Experimental unilateral intracerebral hemorrhage induces delayed bilateral neurodegeneration of sciatic nerve fibres in rats

Abstract

Pathological processes, such as inflammatory effects, oxidative stress, apoptosis and cytotoxicity of blood after an intracerebral hemorrhage (ICH), generally contribute to a secondary injury. One of the secondary ICH consequences in the nervous system may be delayed neurodegeneration of the peripheral nerves. Therefore, the aim of our study was to investigate possible structural changes in the sciatic nerve and changes in the conduction velocity via this nerve at different terms after experimental ICH in male Wistar rats. Intracerebral hemorrhage was provided by direct injection of autologous blood into the capsula interna. On the 10th day after ICH mean conduction velocity in sciatic nerve was 15% smaller compared to the control. On the 30th and 90th days after ICH, highly significant decreases in the conduction velocity by 62% and 60%, respectively in comparison with the control group of animals were observed. The data of morphometric analysis demonstrated significant decreases in the mean diameter and density of myelinated fibres at all examined terms after ICH. A number of the myelin sheaths were swollen and lost their regular laminations. Axoplasmic and myelin degenerations were the most frequent events in these nerve fibres; reductions of the diameter of the axis cylinders were also observed. In the contralateral nerve (related to the hemisphere with ICH), negative changes were greater, while the ipsilateral nerve was also subjected to those. Our data demonstrate that the consequences of unilateral ICH in the capsula interna induce bilateral negative changes in the peripheral nervous system of rats.

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

“…The sciatic nerve, on the background of Hypothyroidism + Thyroxine + Miacalcic (subgroup IIIb), underwent the phases of regeneration and degeneration faster, which was associated with no significant delay in the progression of degenerative changes, characteristic of the morphological alterations in the damaged nerve in hypothyroid rats (subgroup IIIa). The onset of regeneration was delayed due to low phagocytic activity and the absence of apoptosis in Schwann cells [22,23]. Further destruction of damaged myelin fibers took place at a slower pace and had a distinct course which differed from the progression of degeneration in rats of subgroup Ia and subgroup IIIa.…”