Pathogenesis of Binswanger chronic progressive subcortical encephalopathy

Reuck, Jacques De; Crevits, Luc; Coster, W. De; Sieben, G.; Eecken, H. vander

doi:10.1212/wnl.30.9.920

Cited by 167 publications

(57 citation statements)

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“…In our MDD sample, atrophy appears to be independent of both overall medical burden and cerebrovascular risk factors. However, chronic ischemic changes have been shown to lead to atrophy, predominantly in the white matter, resulting in well recognized clinical/cognitive disturbances (DeReuck et al 1980;Fisher 1989;Huang et al 1985;Loizou et al 1981). The structure of subcortical nuclei may also be influenced by chronic hypertension and lacunar infarcts (Schmidt et al 1991;Hastak and Hachinski 1992).…”

Section: Discussionmentioning

confidence: 99%

Atrophy and High Intensity Lesions Complementary Neurobiological Mechanisms in Late-Life Major Depression

Kumar

Bilker

Jin

et al. 2000

Neuropsychopharmacology

166

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The primary objective of our study was to examine the role of atrophy, high intensity lesions and medical comorbidity in the pathophysiology of major depressive disorder in the elderly (late-life MDD). Our sample was comprised of 51 patients with late-life MDD and 30 non-depressed controls.All subjects were scanned on 1.5 tesla magnetic resonance imaging scanner (MRI) Depression is one of the most common mental disorders in the elderly (Alexopolous et al. 1988;Beck and Koenig 1996;Blazer et al. 1987;Blazer 1989Blazer , 1994Koenig et al. 1993;Oxman et al. 1987;Parmalee et al. 1989;Ruegg et al. 1988;Sherbourne et al. 1994). The prevalence of major depressive disorder (MDD) is estimated to be approximately 1-2 percent in community settings and strikingly higher in inpatient and long term care settings (Blazer et al. 1987;Koenig et al. 1993;Parmalee et al. 1989). The prevalence of other clinically significant forms of depression, that do not meet the severity criteria for MDD, lies between 5 and 15 percent in all major clinical settings (Beck and Koenig 1996;Blazer et al. 1987, Blazer 1994Parmalee et al. 1989). Anatomical and physiological neuroimaging approaches have been utilized to study the neurobiological correlates of MDD and minor depression in the elderly (Coffey et al. 1990;Coffey et al. 1993;Greenwald et al. 1996;Krishnan et al. 1988;Krishnan 1993;Kumar et al. 1997a;Lesser et al. 1994;Sackheim et al. 1993;Sheline et al. 1996). Glucose hypometabolism and Lesser et al. 1994;Sackheim et al. 1993). Using magnetic resonance imaging (MRI), investigators have demonstrated neuroanatomical abnormalities including smaller focal brain volumes and larger high intensity lesion volumes in patients with both late-life major and minor depression when compared with non-depressed controls (Coffey et al. 1990;Coffey et al. 1993;Greenwald et al. 1996;Krishnan et al. 1988;Krishnan 1993;Kumar et al. 1997aKumar et al. , 1997bKumar et al. , 1998Sheline et al. 1996).Despite these observations, the precise nature and extent of the neuroanatomical changes in elderly patients with MDD remains unresolved (Jeste et al. 1988;Morris and Rapoport 1990).Late-life MDD is also consistently associated with medical comorbidity (Berkman et al 1986;Gierz and Jeste 1993;Katz et al. 1994;Katz 1996;Lacro and Jeste 1994;Rodin and Voshart 1986). A broad spectrum of medical disorders including cardiovascular, musculoskeletal, gastrointestinal, pulmonary and metabolic disturbances are associated with both major and minor forms of depression (Alexopolous et al. 1988;Katz et al. 1994;Koenig et al. 1993;Lacro and Jeste 1994). Despite this association, the relationship between neuroanatomical abnormalities and medical disorders in late-life and their relative contributions to the pathophysiology of mood disorders remain unknown.In an earlier report, we demonstrated that the odds of developing MDD in late-life increased with overall medical burden and larger whole brain cerebrospinal fluid (CSF) volume (Kumar et al. 1997a). However, only global measures ...

