Correlations of leuko-araiosis with cerebral atrophy and perfusion in elderly normal subjects and demented patients.

Kawamura, Jun; Meyer, John Stirling; Ichijo, M; Kobari, Masahiro; Terayama, Yasuo; Weathers, Susan

doi:10.1136/jnnp.56.2.182

Cited by 44 publications

(29 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…19 -25 Several earlier studies reported reduced cerebral blood flow in AD. [5][6][7][22][23][24][25]28,29 Pavics et al, 30 studying regional cerebral blood flow, showed that bilateral cerebral hypoperfusion occurs in the temporal and/or parietal region in 70% (23/33) of patients with AD and in 33% (6/18) of patients with vascular dementia. Many authors have concluded that diffuse cerebral hypoperfusion is responsible for leukoaraiosis in AD.…”

Section: Discussionmentioning

confidence: 99%

Cerebral Hypoperfusion Generates Cortical Watershed Microinfarcts in Alzheimer Disease

Suter

Sunthorn²,

Kraftsik³

et al. 2002

Stroke

204

175

View full text Add to dashboard Cite

Background and Purpose-The watershed cortical areas are the first to be deprived of sufficient blood flow in the event of cerebral hypoperfusion and will be the sites of watershed microinfarcts. Cerebral hypoperfusion is associated with Alzheimer disease (AD), but information regarding the occurrence of watershed cortical infarcts in AD is lacking. Methods-Brains of 184 autopsy cases (105 definite AD cases and 79 age-matched controls) were selected and analyzed by histochemical and immunohistochemical techniques. The 3-dimensional reconstruction of the whole cerebrum, with 3-mm spaced serial sections, was performed in 6 AD cases to study the intrahemispheric and interhemispheric distribution of the cortical microinfarcts. Results-A significant association (Pϭ0.001) was found between the occurrence of watershed cortical infarcts and AD (32.4% versus 2.5% in controls). The microinfarcts were restricted to the watershed cortical zones. Congophilic angiopathy was revealed to be an important risk factor. Perturbed hemodynamic factors (eg, decreased blood pressure) may play a role in the genesis of cortical watershed microinfarcts. Conclusions-In

show abstract

Section: Discussionmentioning

confidence: 99%

Cerebral Hypoperfusion Generates Cortical Watershed Microinfarcts in Alzheimer Disease

Suter

Sunthorn²,

Kraftsik³

et al. 2002

Stroke

204

175

View full text Add to dashboard Cite

show abstract

“…In other studies, radiological WMD as such occurring with dementia has been found to concur with an increased prevalence of systemic hypotension and heart failure, in a clinical setting different from that of brain infarction [25,26]. Several investigators underscore the possibility of a vascular aetiopathogenesis of the white matter changes in AD [2,27,28], some by suggesting a role of the AD-associated amyloid angiopathy. In the present study, the lack of correlation between severity of WMD and grey matter AE also extends to a lack of correlation with the corticomeningeal amyloidosis.…”

Section: Discussionmentioning

confidence: 99%

Neuropathology of White Matter Changes in Alzheimer’s Disease and Vascular Dementia

Englund¹

1998

Dement Geriatr Cogn Disord

198

167

View full text Add to dashboard Cite

Morphological white matter changes were investigated in clinically and neuropathologically diagnosed cases of Alzheimer’s disease (AD; 60 cases) and vascular dementia (VaD; 40 cases). In 33 of 60 AD cases, a white matter disease (WMD) characterized by tissue rarefaction, mild gliosis and a non-amyloid small-vessel sclerosis occurred in the central, preferentially frontal deep white matter. The mean vessel density was significantly lower than in normal control case frontal white matter. The presence of WMD did not parallel the severity of grey matter Alzheimer encephalopathy. In 25 of 60 AD cases, white matter degeneration with signs of both condensation and rarefaction of tissue elements was seen subjacent to advanced cortical degeneration in the temporal lobes. It concurred with WMD in only 13 cases and was judged to be of anterograde, Wallerian type and not related to angiopathy. In VaD, similar changes occurred, accompanied by several types of focal and topographically related lesions. For diffuse white matter pathology of similar appearance in vascular and neurodegenerative disease with dementia, there may be various at least partly contrasting aetiologies, which can be differentiated by the presence of even minor focal lesions in some cases. For the recognition of such subtle variations in the spectrum of WMD, modern imaging techniques are crucial for detailed clinical diagnosis and attempts at therapeutic intervention.

