic administration, experimental mercury intoxication, hypothyroidism, and their correction. In all groups, degeneration was observed, but a noteworthy delay in degenerative processes was observed specifically in cases involving delayed surgical nerve connection, mercurialism, and hypothyroidism, possibly due to the inhibition of Schwann cells. This led to a delayed regeneration process. However, the regeneration of the damaged nerve was significantly accelerated when the experimental pathological condition was corrected.