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Dr . Sunny LohiaDr . Sunny Lohia
Encephalitis usually affects the meninges as well as the brain, the
term MENINGOENCEPHALITIS is more accurate.
Inflammation of meninges
An acute inflammatory process affecting the brain parenchyma.
Encephalopathy syndrome of altered mental status,
manifesting as reduced consciousness or altered behaviour.
Viral infection is the most common and important cause of encephalitis.
Most common cause in world- Japanese encephalitis
Most common cause in asia – Entero virus
Most common cause in india - Japanese encephalitis
Most common causes of endemic VE- HHV
Most common causes of epidemic VE-HSV
Cause of encephalitis in immuno-competent hosts - Varicella,
herpes zoster, HHV 6 and 7, and EBV
Severe and Fatal Encephalitis- Arbo viruses and HSV
•Cat Scratch Disease
•Progressive multifocal -
• Post Vaccine
Causes ofCauses of
CAUSES of ENCEPHALITIS
Mode of transmission
Exposure to viruses can occur through:
Breathing in respiratory droplets from Infected person
Contaminated food or drink
Mosquito, tick, and other insect bites
Neurological damage is caused by direct invasion &
destruction of neural tissue or by host reaction to viral
There are varying degree of parenchymal & maningeal
inflammation, edema & necrosis.
Temporal lobe is often severly affected by HSV.
Arbo virus tends to affect entire brain.
Rabies virus mostly affect basal structures (hippocampus).
Fever that is
not very high
Some patients may have symptoms of a cold or stomach infection before encephalitis
Symptoms in Newborns and Infants
Symptoms in newborns and younger infants may not be
easy to recognize :
Irritability and crying more often
Bulging ant fontanelle
Loss of consciousness, poor responsiveness, stupor, coma
Muscle weakness or paralysis
Sudden change in mental functions:
"Flat" mood, lack of mood
Less interest in daily activities
Memory loss (amnesia),
Clinical presentation of non specific prodrome followed by
progressive CNS symptoms.
EEG: Diffuse slow-wave activity.
CT/MRI: Swelling of the brain parenchyma.
Pleocytosis : Initially Polymorphs & later mononuclear cells predominate.
Increased or normal protein.
Isolation of virus from serum
Detection of viral DNA or RNA by PCR
Specific IgM Antibody level
CSF to Serum Ratio of Anti HSV IgG
Primary test for CMV, HSV, VZV, EBV
Sensitive(>90%) and specific(100%) for HSV
Positivity increases with duration of illness
Not affected by less than 1 week of therapy
Next specific for entero-viruses
Not established for EBV
MRI brain (T2W image): right temporal lobe high signal in a
patient with herpes encephalitis
10% may have normal MRI.
Meningitis vs Encephalitis
Constitutional symptoms Encephalitis Meningitis
Fever Yes Yes
Headache, nausea, vomitting, lethargy Yes Yes
Photophobia, neck stiffness No Yes
seizures Yes Minimal
Cranial nerve palsies Yes No
Altered mental status yes minimal
Encephalopathy vs Encephalitis
Fever Uncommon Common
Headache Uncommon Common
Depressed mental status Steady deterioration May fluctuate
Focal neurological signs Uncommon Common
Type of seizure Generalised Generalised or focal
Blood Leucocytosis uncommon Leucocytosis common
CSF Pleocytosis uncommon Pleocytosis common
EEG Diffuse slowing Diffuse slowing and focal
MRI Often normal Focal abnormalities
Reduction in room light, visitors, & noise
Maintain airway, breathing and circulation.
Control of seizures.
Treatment of raised ICT.
Manage fever ((Never give aspirin)Never give aspirin)..
Maintain fluid & electrolyte balance.
Maintain blood-sugar level.
Feeding: NPO initially then NG Tube Feeding.
Methyl-prednisolone or dexa-methasone must be given to children
with suspected ADEM.
Available in oral and suspension form and IV formulation
Very poor bioavailability – required frequent dosing
10 mg/kg IV every 8 hrs for 14 days (30 mg/kg/day)
Additional 7 days in case of positive CSF PCR at 14 days.
VALACYCLOVIR – prodrug of acyclovir
FAMCICLOVIR – prodrug of penciclovir
Resistance to acyclovir and penciclovir occur in
Both have very
Most children completely recover from viral
encephalitis, although prognosis depends on severity
of illness, causative organism and age of child.
