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Binswanger's disease

Binswanger's disease is a rare form of multi-infarct dementia caused by damage to deep white brain matter. It is characterized by loss of memory and intellectual function and by changes in mood. more...

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Binswanger's disease is one of the neurological syndromes associated with hypertension. It is uncommon, but obviously devastating. The histologic findings are diffuse, irregular loss of axons and myelin accompanied by widespread gliosis. Small infarcts may be seen in the frontal lobes. The pathologic mechanism may be damage caused by severe atherosclerosis.

A patient with long term severe hypertension develops progressive dementia. CT scans of the head demonstrate a diffuse loss of deep hemispheric white matter.

Binswanger's disease has no known treatment, let alone cure, although drugs used to treat high blood pressure, depression, arrhythmia and low blood pressure are used to treat the condition's symptoms.


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Cerebrovascular disease and cognitive dysfunction
From Neurological Research, 6/1/02 by Lanzino, Giuseppe

As the general population ages, the progressive cognitive decline that occurs with aging and dementia is having a significant socioeconomic impact on society. Vascular dementia associated with cerebral vascular disease is now the third most common cause of dementia. Recent evidence has revealed a new and significant etiopathogenetic role of cerebrovascular pathology, as well as newly determined risk factors for the development of neurocognitive deficits and other forms of dementia including Alzheimer's disease. In this article, we summarize the experimental and clinical data linking cerebrovascular pathology to neurocognitive decline and dementia. [Neurol Res 2002; 24: 331-336]

Keywords: Cerebral ischemia; chronic cerebral hypo perfusion; dementia; elderly; Alzheimer's disease; carotid stenosis; neuropsychological tests


Life expectancy has dramatically improved in the past century. Currently, the elderly population constitutes a large proportion of the general population, and their number is projected to increase as the 'baby boomers' grow older and become senior boomers. As a result of the aging process, the progressive cognitive decline in elderly people and the development of frank dementia have emerged to be a significant socioeconomic problem, receiving much social and medical attention.

Vascular dementia has long been recognized as one of the causes of cognitive decline secondary to cerebrovascular disease. In the past decade, however, mounting evidence has linked cerebrovascular disease to cognitive decline in a greater proportion of individuals than can be classified under the category of vascular dementia, including those with frank Alzeheimer's disease (AD)1-3. In this review we summarize the experimental and clinical evidence strongly suggesting a possible etiological role of cerebrovascular pathology in cognitive dysfunction observed in elderly patients and in patients with dementia of any etiology.


In order to maintain and carry on its cellular and molecular needs normal brain function is critically dependent upon an adequate supply of energy sources. It is conceivable that cognitive decline can be the consequence of conditions (such as chronic ischemia or protracted hypoperfusion) in which this source of energy is sub-optimally available for extended periods of time4. Similarly, protracted decreased blood flow to the brain might trigger some of the changes observed in clinical dementia syndromes, including AD. Several experimental data support these hypotheses.

Rats submitted to permanent bilateral carotid occlusion display a significant and protracted decrease in spatial memory5. In these rats, ischemic-sensitive hippocampus neurons show spotty areas of neuronal death6. These neurons are critical for memory, and therefore their destruction can precipitate cognitive impairment. In an experimental rat model of chronic hypoperfusion, de la Torre et al.4 have been able to mimic the metabolic, anatomic, and cognitive pathology reported in Alzheimer's patients. Moreover, rats subjected to 2-vessel occlusion for 12 months develop significant capillary abnormalities selectively in CAl as determined ultrastructurally5. Findings from this study suggest that the microvessel changes may actually precede the degeneration observed in the ischemic sensitive-neurons in that area and possibly cause it. This wealth of data strengthens the hypothesis that chronic hypoperfusion leads to cognitive impairment7,8.

The changes observed in rats after the establishment of chronic hypo perfusion are not necessarily permanent and promptly regress if adequate flow is re-established. After eight weeks of bilateral carotid occlusion, visuospatial impairment in aging rats was reversed by reestablishing flow with carotid reanastomosis9. This observation, should it hold true for humans, could have obvious clinical significance.

The effects of critical flow threshold are related to age. In a 3-VO model in rats, de la Torre et al.10 demonstrated that young rats over time recover from visuo-spatial deficits induced by nine weeks of chronic bilateral hypoperfusion. On the other hand, middle aged rats not only did not recover, but went on to develop progressive deterioration of the CA1 hippocampus sector and eventual necrosis of the parietal and temporal cortex11.

