Magnetic resonance findings in patients with early-onset Alzheimer's disease

McDonald, William M.; Ranga, K.; Krishnan, Ranga; Doraiswamy, P. Murali; Figiel, Gary S.; Husain, Mustafa M.; Boyko, Orest B.; Heyman, Albert

doi:10.1016/0006-3223(91)90199-v

Cited by 42 publications

(18 citation statements)

References 26 publications

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“…The PVH scores correlated significantly with systolic arterial blood pressure, but differences in blood pressure could not explain the differences in PVHs between the two groups. The low frequency of PVHs in our group of healthy subjects without major cerebrovascular risk factors corresponds to that reported by Fazekas et al 25 The increased frequency and extension of PVHs in patients with Alzheimer's disease, which suggested that PVHs may be associated with the Alzheimer's disease process, is in agreement with the findings of McDonald et al 26 By contrast, Leys et al, 6 Kozachuk et al,5 and Fazekas et al27 failed to find any difference in PVHs between patients with Alzheimer's disease and healthy subjects. Scheltens et al7 found increased severity of PVHs in his group of patients with Alzheimer's disease and with senile onset of disease, but not in presenile onset Alzheimer's disease.…”

Section: Discussionsupporting

confidence: 93%

White matter magnetic resonance hyperintensities in dementia of the Alzheimer type: morphological and regional cerebral blood flow correlates.

Waldemar

Christiansen

Larsson

et al. 1994

Journal of Neurology, Neurosurgery & Psychiatry

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In a prospective MRI study the presence, appearance, volume, and regional cerebral blood flow (rCBF) correlates of periventricular hyperintensities (PVHs) and deep white matter hyperintensities (DWMHs) were examined in 18 patients with probable Alzheimer's disease and in 10 age matched healthy control subjects, all without major cerebrovascular risk factors. The 133Xe inhalation method and the [9"-Tc]-d,l-hexamethyl-propyleneamine-oxime (HMPAO) technique with single photon emission computed tomography (SPECT) were used to measure rCBF. Rating scores for PVHs were significantly higher in the Alzheimer's disease group (p < 0.01) and correlated significantly with the volume ofventricles (p < 0.05) and with systolic arterial blood pressure (p < 0.01), but not with rCBF.By contrast, there was no significant difference in the rating scores or volumes of DWMHs between the two groups, although three patients had extensive DWMH lesions in the central white matter. In the group of patients with Alzheimer's disease as a whole, the volume of DWMHs correlated well with rCBF in the hippocampal region (r = -0-72; p < 0'001), but not (0-79 (1-55)) (5-39 (11 3)) Total volume of ventricles (cm3) 24-5 (8 9-56 2) 46-9 (18-6-127-2) NS (mean (SD)) (31-1 (17-8)) (54-2 (33-1)) Values are median (range) unless stated otherwise. Control = healthy control subjects; Alzheimer's disease = patients with a clinical diagnosis of probable Alzheimer's disease; MMSE = mini mental state examination'4; GDS = global deterioration scale'5; PVH = periventricular hyperintensities; DWMH = deep white matter hyperintensities. **p < 0-01, NS = nonsignificant (patients with Alzheimer's disease v control subjects, Wilcoxon two sample rank sum test). study reported elsewhere,8 and the present report includes only patients in whom a cranial MRI study was available. In one patient (case 04-19), the diagnosis was later confirmed by postmortem neuropathological examination. All patients underwent an extensive study programme to rule out any other disorders that might be associated with dementia, cognitive dysfunction, or altered rCBF.8 Briefly, cranial x ray CT was without focal pathology and without periventricular hypodensity in all patients. No patient had a history of psychiatric or neurological disease, except for Alzheimer's disease. All patients had Hamilton" depression scores below or at 10. Cerebrovascular risk factors were minimised: patients with diabetes mellitus, moderate to severe impairment of cardiac or pulmonary function, significant stenosis of the carotid arteries on Doppler examination, chronic arterial hypertension, or increased cholesterol concentrations in the blood were excluded. Resting systolic/diastolic blood pressure was below 180/100 on the study day. The severity of dementia was documented (

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Section: Discussionsupporting

confidence: 93%

White matter magnetic resonance hyperintensities in dementia of the Alzheimer type: morphological and regional cerebral blood flow correlates.

