There are five types of encephalopathy, two benign and three malignant. Typically they occur a mean of two weeks post influenza, and are not associated with CNS inflammation. They include:
1) MERS (mild encephalopathy with reversible splenial lesion)- influenza symptoms, then prodrome of decreased level of consciousness, seizures, CSF pleocytosis, EEG abnormal, often within 103 days, and total resolution within one month with or without therapy. Agents include infl A and B, Legionella, Staph and Strep species, and E Coli. Splenial lesion is thought to represent intramyelinc edema with fiber separation.
2) HSES (hemorrhagic shock and encephalopathy syndrome (peds only)) shock, seizures, coma, DIC, diarrhea, drop HB/platelets, elevated LFT's, renal dysfunction, acidoses, negative blood and CSF cultures. "Definite" all 9 criteria are met, "probably" is 7-8 criteria met. Originally defined by Levin et al, 1982. Biphasic course with improvement then deterioration may occur. Abnormal EEG, diffuse cerebral edema, hemorrhagic necrosis occur. Morbidity plusmortality may > 90 percent.
3) ANE-- Acute necrotizing encephalopathy (pediatric and adults)-- most common complication of influenza. Course is fever, URI prodrome, then rapid and severe decline in consciousness often with seizures at onset and within 1-3 days of onset of systemic symptoms. CSF shows mild pleocytosis, limited utility. MRI shows severe symmetric, diffusion restricting lesions in both thalami, rostral midbrain tegmentum, putamena, periventricular white matter and cerebellar hemispheres. Decreased flow without stenosis or emboli is seen in thalamaperforators, SCA's , and deep internal and great cerebral veins. Early steroid therapy aids survival among patients without brainstem lesions.
4) (AESD) Acute encephalopathy with seizures and late restricted diffusion-- predominantly a pediatric diagnosis with variable features and prognosis and several eponyms
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