1. Encephalitis is an inflammation of the brain parenchyma that presents as diffuse or focal neurological dysfunction. It is usually caused by a viral infection, though bacteria, fungi, and other causes can also produce encephalitis. 2. Common viruses that cause encephalitis include herpes simplex virus, varicella zoster virus, mumps virus, measles virus, and West Nile virus. The virus enters the brain either through bloodstream spread or travel along neural pathways. 3. Symptoms of encephalitis include altered mental status, personality changes, seizures, focal neurological deficits, and headache. Diagnosis involves blood and CSF tests to identify infectious agents and brain imaging to examine abnormalities

1. Encephalitis
Presented by:
Dr. Mona Mohammed Ali
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3. Introduction:
• Encephalitis, an inflammation of the brain parenchyma, presents as diffuse and/or
focal neuropsychological dysfunction.
• Although it primarily involves the brain, the meninges are frequently involved
(meningoencephalitis).
• From an epidemiologic and pathophysiologic perspective, encephalitis is distinct
from meningitis
• It is also distinct from cerebritis.
• Cerebritis describes the stage preceding abscess formation and implies a highly
destructive bacterial infection of brain tissue, whereas acute encephalitis is most
commonly a viral infection with parenchymal damage varying from mild to
profound.
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4. Etiology:
• Bacterial, fungal, and autoimmune disorders can produce
encephalitis, but most cases are viral in origin.
• The cause of encephalitis is usually infectious in nature.
• Viral agents, such as HSV types 1 and 2 (the latter much more
common in neonates than adults), VZV, EBV, measles virus (PIE
and SSPE), mumps virus, and rubella virus, are spread through
person-to-person contact.
• Human herpes virus 6 may also be a causative agent.
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5. Etiology:
The CDC has confirmed that WNV( West Nile Virus) can be transmitted by means of
organ transplantation and via blood transfusions.
Important animal vectors for some types of encephalitis include:
1- mosquitoes and ticks, which spread the arbovirus group.
2- warm-blooded mammals, which are vectors for rabies and lymphocytic
choriomeningitis (LCM).
Bacterial pathogens, such as Mycoplasma species and those causing rickettsial disease
or catscratch disease, are rare and invariably involve inflammation of the meninges
out of proportion to their encephalitic components.
Noninfectious causes include the demyelinating process in acute disseminated
encephalitis.
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6. Pathophysiology:
• In general, the virus replicates outside the CNS and gains entry
to the CNS either by hematogenous spread or by travel along
neural pathways (e.g., rabies virus, HSV, VZV).
• Once across the blood-brain barrier, the virus enters neural
cells, with resultant disruption in cell functioning, perivascular
congestion, hemorrhage, and a diffuse inflammatory response
that disproportionately affects gray matter over white matter.
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7. Pathophysiology (continued):
• Regional tropism associated with certain viruses is due to neuron cell
membrane receptors found only in specific portions of the brain, with
more intense focal pathology in these areas. A classic example is the
HSV predilection for the inferior and medial temporal lobes.
• In contrast to viruses that invade gray matter directly, acute
disseminated encephalitis and postinfectious encephalomyelitis (PIE),
most commonly due to measles infection and associated with Epstein-
Barr virus (EBV) and CMV infections, are immune-mediated processes
that result in multifocal demyelination of perivenous white matter.
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8. C/F
• The viral prodrome typically consists of fever, headache, nausea and
vomiting, lethargy, and myalgias.
• Manifestations associated with specific types of encephalitis include the
following:
1. Encephalitis caused by varicella-zoster virus (VZV), Epstein-Barr virus
(EBV), cytomegalovirus (CMV), measles virus, or mumps virus: Rash,
lymphadenopathy, hepatosplenomegaly, and parotid enlargement.
2. St Louis encephalitis: Dysuria and pyuria.
3. West Nile encephalitis (WNE): Extreme lethargy.
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9. C/F
• The classic presentation is encephalopathy with diffuse or focal neurologic
symptoms, including the following:
1. Behavioral and personality changes, with decreased level of consciousness.
2. Neck pain, stiffness.
3. Photophobia.
4. Lethargy.
5. Generalized or focal seizures (60% of children with California virus encephalitis
[CE]).
6. Acute confusion or amnestic states.
7. Flaccid paralysis (10% of patients with WNE).
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10. C/F
• The signs of encephalitis may be diffuse or focal. Typical findings include the following:
1. Altered mental status.
2. Personality changes (very common).
3. Focal findings (e.g., hemiparesis, focal seizures, and autonomic dysfunction).
4. Movement disorders (e.g., St Louis encephalitis, eastern equine encephalitis, and western equine
encephalitis).
5. Ataxia.
6. Cranial nerve defects.
7. Dysphagia, particularly in rabies.
8. Meningismus (less common and less pronounced than in meningitis).
9. Unilateral sensorimotor dysfunction (postinfectious encephalomyelitis.)
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11. C/F
• Findings of herpes simplex virus (HSV) infection in neonates may include the
following:
1. Herpetic skin lesions over the presenting surface from birth or with breaks in the
skin, such as those resulting from fetal scalp monitors.
2. Keratoconjunctivitis.
3. Oropharyngeal involvement, particularly buccal mucosa and tongue.
4. Encephalitis symptoms (e.g., seizures, irritability, change in attentiveness, and bulging
fontanels).
5. Additional signs of disseminated, severe HSV include jaundice, hepatomegaly, and
shock.
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12. C/F
• Encephalitis may be associated with a number of complications,
including the following:
1. Seizures.
2. Syndrome of inappropriate secretion of antidiuretic hormone
(SIADH).
