Why do frontal lobe symptoms predominate in vascular dementia with lacunes?

Ishii, Nobuyoshi; Nishihara, Yunosuke; Imamura, Tohru

doi:10.1212/wnl.36.3.340

Cited by 266 publications

(64 citation statements)

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“…Compared to patients with AD, VaD patients suffer severe WM damage, arteriosclerosis-like changes, WM vacuolization and demyelination particularly in the periventricular region (Erkinjuntti, et al, 1996). Also, the periventricular frontal lobe and caudate head suffers from the highest density and frequency of lacunar infarction (Ishii, et al, 1986). This periventricular WM damage which disrupts the neuronal connections to the frontal lobe may be central to VaD induced cognitive deficits (Sultzer, et al, 1995).…”

Section: Discussionmentioning

confidence: 99%

White matter damage and glymphatic dysfunction in a model of vascular dementia in rats with no prior vascular pathologies

Venkat

Chopp

Zacharek

et al. 2017

Neurobiology of Aging

103

130

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We investigated cognitive function, axonal/white matter (WM) changes and glymphatic function of vascular dementia (VaD) using a multiple microinfarction (MMI) model in retired breeder (RB) rats. The MMI model induces significant (p<0.05) cognitive decline that worsens with age starting at 2 weeks, which persists until at least 6 weeks after MMI. RB rats subjected to MMI exhibit significant axonal/WM damage identified by decreased myelin thickness, oligodendrocyte progenitor cell numbers, axon density, synaptic protein expression in the cortex and striatum, cortical neuronal branching, and dendritic spine density in the cortex and hippocampus compared with age matched controls. MMI evokes significant dilation of perivascular spaces as well as water channel dysfunction indicated by decreased Aquaporin-4 (AQP-4) expression around blood vessels. MMI induced glymphatic dysfunction with delayed cerebrospinal fluid (CSF) penetration into the brain parenchyma via paravascular pathways as well as delayed waste clearance from the brain. The MMI model in RB rats decreases AQP-4 and induces glymphatic dysfunction which may play an important role in MMI induced axonal/WM damage and cognitive deficits.

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Section: Discussionmentioning

confidence: 99%

White matter damage and glymphatic dysfunction in a model of vascular dementia in rats with no prior vascular pathologies

Venkat

Chopp

Zacharek

et al. 2017

Neurobiology of Aging

103

130

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“…Although the ischemic lesions occur in diffuse and extensive. white matter in Binswanger's disease and multiple lacuna dementia, frontal white matter is preferentially and 200 severely affected (Ishii et al, 1986). Electron microscopy studies in Binswanger's disease have revealed a significant decrease of nerve fibers in the anterior white matter and the genu of the corpus callosum, but not in the splenium (Yamanouchi et aZ., 1989;.…”

Section: Discussionmentioning

confidence: 99%

Regional differences in diffusion abnormality in cerebral white matter lesions in patients with vascular dementia of the Binswanger type and Alzheimer's disease

Hanyu

Imon

Sakurai

et al. 1999

Euro J of Neurology

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We investigated changes in water diffusion in the cerebral white matter of 14 patients with vascular dementia of the Binswanger type (VDBT) and ten patients with Alzheimer's disease (AD) with periventricular hyperintensity (PVH) lesions using diffusion-weighted magnetic resonance imaging (MRI) and studied the pathophysiological differences between white matter lesions found in these two conditions. Apparent diffusion coefficients (ADCs) in the anterior and posterior white matter and the genu and splenium of the corpus callosum were significantly higher in both groups of patients than in the 12 age-matched controls, and ADC values in VDBT and AD groups were almost the same. ADC ratios, defined as diffusion restricted perpendicular to the direction of nerve fibers, were also significantly higher in the patients than in the control subjects. However, there were regional differences in ADC ratios in the two conditions, with ratios in VDBT being higher in the anterior portions of the white matter but ratios in AD were higher in the posterior portions. The diffusion-weighted MRI technique may be useful in the differential diagnosis of VDBT and AD with white matter lesions.

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“…Subcortical VaD incorporates two clinical entities – ‘Binswanger’s disease’ and ‘the lacunar state’ [21, 22, 23, 24, 25]. The ischaemic lesions in VaD affect especially the prefrontal subcortical circuit [26], which explains the main cognitive, behavioural and clinical neurological features.…”

Section: Subcortical Vascular Dementiamentioning

confidence: 99%

Subcortical Vascular Dementia

Erkinjuntti

2002

Cerebrovasc Dis

111

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Vascular dementia (VaD) incorporates different vascular mechanisms and changes in the brain, and has different causes and clinical manifestations. Current criteria for VaD select an aetiologically and clinically heterogeneous group and this definitional heterogeneity has affected clinical trial results. Focus on a more homogeneous group, such as that with subcortical (ischaemic) VaD, could be an alternative in clinical drug trials. This subtype incorporates two small vessel clinical entities – ‘Binswanger’s disease’ and ‘the lacunar state’. It comprises small vessel disease as the primary vascular aetiology, lacunar infarct(s) and ischaemic white matter lesions as the primary type of brain lesions, subcortical location as the primary location of lesions, and the subcortical clinical syndrome as the primary clinical manifestation. Subcortical VaD is expected to show a more predictable clinical picture, natural history, outcome and treatment responses.

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Why do frontal lobe symptoms predominate in vascular dementia with lacunes?

Cited by 266 publications

References 0 publications

White matter damage and glymphatic dysfunction in a model of vascular dementia in rats with no prior vascular pathologies

White matter damage and glymphatic dysfunction in a model of vascular dementia in rats with no prior vascular pathologies

Regional differences in diffusion abnormality in cerebral white matter lesions in patients with vascular dementia of the Binswanger type and Alzheimer's disease

Subcortical Vascular Dementia

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