Viral Encephalitis

Abstract

Patients with viral infections of the central nervous system are encountered daily, but it is often difficult to establish a correct differential diagnosis. This paper attempts to “reorganize” our knowledge of such infections.

Our starting point was virology, defining the different viruses according to the latest classifications, distinguishing RNA viruses from DNA viruses, assessing capsid shape and dividing each family into genera and species of interest. We then determined the pathophysiology: from initial viraemia we considered the mechanisms of CNS penetration and the pathological changes which ensue. The different species of viruses were found to behave in a broadly similar fashion, accounting for the often very similar radiological findings which make differential diagnosis arduous even for the expert.

Lastly, we studied the different forms of slow and acute encephalitis aiming to separate crucial information from useful findings which together with clinical presentation will aid diagnosis.

Among the acute forms of encephalitis, the main group comprises herpes encephalitis caused by herpes simplex virus types 1 and 2, cytomegalovirus and varicella-zoster virus. HS1 is usually responsible for severe necrotising meningo-encephalitis; type 2 often presents symmetrical malacic areas in the white matter with little involvement of the grey matter. Cytomegalovirus, which is dangerous mainly to the fetus and neonate, is responsible for dystrophic calcifications and neuronal migration disorders, sometimes resulting in lissencephaly; in immunodepressed patients, it causes atrophy and leukencephalopathy without damage to the brain barrier. Varicella-zoster virus is responsible for transverse myelitis, asectic meningitis and meningo-encephalitis, often presenting a characteristic subtentorial location, sometimes complicated by patchy haemorrhagic lesions.

The slow forms of encephalitis include subacute sclerosing panencephalitis caused by measles-like paramyxovirus which presents aspecific signs from neuronal degeneration to atrophy. HIV encephalitis causes atrophy and leucoencephalopathy without damage to the blood brain barrier. Progressive multifocal leucoencephalopathy caused by papavirus is characterized by involvement of the subcortical oligodendrocytes resulting in a leucoencephalopathy presenting a typical finger shape often in a subtentorial site.