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ENCEPHALITIS
_SANTHOSHI
◦Is an inflammatory process of brain parenchyma.
◦Occurs most often in the first year of life
◦M/C in world and in INDIA _ Japanese encephalitis
◦In immunocompetent host- Vaicella , EBV, herpes
Etiology
◦RNA viruses- mumps, measles,
rubella,enteroviruses
◦DNA viruses- herpes simplex, cytomegalovirus,
Epstein barre virus
◦ARTHROPOD BORNE viruses- Japanese Bvirus,
west Nile, equine viruses
◦HIV, Rabies, lymphocytic choriomeningitis, dengue
virus
Cont…
◦Rickettsia, fungi (cryptococcus), protozoa (T gondii),
bacteria(tb meninges, listeria )
◦Non infectious causes- ADEM( ac. Disseminated
encephalomyelitis) allergy( post vaccine), Heat
hyperpyrexia, antibody associated encephalitis ,
electrolyte imbalance, toxins, metabolic disorders
Mode of transmission
◦Respiratory droplets
◦ contaminated food&
drinK
◦Mosquito, tick & other
insect bites
◦Skin contact
Pathogenesis
◦Neural damage is caused by direct invasion & destruction
of neural tissue or by host reactions to the antigens.
◦The damage leads to parenchyma & meningeal
inflammation , oedema & necrosis
◦HSV- affects temporal lobe
◦Arbo virus_ entire brain
◦Rabies virus- hippocampus
Pathological changes
◦Gross- brain shows diffuse oedema, congestion,
hemorrhages
◦Microscopic- perivascular cuffing with
lymphocytes & neutrophils
◦Necrosis & degeneration of neurons with
neuronophagocytosis.
Clinical features
◦Features depends on- severity of infection
-host susceptibility
- agent localization
- presence of raised
Intracranial pressure
Initial symptoms
◦Onset- sudden but may be gradual.
◦ High fever, head ache, mental confusion, vomiting,
irritability, loss of consciousness, seizures.
◦Ocular palsies, hemiplegia, speech dysfunction,
&cerebellar symptons
◦Raised ICT –decerebration
- cardiorespiratory insufficiency
-hyperventilation
- autonomic dysfunction
◦Extrapyramidal symptoms are common with JE
◦Lateralization to one side with temporalorfrontal
involvement- Herpes encephalitis
◦Brain swelling leads to herniation at tentorial
hiatus.
◦Compression of midbrain cause deterioration in
consciousness, ptosis, pupillary abnormalities,
6th palsy , ophthalmoplegia, cheynestoke
breathing hyperventilation & bradycardia.
Symptoms-in newborn & infants
◦Irritability
◦Body stiffness
◦Poor feeding
◦Bulging fontanellE
◦Vomiting
Emergency symptoms
◦Loss of consciousness, stupor, coma.
◦Muscle weakness, paralysis, seizures.
◦Severe head ache,high fever.
◦Sudden change in mental function Like flat
mood , loss of interest in daily activities,
memory loss
Encephalitis - clinical presentation

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Encephalitis - clinical presentation

  • 2. ◦Is an inflammatory process of brain parenchyma. ◦Occurs most often in the first year of life ◦M/C in world and in INDIA _ Japanese encephalitis ◦In immunocompetent host- Vaicella , EBV, herpes
  • 3. Etiology ◦RNA viruses- mumps, measles, rubella,enteroviruses ◦DNA viruses- herpes simplex, cytomegalovirus, Epstein barre virus ◦ARTHROPOD BORNE viruses- Japanese Bvirus, west Nile, equine viruses ◦HIV, Rabies, lymphocytic choriomeningitis, dengue virus
  • 4. Cont… ◦Rickettsia, fungi (cryptococcus), protozoa (T gondii), bacteria(tb meninges, listeria ) ◦Non infectious causes- ADEM( ac. Disseminated encephalomyelitis) allergy( post vaccine), Heat hyperpyrexia, antibody associated encephalitis , electrolyte imbalance, toxins, metabolic disorders
  • 5. Mode of transmission ◦Respiratory droplets ◦ contaminated food& drinK ◦Mosquito, tick & other insect bites ◦Skin contact
  • 6. Pathogenesis ◦Neural damage is caused by direct invasion & destruction of neural tissue or by host reactions to the antigens. ◦The damage leads to parenchyma & meningeal inflammation , oedema & necrosis ◦HSV- affects temporal lobe ◦Arbo virus_ entire brain ◦Rabies virus- hippocampus
  • 7. Pathological changes ◦Gross- brain shows diffuse oedema, congestion, hemorrhages
  • 8. ◦Microscopic- perivascular cuffing with lymphocytes & neutrophils ◦Necrosis & degeneration of neurons with neuronophagocytosis.
  • 9. Clinical features ◦Features depends on- severity of infection -host susceptibility - agent localization - presence of raised Intracranial pressure
  • 10. Initial symptoms ◦Onset- sudden but may be gradual. ◦ High fever, head ache, mental confusion, vomiting, irritability, loss of consciousness, seizures. ◦Ocular palsies, hemiplegia, speech dysfunction, &cerebellar symptons
  • 11. ◦Raised ICT –decerebration - cardiorespiratory insufficiency -hyperventilation - autonomic dysfunction ◦Extrapyramidal symptoms are common with JE ◦Lateralization to one side with temporalorfrontal involvement- Herpes encephalitis
  • 12. ◦Brain swelling leads to herniation at tentorial hiatus. ◦Compression of midbrain cause deterioration in consciousness, ptosis, pupillary abnormalities, 6th palsy , ophthalmoplegia, cheynestoke breathing hyperventilation & bradycardia.
  • 13. Symptoms-in newborn & infants ◦Irritability ◦Body stiffness ◦Poor feeding ◦Bulging fontanellE ◦Vomiting
  • 14. Emergency symptoms ◦Loss of consciousness, stupor, coma. ◦Muscle weakness, paralysis, seizures. ◦Severe head ache,high fever. ◦Sudden change in mental function Like flat mood , loss of interest in daily activities, memory loss