Lecturer

(Deptt. of pediatrics)
MGIMS Sevagram
n An inflammatory process that affects the brain tissue.
n It is almost always accompanied by inflammation of
adjacent meninges ,thus the term
meningoencephalitis.
n Encephalopathy implies cerebral dysfunction due to
circulating toxins, poisons, abnormal metabolites, or
intrinsic biochemical disorders affecting the neurons
but without inflammatory response.
A. Viruses: spread person to
person:
Harpies simplex1 &2.
Varicella zoster.
Mumps, Measles, Variola
Epstien -Barr Virus, CMV
Influenza virus, Enterovirus
Rubella, Adenovirus
HHV6
B. Spread by mosquitoes or
ticks
Japanese B encephalitis
Kyasanur forest disease.
Dengue virus
West Nile virus
Equine encephalitis virus
St.louis encephalitis
 Etiology cont…..
Spread by warm blooded Others
mammals
Rabies HIV
Lymphocytic Slow virus infections, prion
Choriomeningitis virus disease
 Etiology cont…..
Bacteria: Others:
H.Influenzae Chlamydia, Rickettsia, mycoplasma.
N.Meningitidis Fungi:
S.pneumonae, M.tuberculosis Cryptococus neoformans,
Spirochetes; borrelia,leptospira, coccidiodomycosis, blastomycosis.
Trponema pallidum.

Protozoa: Helminths:
Plasmodium falciparum, Schistosoma
Acanthamoeba, Naegleria
n Factors affect the epidemiology are; age, geographical
location, season, climate, and host immunocompetence.

n Incidence of encephalitis differs greatly in different

countries and in different seasons of the year.

n JE transmitted in our country by female mosquitoes Culex

triaenorhynchus and culex vishnui.

n Herpies tends to occur worldwide with little seasonal

variation.
n Primary: direct invasion and replication of virus
leading to tissue necrosis.
n Para infectious: A post infectious inflammatory
response characterized by immune mediated CNS
damage, demyelination with preservation of neurons
and axones.
n Many viruses caused widespread inflammation
,cerebral edema and necrosis.
n Some such as rabies and harpies virus have
predisposition to involve specific areas of the brain
namely basal ganglia and temporal lobe.
n Harpies virus have
predisposition to
involve specific areas
of the brain namely
temporal lobe.
n Determined by the:
1.severelty of involvement and anatomic location of affected
portion of the nervous system.
2.Inherent pathogenesis of offending agent.
3.Immune and other reactive mechanisms of the patient.
n Clinical manifestations may vary from inapparent mild
abortive illness or aseptic meningitis syndrome to severe
encephalopathy with or without radiculitis.
n Onset usually acute, but sign and symptoms of CNS
involvement often are preceded by a non specific ,acute
febrile illness.
 Clinical features cont……
n In Older children: headache and malaise.
n Infants are typically are irritable and lethargic.
n Fever, nausea, vomiting, neck pain, and photophobia are common.
n Alteration of consciousness ranges from mild lethargy and confusion to
coma.
n Evidence of brain parenchymal involvement is the hallmark of
encephalitis.
n Children with encephalitis may demonstrate evidence of diffuse disease
e.g. behavioral or personality changes ,decreased consciousness, and
generalized seizures or localized changes e.g. focal seizures ,
hemi paresis, movement disorders ,cranial nerve deficits and ataxia.
 Clinical features cont……
n Neurological abnormalities may be stationary ,progressive
,or fluctuating.
n Sudden severe rise of ICT may result in decerebration
cardio respiratory insufficiency, hyperventilation and
autonomic dysfunction.
n Uncontrolled cerebral edema may lead to herniation at
tentorial hiatus ,compression of the midbrain causing
deterioration of consciousness, papillary changes,ptosis,6th
nerve palsy, Ophthalmoplegia, paralysis of upward gaze,
cheyne-stroke breathing ,hyperventilation and bradycardia.
n Herniation of cerebellum through the foramen magnum
causes distortion and compression of medulla oblongata
with severe disturbances of vital centers leading to
respiratory or cardiac arrest.
n Course of encephalitis varies from that of fulminating
type, ending in death in 2 to 4 days,
n to that of a mild form in which illness subsides in 1 or 2
weeks with complete recovery.
n Typically this stage lasts for 7-10 days after which there is
gradual recovery with or without sequelae.
n Ds usually made on clinical presentation of a non-specific
prodrome followed by progressive CNS involvement.
n Presence of focal features favors the possibility of harpies
encephalitis.
n History is taken for prior viral infections, exanthema
(echovirus, coxsackievirus, varicella zoster virus, measles,
rubella) or recent vaccination.
n History of bite from a potentially rabid animal, travel history,
exposure to mosquitoes, rodents and ticks, the season in
which illness occurs and the disease prevalent in
community may provide clues to the diagnosis.
n Pressure: normal to slightly elevated.
n Usually there is lymphocytic pleocytosis(5-500 cells/mm3).
n Rarely more than 1,000 cells/mm3 may be seen in conditions
like eastern equine encephalitis and lymphocytic
choriomeningitis.
n Early in the disease cells might be polymorphonuclear ,later
mononuclear cells predominate.
n Some patients of HSE may show a xanthochromic or bloody
CSF ,usually with less than 500 RBCs/cmm.
n Protein contents is mildly elevated (50-200mg/dl).
n Glucose content is normal or slightly decreased.
n CSF should be cultured for viruses, bacteria, fungi and mycobacteria.
n Lab methods include to diagnose CNS viral infection: isolation of
virus, detection of viral antigen, or its nucleic acids and serology.
n Workup includes: viral culture of respiratory secretions ,throat swab,
CSF, blood ,urine, stool, swab from skin rash and brain tissue taken as
early as possible in the illness.
n Detection of viral antigen can be done in brain tissue or CSF.
n Detection of antibodies in CSF and CSF to blood ratio of specific IgG
can be helpful in diagnosing the HSV infection.
n Single serum IgM value or paired sera (acute and convalescent) to
show rising titers of IgG are also helpful.
n PCR to detect viral nucleic acids in CSF is provide a rapid ,accurate
diagnosis.
n May be helpful in patients with:
1.markedly neurological function,where it detect seizure and
monitor the effect of antiepileptics.
2.suspected HSV infection where characteristics periodic
sharp waves repeating every 0.5-4 sec. are found.
n EEG abn. May be deffuse or temporo- frontal, unilateral, or
bilateral, and are always accompanied by diffuse or
temporally accentuated excess Delta activity.
n It is helpful to separate viral encephalitis from metabolic or
toxic disorders.
n MRI is sensitive than CT scan to identifies the lesions of
encephalitis.
n In JE, CT scan shows non-enhancing low density areas in
thalamus, basal ganglia, midbrain, pons and medulla.
n Bilateral hemorrhagic thalamic involvement is characteristic
of JE in endemic areas.
n HSE
.

