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Acute disseminated encephalomyelitis
Encephalitis is inflammation of the parenchyma of the brain, resulting from

direct viral invasion.
Acute disseminated encephalomyelitis is brain and spinal cord inflammation

caused by a hypersensitivity reaction to a virus or another foreign protein.
Both disorders are usually triggered by viruses.
Symptoms include fever, headache, and altered mental status, often

accompanied by seizures or focal neurologic deficits.
Diagnosis requires cerebrospinal fluid analysis and neuroimaging.
Treatment is supportive and, for certain causes, includes antiviral drugs.
Etiology of Encephalitis
Encephalitis is usually a primary manifestation or a secondary (postinfectious) immunologic
complication of viral infection.
Primary viral infection

Viruses causing primary encephalitis directly invade the brain. These infections may be
 Epidemic (eg, due to arbovirus, echovirus, coxsackievirus, or poliovirus [in some

underdeveloped countries])
 Sporadic (eg, due to cytomegalovirus or to herpes simplex, varicella-zoster, lymphocytic
choriomeningitis, rabies, or mumps virus)
 Rabies remains a significant cause of encephalitis in developing countries
 Encephalitis can also occur as a late reactivation of latent or subclinical viral infection. The
best known types are
 HIV-associated encephalopathy and dementia

 Subacute sclerosing panencephalitis (which occurs years after a measles infection and is
thought to represent reactivation of the original infection; it is now rare in Western countries)
 Progressive multifocal leukoencephalopathy (which is caused by reactivation of JC virus;
particularly in AIDS or immunosuppressed patients)
 Herpes simplex type 1 and herpes zoster encephalitis
Immunologic reaction
Encephalitis can occur as a secondary immunologic complication of certain viral infections or
vaccinations.
Inflammatory demyelination of the brain and spinal cord can occur 1 to 3 weeks later (as acute
disseminated encephalomyelitis); the immune system attacks one or more central nervous
system (CNS) antigens that resemble proteins of the infectious agent.
The most common causes of this complication used to be measles, rubella, chickenpox, and
mumps (all now uncommon because childhood vaccination is widespread); smallpox vaccine; and
live-virus vaccines (eg, the older rabies vaccines prepared from sheep or goat brain). In the US,
most cases now result from influenza A or B virus, enteroviruses, Epstein-Barr virus, hepatitis
A or hepatitis B virus, or HIV. Immunologically mediated encephalitis also occurs in patients with
cancer and other autoimmune disorders.
Rarely, apparent encephalitis has developed in patients with COVID-19, caused by the novel
pandemic severe acute respiratory syndrome coronavirus (SARS-CoV2); the mechanism is not
clear, but an immunologic contribution to the mechanism of apparent encephalitis is possible, as is
direct viral invasion of the brain.
Encephalopathies caused by autoantibodies to neuronal membrane proteins (eg, N-methyl-D-

aspartate [NMDA] receptors) may mimic viral encephalitis. Some evidence suggests that anti-
NMDA receptor encephalitis is a more common type of encephalitis than was previously thought. It
occasionally develops after encephalitis due to herpes simplex virus, even when the encephalitis
was successfully treated.
Pathophysiology of Encephalitis
In acute encephalitis, inflammation and edema occur in infected areas throughout the cerebral
hemispheres, brain stem, cerebellum, and, occasionally, spinal cord.
Petechial hemorrhages may be present in severe infections. Direct viral invasion of the brain
usually damages neurons, sometimes producing microscopically visible inclusion bodies.
Severe infection, particularly untreated herpes simplex virus (HSV) encephalitis, can cause brain
hemorrhagic necrosis.
Acute disseminated encephalomyelitis is characterized by multifocal areas of perivenous

demyelination and absence of virus in the brain.
Symptoms and Signs of Encephalitis

