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ENCEPHALITIS

Dr.Hemant
(PT-NEURO)
Encephalitis
 An inflammation of the brain parenchyma, presents
as diffuse and/or focal neuropsychological
dysfunction
 Viral infection is the most common and important cause, with
over 100 viruses implicated worldwide
 Incidence of 3.5-7.4 per 100,000 persons per year
CAUSES
VIRUS -
• Arboviruses – examples: Japanese encephalitis; St. Louis
encephalitis virus; West Nile encephalitis virus; Eastern,
Western and Venzuelan equine encephalitis virus; tick borne
encephalitis virus
• Herpes viruses – HSV-1, HSV-2, varicella zoster virus,
cytomegalovirus, Epstein-Barr virus, human herpes virus 6
• Adenoviruses
• Influenza A
• Enteroviruses, poliovirus
• Measles, mumps, and rubella viruses
• Rabies
• Bunyaviruses – examples: La Crosse strain of California
virus
• Reoviruses – example: Colorado tick fever virus
• Arenaviruses – example: lymphocytic choriomeningitis virus
Japanese Encephalitis
 Most important cause of
arboviral encephalitis
worldwide, with over 45,000
cases reported annually
 Transmitted by culex mosquito,
which breeds in rice fields
› Mosquitoes become infected
by feeding on domestic pigs
and wild birds infected with
Japanese encephalitis virus
› Infected mosquitoes transmit
virus to humans and animals
during the feeding process
History of Japanese Encephalitis
 1800s – recognized in Japan
 1924 – Japan epidemic. 6125 cases, 3797 deaths
 1935 – virus isolated in brain of Japanese patient who died
of encephalitis
 1938 – virus isolated from Culex mosquitoes in Japan
 1948 – Japan outbreak
 1949 – Korea outbreak
 1966 – China outbreak
 Today – extremely prevalent in South East Asia 30,000-
50,000 cases reported each year
Causes
 Bacteria
 H. influenza
 S.pneumoniae
 N. meningitidis

 M. tuberculosis

 Mycoplasma pneumoniae

 Others
 Rickettsia, Spirochete & Malaria
Clinical manifestation
 Initial Signs
 Fever

 Headache

 Malaise

 Anorexia

 Nauseaand Vomiting
 Abdominal pain
Clinical manifestation
 Developing Signs
 Altered LOC – mild lethargy to deep coma
 AMS – confused, delirious, disoriented

 Mental aberrations :
 hallucinations
 personality change
 behavioral disorders ; occasionally frank psychosis
 Focal or general seizures in >50% severe cases.
 Severe focused neurologic deficits
Clinical manifestation
 Neurologic Signs
 Most Common
 Aphasia
 Ataxia
 Hemiparesis with hyperactive tendon reflexes
 Involuntary movements
 Cranial nerve deficits (ocular palsies, facial weakness)
Diagnosis
 Patient History
 Physical exam

 Work up
Patient History
 Prodromal illness, recent vaccination, development
of few days → Acute Disseminated
Encephalomyelitis (ADEM)
 Biphasic onset : systemic illness then CNS disease →
Enterovirus encephalitis
 Abrupt onset, rapid progression over few days →
HSV encephalitis
Patient History
 Recent travel and the geographical :
› Africa → Cerebral malaria
› Asia → Japanese encephalitis
› High risk regions of Europe and USA → Lyme disease
 Recent animal bites → Tick borne encephalitis or
Rabies
 Occupation
› Forest worker, exposed to tick bites
› Medical personnel, possible exposure to infectious
diseases
Patient History

 Season
› Japanese encephalitis : rainy season
› Arbovirus infections are : summer and fall
 Predisposing factors :
› Immunosuppression caused by disease and/or drug
treatment
› Organ transplant → Opportunistic infections
› HIV → CNS infections
 HSV-2 encephalitis and CMV infection
 Drug ingestion and/or abuse
 Trauma
Physical exam

