Binswanger's Disease Research Articles

P3-161 Cotton-wool plaques, plaque-like angiopathy, neurofibrillary tangles and leukoencephalopathy in a Japanese man clinically presenting with binswanger's disease

P3-161 Cotton-wool plaques, plaque-like angiopathy, neurofibrillary tangles and leukoencephalopathy in a Japanese man clinically presenting with binswanger's disease

The neuropathology of vascular dementia

Ischemic infarction is the main lesion underlying vascular dementia (VaD) but cases also occur after brain hemorrhage, as well as with hypoperfusive brain ischemia. Ischemic strokes include large-vessel cortico-subcortical strokes and lacunes resulting from small-vessel disease. Arteriolosclerosis and fibrinoid necrosis are the most common forms of small-vessel disease in the elderly. Although it was originally proposed that vascular dementia could result from repeated strokes with loss of >100 mL of brain tissue loss (multi-infarct dementia), it is currently held that the location of the stroke is probably more relevant to cognitive loss and dementia. In fact, a single, strategically located stroke may interrupt cortico-subcortical circuits important for memory and cognition. Hypoperfusive lesions include border-zone cortico-subcortical infarcts, temporal lobe sclerosis, and periventricular incomplete ischemic leukoencephalopathy. The latter two lesions are commonly seen in the elderly as a result of narrowing and tortuosity of medullary arterioles irrigating these distal territories, plus cardiac pump failure. Binswanger disease is characterized by extensive periventricular ischemic leukoencephalopathy that spares the arcuate U-fibers, and presence of lacunar strokes. CADASIL is a genetic form of vascular dementia characterized by a cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy. CADASIL is due to a mutation of the Notch3 gene in chromosome 19. Intracerebral hemorrhages in strategic locations may produce vascular dementia. Lesions in the basal forebrain that damage cholinergic nuclei, such as those resulting from a ruptured aneurysm of the anterior communicating artery, may produce vascular dementia. Some patients with subarachnoid hemorrhage develop normal-pressure hydrocephalus. Cerebral amyloid angiopathy (congophilic angiopathy) may cause lobar hemorrhages and dementia. Vascular lesions, in particular, microinfarcts, are frequently found in patients with a clinical diagnosis of Alzheimer disease. These mixed forms of dementia are likely to become the most common form of dementia in the elderly.

Controversies in vascular dementia

The main controversies in the field of vascular dementia (VaD) include the nosological classification of this disorder, the definition of dementia, the differences between the different sets of diagnostic criteria, the concept of Binswanger disease, the role of vascular lesions in Alzheimer disease, and the results of cholinesterase trials in VaD. Vascular Cognitive Disorder (VCD) is the most current nosological classification for the global diagnostic category of cognitive impairment of vascular origin, ranging from mild cognitive impairment (MCI) to vascular dementia. It includes specific disease entities such as poststroke VaD, CADASIL, Binswanger disease, and AD plus CVD. Vascular cognitive impairment (VCI) is limited to cases of vascular MCI without dementia, by analogy with the concept of amnesic MCI, currently considered the earliest clinically diagnosable stage of Alzheimer disease (AD). The main problem of VaD stems from the currently accepted definition of dementia that requires memory loss as the sine qua non for the diagnosis. This may result in over-sampling of patients with AD worsened by stroke (AD+CVD). We have proposed an operational definition of dementia in VaD based on the presence of abnormal executive control function, severe enough to interfere with social or occupational functioning. This may increase the sensitivity and specificity of the NINDS-AIREIN criteria. In donepezil trials in VaD that excluded prestroke MCI, the placebo groups were different from those in AD without CVD, and in AD+CVD trials.

