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Clive Ballard - One of the best experts on this subject based on the ideXlab platform.
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hypertension is a potential risk factor for Vascular Dementia systematic review
International Journal of Geriatric Psychiatry, 2011Co-Authors: Sally I Sharp, Dag Aarsland, Sarah Day, Hogne Sonnesyn, Clive BallardAbstract:OBJECTIVE: The aim of the study was to conduct a meta-analysis of epidemiological and case control studies to determine whether arterial hypertension is specifically associated with an increased risk of Vascular Dementia (VaD). DESIGN: Longitudinal and cross-sectional prospective studies using operationalised criteria to define VaD and hypertension, with a normal control comparison group were systematically reviewed. Cochrane Library, Embase, Medline, and PsycInfo data sources were searched along with reference lists of included articles and reviews. Original, prevalence or incidence studies were included if operationalised criteria for hypertension and VaD as well as number of cases with and without hypertension in VaD and non-demented groups were provided. Intervention studies and post-stroke and CADASIL studies were excluded. RESULTS: Eleven studies recruiting either volunteers or clinical patients, or which were population-based, examined a total of 768 people with VaD and 9857 control cases. A meta-analysis of the six longitudinal studies showed that hypertension was significantly associated with increased risk of incident VaD (odds ratio, OR: 1.59, CI: 1.29-1.95, p < 0.0001). A similar association between hypertension and the risk of prevalent VaD was found in the five cross-sectional studies (OR: 4.84, CI: 3.52-6.67, p < 0.00001). CONCLUSIONS: Hypertension significantly increases the risk of Vascular Dementia. The current meta-analysis highlights the potential importance of rigorous treatment of hypertension as a key measure to help prevent the development of VaD. Copyright © 2010 John Wiley & Sons, Ltd.
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is physical activity a potential preventive factor for Vascular Dementia a systematic review
Aging & Mental Health, 2010Co-Authors: Dag Aarsland, Farzaneh S Sardahaee, Sigmund A Anderssen, Clive BallardAbstract:Background: Physical exercise has several beneficial effects, including reduced risk for Alzheimer's disease. Although several studies of potential risk factors for Vascular Dementia (VaD) exist, including physical activity, the studies have usually included few participants and there are no meta-analyses addressing this key topic. Methods: The MEDLINE database was searched using the key words ‘physical exercise’ ‘activity’ or ‘walking’ in combination with ‘Dementia’ and ‘Vascular Dementia’. Potentially relevant studies were assessed and summarised by two of the authors, and longitudinal studies with operationalised definition of physical activity providing risk for VaD in both groups were included in the meta-analysis using pooled estimates from a random effects model. Results: A total of 24 longitudinal studies, including 1378 patients with VaD, were included in the review. The majority of individual studies did not report significant associations. Five studies fulfilled criteria for meta-analysis, incl...
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efficacy safety and tolerability of rivastigmine capsules in patients with probable Vascular Dementia the vantage study
Current Medical Research and Opinion, 2008Co-Authors: Clive Ballard, M Sauter, Philip Scheltens, Frederik Barkhof, E C W Van Straaten, W M Van Der Flier, C Hsu, Roger LaneAbstract:ABSTRACTObjective: The aim was to evaluate the efficacy, safety and tolerability of rivastigmine capsules in patients diagnosed with probable Vascular Dementia (VaD).Methods: VantagE (Vascular Dementia trial studying Exelon) was a 24-week, multicentre, double-blind study. VaD patients aged 50–85 years were randomized to rivastigmine capsules (3–12 mg/day) or placebo. Efficacy assessments included global and cognitive performances, activities of daily living and neuropsychiatric symptoms. Adverse events were recorded. Additional exploratory analyses determined whether heterogeneity in pathologies and symptoms extended to differential treatment effects.Trial registration: NCT00099216.Results: 710 patients were randomized. Rivastigmine demonstrated superiority over placebo on three measures of cognitive performance (Vascular Dementia Assessment Scale, Alzheimer's Disease Assessment Scale cognitive subscale, Mini-Mental State Examination; all p ≤ 0.05, intent-to-treat population [ITT]), but not other outcomes...