n 3 y male presented with fever & unconscious.

n Bilateral asymmetrical hypodense area in the temporal region with hyperdense focus.
n Herpes encephalitis.
n Bilaterally hypo dense lesions in basal ganglia
suggestive of JE.
n Bacterial or tuberculous meningitis
n Cerebral malaria.
n Encephalitis or meningoencephalitis due to leptospira spp,
mycoplasma pneumonea Aracanthamoeba.
n Brain abscess.
n Reye syndrome.
n Enteric encephalopathy.
n Electrolyte and metabolic encephalopathy.
n Drug ingestion.
n Cerebral vascular disorders.
nMain objectives of treatment;
1.To reduce the raised ICT.
2.To optimize systemic arterial pressure to maintain
adequate cerebral perfusion pressure.
3.Prevention of secondary complications.
n 1.avoiding situations that increases the
ICP.
n 2.Therapeutic measures to decrease ICP.
n 1.Position and general care of patient- A 15-300 head up tilt with head
kept in the midline position facilitates venous return from head,
decreases ICP and improves cerebral perfusion pressure.
n 2.Temperature control: Raised temp. increases the ICP by increasing
cerebral metabolism ,cerebral blood flow and cerebral edema.
n It should be controlled by cooling mattresses and paracetamol.
n 3.Role of sedation: Pain and arousal cause elevated ICP by increasing
cerebral blood flow.
n It play a imp. role in prevention of worsening of ICP by this
mechanism.
n Seizure control: Seizure increases ICP by increasing cerebral
metabolism and cerebral blood flow.
n Midazolam and diazepam is effective for emergency use.
n Pt. should kept nil by orally for first 24 hours.
n Pt. should receive IV fluids as n.5 in 5%
dextrose in normal maintenance requirement.
n If pt, develop SIADH than 2/3 of maintenance
are given.
n 1. Hyperventilation: After Endotracheal intubation with
maintenance of Paco2 between 25-30 mmHg effectively
reduces ICP by causing cerebral vasoconstriction.
n Drop in ICP occur within 1 to 5 minutes of initiation of
hyperventilation.
n 2.Mannitol:it is most commonly used agent for control of
raised ICP.
n DOSE: 0.25 to 1.0 g/kg body weight every 4-6 hours, or
20% mannitol 5 ml/kg over 5-10 min. followed by 3 ml/kg
BW 6 hourly till 48 hours.
n Acetazolamide in dose of 20-50 mg/kg /day in 3 to 4 doses .oral
glycerol 1ml/kg/dose 8 hourly may be used if ICP is elevated beyond
48 hours.
n Furosemide can be used in a dose of 1 mg/kg IV q 12 hourly.
n Barbiturates are generally used only when standard therapy consisting
of osmotic agents, hyperventilation and head position failed to control
the ICP.
n Dexamethasone: use of corticosteroid is controversial.
n CSF removal by an external ventricular drain: can be used only when it
has reached dangerous levels. it gives only a temporary relief for
raised ICP in pt. with acute hydrocephalus.
n Maintenance of cerebral perfusion: it is essential to
prevent cerebral ischemia.
n Normal cerebral perfusion in an infant is in the range of
30 mmHg.
n Hence it should be:
n >30 mmHg in infants <6mon.
n >40 mmHg in older children.
n >60 mmHg in adolescents.
n Feeding; should be started once the sensorium
improved.
n Pt. should be managed in ICU.
n Aim is to evaluate cardio-respiratory stability and detect
acute life threatening.
n Vitals including; temp. pulse, respiration, BP, neurological
status, head size, body weight, and urine are recorded
carefully.
Virus Drug Dose
HSV Acyclovir 10 mg/kg, q 8 hr, IV for 14-
21 days.

VZV Acyclovir 10-15 mg/kg, q 8 hr, IV for

7-10 days.
CMV Gancyclovir 7.5 mg/ k/ d, q 8hr, for14-
21days.

Influenza Amantadine 100 mg twice daily,for 5-7

days.
Rimantadine <14 yrs not recommended.
n Prognosis in all encephalitis is guarded with respect
to immediate outcome and sequelae.
n Sequelae involving CNS include intellectual, motor,
psychiatric, epileptic, visual or auditory.
n Predictor of poor outcome are: young age, low
GCS, abn. oculocephalic response, focal
neurological signs, reduction in cerebral perfusion
pressure, abn. Neuroimaging study, and unilateral
hyper perfusion on SPECT suggest a poor
prognosis.