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By,
Ms. Ekta. S. Patel
II Year M.Sc (N)
MSN (Neuroscience)
Encephalitis is an inflammation of cerebral tissue,
typically accompanied by meningeal inflammation.
Meningoencephalitis is most commonly caused by
a viral infection. Like meningitis, encephalitis can
be infectious or noninfectious and acute, subacute,
or chronic.
Encephalitis is an inflammation of the brain that is
caused especially by infection with a virus (such as
herpes simplex or West Nile virus) or less
commonly by bacterial or fungal infection or
autoimmune reaction.
The exact cause of encephalitis is often unknown.
But when a cause is known, the most common is a
viral infection. Bacterial infections and
noninfectious inflammatory conditions also can
cause encephalitis.
There are two main types of encephalitis:
This condition occurs when a virus or other agent
directly infects the brain. The infection may be
concentrated in one area or widespread. A primary
infection may be a reactivation of a virus that had
been inactive after a previous illness.
This condition results from a faulty immune system
reaction to an infection elsewhere in the body.
Instead of attacking only the cells causing the
infection, the immune system also mistakenly
attacks healthy cells in the brain. Also known as
post-infection encephalitis, secondary encephalitis
often occurs two to three weeks after the initial
infection.
The viruses that can cause encephalitis include:
Herpes simplex virus (HSV). Both HSV type 1 —
associated with cold sores and fever blisters
around your mouth — and HSV type 2 —
associated with genital herpes — can cause
encephalitis. Encephalitis caused by HSV type 1 is
rare but can result in significant brain damage or
death.
Other herpes viruses. These include the Epstein-
Barr virus, which commonly causes infectious
mononucleosis, and the varicella-zoster virus,
which commonly causes chickenpox and shingles.
Enteroviruses. These viruses include the
poliovirus and the coxsackievirus, which usually
cause an illness with flu-like symptoms, eye
inflammation and abdominal pain.
Mosquito-borne viruses. These viruses can
cause infections such as West Nile, La Crosse, St.
Louis, western equine and eastern equine
encephalitis. Symptoms of an infection might
appear within a few days to a couple of weeks
after exposure to a mosquito-borne virus.
Tick-borne viruses. The Powassan virus is
carried by ticks and causes encephalitis in the
Midwestern United States. Symptoms usually
appear about a week after a bite from an infected
tick.
Rabies virus. Infection with the rabies virus, which
is usually transmitted by a bite from an infected
animal, causes a rapid progression to encephalitis
once symptoms begin. Rabies is a rare cause of
encephalitis in the United States.
Childhood infections. Common childhood
infections — such as measles (rubeola), mumps
and German measles (rubella) — used to be fairly
common causes of secondary encephalitis. These
causes are now rare in the United States due to
the availability of vaccinations for these diseases.
Anyone can develop encephalitis. Factors that may
increase the risk include:
Age. Some types of encephalitis are more
common or more severe in certain age groups. In
general, young children and older adults are at
greater risk of most types of viral encephalitis.
Weakened immune system. People who have
HIV/AIDS, take immune-suppressing drugs or
have another condition causing a weakened
immune system are at increased risk of
encephalitis.
Geographical regions. Mosquito- or tick-borne
viruses are common in particular geographical
regions.
Season of the year. Mosquito- and tick-borne
diseases tend to be more common in summer in
many areas of the United States.
Signs and symptoms may develop hours or weeks
after exposure.
Classic symptoms include fever, headache, and
brain aberration (eg, disorientation, neurologic
deficits, seizures).
Increased ICP may result in alteration in
consciousness, nausea, and vomiting.
Motor weakness, such as hemiparesis, may be
detected.
Increased deep tendon reflexes and extensor
plantar response are noted.
Bizarre behavior and personality changes may
present at onset.
Hypothalamic-pituitary involvement may result in
hypothermia, diabetes insipidus, SIADH
Neurologic symptoms may include superior
quadrant visual field defects, aphasia, dysphagia,
ataxia, and paresthesias.