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towards defining the neuropathological substrates of Vascular Dementia
Journal of the Neurological Sciences, 2004Co-Authors: Raj N Kalaria, R H Perry, Clive Ballard, P G Ince, Rose Anne Kenny, Tuomo PolvikoskiAbstract:CerebroVascular disease is highly heterogeneous but can culminate in Vascular cognitive impairment or Vascular Dementia (VaD). As much as the clinical diagnosis warrants scrutiny, the neuropathological substrates of VaD also need to be better defined. Atherosclerosis and small vessel disease are the main causes of brain infarction. Lacunar infarcts or multiple microinfarcts in the basal ganglia, thalamus, brainstem and white matter are associated with more than half of VaD cases consistent with subcortical ischaemic VaD. White matter changes including regions of incomplete infarction are usually widespread in VaD, but their contribution to impairment is not explicit. Other pathologies including hippocampal injury and Alzheimer type of lesions may also modify the course of Dementia. Similar to other common Dementias consensus criteria for VaD need unambiguous definition to impact on preventative and treatment strategies and are critical for selective recruitment to clinical trials.
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progressive brain atrophy on serial mri in Dementia with lewy bodies ad and Vascular Dementia
Neurology, 2001Co-Authors: John T Obrien, Clive Ballard, Robert Barber, A Gholkar, Ian G Mckeith, S M Paling, E D Williams, William R Crum, Martin N RossorAbstract:The authors determined rates of brain atrophy, as assessed by the boundary shift integral on serial MRI, in patients with Dementia with Lewy Bodies (DLB, n = 10), AD (n = 9), Vascular Dementia (VaD, n = 9), and age-matched controls (n = 20). Mean % ± SD atrophy rates per year were as follows: DLB, 1.4 ± 1.1; AD, 2.0 ± 0.9; VaD, 1.9 ± 1.1; and controls, 0.5 ± 0.7. Dementia subjects had higher rates than controls ( p
Helena C Chui - One of the best experts on this subject based on the ideXlab platform.
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subcortical ischemic Vascular Dementia
Neurologic Clinics, 2007Co-Authors: Helena C ChuiAbstract:Subcortical ischemic Vascular Dementia (SIVD) has been proposed as a subtype of Vascular cognitive impairment. MRI often discloses "silent" hyperintensities in 20% to 40% of community-dwelling elderly. Efforts to relate MRI-measured lacunes and white matter changes to cognitive impairment have not been straightforward. The possibility that Alzheimer's disease pathology contributes to cognitive impairment increases with age. A rare disorder known as cerebral autosomal dominant arteriopathy with subcortical infarctions and leukoencephalopathy (CADASIL) provides an opportunity to study SIVD in the absence of Alzheimer's disease. Lacunes and deep white matter changes are associated with dysexecutive syndrome. Hypertension, the leading risk factor for sporadic SIVD, is treatable. High priority must be given to reducing Vascular risk profiles.
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correlates of hippocampal neuron number in alzheimer s disease and ischemic Vascular Dementia
Annals of Neurology, 2005Co-Authors: Chris Zarow, Harry V Vinters, William G Ellis, Michael W Weiner, Dan M Mungas, Lon R White, Helena C ChuiAbstract:The cornu ammonis 1 region of the hippocampus (CA1) sector of hippocampus is vulnerable to both Alzheimer's disease (AD)-type neurofibrillary degeneration and anoxia-ischemia. The objective of this article is to compare number and size of neurons in CA1 in AD versus ischemic Vascular Dementia. Unbiased stereological methods were used to estimate the number and volume of neurons in 28 autopsy-derived brain samples. For each case, the entire hippocampus from one cerebral hemisphere was sliced into 5mm slabs (5-7 slabs/case), cut into 50 microm sections, and stained with gallocyanine. Using the optical dissector, we systematically sampled the number and size of neurons throughout the extent of CA1 and CA2. The total number of neurons was significantly less in AD compared with ischemic Vascular Dementia (p < 0.02), but there was no significant difference in neuron size. The greatest loss of neurons was observed in two cases with combined AD and hippocampal sclerosis. Regardless of causative diagnosis, the number of CA1 neurons correlates with magnetic resonance imaging-derived hippocampal volume (r = 0.72; p < 0.001) and memory score (r = 0.62; p < 0.01). We conclude that although CA1 neuron loss is more consistently observed in AD than ischemic Vascular Dementia, severity of loss shows the expected correlation with structure and function across causative subtype. Reductions in magnetic resonance imaging-derived hippocampal volume reflect loss, rather than shrinkage, of CA1 neurons.
