脑炎及化脑讲义.pdf

page 1 encephalitisencephalitis and and and and meningitismeningitismeningitismeningitis 脑炎及脑膜炎脑炎及脑膜炎 zhang xinqing xuanwu hospital zhang xinqing xuanwu hospital page 2 definitions meningitis inflammation of the meninges encephalitis infection of the brain parenchyma meningoencephalitis inflammation of brain + meninges encephalitis 脑炎 page 4 viral encephalitis encephalitis is an acute inflammatory process affecting the brain 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 page 5 causes of viral encephalitis herpes viruses hsv-1, hsv-2, varicella zoster virus, cytomegalovirus adenoviruses influenza a enteroviruses, poliovirus measles, mumps, and rubella viruses rabies arboviruses examples: japanese encephalitis; west nile encephalitis virus; eastern, western and venzuelan equine encephalitis virus; tick borne encephalitis virus bunya viruses reoviruses example: colorado tick fever virus arenaviruses example: lymphocytic choriomeningitis virus page 6 clinical manifestations signs and symptoms of viral encephalitis common fever headache(dull), nausea, vomiting, malaise mental changes, confusion, delirium, lethargy ,stupor seizures: generalized or focal hyperreflexia, babinski signs, spasticity mild stiff neck page 7 clinical manifestations less common coma tremors of arm or face, pakinsonism hemiparesis aphasia cranial nerve palsies ataxia papilledema visual loss rare peripheral neuropathy signs and symptoms of viral encephalitis page 8 laboratory findings the blood leukocyte count is often elevated lumbar 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 page 9 laboratory findings the eeg is always abnormal and shows diffuse background slowing with occasional epileptiform or electrographic seizure activity mri studies often show areas of increased signal intensity on t2-weighted images. the ct scan may appear normal early, and later may show cerebral edema, necrosis or hemorrhage page 10 diagnosis the 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 page 11 diagnosis the 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 page 12 mortality rate and frequency of neurologic sequelae mortality rate and frequency of neurologic sequelae virus approximate mortality rate(%) rate of neurological sequlae(%) herpes simplex virus arboviruses eastern equine western equine enteroviruses mumps virus varicella-zoster virus rabies virus 70 untreated, 20-30treated 20-40 75 100 page 13 herpes simplex encephalitis herpes simplex encephalitis (单纯疱疹性脑炎) page 14 etiology hsv 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 hsv type 2 encephalitis causes neonatal hse by passage through the birth canal of a mother with active genital lesions page 15 pathology hse type 1 encephalitis is an acute, necrotizing, asymmetric hemorrhagic process with lymphocytic and plasma cell reaction it usually involves the medial temporal and frontal lobes inclusions may be seen in neurons and glia page 16 clinical findings acute onset rapid progression over several days headache, fever, vomiting, fatigue, behavioral disorders, memory loss, aphasia, hemiparesis focal or generalized seizures coma, even death eeg csf diffuse slow wave activities periodic slow-wave complexes arising from one or both temporal lobes increased 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 page 18 ct or mri mri: may show hyperintensity in temporal lobe, frontal lobes, insular cortex, or cerebral convexity on t2- weighted images ct: is less sensitive and may be normal during early phase and become abnormal later similar to the mri page 19 diagnosis hse 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 page 20 diagnosis the 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 page 21 treatment and prognosis treatment acyclovir given intravenously at a dosage of 10mg/kg every 8 hours, continued for 14 days symptomatic and supportive therapy prognosis up to 50% untreated cases die early treatment with acyclovir can reduce the mortality rate to 20% to 30% page 22 differential diagnosis tumor subacute or chronic onset slowly progressive course ct scan or mri may be helpful acute demyelinated encephalopathy acute or subacute onset upper respiratory tract infection and fever may be present mri shows lesion in white matter page 23 varicella-zoster encephalitis varicella-zoster encephalitis 水痘带状疱疹脑炎 page 24 pathology multifocal necrotic encephalomyelitis neuronal degeneration demyelination vasculitis involving medium and small blood vessels of the cns result in multiple brain infarction mainly in subcortical white matter page 25 laboratory findings csf: mildly elevated white cell counts and protein concentration particular antibody can be detected ct: multifocal ischemic and hemorrhagic necrosis mainly focused on white matter dsa: pearl stenosis in the proximal part of middle cerebral artery page 26 diagnosis and treatment diagnosis detection of vzv dna in csf by pcr assay detection of viral antibody brain biopsy with characteristic histopathologic changes treatment with acyclovir for 14-21 days usually 30mg/kg per