Researchers at the Children’s Hospital, University of Oxford, and Alder Hey Children’s NHS Foundation Trust, Liverpool, UK review the literature on encephalitis and suggest a management strategy. Encephalitis, defined as inflammation of brain parenchyma, is associated directly or indirectly with infectious agents (viruses or other microorganisms, fungi, parasites, rickettsiae) or caused by other inflammatory or immune-mediated pathologies (eg. ADEM, paraneoplastic, NMDAR encephalitis, voltage gated K channel limbic encephalitis). Herpes simplex virus (HSV) type 1 is the most common cause of sporadic encephalitis, either primary infection or via reactivation of virus in the trigeminal ganglion. Enteroviruses such as polio and arboviruses (Japanese encephalitis virus and West Nile virus) enter the brain across the blood-brain barrier. Etiology is undefined in 60% cases of encephalitis.

CSF should be sent: 1) to microbiology lab for microscopy, culture and sensitivity analysis; 2) to virology lab for PCR for HSV types 1 and 2, VZV, HHV-6 and -7, CMV, EBV, enteroviruses, respiratory viruses, HIV and C pneumonia; 3) to biochemistry for glucose (with paired plasma sample), lactate and oligoclonal bands; and 4) stored sample for future tests. Up to 10% of patients with viral encephalitis have a normal CSF. Some patients have a mononuclear pleocytosis and moderately elevated protein in the CSF, or raised red blood cell count (hemorrhagic encephalitis). Eosinophils suggest infection with helminthes, toxoplasma, Rickettsiae, or M pneumonia. Low CSF glucose suggests a bacterial, fungal or protozoal etiology. PCR may be negative early and after acyclovir. [1]

COMMENT. This excellent review also refers to the value and indications for EEG and MRI in diagnosis of encephalitis, treatment including acyclovir, and prognosis.