神经影像与临床课件

,*,单击此处编辑母版文本样式,第二级,第三级,第四级,第五级,单击此处编辑母版标题样式,imaging and clinical 10,imaging and clinical 10,Leukoaraiosis,(,脑白质疏松症,),represents a,heterogeneous diffuse,anomaly,of,cerebral white matter l,ocalized,predominantly,periventricular, detected by,CT,scan,(,hypodensity,) or,MRI,(,hyperintensity,on,T2,weighted images or,FLAIR,). Leukoaraiosis affects,approximately,7%,of cases with,ischemic stroke,20%,in those with,lacunar infarcts,30-40%,of patients,with,dementia,and,2/3,of patients with,vascular,dementia,. Also in,old people,is in association,with,vascular risk factors,like,arterial hypertension,.,Pathophysiology: in region with leukoaraiosis,there are areas of,demyelination,increased,perivascular,space,gliosis,and,axonal loss,. Initially it was,thought that demyelination was,secondary to incomplete,ischemia but PET scan revealed the los,as,totality,of,nervous fibers,.,Leukoaraiosis(脑白质疏松症) repr,The same images also,appear in,obstructive hydrocephalus,disseminated,metastasis,of,white matter,and,lymphomas,.,Cerebral white matter is vascularised by penetrating,arteries and arterioles which are branches of,larger superficial cerebral arteries. Structural modification of these arteries are as follow: from,concentric,hyaline deposits,of artery wall, to,lipo,-,hyalinosis,(it is referred to severe,disorganisation,of,vascular bed with,macrophage presence,) and,fibrinoid,necrosis,. In asymptomatic elders the lumen of,these arteries are decreased significantly. Pathological,studies suggest that,leukoaraiosis,is one of the,manifestations of,cerebral small vessels disease,.,From this point of view it can be explained the relation,between leukoaraiosis and lacunar infarcts.,The same images also appea,Age,and,arterial hypertension,are associated,more frequently with,ischemic leukoaraiosis, where,hypercholesterolemia,diabetes mellitus, and,myocardial,infarction,are associated more frequent with,isolated lacunar infarcts,. So suggested,non-atheromatosis,pathogenesis,of,cerebral small arteries,implicated,in,ischemic leukoaraiosis,.,Staging of leukoaraiosis in grades according,to lesion severity and their advancement is done with the help of cerebral,MRI scan:,Stage I:,hyperintense lesions on,T2,weighted,and,FLAIR,images are,spot,-like and are located,in neighborhood of,frontal horns,of,lateral,ventricles,.,Stage II:,white matter lesions are located,around,subependymal region,of,lateral ventricles,.,Stage III,: white matter lesion on,T2,weighted,and,FLAIR,are the,same,as in stage,II,in,addition,focal spot,-like lesion of,deep white,matter,.,Stage IV,:,hyperintense,white matter lesions,on,T2,weighted and,FLAIR,images are,extended,fusiform,and,i,nterconnected,.,Age and arterial hypertensi,FLAIR images of single subcortical leukoaraiosis (SLA) (a), multiple SLA (b), large multiple SLA (c), and periventricular leukoaraiosis (PLA) (c). Arrow heads and arrows show SLA and PLA, respectively.,Leukoaraiosis in 1 region (frontal) marked by arrow,Advanced Leukoaraiosis (in bilateral frontal and occipital regions) marked by arrows,FLAIR images of single subcort,Patient S.B., 60 years, smoker, history of,myocardial infarction, admitted for vertigo, memory,disturbances and headache. MRI scan shows:,leukoaraiosis,stage I, deep parietal lacunar infarct on right side.,Stage I:,hyperintense lesions on,T2,weighted,and,FLAIR,images are,spot,-like and are located,in neighborhood of,frontal horns,of,lateral,ventricles,.,Patient S.B., 60 years, smok,Patient L.H., 65 year, with untreated arterial,hypertension, smoker, admitted for left hemiplegia,suddenly occurred. Cerebral MRI scan shows primary,right temporo-parietal primary intracerebral hematoma,mixed cerebral atrophy,leukoaraiosis stage II.,Stage II:,white matter lesions are located,around,subependymal region,of,lateral ventricles,.,Patient L.H., 65 year, wit,Patient C.N., 63 years, with arterial hypertension,diabetes mellitus, peripheral arterial disease,gait abnormalities for one year, frequent falling and,memory disturbances. Cerebral MRI scan shows: mixed,brain atrophy and,leukoaraiosis stage II.,Patient C.N., 63 years, wit,Patient P.I., 70 years, with arterial hypertension,diabetes mellitus, with left posterior cerebral arterial,ischemic stroke in the last 3 years, admitted for right,hemiparesis and mixed aphasia. Cerebral MRI shows acute,left middle cerebral arterial stroke, old posterior cerebral,arterial stroke on left side and leukoaraiosis stage III.,Stage III,: white matter lesion on,T2,weighted,and,FLAIR,are the,same,as in stage,II,in,addition,focal spot,-like lesion of,deep white,matter,.,Patient P.I., 70 years, wit,Patient M.G., 71 years, known with arterial,hypertension, dyslipidemia, history of bilateral PCA,Infarcts (first one in 2004 and the second in 2008),cortical blindness, with sphincter abnormalities for some,months, gait