Aseptic meningitis  definition: When the CSF culture was negative.  CSF: pressure mmh2o: normal or slightly elevated. leukocytes : PMN early mononuclear.

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Presentation transcript:

Aseptic meningitis  definition: When the CSF culture was negative.  CSF: pressure mmh2o: normal or slightly elevated. leukocytes : PMN early mononuclear later.rarly >1000 Protein mg /dl: Glucose mg/dl: generally normal may be depressed to40. (15-20%) Entroviruse recoverd by CSF culture or PCR HSV by PCR. CSF

Aseptic meningitis  Refer principally to viral meningitis.  Other infection.( Lyme disease,syphlis,TB)  Parameningeal infection: (brain abscess, epidural abscess,venus sinus empyema)  Chemical (NSAID,anti-inflamatory, IVig)  Autoimmune disorders

Encephalitis Inflammatory of brain parenchyma lead to cerebral dysfunction.  May be diffuse, or localized 1.Acute 2.Post infection encephalomyelitis 3.Chronic degenerative,slow viral infection.

Encephalitis  it has 2 mechanism. 1.Direct infection. 2.Immune mediated response in the CNS that begins several days after the extraneural manifestation of infection.

Encephalitis  Viruses are the principal causes of acute infection encephlitis.  Metabolic.  Toxic.  Neoplastic disorder.  HIV is an important cause of enceplalitis more commonly insidious in onset.

ADEM ( Acute disseminated encephalomyelitis)  ADEM abrupt development.  mutiple neurologic signs related to an inflammatory and demyelinating disorder of brain and spinal cord.  Childhood viral infection. ( measles, chickenpox, or vaccination)  Resembles to MS.  Relapses occurred in 14% within in 1 year.

Clinical manifestation encephalitis  Prodrome of nonspecific symptoms. (cough, sore throat, fever, headache, abdominal complaint)  Progressive lethargy, behavioral change, neurologic deficits.  Seizures are common.  Maculopapular rash.  Coma, transverse myelitis, Polio- like illness, periferal neuropathy.

Laboratory  CSF shows: lymphocytic pleocytosis. Slight elevatin protein. Normal glucose. The CSF occasionally may be normal.  In HSV protein and RBC increased.  Extreme elevated of protien and reduction of glucose (TB, carcinomatoseis, cryptococcal infection)

Laboratory  EEG: temporal lobe characteristic HSV infection.  Serologic studies. (arbovirus, EBV, mycoplasma, cat-scratch, Lyme)  culture stool and CSF,nasopharyngeal.  PCR test for HSV,entrovirus and other virus.  The cause of encephalitis In 1/3 of cases is undetermined.

Laboratory  Brain biopsy may be necessary for definitive diagnosis. 1.in patients with focal neurologic finding 2.Severe encephalopathy with no clinical improvement if diagnosis is obscure. 3.HSV,rabis encephalitis,prion related disease (kuru, jakob) diagnosed with culture of brain biopsy. 4.Identify arbovirus, entrovirus, TB, fungal infection. 5.Non infection illness ( primary CNS vasculopathies,malignancies)

Differential diagnosis  Diagnosis established with :  Neurologic signs. epidemiology, evidence of infection in CSF, EEG, brain imaging  brain biopsy diagnostic but seldom performed.

Treatment  There is no specific therapy exception of HSV and HIV. Treatment is supportive (siezure, electerolyte abnormality, airway monitoring, increased ICP  ADEM:high-dose IV corticosteroids.  IV acyclovir is choice for HSV.  M,pneumonia may be trated with doxycycline, erythromycin, azithromycin, clarithromycin??

complication  Symptoms resolve over several days to 2-3 weeks.  Recover without sequelae in 2/3 before dischrge from hospital.  neurologic sequelae(spasticity,cognitive impairment, weakness, ataxia, seizure. ( gradually recover some or all)  death.  Mortality is 5%