Recently, a number of observations have linked the neurodegeneration seen in AD patients to the same pathogenetic mechanisms implicated in ischemiainduced neuronal death. For example, increased markers of oxidation, reduced activities of anti-oxidant enzymes, and decreased energy metabolism (all processes well-established in the pathophysiology of cerebral ischemia) have been observed in AD. These changes imply that mitochondria and oxidative damage contribute to the neurodegeneration in AD12,13. Similarly, patients with AD whose therapeutic regimen includes vitamin E (a fat-soluble free-radical scavenger utilized to inhibit biochemical oxidative stress and lipid peroxidation) have shown some clinical improvements14. A closer link than previously considered between the pathophysiology of cerebral ischemia and AD is suggested by the observation that amyloid precursor protein (a marker of AD) accumulates in regions of neurodegeneration following focal cerebral ischemia in the rat15.

In an attempt to explain these experimental data, de la Torre4 hypothesized that advanced aging interacts with other risk factors for Alzheimer's disease to cause a Critically Attained Threshold of Cerebral Hypoperfusion (the CATCH hypothesis) that will subsequently affect the microcirculation and delivery of energy substrates required for optimal brain function.


The concept of cognitive decline associated with aging and the development of frank dementia is undergoing rapid and radical revision. In the early part of last century, a long-standing belief was that senile cognitive decline associated with senility was the result of cerebrovascular diseases, i.e., 'hardening of the vessels'. However, no convincing proof of such belief has ever been provided. It has long been recognized that a group of patients suffering from dementia demonstrate a stepwise, progressive deterioration consistent with multiple ischemic events, thus the name of 'multi-infarct dementia' or vascular dementia. Otto Binswanger16 was the first to point out the relationship between a slowly progressive, subcortical vascular encephalopathy with focal neurological deficits and vascular white matter lesions. The term 'Binswanger's disease' has classically been used to indicate this disorder. Traditionally, this type of dementia has been differentiated from the more common form of dementia known as Alzheimer's disease.

The notion that Binswanger's disease or vascular dementia is rare is now being challenged with the advent of CT and MRI17. These sophisticated imaging techniques have led to the in vivo diagnosis of white matter changes in patients with cognitive decline and frank dementia, and also demonstrated that these pathological changes occur more frequently than previously thought. A more descriptive term 'leukoakariosis' (from the Greek leuko=white, ariosis= rarefaction) instead of 'Binswanger's disease' has been proposed to indicate these neuroradiological changes17. It has also become evident that a clear-cut differentiation between vascular and other dementias including the Alzheimer's type is not so well-defined. In fact, several mixed forms may exist.

A new concept of cognitive decline is emerging. It is now considered by some authors as a relentless process, often associated with aging, with different degrees of expression and multifactor etiopathogenesis. As one of the predisposing factors, cerebrovascular pathology is receiving a great degree of attention because most factors favoring the development of cerebrovascular pathology can be treated or prevented, possibly affecting the development of ensuing cognitive decline. For example, a strong association between the risk factors found in vascular dementia (which, to some extent, are the same for ischemic stroke and cerebrovascular diseases at large) and in Alzheimer's disease has been noted. These risk factors share a similar morbid outcome despite their widely different pathologic etiologies and clinical course. A common denominator to these factors is impairment or reduction of cerebral perfusion4.

Changes in autoregulation, which occur with aging are also being investigated for their possible role in cognitive decline18,19. If coupled with levels of arterial blood pressure below the minimum required to maintain adequate perfusion (> 50 cc 100 g^sup -1^ min^sup -1^), changes in autoregulation may produce hypoperfusion and ischemia, especially in border zones and vulnerable areas20,21. The importance of changes in the regulation of blood pressure is supported by the increasing prevalence of low and labile blood pressure in patients at a late stage of vascular dementia and AD22. A positive association between cognitive performance and blood pressure after the age of 75 has been reported . Similarly, a recent study found an inverse association for blood pressure measured four years before diagnosis and the risk of developing AD24. In elderly patients suffering from cardiac arrhythmias and hypotension, persistent chronic cerebral hypoperfusion is responsible for the cognitive impairment observed22,25.

Additional evidence linking Alzheimer's disease and stroke is provided by the observation that the two disorders share one critical genetic risk factor. The ^sup epsilon^4 allele of the apolipoprotein E gene (APOE) is associated with an increased risk of ischemic stroke26. This same allele has also been firmly established as a major risk factor for late-onset AD27,28. A recent report further suggests the potential association of metabolic disorder and the development of dementia. Reman et al.29 showed that people aged 50-60 years with normal APOE ^sup epsilon^4 had decline in glucose metabolism. The areas involved include the prefrontal cortex, temporal lobe, posterior cingulated gyrus, basal forebrain, thalamus and para-hippocampal gyrus.

