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

Ishii, Nobuyoshi; Nishihara, Yunosuke; Imamura, Toru

doi:10.1097/00002093-198701000-00041

Cited by 59 publications

(87 citation statements)

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“…It has been postulated that hydrocephalus may directly compress and therefore impede the corticospinal fibers controlling the leg movements and/or frontopontocerebellar fibers as they descend close to the lateral ventricle [12,36]. Others have suggested that ventricular enlargement interrupts the cortical-subcortical basal ganglia loop, which connects the frontal cortex and basal ganglia, thus resulting in frontal lobe-like gait disturbance with marked disequilibrium [1,3,28].…”

Section: Discussionmentioning

confidence: 99%

Correlation of midbrain diameter and gait disturbance in patients with idiopathic normal pressure hydrocephalus

et al. 2005

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The clinical elements of the NPH gait can be summarized as a hypokinetic gait which is characterized by diminished gait velocity, reduced stride length, reduced step height, and dynamic disequilibrium [17,28,31,34]. Patients with many other neurodegenerative diseases, such as Parkinson's disease, subcortical arteriosclerotic encephalopathy, progressive supranuclear palsy (PSP), and corticobasal degeneration, may develop hypokinetic gait during the disease progression [4,35,37] ■ Abstract Background and purpose Although gait disturbance is an important feature of idiopathic normal pressure hydrocephalus (NPH), only tentative theories have been offered to explain its pathophysiology. It has been suggested that the mesencephalic locomotor region is the anatomical substrate for the development of the hypokinetic NPH gait. To investigate this possibility, we evaluated the correlation between gait disturbance and midbrain diameter. Methods We enrolled 21 patients with NPH and 20 age-matched control subjects for the study. The maximal diameter of the midbrain and pons, and the width of the lateral and third ventricles were measured using midsagittal T1-weighted MRI and axial T2-weighted MRI, respectively. Gait disturbance, cognitive dysfunction, and incontinence were semiquantified. Results The maximal midbrain diameter was significantly smaller in the NPH group than in the controls (14.8 ± 0.9 vs. 17.1 ± 0.7 mm, p < 0.001). There were inverse correlations between the midbrain diameter and the widths of the two ventricles (r = -0.562, p = 0.008 for the third ventricle, and r = -0.510, p = 0.018 for the lateral ventricle). The severity of gait disturbance was negatively correlated with the midbrain diameter (r = -0.598, p = 0.004), but the degree of cognitive dysfunction and incontinence showed no significant correlation with midbrain diameter or ventricular width. Conclusions This study suggests that midbrain atrophy is significantly associated with gait disturbance in NPH.

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Section: Discussionmentioning

confidence: 99%

Correlation of midbrain diameter and gait disturbance in patients with idiopathic normal pressure hydrocephalus

et al. 2005

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“…Lacunae often occur in subcortical gray matter nuclei (e.g., thalamus, caudate) necessary for filtering/disengaging attention (23). Leukoaraiosis and lacunae mark chronic small brain vessel disease (24) and are contributors to insidious executive dysfunction (25).…”

Section: Introductionmentioning

confidence: 99%

A Pilot Study Evaluating Presurgery Neuroanatomical Biomarkers for Postoperative Cognitive Decline After Total Knee Arthroplasty in Older Adults

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Schmalfuss

et al. 2014

Survey of Anesthesiology

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Background-Total knee arthroplasty improves quality of life but is associated with postoperative cognitive dysfunction in older adults. This prospective longitudinal pilot study with a parallel control group tested the hypotheses that: 1) nondemented adults would exhibit primary memory and executive difficulties after total knee arthroplasty, and 2) reduced preoperative hippocampus/entorhinal volume would predict postoperative memory change, whereas preoperative leukoaraiosis and lacunae volumes would predict postoperative executive dysfunction.

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“…Progression of subcortical WMH volume is associated with the decreased performance in the Logical Memory Testing [17] . Postmortem studies in 30 cases of VAD have revealed that both lacunes and diffuse softening are predominant in the frontal lobes [18] , which probably results from ischemic interruption in parallel circuits from the prefrontal cortex to the basal ganglia and in the corresponding thalamocortical connections.…”

Section: Vascular Cognitive Impairment Vascular Dementiamentioning

confidence: 99%

The clinical manifestations and pathophysiology of cerebral small vessel disease

Zhang

Wang

2010

Neurosci. Bull.

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Small vessel disease (SVD) is responsible for brain chronic circular disorder, and accounts for 20%-30% cases of ischemic stroke as well as cerebral hemorrhage, and to a great extent, encephalopathy. Binswanger's disease and multiple small strokes, which are common in older people, are also closely associated with SVD. These disorders often cause decline in cognition, vascular dementia, impairment in gait and balance, mood depression, and urinary incontinence, and often brings great social and economic burdens. SVD-related encephalopathy increases the incidences of fall, disability and death in elderly people. With the aging of the society, more attention should be paid to the importance of early diagnosis and prophylactic treatment of SVD. Here the clinical manifestations and pathophysiology of SVD are reviewed.

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

Cited by 59 publications

References 0 publications

Correlation of midbrain diameter and gait disturbance in patients with idiopathic normal pressure hydrocephalus

Correlation of midbrain diameter and gait disturbance in patients with idiopathic normal pressure hydrocephalus

A Pilot Study Evaluating Presurgery Neuroanatomical Biomarkers for Postoperative Cognitive Decline After Total Knee Arthroplasty in Older Adults

The clinical manifestations and pathophysiology of cerebral small vessel disease

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