Potential deficits- intellectual, motor, psychiatric,
epileptic, visual or auditory in nature.
10% of children younger than 2 years of age with
entero-viral CNS infections suffers acute
complications as seizures, increased ICP , coma.
Almost all have favourable long term neurological
Effective viral vaccines
Control of insect vector
Eradications of insect breeding sites
Insect repllents- DEET
One of the commonest cause of AES, mainly
prevalent in Assam, West Bengal, Uttar Pradesh and
Primarily affects children under age 15.
Acute onset, fulminant course, and high mortality & morbidity.
70% of patients either die or survive with long term
Group-B arbo virus (Flavi virus).
Single stranded RNA virus.
Transmitted by culex mosquitoes(Zoonotic Disease).
Peak season : june to september
Man is an incidental dead end host.
Man-to-man transmission not reported.
Pigs are amplifier of virus.
Incubation Period: 5-15 days.
Cases represent tip of iceberg.
Case Fatality Rate: 10 –70%.
Incidence: 1- 10/10, 000 population.
IN HUMANS, prior dengue virus infection provides partial
protection from clinical Japanese Encephalitis
there is no specific treatment for JE.
The treatment is intensive supportive care, including control of
Vaccination against JE is advised in endemic areas.
There are 4 main types of JE vaccines currently in use
inactivated mouse brain-derived vaccines,
inactivated Vero cell-derived vaccines,
live attenuated vaccines
live recombinant vaccines.
In such areas, it is given routinely to children above 1 year of
Protective immunity develops in about a month’s time after
the second dose.
Revaccination after 3 yrs.
Best used in inter-epidemic period.
JE vaccine not recommended for routine use.
ADEM is an initial inflammatory , demyelinating event
with multifocal neurological deficits, typically
accompanied by encephalopathy.
Most common age group – 5 to 8 years.
More common in males.
0.07-0.4 /lakh pediatric population.
It maybe induced by infectious exposure or vaccine may
trigger production of CNS auto-antigens.
Lethargy, fever, headache, vomiting , meningeal signs, and
seizures including s. Epilepticus .
Encephalopathy is hallmark of ADEM , ranging from
ongoing confusion to persistent irritability to coma.
Focal neurological signs include visual loss, cranial
neuropathies, ataxia, motor and sensory deficits with
concurrent spinal cord demyelination.
CSF – Pleocytosis with lymphocytic or monocytic
CSF protein can be elevated
In 10% - oligoclonal bands
Elevated CSF immunoglobulin production
EEG- Generalised slowing
Head CT – may be normal or show hypodense regions.
BRAIN MRI – large , multifocal and sometimes confluent
or edematous mass like tumefactive T2 lesions with
variable enhancement within white and often grey matter
of cerebral hemispheres, cerebellum , and brain stem.
Spinal cord may have abnormal T2 signal or
enhancement, with or without clinical signs of myelitis.
High dose IV Steroid-Methylprednisolone 20-30mg/kg/day
for 5 days with a max dose of 1000mg/day.
Oral prednisolone taper over 1 month may prevent
IVIG- 2gm/kg/day over 2-5 days
Many children experience full recovery but some are left with residual
motor and/or cognitive deficit.
Can occur at all ages.
These disorders associated with antibodies against
neuronal cell surface proteins and synaptic receptors.
Most of these are severe and potentially fatal.
Mechanisms that trigger the antibodies production are
Brain MRI –
•Abnormal in 35%
•Nonspecific cortical &
sub-cortical T2 FLAIR
EEG – abnormal in all cases
Focal or diffuse slow
activity in delta & theta range.
characteristic EEG in
children “extreme delta
CSF –abnormal in 80% cases
Moderate lymphocytic pleocytosis & less frequently
increased protein synthesis and oligoclonal bands.
Diagnosis established by demonstrating NMDAR
antibodies in CSF or serum(sensitivity higher in CSF
100% vs 85%)
Presence of underlying tumour, mostly teratoma is age &
In few patients anti NMDAR occur after variety of
pathogen like M. pneumoniae, HSV 1 & 6 , entero virus &
Mortality rate – 7%
Substantial or full recovery – 80%
Recovery is usually slow can take upto 2 years.
Relapse rate – 15%