An infection of the brain parenchyma commonly associated with meningitis (“meningoencephalitis”). Clinical features are those of viral meningitis plus evidence of brain tissue involvement, commonly including altered consciousness such as behavioral changes and hallucinations; seizures; and focal neurologic findings such as aphasia, hemiparesis, involuntary movements, and cranial nerve deficits.
The same organisms responsible for viral meningitis are also responsible for encephalitis, although relative frequencies differ. The most common causes of sporadic encephalitis in immunocompetent adults are herpesviruses (HSV, VZV, EBV) (Table 194-5 Viruses Causing Acute Encephalitis in North America). HSV encephalitis should be considered when focal findings are present and when involvement of the inferomedial frontotemporal regions of the brain is likely (olfactory hallucinations, anosmia, bizarre behavior, or memory disturbance). Epidemics of encephalitis are usually caused by arboviruses. WNV has been responsible for the majority of arbovirus meningitis and encephalitis cases in the United States since 2002. Prominent motor manifestations, including acute poliomyelitis-like paralysis, may occur with WNV.
CSF studies are essential; typical CSF profile is similar to viral meningitis. CSF PCR tests allow for rapid and reliable diagnosis of HSV, EBV, CMV, HHV-6, and enteroviruses. In VZV CNS infection, CSF PCR and detection of virus-specific IgM or intrathecal antibody synthesis both provide important aids to diagnosis. Unbiased rapid parallel sequencing technologies capable of identifying infectious genomes in CSF, brain, and other tissues have recently shown great promise for rapid diagnosis of obscure cases. CSF virus cultures are generally negative. For viruses with low seroprevalence rates, diagnosis of acute viral infection can be made by documenting seroconversion between acute-phase and convalescent sera (typically obtained after 2-4 weeks) or by demonstrating the presence of virus-specific IgM antibodies. Demonstration of WNV IgM antibodies in the CSF is diagnostic of WNV encephalitis.
MRI is the neuroimaging procedure of choice and demonstrates areas of increased T2 signal. Bitemporal and orbitofrontal areas of increased signal are seen in HSV encephalitis, but are not diagnostic (Fig. 194-2. Coronal Flair Magnetic Resonance Image from a Pt with Herpes Simplex Encephalitis). The EEG may suggest seizures or show temporally predominant periodic spikes on a slow, low-amplitude background suggestive of HSV encephalitis.
Brain biopsy is now used only when CSF PCR studies fail to identify the cause, focal abnormalities on MRI are present, and progressive clinical deterioration occurs despite treatment with acyclovir and supportive therapy.
Includes both infectious and noninfectious causes of encephalitis, including vascular diseases; abscess and empyema; fungal (Cryptococcus and Mucor), spirochetal (Leptospira), rickettsial, bacterial (Listeria), tuberculous, and mycoplasmal infections; tumors; toxic encephalopathy; SLE; and ADEM; as well as an increasing number of antibodies that cause paraneoplastic autoimmune encephalitis (Chap. 79 Neurologic Paraneoplastic Syndromes).
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Viral Encephalitis
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