Cerebral blood flow patterns in Binswanger's disease: a SPECT study using three-dimensional stereotactic surface projections

We investigated regional cerebral blood flow (rCBF) patterns in Binswanger's disease (BD) patients using single photon emission computed tomography (SPECT). SPECT data on 22 patients with BD were analyzed using three-dimensional stereotactic surface projections (3D-SSP) and were compared with those of 22 patients with Alzheimer's disease (AD). rCBF patterns in patients with BD were different from those with AD. The BD group had greater CBF reduction in the frontal and anterior cingulate cortices, while the AD group had greater CBF reduction in the temporoparietal and posterior cingulate cortices. However, the rCBF pattern of each patient was more variable, and could be divided into three patterns: anterior cerebral hypoperfusion, posterior cerebral hypoperfusion, and diffuse cerebral hypoperfusion patterns. A distinct CBF reduction in the temporoparietal and/or posterior cingulate cortices, indistinguishable from the CBF pattern observed in AD, was demonstrated in 8 of 22 (36%) patients with BD, in particular there was bilateral hemispheric involvement with a diffuse hypoperfusion pattern. Although no pathological confirmation could be performed, some of the BD patients with CBF reduction in the posterior cerebral cortices may represent additional changes in the brain due to AD. In the future, a longitudinal study including pathology will be needed to determine whether these patients have coexisting AD pathology.

Topographical and cytopathological lesion analysis of the white matter in Binswanger?s disease brains

The purpose of the present study was to document the topographical and cytopathological lesions in the white matter (WM) of Binswanger's disease (BD) brains. Subcortical WM lesions in each lobe and fiber bundle lesions related to the medial thalamic and hippocampal structures in clinicopathologically proven BD brains were evaluated by Klüver-Barrera staining using a grading score. Lesions in the frontal subcortical WM of BD brains, brains from non-neurological patients, and brains with cerebral hemorrhage or large cortical infarcts were also examined immunohistochemically using molecular markers for axonal flow damage: amyloid precursor protein (APP); and for demyelinating axonopathy: encephalitogenic peptide (EP). Our results indicated that the WM lesions in BD were significantly more prominent in the frontal periventricular and subcortical regions as compared with other subcortical WM lesions, in the order of the parietal, occipital and temporal lobes. Fiber bundle lesions in the capsular genu, including the anterior thalamic peduncle, were also significantly more prominent in BD brains as compared with the other bundle lesions. Furthermore, the frequency of damaged nerve fibers labeled by the EP antiserum and APP immunoreactive fibers was significantly higher in BD brains as compared with the control brains. The grading scores for the WM damage correlated significantly with those for the APP and EP immunoreactive fibers in all brains, including the control brains. The axonal damage in the frontal WM lesions of the BD brains was clearly revealed in our study using immunohistochemistry for APP and EP.

Effects of transforming growth factor beta receptor 1 (TGFβ R1) on demyelination and vascular pathology in Binswanger's disease and other forms of vascular dementia

Pleomorphic xanthoastrocytoma (PXA) is a rare astrocytic neoplasm that usually arises in children and young adults. Typically, lesions of PXA are superficially located in the cerebral hemispheres. Herein, we report two extremely rare patients with PXA arising from suprasellar regions. One of the patients is a 29-year-old man admitted to our hospital with a history of progressive headache for 1 month. The patient’s brain MRI revealed a large tumor arising from the suprasellar cistern of the third ventricle. The second patient, a 52-year-old woman, presented with progressive dizziness and visual disturbance that had developed over the course of 1 year. The MRI revealed a well-enhanced suprasellar solid mass measuring 1.4 × 1.2 × 1.4 cm. Both patients underwent surgical removal of their tumors, and both patients showed similar microscopic structures and immunohistochemical phenotypes: the tumor cells were pleomorphic with mixtures of spindle-shaped, and multinuclear giant cells. In addition, eosinophilic granular bodies and xanthomatous cells were seen on section. Immunohistochemistry was positive for GFAP, S-100, and CD34, and was negative for IDH 1, CK, and Syn. The Ki-67 proliferation index was less than 1%. Silver impregnation revealed reticulin fibers surrounding the individual tumor cells, and small cell groups. Based on these findings, the two patients were diagnosed with PXA in the suprasellar region. To date, only five such patients have been reported in the literature. PXA should be included in the differential diagnosis for tumors arising in the sellar region.