The patient with brainstem encephalitis may
present with nystagmus, decreased extraocular
movements, hearing loss, dysphagia, dysarthria,
respiratory abnormalities, and motor involvement.
Limbic encephalitis may cause mood and
personality changes that progress to severe
memory loss and delirium.
In WNV, about two-thirds of symptomatic patients
have encephalitis with signs and symptoms of
fever, vomiting, headache, nuchal rigidity,
decreased LOC, cranial nerve dysfunction, and an
erythematous rash. Seizures are uncommon.
Lumbar puncture, with evaluation of CSF, is
performed to detect leukocytosis, increased
mononuclear cell pleocytosis, increased proteins,
and normal or slightly lowered glucose.
Polymerase chain reaction analysis of the virus'
deoxyribonucleic acid (DNA), and the detection of
intrathecally produced viral antibodies, are
essential in diagnosing the specific virus (eg,
herpes simplex virus, cytomegalovirus). Arbovirus-
specific immunoglobulin (IgM) in CSF and a
fourfold change in specific IgG antibody are
diagnostic for arboviral encephalitis.
EEG may demonstrate slow brain wave complexes
in encephalitis.
Gadolinium-enhanced MRI differentiates postinfectious
encephalomyelitis from acute viral encephalitis.
 Enhanced multifocal white matter lesions are seen in
encephalomyelitis, which may remain for months after
clinical recovery.
 Herpes simplex virus encephalitis typically causes medial-
temporal and orbital-frontal lobe inflammation and necrosis;
low-density abnormalities may be present in the temporal
lobes. An MRI is preferred compared to a CT scan.
 Cytomegalovirus, seen in patients who have advanced HIV
disease, may have enhanced periventricular areas.
Brain tissue biopsy indicates presence of infectious
organisms.
WNV can have pleocytosis, and may be seen on
an MRI with enhancement of the meninges and
periventricular areas. The assay, WNV ELISA, can
be done from blood or CSF; a cell culture can also
be diagnostic.
Differentiate acute viral encephalitis from
noninfectious diseases such as sarcoidosis,
vasculitis, systemic lupus erythematosus, and
others.
In patients who are immunosuppressed, such as HIV-positive
patients, differentiate acute viral encephalitis from
cytomegalovirus encephalitis, toxoplasmic encephalitis, and
fungal infections.
 Patients with cytomegalovirus may be treated with
ganciclovir (Cytovene) and foscarnet (Foscavir), commonly
used to treat cytomegalovirus retinitis in HIV-positive
patients.
 Pyrimethamine (Daraprim) and sulfadoxine (Fansidar) are
commonly used to treat Toxoplasma encephalitis.
 When encephalomyelitis develops, supportive care is
indicated because there is no known treatment;
corticosteroids may be used.
I.V. acyclovir over 10 to 21 days is indicated for
herpes simplex virus. Mothers who have genital
herpes simplex may be treated with acyclovir
during the third trimester to avoid shedding the
virus to their babies.
Anticonvulsants manage seizures.
Sequelae of the herpes simplex virus may cause
temporal lobe swelling, which can result in
compression of the brain stem. This virus may also
cause aphasia, major motor and sensory deficits,
and Korsakoff's psychosis (amnestic syndrome).
Relapse of encephalitis may be seen after initial
improvement and completion of antiviral therapy.
Mortality and morbidity depend on the infectious
agent, host status, and other considerations.
Obtain patient history of recent infection, animal exposure,
tick or mosquito bite, recent travel, exposure to ill contacts.
Before delivery, women should be questioned regarding a
history of congenital herpes simplex virus and examined
for evidence of this virus; a cesarean delivery should be
explored with the physician.
Strict standard precautions should be adhered to in
order to contain drainage from herpetic lesions.
Vesicular lesions or rashes on neonates should be
reported immediately because these could indicate
active herpes simplex infection.
Perform a complete clinical assessment.