and memory diffi culties aggravated. Cerebral,MRI scan shows: mixed brain atrophy,leukoaraiosis,stage II-III,bilateral old occipital ischemic lesions.,Patient M.G., 71 years, kno,Patient G.V., 68 years, history of untreated,arterial hypertension of 10 years, with gait apraxia,dementia, phonation abnormalities for about one year.,Cerebral MRI shows mixed brain atrophy and,l,eukoaraiosis,stage IV,.,Stage IV,:,hyperintense,white matter lesions,on,T2,weighted and,FLAIR,images are,extended,fusiform,and,i,nterconnected,.,Patient G.V., 68 years, his,Forms of white matter lesions (WML); small caps (A), large caps (B), extending caps (C), thin lining (D), smooth halo (E), irregular,periventricular WML (F), punctuate deep WML (G), deep WML beginning confluence (H), confluent deep WML (I),Forms of white matter lesi,With the help of MRI scan leukoaraiosis was,classified in 4 stages, according to severity,and extension (Brand-Zawadzki).,Stage II was present frequently in patients,with acute stroke.,Stage III was in patients with chronic vascular,lesions.,Stage IV in our studied group was found in,those with Binswanger disease.,Severity of leukoaraiosis increases with age.,Severity of neurologic symptoms is in direct,proportion with severity of leukoaraiosis,Leukoaraiosis is a risk factor for cognitive,decline, in our study this affect was accentuated,due to association with brain atrophy in,66% of all cases.,Presence of leukoaraiosis is associated with,increased risk of stroke,recurrence.,With the help of MRI scan leuk,Progressive multifocal leukoencephalopathy,(PML：,进行性多灶性白质脑病,),is a,demyelinating disease,which results from the,JC virus（,多瘤病毒,）,infecting,oligodendrocytes（,少突胶质细胞,）,. It is considered the most common clinical manifestation of JC virus infection in the brain .,Epidemiology,PML is strongly associated with,immunosuppressed states, particularly AIDS but also can occur in,transplant patients,and . Incidence in non HIV settings are thought to be increasing. Primary PML developing in an immunocompetent patient is very rare.,In AIDS, it typically develops in patients with CD4 counts of 50 - 100 cells/uL, and is found in approximately 5% of autopsies of patients who died from AIDS .,More recently it has also been associated with Natalizumab (Tysabri TM), an IgG monoclonal antibody used in the treatment of relapsing remitting multiple sclerosis,Progressive multifocal leuk,Clinical presentation,Patients with PML present with various neurological symptoms. It typically spares the,optic nerve,and the,spinal cord,. The most frequently encoutered symptoms include :,altered mental status,motor deficits,limb and gait ataxia,visual symptoms,(diplopia & hemianopia),seizure,(as PML can also involve the grey matter),The final diagnosis is established with brain biopsy (specificity : 100%, sensitivity : 65-95%).,Clinical presentation,Pathology,Lesions tend to have a,confluent,bilateral,but,asymmetrical cerebral involvement,. Lesions were distributed throughout the,brain, including the,brain,stem,and,basal ganglia,. While the condition invariably involves white matter, lesions can also involve grey matter .,Histology reveals,demyelinating plaques,involving the,subcortical U-fibers,with sparing of the,cortex,and,deep gray matter,. Other findings include infected,oligodendrocytes,with,enlarged amphophilic nuclei,located at the,periphery,of the lesions, macrophages containing phagocytosed cellular debris and myelin, and reactive gliosis with enlarged astrocytes,Pathology,Radiographic features,CT,Asymmetric focal zones of low attenuation involving the peri-ventricular and sub-cortical white matter. This is in distinction to the more symmetrical hypo-attenuation seen in HIV encephalopathy.,MRI,Typically seen as,multifocal,asymmetric peri-ventricular,and,sub-cortical involvement,. There is,little or no mass effect,. The,U-fibers,are,commonly involved,.,T1,: involved regions are usually,hypo,-intense,T2,: involved regions are,hyper,-intense, T1,C+ (Gd),: typically there is,no enhancement, however if present it may be associated with improved survival,Radiographic features,MR spectroscopy : according to one study spectra of PML lesions were characterised by significantly,reduced NAA,lactate presence, and by significantly,increased,Cho,and,lipids,compared with control group values,Treatment and prognosis,Prognosis is generally is poor with an inexorable neurologic decline leading to coma and death occurring in the majority of patients with PML . If untreated, PML is usually fatal within 1 year. Treatment with highly active antiretroviral therapy (HAART) may prolong survival. Some reports also state some benefit with cytarabine.,MR spectroscopy : according t,弓形纤维,短联合纤维束,弓形纤维短联合纤维束,神经影像与临床课件,神经影像与临床课件,神经影像与临床课件,神经影像与临床课件,神经影像与临床课件,神经影像与临床课件,神经影像与临床课件,神经影像与临床课件,神经影像与临床课件,神经影像与临床课件,神经影像与临床课件,