2. ๏ Definition of terms
๏ Differential diagnosis
๏ Points from history/epidemiology
๏ Investigations
๏ Supportive management
๏ Specific management
๏ Autoimmune encephalitis
3. ENCEPHALOPATHY
โข Diffuse disturbance of brain function without inflammation
ENCEPHALITIS
โข Dysfunction of brain associated with inflammation
FEBRILE ENCEPHALOPATHY
โข a/c onset of fever (<1wk)+alteration of consciousness >12
hrs
4. Febrile
inflammation
ENCEPHALOPATHY
Temp >380C Cellular CSF
Seizures
Alteration of cerebral Imaging /EEG
function suggestive of
Focal neurological signs inflammation
5. ๏ Clinically, a case of Acute Encephalitis Syndrome (AES)
is defined as a person of any age, at any time of year with
the acute onset of fever and at least one of:
๏ a) change in mental status (including symptoms such as
confusion, disorientation, coma, or inability to talk);
๏ b) New onset of seizures (excluding simple febrile seizures.
๏ ( A simple febrile seizure is defined as a seizure that occurs in a child aged 6
months to less than 6 years old, whose only finding is fever and a single
generalized convulsion lasting less than 15 minutes, and who recovers
consciousness within 60 minutes of the seizure)
Bull World Health Organ 2008, 86(3):178-186.
11. ๏ Features of infection
๏ Evidence of CNS involvement
๏ Features of raised intracranial tension
๏ Signs and symptoms of meningeal irritation
12. โข HSV is sporadic
epidemiology โข JE epidemics
h/o animal bites โข Rabies
โข JE
Mosquito bites โข Dengue
โข Chikun Gunya
Working/playing โข Leptospirosis
in dirty water
Contact withTB โข TBM
23. BACTERIAL โข PMN
MENINGITIS โข High protein, low sugar, gram stain
โข Few lymphocytes
ASEPTIC โข Normal protein
MENINGITIS โข Normal sugar
โข lymphocytic
VIRAL
โข Normal sugar, normal to slightly
ENCEPHALITIS raised protein
โข Opalescent, cob web
TUBERCULOUS โข Lymphocytic
MENINGITIS โข High protein. Low sugar
24. ๏ Take at least 5 ml of CSF
๏ Be sure that it is not mixed with blood
๏ Sensitivity and specificity are relatively good
๏ Can be negative very early in HSV and after
10 days of treatment
๏ Never stop Acyclovir before repeating once
more after 72hrs โ if clinical history, EEG and
imaging are suggestive
๏ Serum/CSF Ig M antibodies useful in JE
๏ Paired samples โ 4 fold rise in titre
25. ๏ MRI is preferable to CT scan-
๏ CTis advised in unstable patients, delirious
children who cannot be kept still for 30 min
31. ๏ Diffuseslowing suggests encephalopathic
process
๏ PLEDS in HSE
๏ Triphasic waves in metabolic encephalopathy
๏ Non convulsive status epilepticus
32.
33. ๏ Should be suspected in confusion, stupor,
unarousable coma
๏ Subtle features like eye blinking, nystagmus,
perioral twitching, automatisms may be seen
๏ May follow convulsive seizures
๏ EEG is the only diagnostic clue
๏ Response to diazepam can be demonstrated
in simultaneous EEG recording
๏ Generalised/complex partial
34.
35. ๏ Maintain
๏ก Normothermia
๏ก Normoglycemia
๏ก Normal electrolyte balance
๏ก Normotension
๏ Management of raised ICT
๏ก minimal stimulation
๏ก Head end elevation
๏ก Avoid hypotonic fluids
๏ก 3% saline
๏ก Mannitol 20% solution
๏ก hyperventilation
36. ๏ Management of
seizures/status
epilepticus
๏ Identify SIADH and
manage
๏ Rapid correction of
hyponatremia may
lead to central
pontine
myelinolysis
38. ๏ HSE โACYCLOVIR I/V 10 mg/kg/dose 8 hrly
x 14 -21 days. (500 mg/m2)Neonates 20
mg/kg/dose
๏ Oral acyclovir has very low bioavailability
๏ Oral valacyclovir can be used
๏ก Very costly
๏ Empirical acyclovir
๏ Repeat LP after 72 hrs if initial PCR is
negative โ and stop Acyclovir after that.
๏ Other drugs effective - foscarnet
40. ๏ Even in best centres a definite diagnosis of
encephalitis is reached only in 42% of cases
(Granerod et al)
๏ ADEM in 21%
๏ 1% autoimmune encephalitis
๏ 37% no definite diagnoses
๏ก Undiagnosed viral infections
๏ก Autoimmune causes
๏ก Unidentified metabolic causes
41. ๏ Poorly understood CNS condition
๏ Manifests lethargy โdelirium
๏ Pathogenesis
๏ก bacterial invasion of brain
๏ก endotoxins
๏ก derangement of neurotransmitter and
๏ก amino acid and microvascular changes
๏ Prognosis---serious
๏ May be seen in patient with
๏ 1. mechnical ventilation
๏ 2.critical ill patient in micu (sedatives, neuromuscular
blocking agents, dyselectrolytemia,hepatic failure may
contribute)
42. ๏ MANIFESTATION MAY BE HIV VIRUS
ITSELF OR ITS NEUROLOGICAL
COMPLICATION D/T OPPORTUNISTIC
INFECTION LIKE
๏ 1. CNS tuberculosis
๏ 2. cytomegalo virus encephalitis
๏ 3. toxoplasmosis
๏ 4. cryptococcal meningitis
๏ 5.syphilis
๏ 6.tumours (primary CNS lymphoma )or drug
related complications
43. ๏ง The potentially fatal complication of
falciparum malaria ( most important cause of
unarousable coma in febrile patients in
endemic area )
๏ง SUSCEPTIBILITY
๏ง - childrens
๏ง - pregnant women
๏ง - non โ immune adults
๏ง 20 % all severe falciparum malaria requires
ICU admission
44. ๏ Selective cytoadherence and
sequestration of parasitized RBCโS in
cerebral venules and
๏ toxin release at schizont rupture are
possible pathological mechanism
๏ Systemic complications like hypoglycemia
may contribute to development of coma
๏ Diagnosis โ PS for MP
๏ Treatment โ artesunate is better than
quinine
45. ๏ often presents with fever
๏ behavioural abnormalities
๏ psychosis
๏ movement disorders
๏ seizures/status
๏ May be paraneoplastic โ
teratoma ovary in young
females
๏ Often no tumour is
identified
๏ Antibodies to NMDA
,VGKC receptors
๏ Treatment โ IVIG,
plasmapheresis
47. ๏ A variety of infective and non infective conditions
in children can present as acute febrile
encephalopathy
๏ Stabilisation of patient and supportive
management helps a lot in reducing morbidity and
mortality
๏ Identification of specific etiology helps in
institution of specific therapy
๏ Awareness of Autoimmune encephalitis is
important โ another treatable cause like ADEM
๏ In a significant proportion of cases aetiology is yet
to be identified