3. Increased intracranial pressure (ICP).
4. Coma.
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13. Diagnosis:
• Blood and urine tests that may be helpful include the following:
1. Complete blood count (CBC).
2. Serum electrolyte levels.
3. Serum glucose level.
4. Blood urea nitrogen (BUN) and creatinine levels.
5. Urine electrolyte levels.
6. Urine or serum toxicology screening.
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14. Diagnosis:
• A lumbar puncture (LP) should be performed in all cases of suspected viral encephalitis.
• Studies that may be ordered to identify the infectious agent include the following:
1. HSV cultures of suspicious lesions and a Tzanck smear.
2. Viral cultures of CSF, including HSV.
3. Blood cultures for bacterial pathogens.
4. Complement fixation antibodies to identify arbovirus.
5. Heterophile antibody and cold agglutinin testing for EBV.
6. Serologic tests for Toxoplasma.
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15. Diagnosis:
• CSF analysis is essential. Parameters to be evaluated include the
following:
1. Pressure.
2. Cell counts.
3. Microorganisms.
4. Glucose.
5. Protein.
6. Brain biopsy is the diagnostic standard (96% sensitivity, 100%
specificity).
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16. Diagnosis:
• Imaging modalities that may be helpful include the
following:
1. CT
2. MRI
3. EEG
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17. Management:
• Management in the prehospital setting includes the following:
1. Evaluation and treatment for shock or hypotension.
2. Airway protection (in patients with altered mental status).
3. Seizure precautions.
4. Oxygen and IV access secured en route to the hospital (all
patients).
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18. Management:
• In the emergency department (ED), beyond supportive care, viral encephalitides are not
treatable, with the exceptions of HSV and VZV encephalitis. Important initial measures
include the following:
1. Administration of the first dose or doses of acyclovir, with or without antibiotics or
steroids, as quickly as possible; the standard for acute bacterial meningitis is initiation
of treatment within 30 minutes of arrival.
2. Consideration of an ED triage protocol to identify patients at risk for HSV encephalitis.
3. Collection of laboratory samples and blood cultures before the start of IV therapy.
4. Neuroimaging (e.g., MRI or, if that is unavailable, contrast-enhanced head CT) before
LP.
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19. Management
• Additional treatment considerations include the following:
1. Management of hydrocephalus and increased ICP.
2. Treatment of systemic complications (e.g., hypotension or
shock, hypoxemia, hyponatremia, and exacerbation of chronic
diseases.)
3. Empiric treatment of HSV meningoencephalitis and VZV
encephalitis.
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20. Management
• Medication Summary:
• The goals of pharmacotherapy are to reduce morbidity and
prevent complications.
• Antivirals are used to manage treatable viral encephalitides.
• Corticosteroids may be considered for postinfectious or
noninfectious encephalitis.
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21. Management
• Antiviral:
• The goal of the use of antivirals for herpes simplex encephalitis (HSE) and varicella-
zoster encephalitis is to shorten the clinical course, prevent complications, prevent
the development of latency and/or subsequent recurrences, decrease transmission,
and eliminate established latency.
• Acyclovir (Zovirax):
• Acyclovir has demonstrated inhibitory activity directed against both herpes simplex
virus type 1 (HSV-1) and HSV-2, and infected cells selectively take it up.
• Foscarnet (Foscavir): may be used.
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22. Management
• Corticosteroids:
• Corticosteroids are anti-inflammatory agents used for treatment of postinfectious
encephalitis and acute disseminated encephalitis. These drugs are commonly
presented as treatment alternatives, though supporting data are limited.
• Dexamethasone:
• Dexamethasone is used to treat various allergic and inflammatory diseases. It may
decrease inflammation by suppressing migration of polymorphonuclear leukocytes
and reversing increased capillary permeability.
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23. Management
• Diuretics:
• These agents are used in patients with hydrocephalus and
increased intracranial pressure (ICP) when more aggressive
diuresis is desired.
• Furosemide (Lasix) is an example.
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24. Management
• Mannitol (Osmitrol):
• Mannitol may reduce pressure in the subarachnoid space by creating an osmotic
gradient between cerebrospinal fluid in the arachnoid space and plasma. This agent
is not intended for long-term use.
• Initially assess for adequate renal function in adults by administering a test dose of
200 mg/kg, given IV over 3-5 minutes. This should produce a urine flow of at least
30-50 ml/h of urine over 2-3 hours.
• In children, assess for adequate renal function by administering a test dose of 200
mg/kg, given IV over 3-5 minutes. This should produce a urine flow of at least 1
mL/kg over 1-3 hours.
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25. Management
• Benzodiazepines:
• These agents are used to treat seizures associated
with encephalitis.
• Lorazepam (Ativan) is an example.
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26. Prognosis:
• The prognosis is dependent on the virulence of the virus
and the patient’s health status.
• Extremes of age (< 1 y or >55 y), immune-compromised
status, and preexisting neurologic conditions are
associated with poorer outcomes.
• Untreated HSE has a mortality of 50-75%, and virtually
all untreated or late-treatment survivors have long-term
motor and mental disabilities.
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27. Prognosis :
• The mortality in treated HSE averages 20%, and the
neurologic outcome correlates with the neurological
disability present at the time of the first dose of acyclovir
or comparable antiviral agents.
• Approximately 40% of survivors have minor-to-major
learning disabilities, memory impairment,
neuropsychiatric abnormalities, epilepsy, fine-motor-
control deficits, and dysarthria.
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28. THANKS
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