Fever, headache, and altered mental status
Accompanied by seizures and focal neurologic deficits.
A gastrointestinal (GI) or respiratory prodrome may precede these symptoms.
Meningeal signs- .
Status epilepticus, particularly convulsive status epilepticus, or coma suggests severe brain
inflammation and a poor prognosis.
Olfactory seizures, manifested as an aura of foul smells (rotten eggs, burnt meat), indicate
temporal lobe involvement and suggest HSV encephalitis.
Diagnosis of Encephalitis
 MRI
 Cerebrospinal fluid (CSF) testing  CSF analysis (including polymerase chain reaction
[PCR] for HSV and other viruses) are usually done,
 Serologic tests to identify the causative virus.
X- RAY
MRI
Contrast-enhanced MRI is sensitive for early HSV encephalitis, - showing edema in the
orbitofrontal and temporal areas,
MRI shows demyelination in progressive multifocal leukoencephalopathy and may show basal
ganglia and thalamic abnormalities
MRI can also exclude lesions that mimic viral encephalitis (eg, brain abscess, sagittal sinus
thrombosis).
CSF testing
Lumbar puncture (spinal tap) is done.
CSF is characterized by lymphocytic pleocytosis, normal glucose, mildly elevated protein, and an
absence of pathogens after Gram staining and culture (similar to CSF in aseptic meningitis).
Pleocytosis may be polymorphonuclear in severe infections.
CSF glucose levels may be low when the cause is varicella-zoster virus, mumps, or lymphocytic
choriomeningitis virus.
PCR testing of CSF is the diagnostic test of choice for HSV-1, HSV-2, varicella-zoster virus,
cytomegalovirus, enteroviruses, and JC virus. PCR for HSV in CSF is particularly sensitive and
specific.
CSF viral cultures grow enteroviruses but not most other viruses.
CSF viral IgM titers are often useful for diagnosing acute infection. CSF IgG and IgM titers may be
more sensitive than PCR for varicella-zoster virus encephalitis.
Brain biopsy
Brain biopsy may be indicated for patients who
 Are worsening
 Are responding poorly to treatment with acyclovir or another antimicrobial

 Have a lesion that is still undiagnosed
Treatment of Encephalitis
 Supportive care
 Acyclovir for HSV or varicella-zoster virus encephalitis

Supportive therapy for encephalitis includes treatment of fever, dehydration, electrolyte disorders,
and seizures. Euvolemia should be maintained.
Acyclovir 10 mg/kg IV every 8 hours should be started promptly and continued usually for 14 days
or until infection with these viruses is excluded.
Giving acyclovir IV slowly over 1 hour with adequate hydration helps prevent nephrotoxicity.
Cytomegalovirus encephalitis can be treated with ganciclovir and/or other antiviral drugs.
If encephalitis is due to an immunologic reaction (eg, acute disseminated encephalomyelitis

[postinfectious encephalomyelitis]), treatment should be begun immediately; it may include
corticosteroids (prednisone or methylprednisolone) and plasma exchange or IV immune globulin.

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Acute disseminated encephalomyelitis

Encephalitis is inflammation of the parenchyma of the brain, resulting from

Acute disseminated encephalomyelitis is brain and spinal cord inflammation

Both disorders are usually triggered by viruses.

Symptoms include fever, headache, and altered mental status, often

Diagnosis requires cerebrospinal fluid analysis and neuroimaging.

Treatment is supportive and, for certain causes, includes antiviral drugs.

Primary viral infection

 Epidemic (eg, due to arbovirus, echovirus, coxsackievirus, or poliovirus [in some

 HIV-associated encephalopathy and dementia

Encephalopathies caused by autoantibodies to neuronal membrane proteins (eg, N-methyl-D-

Acute disseminated encephalomyelitis is characterized by multifocal areas of perivenous

Symptoms and Signs of Encephalitis

Accompanied by seizures and focal neurologic deficits.

A gastrointestinal (GI) or respiratory prodrome may precede these symptoms.

 Serologic tests to identify the causative virus.

Pleocytosis may be polymorphonuclear in severe infections.

 Are responding poorly to treatment with acyclovir or another antimicrobial

 Acyclovir for HSV or varicella-zoster virus encephalitis

If encephalitis is due to an immunologic reaction (eg, acute disseminated encephalomyelitis

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