Risk for Injury related to seizures and cerebral
edema
Ineffective Tissue Perfusion (cerebral) related to
disease process
Hyperthermia related to infectious process
Disturbed Thought Processes due to personality
changes
Risk of Infection related to transmittal

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Encephalitis

  • 1. By, Ms. Ekta. S. Patel II Year M.Sc (N) MSN (Neuroscience)
  • 2. Encephalitis is an inflammation of cerebral tissue, typically accompanied by meningeal inflammation. Meningoencephalitis is most commonly caused by a viral infection. Like meningitis, encephalitis can be infectious or noninfectious and acute, subacute, or chronic.
  • 3. Encephalitis is an inflammation of the brain that is caused especially by infection with a virus (such as herpes simplex or West Nile virus) or less commonly by bacterial or fungal infection or autoimmune reaction.
  • 4. The exact cause of encephalitis is often unknown. But when a cause is known, the most common is a viral infection. Bacterial infections and noninfectious inflammatory conditions also can cause encephalitis. There are two main types of encephalitis:
  • 5. This condition occurs when a virus or other agent directly infects the brain. The infection may be concentrated in one area or widespread. A primary infection may be a reactivation of a virus that had been inactive after a previous illness.
  • 6. This condition results from a faulty immune system reaction to an infection elsewhere in the body. Instead of attacking only the cells causing the infection, the immune system also mistakenly attacks healthy cells in the brain. Also known as post-infection encephalitis, secondary encephalitis often occurs two to three weeks after the initial infection.
  • 7. The viruses that can cause encephalitis include: Herpes simplex virus (HSV). Both HSV type 1 — associated with cold sores and fever blisters around your mouth — and HSV type 2 — associated with genital herpes — can cause encephalitis. Encephalitis caused by HSV type 1 is rare but can result in significant brain damage or death.
  • 8. Other herpes viruses. These include the Epstein- Barr virus, which commonly causes infectious mononucleosis, and the varicella-zoster virus, which commonly causes chickenpox and shingles.
  • 9. Enteroviruses. These viruses include the poliovirus and the coxsackievirus, which usually cause an illness with flu-like symptoms, eye inflammation and abdominal pain.
  • 10. Mosquito-borne viruses. These viruses can cause infections such as West Nile, La Crosse, St. Louis, western equine and eastern equine encephalitis. Symptoms of an infection might appear within a few days to a couple of weeks after exposure to a mosquito-borne virus.
  • 11. Tick-borne viruses. The Powassan virus is carried by ticks and causes encephalitis in the Midwestern United States. Symptoms usually appear about a week after a bite from an infected tick.
  • 12. Rabies virus. Infection with the rabies virus, which is usually transmitted by a bite from an infected animal, causes a rapid progression to encephalitis once symptoms begin. Rabies is a rare cause of encephalitis in the United States.
  • 13. Childhood infections. Common childhood infections — such as measles (rubeola), mumps and German measles (rubella) — used to be fairly common causes of secondary encephalitis. These causes are now rare in the United States due to the availability of vaccinations for these diseases.
  • 14. Anyone can develop encephalitis. Factors that may increase the risk include: Age. Some types of encephalitis are more common or more severe in certain age groups. In general, young children and older adults are at greater risk of most types of viral encephalitis.
  • 15. Weakened immune system. People who have HIV/AIDS, take immune-suppressing drugs or have another condition causing a weakened immune system are at increased risk of encephalitis.
  • 16. Geographical regions. Mosquito- or tick-borne viruses are common in particular geographical regions.
  • 17. Season of the year. Mosquito- and tick-borne diseases tend to be more common in summer in many areas of the United States.
  • 18. Signs and symptoms may develop hours or weeks after exposure. Classic symptoms include fever, headache, and brain aberration (eg, disorientation, neurologic deficits, seizures). Increased ICP may result in alteration in consciousness, nausea, and vomiting.
  • 19. Motor weakness, such as hemiparesis, may be detected. Increased deep tendon reflexes and extensor plantar response are noted. Bizarre behavior and personality changes may present at onset. Hypothalamic-pituitary involvement may result in hypothermia, diabetes insipidus, SIADH
  • 20. Neurologic symptoms may include superior quadrant visual field defects, aphasia, dysphagia, ataxia, and paresthesias. The patient with brainstem encephalitis may present with nystagmus, decreased extraocular movements, hearing loss, dysphagia, dysarthria, respiratory abnormalities, and motor involvement.