show abstract

“…White matter hyperintensities observed in 8% of patients in HT, seem to provide a further interpretative key to the possible etiopathogenetic role of deficient cerebral vascularization which could explain CA: they include atrophic perivascular demyelination, glyosis, and/or lacunar white matter infarcts [30, 31]and are the expression of a chronic state of cerebrovascular insufficiency determining ischemic lesions in the distal or borderline vascular territories [32]. This may be observed in neurologically asymptomatic patients [33], but the incidence and severity are greater in hypertensive nonuremic patients despite adequate antihypertensive treatment [34]. …”

Section: Discussionmentioning

confidence: 99%

Cerebral Imaging Changes in Patients with Chronic Renal Failure Treated Conservatively or in Hemodialysis

Savazzi¹,

Cusmano

Musini³

2001

Nephron

View full text Add to dashboard Cite

Background: Nonuremic patients with apparently normal memory and behavior, studied by means of cerebral computed tomography and found to have cerebral atrophy (CA), evidenced functional intellectual deficits when they underwent psychometric testing. The finding of CA has been repeatedly reported in limited case groups of uremic patients who also demonstrated functional intellectual deficits on the basis of the same tests. This retrospective study considered all diagnostic cerebral computed tomography scans done in our department between 1981 and 1998. Fifty-five uremic patients in conservative treatment (CT) and 111 patients in hemodialysis treatment (HT) were selected on the basis of the following two criteria: primary nephropathy as the cause of uremia and an age ≤55 years to exclude involutive brain changes occurring with age. Aims: The aims of the study were to determine the percent of uremic patients with CA, the characteristics of their CA (cortical or subcortical), and eventual associated morphological lesions. Results: CA was detected in 50.9% (cortical atrophy in 47.3% and subcortical atrophy in 3.6%) of the uremic patients in CT and in 77.5% of those in HT (cortical atrophy in 65.7% and subcortical atrophy in 7.7%). The average degree of CA was 0.872 in the patients in CT and 1.765 in the patients in HT. Thirty-four of the patients in the CT group and 46 in the HT group were hypertensive: these patients had a more severe degree of CA than the nonhypertensive subjects. In the CT group, the degree of CA in the hypertensive patients was 1.205 versus 0.428 for the nonhypertensive subjects. In the HT group, the degree of CA was 2.087 for the hypertensive patients versus 1.538 for the nonhypertensive patients. Of the overall population, 7.8% had ischemic lesions, 9.6% had endocranial calcifications, and 5.4% evidenced periventricular white matter hyperintensities. Conclusions: The high percent of CA found in young uremic patients increased in subjects in HT and, even more so in hypertensive patients. Vascular calcifications, focal ischemia and leukoaraiosis, well-known expressions of a chronic state of cerebrovascular insufficiency, were also found in HT patients; hypertension alone is a recognized accelerator of vascular damage. Thus, early and severe atherosclerosis and related hypoperfusion can be considered as the paramount causes of parenchymal cerebral damage in uremia.

show abstract

Correlations of leuko-araiosis with cerebral atrophy and perfusion in elderly normal subjects and demented patients.

Cited by 44 publications

References 29 publications

Cerebral Hypoperfusion Generates Cortical Watershed Microinfarcts in Alzheimer Disease

Cerebral Hypoperfusion Generates Cortical Watershed Microinfarcts in Alzheimer Disease

Neuropathology of White Matter Changes in Alzheimer’s Disease and Vascular Dementia

Cerebral Imaging Changes in Patients with Chronic Renal Failure Treated Conservatively or in Hemodialysis

Contact Info

Product

Resources

About