 Focal neurological deficit → HSV encephalitis


 Hallucination or aphasia → HSV encephalitis

 Local paresthesia → Rabies encephalitis

 Brain stem signs, Unilateral peripheral motor weakness or


Cerebellar sign → Meliodosis
 Eschar → Scrub typhus

 Parotitis → Mumps

 Systemic sign eg. Rash → Mycoplasma & Enterovirus


Work up
 CBC : usually within the reference range
 Electrolytes : usually within reference range
 Syndrome of inappropriate secretion of antidiuretic
hormone (SIADH)
 Serum glucose : Use this level as a baseline for
determining normal CSF glucose values
Work up
 BUN/creatinine and liver function tests (LFTs) :
Assess organ function and the need to adjust the
antibiotic dose
 Platelet test and a coagulation profile : indicated
in patients with chronic alcohol use, liver disease, or
if DIC is suspected
 Urinary electrolyte test : Perform this assessment if
SIADH is suspected
 Urine and/or serum toxicology screening
Work up
 Lumbar puncture
 CSF examination (Polymorphonuclear cells may
predominate early in the illness but are replaced by
mononuclear cells within hours)
 Viral culture
 Viral PCR may identify the virus
 Serology tests antibodies to an specific virus → JEV,
Dengue, Mycoplasma (4 fold rising )
CSF

 It reveals 5-500 lymphocytes.


 The protein is mildly elevated
 The glucose is normal
EEG
 Certain EEG wave patterns can suggest encephalitis
due to herpes
 Unilateral or Bilateral periodic focal spike with slow
activity background
Imaging
Differential diagnosis
 Metabolic causes
 Drug & Toxicology
 Mass lesion
 Epilepsy
 Subarachnoid hemorrhage
 Acute confusional migraine
 Autoimmune : SLE
 CNS Vasculitis
Differential diagnosis
Encephalopathy Encephalitis
Fever Uncommon Common
Headache Uncommon Common
AMS Steady deterioration May fluctuate
Focal Neurologic Signs Uncommon Common
Types of seizures Generalized Both
Blood: Leukocytosis Uncommon Common
CSF: Pleocytosis Uncommon Common
EEG: Diffuse slowing Common +Focal
MRI Often normal Focal Abn.
Treatment
 No satisfactory treatment exists for the relatively
common acute arboviral encephalitides, which vary
in epidemiology, mortality, and morbidity, if not
clinical presentation
Treatment
 Clinically distinguishing these acute arboviral
encephalitis from the 2 potentially treatable acute
viral encephalitis is important
 Herpes simplex encephalitis (HSE), which is a sporadic
and lethal disease of neonates and the general
population
 Less common varicella-zoster encephalitis, which is
deadly in immunocompromised patients
Treatment
 Specific treatment
 HSV encephalitis : Neonate & infant Acyclovir 60
mg/kg/day IV div 8 hr 14 -21 days, Child & Adult 30
mg/kg/day 14 -21 days
 Varicella zoster encephalitis : Acyclovir

 CMV encephalitis : Gancyclovir or Foscanir

 Others : depend on etiology


Treatment
 Supportive treatment
 Reduce intracranial pressure : restrict fluid ,
hyperventilation( if on ventilator), low body
temperature , steroid ? (Mycoplasma )
 Rest, nutrition, fluids (SIADH), antipyretic, Anticonvulsant

 Acute psychosis : haloperidol


Prognosis
 Depends the virulence of the virus and on variables
associated with the patient's health status, such as
extremes of age, immune status, and preexisting
neurologic conditions
 Rabies, EEE, JE, and untreated HSE have high rates
of mortality and severe morbidity, including mental
retardation, hemiplegia, and seizures
Prognosis
 The mortality rate in treated HSE averages 20%
and is correlated with mental status changes at time
of first dose of acyclovir
 Approximately 40% of survivors have minor-to-
major learning disabilities, memory impairment,
neuropsychiatric abnormalities, epilepsy, fine-motor-
control deficits, and dysarthria
Prevention
 Controlling mosquitoes : Dengue
 Animal vaccination : Rabies virus
 Human vaccination : JEV
Medical/Legal Pitfalls
 Failure to consider HSE in the diagnosis or to initiate
administration of acyclovir in a timely fashion