Encephalitis is an inflammation of the brain parenchyma that causes diffuse or focal neurological dysfunction. It is often caused by viral infections like herpes simplex virus or varicella zoster virus. Diagnostic workup includes imaging tests, lumbar puncture for cerebrospinal fluid analysis, and electroencephalography. Treatment focuses on supportive care and antiviral medications like acyclovir for suspected herpes infections. Prognosis depends on the cause, with viral causes generally having a better outlook than autoimmune or unknown causes.

1. ENCEPHALITIS
Dr Muhammad Abdelmoneim
ICU
Registrar

2. Definition
Encephalitis, an inflammation of the brain parenchyma which presents
as diffuse and/or focal neuropsychological dysfunction

3. Definitions
Meningitis vs Encephalitis
Normal brain function is the distinction
Seizures and postictal state can occur in meningitis
Some times it is difficult to differentiate
Cerebritis describes the stage preceding abscess formation and implies a
highly destructive bacterial infection of brain tissue

4. Etiology
Infectious :
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•
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Viral (HSV-VZV-CMV-EBV-Arboviruses-Ticoviruses)
Parasitic ( Toxoplasmosis)
Bacterial rare ( Mycoplasm)​​
​Non-infectious :
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Post infection (demylinating process)
Autoimmune

5. Epidemiology
•Determining the true incidence of encephalitis is impossible
•HSE, the most common cause of sporadic encephalitis in Western countries,
is relatively rare; the overall incidence is 0.2 per 100,000, with neonatal HSV
infection occurring in 2-3 per 10,000 live births
•The arbovirus group is the most common cause of episodic encephalitis,
with a reported incidence similar to that of HSV
•These statistics may be misleading in that most people bitten by arbovirusinfected insects do not develop clinically apparent illness and, of those who
do, less than 10% develop overt encephalitis

6. Pathophysiology
 Infectious :
Many viruses are transmitted by humans, though most cases of HSE are
thought to be reactivation of HSV lying dormant in the trigeminal ganglia
Mosquitoes or ticks inoculate arbovirus, and rabies virus is transferred via
an infected animal bite or exposure to animal secretions
With some viruses, such as varicella-zoster virus (VZV) and
cytomegalovirus (CMV), an immune-compromised state is usually
necessary to develop clinically apparent encephalitis
In general, the virus replicates outside the CNS and gains entry to the CNS either by hematogenous
spread or by travel along neural pathways (eg, rabies virus, HSV, VZV)

7. Pathophysiology
•Non-infectious :
The etiology of slow virus infections, such as those implicated in the measlesrelated subacute sclerosing panencephalitis (SSPE) and progressive
multifocal leukoencephalopathy (PML), is poorly understood

8. Pathophysiology
•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
•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

9. Pathophysiology
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

10. Presentation
Presentation
Variable
The acuity and severity of the presentation correlate with the prognosis
A history of mosquito or tick bites or exposure to mouse/rat droppings
should be sought
animal bite(s)
A prodrome of several days and consists of fever, headache, nausea and
vomiting, lethargy, and myalgias

11. Presentation
The classic presentation is encephalopathy with diffuse or focal neurologic
symptoms, including
•Behavioral and personality changes, with decreased level of consciousness
•Neck pain, stiffness
•Photophobis
•Lethargy
•Generalized or focal seizures (60% of children with CE)
•Acute confusion or amnestic states
•Flaccid paralysis (10% of patients with WNE)

12. Presentation
•(VZV), (EBV), (CMV), measles virus, or mumps virus includes a prodrome of
rash, lymphadenopathy, hepatosplenomegaly, and parotid enlargement
•Dysuria and pyuria are reported with St Louis encephalitis
•Extreme lethargy has been noted with West Nile encephalitis (WNE)

13. Physical Examination
•Typically
•Altered mental status
•Personality changes are very common
•Focal findings, such as hemiparesis, focal seizures, and autonomic
dysfunction
•Movement disorders (St Louis encephalitis, eastern equine encephalitis
[EEE],
western equine encephalitis [WEE])
•​Ataxia
​
•​Cranial nerve defects

14. Meningismus (less common and less pronounced than in meningitis)
Unilateral sensorimotor dysfunction (postinfectious encephalomyelitis
[PIE])
Dysphagia, particularly in rabies
HSV in neonates (aged 1-45 d) may include the following:
Herpetic skin lesions over the presenting surface from birth or with breaks
in the skin, such as those resulting from fetal scalp monitors
Keratoconjunctivitis
Oropharyngeal involvement, particularly buccal mucosa and tongue
Encephalitis symptoms, such as seizures, irritability, change in level of
attentiveness, bulging fontanelles
Additional signs of disseminated, severe HSV include jaundice,
hepatomegaly, and shock