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subcortical ischaemic Vascular Dementia
Lancet Neurology, 2002Co-Authors: Gustavo C. Roman, Timo Erkinjuntti, Anders Wallin, Leonardo Pantoni, Helena C ChuiAbstract:Summary Vascular Dementia is the second most common type of Dementia. The subcortical ischaemic form (SIVD) frequently causes cognitive impairment and Dementia in elderly people. SIVD results from small-vessel disease, which produces either arteriolar occlusion and lacunes or widespread incomplete infarction of white matter due to critical stenosis of medullary arterioles and hypoperfusion (Binswanger's disease). Symptoms include motor and cognitive dysexecutive slowing, forgetfulness, dysarthria, mood changes, urinary symptoms, and short-stepped gait. These manifestations probably result from ischaemic interruption of parallel circuits from the prefrontal cortex to the basal ganglia and corresponding thalamocortical connections. Brain imaging (computed tomography and magnetic resonance imaging) is essential for correct diagnosis. The main risk factors are advanced age, hypertension, diabetes, smoking, hyperhomocysteinaemia, hyperfibrinogenaemia, and other conditions that can cause brain hypoperfusion such as obstructive sleep apnoea, congestive heart failure, cardiac arrhythmias, and orthostatic hypotension. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leucoencephalopathy (CADASIL) and some forms of cerebral amyloid angiopathy have a genetic basis. Treatment is symptomatic and prevention requires control of treatable risk factors.
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neuropathologic substrates of ischemic Vascular Dementia
Journal of Neuropathology and Experimental Neurology, 2000Co-Authors: Harry V Vinters, William G Ellis, Chris Zarow, Barbara Zaias, William J Jagust, Wendy J Mack, Helena C ChuiAbstract:Ischemic Vascular Dementia (IVD) is a relatively uncommon entity, in the course of which multiple ischemic brain lesions result in progressive cognitive and memory impairment. Ischemic brain lesions may also aggravate the neuropsychologic deficit of Alzheimer disease (AD). In this review we summarize our experience based upon autopsy examination of the central nervous system in 20 patients (age range 68-92 years) enrolled in a longitudinal investigation of structural, neurochemical, functional neuroimaging, and neuropsychologic components of IVD, especially Dementia associated with cerebral microVascular disease. While cystic infarcts were present in the CNS of 5 patients, the most commonly observed neuropathologic abnormalities were lacunar infarcts and microinfarcts--both types of lesion were encountered in over half of patients' brains. Evidence of (remote) hippocampal injury was found in 11/20 patients. Severe atherosclerosis and arterio/ arteriolosclerosis were both associated with the occurrence of multiple lacunar infarcts. Pronounced cerebral amyloid angiopathy (CAA) was noted in a single patient, who also showed other microscopic changes of severe AD. While fairly unusual as a nosologic entity, IVD appears to correlate with widespread small ischemic lesions distributed throughout the CNS. We furthermore propose an approach to quantifying the burden of ischemic Vascular and parenchymal disease that may be associated with a Dementia syndrome. A brief review of neuropathologic features of Vascular Dementia (both familial and sporadic) is presented.
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research criteria for subcortical Vascular Dementia in clinical trials
Journal of Neural Transmission-supplement, 2000Co-Authors: Timo Erkinjuntti, Gustavo C. Roman, Anders Wallin, Helena C Chui, Leonardo Pantoni, P Scheltens, Domenico Inzitari, Kenneth Rockwood, David W DesmondAbstract:Vascular Dementia (VaD) incorporate different Vascular mechanisms and changes in the brain, and have different causes and clinical manifestations. Variation in defining the cognitive syndrome, in Vascular etiologies, and allowable brain changes in current clinical definitions of VaD have resulted in variable estimates of prevalence, of groups of subjects, and of the types and distribution of putative causal brain lesions. Thus current criteria for VaD select an etiologically and clinically heterogeneous group. This definitional heterogeneity may have been a factor in “negative” clinical trials. An alternative for clinical drug trials is to focus on a more homogenous group, such as those with subcortical (ischemic) VaD. This designation incorporates two small vessel clinical entities “Binswanger’s disease” and “the lacunar state”. It comprises small vessel disease as the primary Vascular etiology, lacunar infarct(s) and ischaemic white matter lesions as the primary type of brain lesions, and subcortical location as the primary location of lesions. The subcortical clinical syndrome is the primary clinical manifestation, a definition which still requires additional empirical data. We expect that subcortical VaD show a more predictable clinical picture, natural history, outcome, and treatment responses. We propose a modification of the NINDS-AIREN criteria as a new research criteria for subcortical VaD.
John T Obrien - One of the best experts on this subject based on the ideXlab platform.
