病毒性脑炎英语课件

Viral Encephalitis Zhang Xinqing Xuanwu Hospital The Capital University of Medical Sciences Epidemiology uViral encephalitis occurs in all seasons but peaks in summer and early fall. uViral encephalitis can occur at any age but the elderly and infants tend to have more severe encephalitis Clinical manifestations uThe onset is usually abrupt uclinical course progress rapidly over 1 to 3 days uthe strain of encephalitic virus determines the severity of the signs and symptom uthe table lists the most common signs and symptoms Clinical manifestations Clinical manifestations Laboratory findings uThe blood leukocyte count is often elevated ulumbar puncture findings a lumbar puncture shows a normal or elevated opening pressure the CSF contains 5 to 300WBC/mm3;50 to 200 mg/dl of protein; and normal glucose; bacterial cultures are sterile Laboratory findings uthe EEG is always abnormal and shows diffuse background slowing with occasional epileptiform or electrographic seizure activity uMRI studies often show areas of increased signal intensity on T2-weighted images. uThe CT scan may appear normal early, and later may show cerebral edema, necrosis or hemorrhage Diagnosis uThe clinical diagnosis is made on: acute onset of fever progressive mental status deterioration focal neurological signs and seizures(generalized or focal) CSF containing lymphocytic pleocytosis, normal glucose and elevated protein abnormal MRI abnormal EEG Diagnosis uThe specific etiology of the viral encephalitis is made by: PCR assay of CSF CSF IgM antibodies to some but not all viruses virus is isolation from throat or stool for some viruses acute and convalescent serum antibody titre rise brain biopsy with virus culture ;virus is seldom isolated from CSF Mortality rate and frequency of neurologic sequelae Herpes simplex encephalitis (HSE) Etiology uHSV type 1 encephalitis is the most common type in adults, the virus migrates along nerve axons to trigeminal ganglia, where it persists in a latent form and may be subsequently reactivated uHSV type 2 encephalitis causes neonatal HSE by passage through the birth canal of a mother with active genital lesions Pathology uHSE type 1 encephalitis is an acute, necrotizing, asymmetric hemorrhagic process with lymphocytic and plasma cell reaction. uIt usually involves the medial temporal and frontal lobes. uInclusions may be seen in neurons and glia Clinical findings uAcute onset uRapid progression over several days uHeadache, fever, vomiting, fatigue, behavioral disorders, memory loss, aphasia, hemiparesis uFocal or generalized seizures uComa, even death CSF uIncreased pressure and lymphocytic cell mild protein elevation, normal glucose red blood cells may be seen in some cases viral antibody may be detected by ELISA EEG udiffuse slow wave activities uperiodic slow- wave complexes arising from one or both temporal lobes CT or MRI uMRI: may show hyperintensity in temporal lobe, frontal lobes, insular cortex, or cerebral convexity on T2-weighted images uCT: is less sensitive and may be normal during early phase and become abnormal later similar to the MRI T2-weighted MRI demonstrated hyperintense lesion in the mesial temporal lobe HSE: MRI T1- weighted demonstrated middling intense and hyper intense in T2-weight T1-weighted MRI demonstrates hypointense and T2- weighted demonstrates hyperintense lesion in the mesial temporal lobe Diagnosis uHSE should be clinically suspected if the Acute onset, clinical symptoms Neurological signs EEG shows a characteristic pattern of high- voltage, periodic, lateralizing epileptiform discharges(PLEDS) at a rate of 2-3Hz originating from the temporal lobe. MRI shows focal medial temporal lobe abnormality Diagnosis uThe diagnosis of HSE is conformed by detection of fragments of HSV DNA in CSF or brain biopsy showing diffuse inflammation with intranuclear inclusion bodies identification of HSV particles by electron microscopy viral antigen identification by immunohistochemistry herpes simplex DNA fragments by PCR isolation of HSV from the tissue Treatment and prognosis utreatment Acyclovir given intravenously at a dosage of 10mg/kg every 8 hours, continued for 14 days symptomatic and supportive therapy uprognosis up to 50% untreated cases die early treatment with acyclovir can reduce the mortality rate to 20% to 30% Differential diagnosis uBacterial meningitis: signs of systemic infection CSF: lpressure is