15. Complications
•​Seizures
​
•​Syndrome of inappropriate secretion of antidiuretic hormone (SIADH)
​
•​Increased intracranial pressure (ICP)
​
•Coma

16. Work-up
Most cases are viral in origin
•So in addition to standard test, studies may be performed to identify the
infectious agent causing the encephalitis
•It is important, when possible, to distinguish acute arboviral encephalitides
from potentially treatable acute viral encephalitides (HSE and VZE) as a high
suspicion for these disorders and prompt treatment can reduce the severity of
neurological sequelae and can be lifesaving

17. Work-up
LP should be performed on all patients suspected of having a viral
encephalitis
•Gram staining to rule out bacterial meningitis
•PCR for HSV DNA
100% specific and 75-98% sensitive within the first 25-45 hours. Types 1
and 2 cross-react, but no cross-reactivity with other herpes viruses occurs
•Virul culture when viruses other than HSV are suspected( Mumps, Measles,
Influenza, Parainfluenza) or in case PCR is not available
•Serologic tests for toxoplasmosis can be helpful in light of an abnormal
computed tomography (CT) scan, particularly in the case of single lesions

18. Work-up
CT, MRI, EEG
Performance of a head CT scan with and without contrast agent should be
performed in virtually all patients with encephalitis
This should be done prior to LP if there are focal complaints or findings, signs
to search for evidence of elevated intracranial pressure (ICP), obstructive
hydrocephalus, or mass effect due to focal brain infection

19. (a) CT in the early stages of herpes encephalitis showing reduced attenuation in the right temporal lobe. (b) MR image
showing bilateral changes involving the temporal lobes and right cingulate gyrus.

20. Work-up
•MRI is more sensitive than CT scanning in demonstrating brain abnormalities
earlier in the disease course
•In HSE, MRI may show several foci of increased T2 signal intensity in medial
temporal lobes and inferior frontal gray matter. Head CT commonly shows areas
of edema or petechial hemorrhage in the same areas
•Invovement of the thalamus and basal ganglia may be observed in the setting
of encephalitis due to respiratory virul infection, Creutzfeld-Jacob disease,
arbovirus and TB
•In toxoplasmosis, contrast-enhanced head CT typically reveals several nodular
or ring-enhancing lesions. Because lesions may be missed without contrast,
MRI should be performed in patients for whom use of contrast material is
contraindicated

21. bilateral frontal cortex and subcortical white matter
This is a typical pattern for viral encephalitis

22. Work-up
HSV tends to attack the "limbic system" responsible for the integration of emotion,
memory, and complex behavior
There is a region of very bright signal on MR in the medial temporal lobe at left
(patient's right). This corresponds to an area of active viral leptomeningeal and
brain tissue infection. ( Image was taken 5 days after infection)

23. Work-up
•In HSE, electroencephalography (EEG) often documents characteristic
paroxysmal lateral epileptiform discharges (PLEDs), even before
neuroradiography changes. Eventually, PLEDs are positive in 80% of cases;
however, the presence of PLEDs is not pathognomonic for HSE
•Brain Biopsy
•Although most histologic features are nonspecific, brain biopsy is the criterion
standard because of its 96% sensitivity and 100% specificity.

24. Treatment
•Emergency Department Care
With the important exceptions of HSE and varicella-zoster encephalitis, the
viral encephalitides are not treatable beyond supportive care.
Treatments for T gondii and cytomegalovirus (CMV) encephalitis are available
but generally not initiated in the ED
•The goal of treatment
for acutely ill patients is 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 the initiation of treatment within
30 minutes of arrival

25. Collect laboratory samples and blood cultures before the start of IV therapy.
Even in uncomplicated cases of encephalitis, most authorities recommend a
neuroimaging study (eg, MRI or, if that is not available,CT scan before LP
Management of hydrocephalus and increased intracranial pressure

26. •Empiric adult emergency treatment for herpes simplex virus (HSV)
meningoencephalitis and varicella-zoster virus (VZV) encephalitis consists of
acyclovir 10 mg/kg (infused over 1 h) q8h for 14-21 days
•In HIV-positive patients, consider foscarnet, given the increased incidence
of acyclovir-resistant HSV and herpes zoster virus (HZV)