The Clinical Diagnosis of Vascular Dementia: A Comparison Among Four Classification Systems and a Proposal for a new Paradigm

Throughout the 1990s a variety of schemes for the diagnosis of Vascular Dementia (VaD) were proposed, including the ADDTC criteria for Ischemic Vascular Dementia, the NINDS-AIREN criteria for Vascular Dementia, Bennett's criteria for Binswanger's disease, and the ICD-10 criteria for Vascular Dementia. We undertook a retrospective analysis of a series of ambulatory outpatients with dementia to determine the prevalence with which patients were diagnosed by each of these diagnostic schemes, and to survey the clinical characteristics associated with VaD. We found that the diagnostic schemes for VaD were not interchangeable; patients diagnosed with VaD using one set of criteria were not necessarily diagnosed with VaD using other criteria. The most common clinical characteristics associated with VaD, regardless of the diagnostic scheme that was used, were hypertension, extensive periventricular and deep white matter alterations on MRI (leukoaraiosis), and differential impairment on neuropsychological tests that assess the ability to establish/maintain mental set and visuoconstruction, with relatively higher scores on tests of delayed recognition memory. Interestingly, the majority of VaD patients obtained low scores on the Modified Ischemic Scale, since cortical infarcts and a history of a sudden onset and/or step-wise decline in cognitive function were rare. We conclude that the current diagnostic schemes for VaD do not necessarily consider the heterogeneous nature of VaD. A new paradigm that seeks to describe, in addition to diagnosing dementia associated with cerebrovascular disease is discussed.

Hemodynamic changes in Alzheimer's and Binswanger's diseases as evaluated by second‐derivative finger photoplethysmography

Background: Hemodynamics is often the focus of dementia research, but methodological difficulties have precluded such research. To clarify the role of hemodynamic factors in the pathogenesis of dementing illness, the newly developed, second‐derivative finger photoplethysmography (SD‐PTG), which can provide hemodynamic indices, was studied in 173 patients with dementia.Methods: The subject group consisted of 41 patients with Binswanger's disease (BD group), 31 patients with Alzheimer's disease with severe periventricular lucency (PVL; AD + PVL group), and 101 patients with Alzheimer's disease without PVL. The SD‐PTG findings as well as the clinical findings of each group were compared with those of 114 controls without dementia. The heights of the a‐, b‐, c‐, d‐, and e‐waves on SD‐PTG waveforms were measured, and b/a and d/a ratios were used as indices of distensibility of the aorta and peripheral vascular impedance in the systemic circulation, respectively.Results: The b/a ratio was significantly higher in the BD and AD + PVL groups than in the AD − PVL group (P < 0.01). The d/a ratio was significantly lower in the BD group than in the AD + PVL, AD − PVL, and control groups (P < 0.01). The d/a ratio in the BD group correlated significantly with mini‐mental state examination (MMSE) score (r = 0.47, P = 0.0023).Conclusions: The results indicate that decreased distensibility of the aortic wall is associated with the white matter lesions in both types of dementia, while the low d/a ratio and the correlation between the d/a ratio and the MMSE score in the BD group indicate that increased peripheral impedance was associated with more extensive involvement of the white matter and cognitive decline in Binswanger's disease.

Vascular Dementia: Distinguishing Characteristics, Treatment, and Prevention

Vascular dementia (VaD) is the second-most-common cause of dementia in the elderly, after Alzheimer's disease (AD). VaD is defined as loss of cognitive function resulting from ischemic, hypoperfusive, or hemorrhagic brain lesions due to cerebrovascular disease or cardiovascular pathology. Diagnosis requires the following criteria: cognitive loss, often predominantly subcortical; vascular brain lesions demonstrated by imaging; a temporal link between stroke and dementia; and exclusion of other causes of dementia. Poststroke VaD may be caused by large-vessel disease with multiple strokes (multiinfarct dementia) or by a single stroke (strategic stroke VaD). A common form is subcortical ischemic VaD caused by small-vessel occlusions with multiple lacunas and by hypoperfusive lesions resulting from stenosis of medullary arterioles, as in Binswanger's disease. Unlike with AD, in VaD, executive dysfunction is commonly seen, but memory impairment is mild or may not even be present. The cholinesterase inhibitors used for AD are also useful in VaD. Prevention strategies should focus on reduction of stroke and cardiovascular disease, with attention to control of risk factors such as hypertension, diabetes mellitus, hypercholesterolemia, and hyperhomocysteinemia.