The observation that AD and ischemic stroke share a common genetic risk factor suggests a pathogenetic relationship between the two diseases30. Clinical studies have shown that the association between dementia and atherosclerosis is particularly strong in patients with the apolipoprotein-E ^sup epsilon^4 genotype 31. These data also suggest an interaction between atherosclerosis and apolipoprotein E to the effect that the increase in the prevalence of Alzheimer's disease with atherosclerosis is particularly pronounced in those with the apolipoprotein-E ^sup epsilon^4 genotype31.


Significant information regarding the association between dementia, cerebrovascular risk factors, and white matter changes has been obtained from a series of articles based on findings of the 'Rotterdam Study'. This was a single-center prospective follow-up study in which all residents older than 55 from a Rotterdam, Netherlands, suburb, were invited to take part. The objective was to investigate the cause of chronic and disabling cardiovascular, neurodegenerative, locomotor, and ophthalmologic diseases. Results from this large population-based prospective study have demonstrated an association between chronic ischemia, periventricular lucency or deep white matter lesions on MRI, and cognitive decline32.The site of these white matter subcortical or periventricular lesions is important in determining the type of cognitive dysfunction. Periventricular lesions have a stronger relationship with the deterioration of memory, psychomotor speed and global cognitive function than subcortical lesions33.


An interesting phenomenon recently receiving increased attention is cognitive impairment in the presence of carotid stenosis. A systematic review of the literature addressing cognitive impairment and occlusive carotid disease found 18 studies with adequate control groups34. Of these, 14 reported cognitive deficits. Eleven studies analyzed the cognitive performance of patients who presented with TIAs, and seven of those (64%) concluded that deficits were present. Furthermore all three studies assessing asymptomatic patients with carotid obstruction found cognitive deficits. Hence the absence or resolution of neurological signs does not guarantee undisturbed cognitive functioning in patients with carotid occlusive disease.

The types of cognitive deficits assessed in different studies varies greatly. In a cohort of over 1,200 people aged between 59 and 71, both poor attention skills and impaired performance on the mini-mental state examination were associated with the presence of carotid plaques35. A larger study of 14,000 people found a negative association between the digit symbol subtest (a measure of performance IQ) of the Wechsler Adult Intelligence Scale (WAIS) and carotid wall thickness, a marker of atherosclerosis36. Patients with carotid stenosis selected to undergo carotid endarterectomy (CEA) showed greater impairment in both verbal and performance IQ when compared to controls37-39. Patients with carotid stenosis have also been found to perform worse on the Trailmaking test (TMT), a measure of problem solving, attention, motor control and setsorting, thus encompassing a number of aspects of frontal lobe dysfunction37,40. Similarly, studies that assessed motor speed, reaction time or attention found greater impairment in the carotid stenosis group41-43.

For the most part, the above mentioned studies involved patients previously selected for CEA. No information is available on the prevalence of cognitive impairment in the elderly population at large, i.e., those with unknown carotid occlusive disease. Thus, several details remain largely unexplored including the possible existence of vascular risk factors that may predispose patients to cognitive impairment and the relevant structural factors regarding the extent and type of brain damage (such as differences between patients who are asymptomatic, have suffered TIAs only or stoke); to the presence of unilateral vs. bilateral carotid occlusive disease or the association of compromise of the vertebrobasilar system; and to the degree of collateral circulation. Once these issues have been properly investigated, the results will aid in determining which patients with cognitive impairment may benefit from interventions, such as revascularization.

The possible association between cognitive impairment and carotid stenosis opens new horizons because the hemodynamic compromise associated with carotid stenosis can be corrected by surgical or endovascular means. Several anecdotal cases suggest improvement of cognitive improvement after revascularization. Tatemichi44 reported the case of a 55-year-old man who presented with behavioral and cognitive changes suggestive of frontal lobe dysfunction. Computerized topography scan of the head revealed a right frontal infarction. Cerebral blood flow studies showed profound reduction in the frontal areas. After right-sided extracranial to intracranial bypass, blood flow and metabolism, as well as behavioral and frontal neuropsychological deficits improved44. Similarly a positive effect of CEA upon improving cognitive performance has been suggested by many studies but controversy still exists whether or not CEA improves cognitive function45. It seems that, at the least, CEA results in improvement in specific functions such as verbal fluency and memory45. However, better designed studies are necessary to further analyze this possible relationship. Given the numerous variables involved, this can be done only with a large scale prospective, possibly multi-institutional, study given the numerous variables involved.


