ABSTRACT
Background: Multiple Sclerosis (MS) and its animal model Experimental Allergic Encephalomyelitis (EAE) is an inflammatory demyelinating disease of the central nervous system, in which the myelin sheath has been considered to be the primary target for many years. However, an increasing number of reports have focused on neurodegenerative aspects of the disease pathogenesis. Damage to axons is taken as a key factor of disability in multiple sclerosis, but its pathogenesis is largely unknown. Axonal injury is believed to occur as a consequence of demyelination and was recently shown to be a feature even of the early disease stages. It is evident that the crucial distinction between primary and secondary demyelination depends on the preservation or the destruction of the axons and the neuronal elements. Methods: EAE was induced in the adult healthy guinea pigs by weekly intradermal injections of homologous whole brain and spinal cord antigen together with complete Freund’s adjuvant into the foot pad of the animal. The animals were observed for clinical features of the disease after injection. Results: The histological observation revealed two stages of EAE; an initial inflammatory stage followed by demyelination. The inflammatory lesions were focal and invariably related to blood vessels. The inflammatory lesions consisted of perivascular cuffings with lymphocytes and mononuclear cells in the perivascular space and surrounding parenchyma. Perivascular demyelination was restricted to that part of the white matter which was infiltrated by mononuclear cells. The fibres in demyelinating lesions were demyelinated. Perivascular demyelination is followed by patchy demyelination and large plaques of demyelination. Neuronal and axonal damage, necrosis, tissue degeneration and cavity formation were seen in those animals which died during the acute phase of the disease. These changes were found in the spinal cord, brainstem and cerebellum. Conclusion: The changes observed in results lead to the conclusion that the acute EAE with severity of disease is no more a primary demyelinating disease.