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progressive brain atrophy on serial mri in Dementia with lewy bodies ad and Vascular Dementia
Neurology, 2001Co-Authors: John T Obrien, Clive Ballard, Robert Barber, A Gholkar, Ian G Mckeith, S M Paling, E D Williams, William R Crum, Martin N Rossor, Nick C FoxAbstract:The authors determined rates of brain atrophy, as assessed by the boundary shift integral on serial MRI, in patients with Dementia with Lewy Bodies (DLB, n = 10), AD (n = 9), Vascular Dementia (VaD, n = 9), and age-matched controls (n = 20). Mean % +/- SD atrophy rates per year were as follows: DLB, 1.4 +/- 1.1; AD, 2.0 +/- 0.9; VaD, 1.9 +/- 1.1; and controls, 0.5 +/- 0.7. Dementia subjects had higher rates than controls (p < 0.001), but there were no significant differences between the three Dementia groups. The authors found accelerating atrophy with increasing severity of cognitive impairment, further emphasizing the need for early diagnosis and intervention in Dementia.
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progressive brain atrophy on serial mri in Dementia with lewy bodies ad and Vascular Dementia
Neurology, 2001Co-Authors: John T Obrien, Clive Ballard, Robert Barber, A Gholkar, Ian G Mckeith, S M Paling, E D Williams, William R Crum, Martin N RossorAbstract:The authors determined rates of brain atrophy, as assessed by the boundary shift integral on serial MRI, in patients with Dementia with Lewy Bodies (DLB, n = 10), AD (n = 9), Vascular Dementia (VaD, n = 9), and age-matched controls (n = 20). Mean % ± SD atrophy rates per year were as follows: DLB, 1.4 ± 1.1; AD, 2.0 ± 0.9; VaD, 1.9 ± 1.1; and controls, 0.5 ± 0.7. Dementia subjects had higher rates than controls ( p
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white matter lesions on magnetic resonance imaging in Dementia with lewy bodies alzheimer s disease Vascular Dementia and normal aging
Journal of Neurology Neurosurgery and Psychiatry, 1999Co-Authors: Robert Barber, R H Perry, Clive Ballard, P Scheltens, A Gholkar, Ian G Mckeith, P G Ince, John T ObrienAbstract:OBJECTIVES—Alzheimer's disease and Vascular Dementia are associated with an increase in changes in white matter on MRI. The aims were to investigate whether white matter changes also occur in Dementia with Lewy bodies and to examine the relation between white matter lesions and the cognitive and non-cognitive features of Dementia with Lewy bodies, Alzheimer's disease, and Vascular Dementia. METHODS—Proton density and T2 weighted images were obtained on a 1.0 Tesla MRI scanner in patients with Dementia with Lewy bodies (consensus criteria; n=27, mean age=75.9 years), Alzheimer's disease (NINCDS/ADRDA; n=28, mean age=77.4 years), Vascular Dementia (NINDS/AIREN; n=25, mean age=76.8 years), and normal controls (n=26, mean age=76.2 years). Cognitive function, depressive symptoms, and psychotic features were assessed using a standardised protocol. Periventricular hyperintensities (PVHs), white matter hyperintensities (WMHs) and basal ganglia hyperintensities (BGHs) were visually rated blind to diagnosis using a semiquantitative scale. RESULTS—Periventricular hyperintensities were positively correlated with age and were more severe in all Dementia groups than controls. Total deep hyperintensities scores (WMHs plus BGHs) were significantly higher in all Dementia groups than controls and higher in patients with Vascular Dementia than those with Dementia with Lewy bodies or Alzheimer's disease. In all patients with Dementia, frontal WMHs were associated with higher depression scores and occipital WMHs were associated with an absence of visual hallucinations and delusions. CONCLUSION—In common with Alzheimer's disease and Vascular Dementia, PVHs and WMHs were significantly more extensive in Dementia with Lewy bodies than in controls. This overlap between different Dementias may reflect shared pathological mechanisms. The link between frontal WMHs and depression and the absence of occipital WMHs and psychotic symptoms has important implications for understanding the neurobiological basis of these symptoms.
William J Jagust - One of the best experts on this subject based on the ideXlab platform.
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cerebral blood flow in ischemic Vascular Dementia and alzheimer s disease measured by arterial spin labeling magnetic resonance imaging
Alzheimers & Dementia, 2009Co-Authors: Norbert Schuff, Bruce L Miller, William J Jagust, Shinji Matsumoto, Joseph Kmiecik, Colin Studholme, Antao Du, Frank Ezekiel, Joel H Kramer, Helen C ChuiAbstract:Background The objectives were first to compare the effects of subcortical ischemic Vascular Dementia (SIVD) and Alzheimer's disease (AD) on cerebral blood flow (CBF) and second to analyze the relationship between CBF and subcortical Vascular disease, measured as volume of white matter lesions (WML).