Waldemar

Christiansen

Larsson

et al. 1994

Journal of Neurology, Neurosurgery & Psychiatry

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“…20,58,59 Although WMHs are sometimes reported as being significantly more frequent in AD patients than in control subjects, the increase is attributed to mild periventricular changes of probably nonischemic origin, including caps, halos, and thin lining. 5,7,9,10 Moreover, Scheltens et al 6 reported that compared with WMH in control subjects, WMH was more intense in patients with senile onset AD but not in patients with presenile onset AD and suggested that additional microvascular factors are involved in elderly patients with senile onset AD. Together with those findings in the recent studies, our results suggests that WM changes in AD patients, when they are defined as irregular periventricular or confluent deep WMHs, are superimposed phenomena of ischemic origin.…”

Section: Discussionmentioning

confidence: 99%

Impact of White Matter Changes on Clinical Manifestation of Alzheimer’s Disease

Hirono

Kitagaki

Kazui

et al. 2000

Stroke

177

123

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Background and Purpose-There have been conflicting results involving the clinical significance of white matter changes in patients with Alzheimer's disease (AD). We studied the association between the volume of white matter hyperintensities (WMHs) on T2-weighted images and cognitive, neurological, and neuropsychiatric symptoms. Methods-The subjects were 76 AD patients who had WMHs but no obvious cerebrovascular diseases. We quantified the volume of WMHs by using fast-fluid-attenuated inversion recovery images and whole brain atrophy by using 3D spoiled gradient-echo images. Effects of WMHs and brain atrophy on dementia severity, cognitive function, neuropsychiatric disturbances, and neurological findings were examined. Results-Whole brain atrophy was significantly associated with dementia severity and cognitive disturbances, as well as with grasp reflex and some kinds of neuropsychiatric disturbances. After we controlled for the effects of brain atrophy, duration of symptoms, and demographic factors, we found that WMH volume was not associated with global cognitive disturbances or dementia severity but was significantly associated with urinary incontinence, grasp reflex, and aberrant motor behaviors. Brain atrophy and WMH volume were not significantly correlated either before or after controlling for age, sex, education, and duration of symptoms. WMH volume was associated with hypertension, but brain atrophy was not positively correlated with any vascular risk factors. Conclusions-Our results support the hypothesis that WMHs in AD patients are superimposed phenomena of vascular origin. WMHs contribute to specific neurological and neuropsychiatric manifestations but not to global cognitive impairment, which is more closely associated with brain atrophy. (Stroke. 2000;31:2182-2188.)

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“…9 Similar results were later replicated in a magnetic resonance imaging (MRI) study. 10 In a serial CT study, Kono and colleagues 4 found that progression of cerebral atrophy was greater in patients with EOAD but again they did not study the localisation of the atrophy. Similar results were found in an MRI study by Woo et al…”

mentioning

confidence: 99%

Structural correlates of early and late onset Alzheimer's disease: voxel based morphometric study

Frisoni

2005

Journal of Neurology, Neurosurgery & Psychiatry

167

117

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Objective: To examine the brain structural correlates of age at onset in patients with Alzheimer's disease. Methods: We studied nine patients with early onset (age (65 years), nine with late onset (age .65) Alzheimer's disease (EOAD and LOAD, respectively) of mild-moderate severity, and 26 controls who were stratified into younger (YC, age (65, n = 9) and older (OC, age .65, n = 17) subjects. The patients were closely matched for clinical severity: 3/2/3/1 patients had clinical dementia rating of 0.5/1/2/3, respectively, in both the groups. High resolution magnetic resonance images of the brain of the EOAD and YC groups and the LOAD and OC groups were compared on a voxel by voxel basis with statistical parametric mapping to detect areas specifically atrophic. Results: The patients with EOAD showed greater neocortical atrophy at the temporoparietal junction while the patients with LOAD showed greater hippocampal atrophy. The results could not be accounted for by the apolipoprotein E genotype. Conclusions: Since genetic factors are believed to play a relevant pathogenetic role in EOAD and environmental factors in LOAD, genetic and environmental factors may differentially predispose the neocortical and limbic areas to the development of Alzheimer's neuropathology.

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Magnetic resonance findings in patients with early-onset Alzheimer's disease

Cited by 42 publications

References 26 publications

White matter magnetic resonance hyperintensities in dementia of the Alzheimer type: morphological and regional cerebral blood flow correlates.

White matter magnetic resonance hyperintensities in dementia of the Alzheimer type: morphological and regional cerebral blood flow correlates.

Impact of White Matter Changes on Clinical Manifestation of Alzheimer’s Disease

Structural correlates of early and late onset Alzheimer's disease: voxel based morphometric study

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