  • 21. Limbic encephalitis may cause mood and personality changes that progress to severe memory loss and delirium. In WNV, about two-thirds of symptomatic patients have encephalitis with signs and symptoms of fever, vomiting, headache, nuchal rigidity, decreased LOC, cranial nerve dysfunction, and an erythematous rash. Seizures are uncommon.
  • 22. Lumbar puncture, with evaluation of CSF, is performed to detect leukocytosis, increased mononuclear cell pleocytosis, increased proteins, and normal or slightly lowered glucose.
  • 23. Polymerase chain reaction analysis of the virus' deoxyribonucleic acid (DNA), and the detection of intrathecally produced viral antibodies, are essential in diagnosing the specific virus (eg, herpes simplex virus, cytomegalovirus). Arbovirus- specific immunoglobulin (IgM) in CSF and a fourfold change in specific IgG antibody are diagnostic for arboviral encephalitis. EEG may demonstrate slow brain wave complexes in encephalitis.
  • 24. Gadolinium-enhanced MRI differentiates postinfectious encephalomyelitis from acute viral encephalitis.  Enhanced multifocal white matter lesions are seen in encephalomyelitis, which may remain for months after clinical recovery.  Herpes simplex virus encephalitis typically causes medial- temporal and orbital-frontal lobe inflammation and necrosis; low-density abnormalities may be present in the temporal lobes. An MRI is preferred compared to a CT scan.  Cytomegalovirus, seen in patients who have advanced HIV disease, may have enhanced periventricular areas.
  • 25. Brain tissue biopsy indicates presence of infectious organisms. WNV can have pleocytosis, and may be seen on an MRI with enhancement of the meninges and periventricular areas. The assay, WNV ELISA, can be done from blood or CSF; a cell culture can also be diagnostic.
  • 26. Differentiate acute viral encephalitis from noninfectious diseases such as sarcoidosis, vasculitis, systemic lupus erythematosus, and others.
  • 27. In patients who are immunosuppressed, such as HIV-positive patients, differentiate acute viral encephalitis from cytomegalovirus encephalitis, toxoplasmic encephalitis, and fungal infections.  Patients with cytomegalovirus may be treated with ganciclovir (Cytovene) and foscarnet (Foscavir), commonly used to treat cytomegalovirus retinitis in HIV-positive patients.  Pyrimethamine (Daraprim) and sulfadoxine (Fansidar) are commonly used to treat Toxoplasma encephalitis.  When encephalomyelitis develops, supportive care is indicated because there is no known treatment; corticosteroids may be used.
  • 28. I.V. acyclovir over 10 to 21 days is indicated for herpes simplex virus. Mothers who have genital herpes simplex may be treated with acyclovir during the third trimester to avoid shedding the virus to their babies. Anticonvulsants manage seizures.
  • 29. Sequelae of the herpes simplex virus may cause temporal lobe swelling, which can result in compression of the brain stem. This virus may also cause aphasia, major motor and sensory deficits, and Korsakoff's psychosis (amnestic syndrome).
  • 30. Relapse of encephalitis may be seen after initial improvement and completion of antiviral therapy. Mortality and morbidity depend on the infectious agent, host status, and other considerations.
  • 31. Obtain patient history of recent infection, animal exposure, tick or mosquito bite, recent travel, exposure to ill contacts. Before delivery, women should be questioned regarding a history of congenital herpes simplex virus and examined for evidence of this virus; a cesarean delivery should be explored with the physician.
  • 32. Strict standard precautions should be adhered to in order to contain drainage from herpetic lesions. Vesicular lesions or rashes on neonates should be reported immediately because these could indicate active herpes simplex infection. Perform a complete clinical assessment.
  • 33. Risk for Injury related to seizures and cerebral edema Ineffective Tissue Perfusion (cerebral) related to disease process
  • 34. Hyperthermia related to infectious process Disturbed Thought Processes due to personality changes Risk of Infection related to transmittal