Mental disorders in Binswanger's disease

Subcortical arteriosclerotic encephalopathy, or Binswanger's disease (BD), is a special form of chronic progressive vascular disease of the brain, the main clinical manifestation of which is dementia in combination with a variety of neurological symptoms (subcortical, cerebellar, pseudobulbar and pyramidal syndromes and disorders of other pelvic organs) .). The genesis of the disease, primarily dementia syndrome, is based on diffuse lesion of the white matter (BV) of the cerebral hemispheres, caused by severe arteriosclerosis of the blood vessels supplying it.

Cerebral microbleeds in Binswanger's disease: a gradient-echo T2*-weighted magnetic resonance imaging study

We investigated the incidence and the number of microbleeds (MBs) on T2*-weighted gradient-echo magnetic resonance imaging in 30 Binswanger's disease (BD) patients with diffuse white matter lesions and a varying degree of lacunar infarction, 51 multiple lacunar stroke (MLS) patients with multiple lacunar infarction and no or mild white matter lesions, and 59 elderly controls. MBs were found in 23 (77%) patients with BD, 26 (51%) patients with MLS, and 5 (8%) controls, and the incidence and the number of MBs were significantly greater in the BD group compared with MLS and control groups. Patients with BD had a more widespread location of MBs. More specifically, MBs were commonly found in areas within or surrounded by white matter lesions of the patients with BD. When 81 patients from both the BD and MLS groups were analyzed, logistic regression analysis showed that number of lacunar infarct, severity of white matter hyperintensity, and use of antiplatelet agents were significantly associated with MBs. Patients with BD exhibited a high frequency and number of MBs, indicating advanced bleeding-prone microangiopathy within the brain, which should be taken into account in treatment and management.

Metallothionein I-II immunocytochemical reactivity in Binswanger's encephalopathy.

Binswanger's disease is a subacute form of hypertensive encephalopathy characterized by patchy-confluent myelin loss of the deep hemispheric white matter, associated with marked regressive changes of the oligodendrocytes and variable astroglial reaction. To understand the distribution and the specificity of astrocyte pathology in Binswanger's disease we quantified reactive and degenerating astrocytes in different regions of the deep and subcortical white matter and of the cerebral cortex. Sections of frontal, temporal, parietal, and occipital lobes of 12 histologically proven cases of Binswanger's disease were immunostained with antibodies to glial fibrillary protein (GFAP) and to metallothionein I and II (MT-I-II), markers which specifically identify normal and reactive astrocytes. Control tissues were from 6 elderly patients without neurological diseases. The brains of Binswanger's disease were characterized by few and lightly immunostained astrocytes in the deep white matter, but normal and reactive astrocytes, strongly immunoreactive for GFAP and MT-I-II, were prominent in the subcortical white matter and the cerebral cortex. However, the relative distribution of GFAP positive and MT-I-II positive astrocytes was significantly different between the cerebral cortex and the subcortical white matter, the MT-I-II positive astrocytes being more frequent in the cerebral cortex, and the GFAP positive astrocytes in the subcortical white matter (p < 0.02). The GFAP and MT-I-II expressions in subsets of reactive astrocytes in the cortico-subcortical layers together with regressive astroglial changes in the deep white matter suggest that the dynamic plasticity of astroglia is topographically and biochemically differentiated in vascular dementia of Binswanger type.