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survival following Dementia onset alzheimer s disease and Vascular Dementia
Journal of the Neurological Sciences, 2005Co-Authors: Annette L Fitzpatrick, Lewis H Kuller, Oscar L Lopez, Claudia H Kawas, William J JagustAbstract:Survival following the onset of Dementia has been reported to vary from 3 to over 9 years. We examined mortality in 3602 participants of the CardioVascular Health (CHS) Cognition Study in four US communities evaluated for Dementia incidence between 1992 and 1999 and followed for 6.5 years. By June 2000, 33 of 62 (53.2%) participants who developed Vascular Dementia (VaD) had died compared to 79 of 245 (32.2%) with Alzheimer's disease (AD), 66 of 151 (43.7%) with both AD and VaD, and 429 of 2318 (18.5%) with normal cognition. Using Cox proportional hazards regression with a time-dependent covariate for Dementia status adjusted for age, gender and race, individuals with VaD were more than four times as likely to die during follow-up than those with normal cognition (HR: 4.4, 95% CI: 3.1-6.3). The hazard ratios were 2.1 (95% CI: 1.6-2.7) for AD and 2.5 (95% CI: 1.9-3.3) for both types. Adjusted accelerated life models estimated median survival from Dementia onset to death as 3.9 years for those with VaD, 7.1 years for AD, 5.4 years for mixed Dementia, and 11.0 years for matched controls with normal cognition. While persons with VaD died primarily from cerebroVascular disease, those with AD/mixed Dementia died more frequently from Dementia/failure to thrive.
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neuropathologic substrates of ischemic Vascular Dementia
Journal of Neuropathology and Experimental Neurology, 2000Co-Authors: Harry V Vinters, William G Ellis, Chris Zarow, Barbara Zaias, William J Jagust, Wendy J Mack, Helena C ChuiAbstract:Ischemic Vascular Dementia (IVD) is a relatively uncommon entity, in the course of which multiple ischemic brain lesions result in progressive cognitive and memory impairment. Ischemic brain lesions may also aggravate the neuropsychologic deficit of Alzheimer disease (AD). In this review we summarize our experience based upon autopsy examination of the central nervous system in 20 patients (age range 68-92 years) enrolled in a longitudinal investigation of structural, neurochemical, functional neuroimaging, and neuropsychologic components of IVD, especially Dementia associated with cerebral microVascular disease. While cystic infarcts were present in the CNS of 5 patients, the most commonly observed neuropathologic abnormalities were lacunar infarcts and microinfarcts--both types of lesion were encountered in over half of patients' brains. Evidence of (remote) hippocampal injury was found in 11/20 patients. Severe atherosclerosis and arterio/ arteriolosclerosis were both associated with the occurrence of multiple lacunar infarcts. Pronounced cerebral amyloid angiopathy (CAA) was noted in a single patient, who also showed other microscopic changes of severe AD. While fairly unusual as a nosologic entity, IVD appears to correlate with widespread small ischemic lesions distributed throughout the CNS. We furthermore propose an approach to quantifying the burden of ischemic Vascular and parenchymal disease that may be associated with a Dementia syndrome. A brief review of neuropathologic features of Vascular Dementia (both familial and sporadic) is presented.
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criteria for the diagnosis of ischemic Vascular Dementia proposed by the state of california alzheimer s disease diagnostic and treatment centers
Neurology, 1992Co-Authors: Helena C Chui, William J Jagust, Jeff Victoroff, D Margolin, R Shankle, R KatzmanAbstract:Accurate diagnosis of Vascular Dementia is important for the recognition of underlying pathophysiology and the institution of appropriate therapy. It is also important for the determination of the incidence and prevalence of not only Vascular Dementia but also Alzheimer9s disease (AD), since differentiating between these two entities is often problematic. The State of California Alzheimer9s Disease Diagnostic and Treatment Centers (ADDTC) herein propose criteria for the diagnosis of ischemic Vascular Dementia (IVD). These criteria broaden the conceptualization of Vascular Dementia, include the results of neuroimaging studies, emphasize the importance of neuropathologic confirmation, refine nosology, and identify areas that require further research. Parallel use of the proposed definitions of “possible” and “mixed” categories in the diagnosis of both AD and IVD would ensure compatibility between the National Institute of Neurological and Communicative Disorders and Stroke (NINCDS) criteria for AD and the ADDTC criteria for IVD. Uniform classification of subtypes of IVD will improve the generalizability of individual studies and aid in multicenter collaborations.