Perhaps the most direct relationship between cerebrovascular pathology and cognitive decline can be seen in patients undergoing CABG. In the United States alone, approximately 300,000 open heart surgeries are performed annually46. Using the transcranial Doppler embolus detection technique, the amount of emboli detected during CABG ranges from less than 200 to over 1000. Most emboli are detected during physical manipulation of the heart or aorta, followed by removal of the cross-clamp on the aorta. The composition of such micro-emboli includes air, atheromatous material, and platelet aggregates. The amount of emboli is directly related to the chance of developing cognitive dysfunction. Stump et al.47 reported that if the number of emboli exceeded 100, 79% of the patients suffered neuropsychological deficits. Brain hypoperfusion, which occurs during CABG surgery, also may contribute to the cognitive decline. By applying the stringent criteria developed at the 1994 consensus meeting on assessment of neurobehavioral outcomes after cardiac surgery, a recent meta-analysis of 23 studies showed that 22% of patients had cognitive decline two months after surgery48.


Dementia secondary to a previous stroke is difficult to define for various reasons. Cerebral infarcts and dementia occur with ever-increasing frequency in elderly persons. In fact, they often coexist, both clinically and neuropathologically. However, recent studies show that stroke is an important risk factor for the subsequent development of dementia49. In a population-based study in Rochester, Minnesota, the incidence of dementia after a stroke was nine times higher than expected . If dementia was not observed the first year after a stroke, the risk in the cohort was still twice the risk in the general population. Age, sex (male), and second stroke were significant independent predictors of dementia. It is unclear how the location or the severity of infarct may impact dementia. In another study, Henon et al.51 reported that, after excluding patients with previously diagnosed dementia, about 30% of patients over the age of 40 developed newonset dementia within three years after a stroke. In this study, age, diabetes mellitus, cognitive disturbances prior to stroke, silent infarcts on CT, and severity of clinical deficit at admission were independent predictors of post-stroke dementia51. Tatemichi et al.52 reported that in patients aged over 60 years the prevalence of dementia three months after an ischemic stroke was 26.3%, nine fold higher than controls. Four years after a first lacunar stroke, 23.1 % of patients develop dementia, which is 4-12 times more than controls53. These studies undoubtedly establish a close correlation between stroke and the risk of developing dementia. One hypothesis stated that the vascular event might reveal an underlying symptomatic AD54. It has also been observed that in some patients, cognitive state, likely to be normal before stroke, is impaired immediately after stroke and does not decline over time. In these cases it is possible that the dementia is related to a single infarct located in a 'strategic' area55.

The evidence reviewed thus far has demonstrated that stroke predisposes persons to the development of dementia. Additional studies have shown the inverse to be true as well: patients with AD are also at risk of stroke. In a community-based study, Ferrucci et al.56 found a higher risk of stroke in elderly subjects with dementia than in nondemented subjects; however, the presumed cause of dementia was not specified. In the Rotterdam study, AD patients had an increased intimamedia thickness in the common carotid artery31; a finding that is associated with an increased risk of stroke in the community57.

On the basis of these observations, it can be speculated that ischemic stroke and the pathological changes considered pathognomonic of Alzheimer's disease interact in determining clinical expression and symptoms consistent with AD. In a large and prospective study of elderly nuns, pathological examination was obtained in all deceased subjects58. Among elderly nuns only 57% of those with pathological changes considered pathognomonic of AD suffered from dementia clinically. However, if cortical infarcts were also present, then 75% suffered from clinical dementia. The percentage of subjects with dementia was as high as 93% if small sub-cortical infarcts were present in addition to the pathological changes of AD58. This may suggest that ischemic stroke and neuropathological changes of AD indeed interact in determining the clinical expression of the disease. The location of the infarct (cortical vs. subcortical) may play a clinical role as well.


Although cerebrovascular pathology has long been recognized as responsible for a subset of dementia syndromes classified as vascular dementia, mounting evidence accumulated in the past decade has revealed a significant etiopathogenetic role of cerebrovascular pathology and risk factors in the development of neurocognitive deficits and other forms of dementia including Alzheimer's disease. Improved understanding of the risk factors for cerebrovascular disease may be helpful to assess patients with dementia since many of these factors can be prevented or modified. Similarly, a better understanding of the possible role of hemodynamic compromise secondary to extra or intracranial large vessel occlusion/stenosis may offer new therapeutic options such as surgical and/or endovascular measures.


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Giuseppe Lanzino*, Desiree J. Lanzino* and David Wang^

*Department of Neurosurgery, University of Virginia Health Sciences Center, Charlottesville, VA

^ Department of Neurology, Illinois Neurological Institute, University of Illinois, Peoria, IL, USA

Correspondence and reprint requests to: Giuseppe Lanzino, MD, Department of Neurosurgery, UVA HSC Box 212, Charlottesville, VA 22908, USA. [] Accepted for publication December 2001.

Copyright Forefront Publishing Group Jun 2002
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