Clinical management of viral encephalitis

Abstract

Introduction Most cases of viral encephalitis are acute, although a few viruses can cause chronic progressive encephalitis. Rarely, systemic virus infection may trigger post-infectious encephalomyelitis. Viral encephalitis typically reflects viral invasion of the brain parenchyma. Encephalitis patients usually have alterations in their state of consciousness. Some viruses produce “diffuse” encephalitis in which the predominant features are impaired consciousness, signs of generalized central nervous system (CNS) dysfunction such as generalized seizures, and a cerebral spinal fluid (CSF) pleocytosis. Conversely, other viruses produce “focal encephalitis,” in which altered consciousness and CSF abnormalities are accompanied by prominent focal abnormalities on neuroimaging tests or clinical examination including hemiparesis, aphasia, hemisensory loss, ataxia, focal as well as generalized seizures, and, less often, involuntary movements, visual field defects, and cranial nerve deficits. Personality changes, language, and memory disturbances and psychotic features are frequent. Viral encephalitis must be distinguished from nonviral conditions that can present a similar clinical picture, including Lyme disease, tuberculosis, syphilis, Listeria, Mycoplasma, fungal and parasitic infections, brain abscess, subdural hematoma or abscess, brain tumors, CNS vasculitis, and toxic/metabolic encephalopathies. Viral encephalitis may be epidemic or sporadic (see also Chapter 17). Causes of epidemic viral encephalitis include the togaviruses, enteroviruses (see Chapter 17), mumps and lymphocytic choriomeningitis (LCM) virus (see Chapter 1). The toga-viruses are RNA viruses transmitted by mosquitoes or ticks (arthropod-born) (see Chapters 6, 7, and 20), with a peak incidence in the Northern Hemisphere in the warm summer months.