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Section: Discussionmentioning

confidence: 99%

Atrophy and High Intensity Lesions Complementary Neurobiological Mechanisms in Late-Life Major Depression

Kumar

Bilker

Jin

et al. 2000

Neuropsychopharmacology

166

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“…Alzheimer (10) subsequently reported the microscopic features, including severe gliosis of the white matter and hyalination, intimal fibrosis, and onion-skinning of the long medullary arteries. Chronic hypoperfusion of the periventricular and deep white matter border zones is postulated as the mechanisms of injury (11).…”

Section: A Historymentioning

confidence: 99%

Subcortical Ischemic Vascular Dementia

Chui

2007

Neurologic Clinics

136

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Subcortical ischemic vascular dementia (SIVD) has been proposed as a subtype of vascular cognitive impairment (VCI). The syndrome is defined clinically by cognitive impairment and evidence of subcortical vascular brain injury, including lacunar infarcts and deep white matter changes. SIVD has been traditionally recognized as lacunar state, strategic infarct dementia, and Binswanger syndrome, but these clinical syndromes represent the tip of the iceberg. Proton density magnetic resonance (MRI) often discloses "silent" hyperintensities in 20-40% of community dwelling elderly. Efforts to relate MRI-measured lacunes and white matter changes to cognitive impairment have not been straightforward. The hidden possibility that concomitant Alzheimer disease pathology contributes significantly to cognitive impairment increases with age. Nonetheless, new knowledge is being gained from longitudinal MRI and systematic neuropathological studies. Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukencephalopathy (CADASIL), a rare genetic disorder, provides an opportunity to study pure SIVD in the absence of AD. Dysexecutive syndrome characterized by slowing of mental processing speed, decreased working memory, and impairment of abstract reasoning are associated with lacunes and deep white matter changes. But data related to sensitivity and specificity which would support dysexecutive syndrome as diagnostic criteria are limited. Hypertension, by far the leading risk factor for sporadic SIVD, is eminently treatable. High priority must be given to reducing vascular risk profiles.

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“…According to several authors the white matter alterations in BD are incomplete infarcts due to ischemia resulting from the combination of a localization of the hypertensive vascular changes in the long penetrating arteries and the scarce anastomoses connecting these vessels.U4-16 Furthermore the characteristics of the arterial border zone of the deep cerebral white matter have been outlined. 17 These, together with eventual hypotensive crises may lead to border-zone infarcts in the deep cerebral white matter, 6 and actually the association of these two factors is considered one of the mechanisms responsible for the so called hypoxicischemic leukoencephalopathy, a condition implying tissue changes similar to those of BD in absence of significant alterations in small arteries. 18 Other authors have sustained that the white matter changes in BD might represent the late effect of chronic vasogenic edema secondary to hypertensive encephalopathy.…”

Section: Pathologic Studymentioning

confidence: 99%

Computed Tomography, Magnetic Resonance Imaging and Pathological Correlations in a Case of Binswanger's Disease

Mascalchi

Inzitari²,

Pozzo³

et al. 1989

Can. j. neurol. sci.

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The results of 3 computed tomography (CT) examinations carried out over a 7 year period and of a post-mortem magnetic resonance (MR) study showed aspects of a white matter disease in a hypertensive patient suffering from vascular dementia. Histopathology revealed the primary cause of dementia to be a white matter degeneration sparing the U fibers. Rarefaction of both the myelin sheaths and the axons was present together with severe thickening of the medullary arteries. These findings support the existence of Binswanger's disease (BD) as a distinct variety of arteriosclerotic dementia. CT and MR imaging are valuable aids for diagnosis. However, since there are many other causes of CT and MR demonstrated diffuse white matter degeneration in the elderly, a conclusive diagnosis of BD requires pathological confirmation. RESUME: Tomodensitometrie, imagerie par resonance magnetique nucleaire et correlations anatomopathologiques dans un cas de maladie de Binswanger Trois tomodensitometries faites sur une periode de sept ans et un examen par resonance magnetique nucleaire effectue en post-mortem ont mis en evidence des modifications compatibles avec une leuco-encephalopathie chez un patient hypertendu atteint d'une demence vasculaire. L'histopathologie a montre que la cause primaire de la demence etait une degSnerescence de la substance blanche epargnant les fibres en U. II existait une rarefaction des gaines de myeline et des axones ainsi qu'un epaississement important des arteres medullaires. Ces observations supportent la notion que la maladie de Binswanger (MB) est une variete distincte de d6mence arteriosclereuse. La tomodensitometrie et 1'imagerie par resonance magnetique nucleaire sont des aides precieuses pour le diagnostic. Cependant, comme il existe plusieurs autres causes de degenerescence de la substance blanche chez les sujets ages, qui sont evidentes a la tomodensitometrie et a l'imagerie par resonance magnetique nucleaire, une confirmation anatomopathologique du diagnostique de MB est essentielle.

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Pathogenesis of Binswanger chronic progressive subcortical encephalopathy

Cited by 167 publications

References 0 publications

Atrophy and High Intensity Lesions Complementary Neurobiological Mechanisms in Late-Life Major Depression

Atrophy and High Intensity Lesions Complementary Neurobiological Mechanisms in Late-Life Major Depression

Subcortical Ischemic Vascular Dementia

Computed Tomography, Magnetic Resonance Imaging and Pathological Correlations in a Case of Binswanger's Disease

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