elevated lappearance ranges from slightly turbid to grossly purulent lCSF white cell counts of 1000-10000/ml may be seen lprotein concentration is elevated lglucose is decreased lGram-stained smears of CSF can identify the causative organism Differential diagnosis uTumor subacute or chronic onset slowly progressive course CT scan or MRI may be helpful uAcute demyelinated encephalopathy acute or subacute onset upper respiratory tract infection and fever may be present MRI shows lesion in white matter Varicella-zoster encephalitis Etiology uAfter infection of varicella-zoster virus(VZV), the virus migrates to ganglia(latent infection) uIn condition of lower immunity, the virus is reactivated and causes encephalitis or meningitis Pathology uMultifocal necrotic encephalomyelitis uneuronal degeneration udemyelination uvasculitis involving medium and small blood vessels of the CNS result in multiple brain infarction mainly in subcortical white matter Clinical finding uEncephalitis may be seen in cases with or without skin rash ufever, headache, vomitting, epilepsy, mental disorder, unconsciousness, focal neurologic signs, cognitive impairment usome cases may develop acute stroke symptoms uin severe cases, coma and death may happen Laboratory findings uCSF: mildly elevated white cell counts and protein concentration particular antibody can be detected uCT: multifocal ischemic and hemorrhagic necrosis mainly focused on white matter uDSA: pearl stenosis in the proximal part of middle cerebral artery Diagnosis and treatment uDiagnosis detection of VZV DNA in CSF by PCR assay detection of viral antibody brain biopsy with characteristic histopathologic changes utreatment with acyclovir for 14-21 days usually 30mg/kg per day divided into 3 doses Enterovirus encephalitis Main etiologic agents uCoxsackievirus uEchovirus uEnterovirus upoliovirus Clinical findings uAbacterial meningitis: fever, severe headache, nausea, vomitting, neck stiffness, Kernig sign(+) uencephalitis: fever, headache, unconsciousness, epilepsy, fccal neurologic signs some cases may show mental and behavioral disorders, ataxia, sensory deficits uacute transverse myelitis: abrupt, progressive flaccid paralysis, urinary retention Myelitis Laboratory finding uCSF: pressure is normal or elevated mild lymphocytic cell counts increase protein concentration is mildly elevated particular antibody can be detected Diagnosis and treatment uDefinite diagnosis: depend on isolation of CSF virus uTreatment: prevention of viral fecal-oral transmission supportive therapy no specific drugs It is self-limited disease, and usually recovers after 1 week Progressive multifocal leukoencephalopathy (PML) Etiology uThe JC virus is the cause of PML uThe virus become latent in the kidney and other sites uthe virus appears to reactivate when immunosuppression from AIDS, chronic leukemia, etc presents Pathology uDiffuse and pachy demyelination of white matter of the cerebral hemisphere usometimes brainstem and cerebellum are also involved Clinical findings uHemiparesis, aphasia, visual deficits, dysarthria and dementia uCommon in patients with AIDS, lymphoma or leukemia, carcinoma, or pharmacologic immunosuppression following organ transplantation uSubacute onset, progressive course, leading to death in 3-6 months Laboratory findings uCSF is usually normal uCT scan or MRI shows mutifocal white matter abnormalities Diagnosis and treatment uThe diagnosis is established by brain biopsy with chacteritic histopathology uappropriate clinical setting with MRI or CT brain lesions is suggestive uJC virus genome fragments detected by PCR assay is suggestive uno antiviral drug has proven efficacy ucytarabine may be helpful umost patients die within 6 months of diagnosis Subacute sclerosing panencephalitis (SSPE) Etiology and pathology uEtiology It is a childhood disease a typical measles infection is cause upathology diffuse inflammatory lesions in white and gray matter, and brainstem, cerebellum, cervical spinal cord can also be involved perivascular lymphocytic infiltration, and microglial proliferation intranuclear or intracytoplasmic inclussions may be seen Clinical findings uChildren less 12 years usually affected, about a half of cases have infective history of measles uthe latency is usually 5 to 8 years uslow onset, 8 to 12 months courses ufour phases of clinical courses Clinical findings ufour phases of clinical courses