Robert Barber - One of the best experts on this subject based on the ideXlab platform.
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progressive brain atrophy on serial mri in Dementia with lewy bodies ad and Vascular Dementia
Neurology, 2001Co-Authors: John T Obrien, Clive Ballard, Robert Barber, A Gholkar, Ian G Mckeith, S M Paling, E D Williams, William R Crum, Martin N Rossor, Nick C FoxAbstract:The authors determined rates of brain atrophy, as assessed by the boundary shift integral on serial MRI, in patients with Dementia with Lewy Bodies (DLB, n = 10), AD (n = 9), Vascular Dementia (VaD, n = 9), and age-matched controls (n = 20). Mean % +/- SD atrophy rates per year were as follows: DLB, 1.4 +/- 1.1; AD, 2.0 +/- 0.9; VaD, 1.9 +/- 1.1; and controls, 0.5 +/- 0.7. Dementia subjects had higher rates than controls (p < 0.001), but there were no significant differences between the three Dementia groups. The authors found accelerating atrophy with increasing severity of cognitive impairment, further emphasizing the need for early diagnosis and intervention in Dementia.
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progressive brain atrophy on serial mri in Dementia with lewy bodies ad and Vascular Dementia
Neurology, 2001Co-Authors: John T Obrien, Clive Ballard, Robert Barber, A Gholkar, Ian G Mckeith, S M Paling, E D Williams, William R Crum, Martin N RossorAbstract:The authors determined rates of brain atrophy, as assessed by the boundary shift integral on serial MRI, in patients with Dementia with Lewy Bodies (DLB, n = 10), AD (n = 9), Vascular Dementia (VaD, n = 9), and age-matched controls (n = 20). Mean % ± SD atrophy rates per year were as follows: DLB, 1.4 ± 1.1; AD, 2.0 ± 0.9; VaD, 1.9 ± 1.1; and controls, 0.5 ± 0.7. Dementia subjects had higher rates than controls ( p
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white matter lesions on magnetic resonance imaging in Dementia with lewy bodies alzheimer s disease Vascular Dementia and normal aging
Journal of Neurology Neurosurgery and Psychiatry, 1999Co-Authors: Robert Barber, R H Perry, Clive Ballard, P Scheltens, A Gholkar, Ian G Mckeith, P G Ince, John T ObrienAbstract:OBJECTIVES—Alzheimer's disease and Vascular Dementia are associated with an increase in changes in white matter on MRI. The aims were to investigate whether white matter changes also occur in Dementia with Lewy bodies and to examine the relation between white matter lesions and the cognitive and non-cognitive features of Dementia with Lewy bodies, Alzheimer's disease, and Vascular Dementia. METHODS—Proton density and T2 weighted images were obtained on a 1.0 Tesla MRI scanner in patients with Dementia with Lewy bodies (consensus criteria; n=27, mean age=75.9 years), Alzheimer's disease (NINCDS/ADRDA; n=28, mean age=77.4 years), Vascular Dementia (NINDS/AIREN; n=25, mean age=76.8 years), and normal controls (n=26, mean age=76.2 years). Cognitive function, depressive symptoms, and psychotic features were assessed using a standardised protocol. Periventricular hyperintensities (PVHs), white matter hyperintensities (WMHs) and basal ganglia hyperintensities (BGHs) were visually rated blind to diagnosis using a semiquantitative scale. RESULTS—Periventricular hyperintensities were positively correlated with age and were more severe in all Dementia groups than controls. Total deep hyperintensities scores (WMHs plus BGHs) were significantly higher in all Dementia groups than controls and higher in patients with Vascular Dementia than those with Dementia with Lewy bodies or Alzheimer's disease. In all patients with Dementia, frontal WMHs were associated with higher depression scores and occipital WMHs were associated with an absence of visual hallucinations and delusions. CONCLUSION—In common with Alzheimer's disease and Vascular Dementia, PVHs and WMHs were significantly more extensive in Dementia with Lewy bodies than in controls. This overlap between different Dementias may reflect shared pathological mechanisms. The link between frontal WMHs and depression and the absence of occipital WMHs and psychotic symptoms has important implications for understanding the neurobiological basis of these symptoms.