day divided into 3 doses page 27 enterovirus encephalitis enterovirus encephalitis 肠道病毒脑炎 page 28 main etiologic agents coxsackievirus echovirus enterovirus poliovirus page 29 clinical findings abacterial meningitis: fever, severe headache, nausea, vomitting, neck stiffness, kernig sign(+) encephalitis: fever, headache, unconsciousness, epilepsy, focal neurologic signs some cases may show mental and behavioral disorders, ataxia, sensory deficits acute transverse myelitis: abrupt, progressive flaccid paralysis, urinary retention page 30 diagnosis and treatment definite diagnosis: depend on isolation of csf virus treatment: prevention of viral fecal-oral transmission supportive therapy no specific drugs it is self-limited disease, and usually recovers after 1 week page 31 subacute sclerosing panencephalitis subacute sclerosing panencephalitis (亚急性硬化性全脑炎) page 32 etiology and pathology etiology it is a childhood disease a typical measles infection is cause pathology 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 page 33 clinical findings children less 12 years usually affected, about a half of cases have infective history of measles the latency is usually 5 to 8 years slow onset, 8 to 12 months courses four phases of clinical courses page 34 clinical findings four phases of clinical courses 1st phase: intelligence decline, personality disorders, irritation and somnolence, lasts for several weeks 2nd phase: movement disorders, myoclonus, and generalized seizures 3rd phase: generalized stiff, opisthotinus, coma, automatic nerve dysfunction 4th phase: decorticate state, high fever, muscular hypotonus, died of all kinds of complication page 35 laboratory findings csf: normal pressure, mildly increased white cell counts and protein concentration eeg: periodic slow wave, sharp and slow wave complex and 5-10s interval ct: enlargement of cerebral ventricles, brain atrophy, multifocal lesions in white matter, no contrast enhancement page 36 diagnosis typical clinical findings characteristic eeg elevated csf igg concentration increased antibody titer in serum or csf isolation of measles in brain biopsy page 37 progressive multifocal leukoencephalopathy progressive multifocal leukoencephalopathy (进行性多灶性白质脑病) page 38 etiology the jc virus is the cause of pml the virus become latent in the kidney and other sites the virus appears to reactivate when immunosuppression from aids, chronic leukemia, etc presents page 39 pathology diffuse and patchy demyelination of white matter of the cerebral hemisphere sometimes brainstem and cerebellum are also involved page 40 clinical findings hemiparesis, aphasia, visual deficits, dysarthria and dementia common in patients with aids, lymphoma or leukemia, carcinoma, or pharmacologic immunosuppression following organ transplantation subacute onset, progressive course, leading to death in 3-6 months page 41 laboratory findings csf is usually normal ct scan or mri shows mutifocal white matter abnormalities page 42 diagnosis and treatment the diagnosis is established by brain biopsy with chacteritic histopathology appropriate clinical setting with mri or ct brain lesions is suggestive jc virus genome fragments detected by pcr assay is suggestive no antiviral drug has proven efficacy cytarabine may be helpful most patients die within 6 months of diagnosis creutzfeldt-jakob disease, cjd 1.sporadic ，scjd： 8090 2.familial，fcjd： 10 3.iatrogenic ，icjd ： 5 4.variantv，cjd： meningitis 脑膜炎 page 45 meningitis infection causing inflammation of the membranes covering the brain and spinal cord medical emergency with significant mortality characteristic pathogens bacterial meningitis or purulent meningitis non-bacterial meningitis often referred to as aseptic meningitis page 46 non-bacterial meningitisnon-bacterial meningitis is referred to as aseptic meningitis e.g. viral meningitis. the most common causes of meningitis are viral infections is referred to as aseptic meningitis e.g. viral meningitis. the most common causes of meningitis are viral infections bacterial meningitis bacterial meningitis is referred to as purulent meningitis. bacterial infections of the meninges are extremely serious illnesses, and may result in death or brain damage even if treat is referred to as purulent meningitis. bacterial infections of the meninges are extremely serious illnesses, and may result in death or brain damage even if treateded classification page 47 causes of meningitis bacterial infections viral infections fungal infections coccidiodes histoplasmosis cryptococcus parasitic angiostrongylus toxoplamosis other infectious borrelia burgdorferi mycobacterium tuberculosis treponema pallidum mycoplasma pneumoniae rickettsia, erlichia, brucella chlamydia page 48 symptoms of meningitis fever headache nausea and vomiting anorexia lethargy back pain altered mental status (seizure, coma) stiff neck meningismus (stiff neck + brudzinski + kernig signs) page 49 viral meningitis summer, fall severe headache vomiting fever stiff neck csf - pleocytosis (monos), protein and glucose are normal page 50