A Clinicopathological Study of Idiopathic Normal Pressure Hydrocephalus

Background: Since Hakim and Adams introduced the clinical entity of normal pressure hydrocephalus (NPH) in 1965, postmortem studies of idiopathic NPH have been few in number. Several autopsy cases reported with clinically probable “idiopathic NPH” were diagnosed with Alzheimer's disease (AD) or Binswanger's disease (BD) neuropathologically. Therefore, the neuropathological study of pathologically confirmed idiopathic NPH remains to be completed both quantitatively and qualitatively. Methods: Out of 239 autopsy cases in Fukushimura Hospital, 13 patients had been diagnosed clinically as having NPH. After excluding seven cases diagnosed neuropathologically with other diseases or secondary NPH, we investigated the clinicopathological findings of six patients with idiopathic NPH. Results: Four patients presented with the complete classic triad consisting of progressive dementia, gait disturbance, and urinary incontinence. All cases exhibited progressive ventricular enlargement with periventricular lucency by computed tomography images. We found (1) diffuse marked dilatation of the lateral ventricles of unknown etiology, and (2) the changes of ependymal cells and subependymal tissue around the callosocaudate angle. Furthermore, no complications were suspected neuropathologically in all cases, such as AD, BD, or Lewy body disease. Conclusion: We experienced six autopsy cases with pathologically confirmed idiopathic NPH. They had two pathological features of NPH but no other pathological disorders that might cause NPH. Several “idiopathic NPH” cases reported previously have been diagnosed neuropathologically with other disorders. However, the presented cases could be clearly distinguished from such “idiopathic NPH.” Therefore, our cases should be defined as idiopathic NPH neuropathologically. By accumulating more cases and investigating further we hope to elucidate the pathogenesis and further develop treatment for idiopathic NPH.

Fibrinogen and the Amount of Leukoaraiosis in Patients with Symptomatic Small-Vessel Disease

We investigated whether there is a direct correlation between plasma fibrinogen levels and the amount of leukoaraiosis (LA) in patients with symptomatic small-vessel disease. The study included 28 patients: 12 with a first-ever lacunar infarction (LI) and 16 with Binswanger’s disease (BD). The mean age was 71 years (SD 8.6), and 21 were men. For each patient, we recorded demographic data, vascular risk factors and the results of blood chemistry analysis including fibrinogen (g/l), hematocrit (decimal fraction) and total serum proteins (g/l). A cerebral MR scan was performed in each patient and an LA score was obtained by an investigator blind to clinical data, using a semiquantified scale in six areas of each cerebral hemisphere (0–4 points in each area, total scoring range 0–48 points). Results: The mean (SD) for the LA score was 18.9 (10.7) and for plasma fibrinogen 3.97 (1.1). Pearson’s and Spearman’s correlation coefficients between fibrinogen and LA score were 0.43 (p = 0.02) and 0.49 (p = 0.007), respectively. Multiple-regression analysis between groups (LI or BD) and fibrinogen versus LA score showed the strongest association for the BD group (p = 0.014) and a direct relation with fibrinogen (p = 0.018). No statistically significant association was found between LA score and age, sex, any vascular risk factor, hematocrit or total serum protein. Conclusion: There is a significant correlation between plasma fibrinogen levels and the amount of LA in patients with symptomatic cerebral small-vessel disease. This result suggests that fibrinogen may be involved in the pathophysiology of LA in these patients.

Clinical Features of CADASIL

Cerebral autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy (CADASIL) is a rare hereditary disease characterized by recurrent transient ischemic attacks, strokes, and vascular dementia. Various mutations in the Notch3 gene cause the disease, whereas the mechanism of how they cause the disorder remains unknown. We recently identified two Japanese CADASIL families with an R141C mutation. The mean age of onset was 44.6, and the main symptoms were recurrent strokes and progressive motor disturbances in extremities, as well as pseudobulbar palsy. Besides those in white matter and basal ganglia, ischemic lesions in temporal edge and corpus callosum were present on magnetic resonance images, which seemed to be characteristic of CADASIL. Moreover, in our cases, nocturnal arterial blood pressure fall was significantly lower in patients compared with control subjects, suggesting that it might be partly associated with ischemic lesions in deep white matter in CADASIL. We also compared Japanese and Caucasian CADASIL cases and found that dementia and pseudobulbar palsy were observed more frequently in Japanese patients, although typical migraine was rather rare. In the present study, we describe the clinical features of CADASIL, hoping to help reveal the mechanism of chronic ischemic brain diseases, including leukoaraiosis or Binswanger's disease.

Vascular dementia in Japan.

Patients with vascular dementia are frequently encountered in Japan reaching nearly 50% of those with senile dementia, which is equal to or even slightly higher than patients with Alzheimer's disease. This contrasts with a much lower ratio of patients with vascular dementia in the United States. The majority of vascular dementia seen in Japan is of the multiple lacunar type or Binswanger disease, often without any episode of stroke. Clinically, those patients tend to have attention deficit and reduction of spontaneous activities. The observed characteristics of vascular dementia likely reflect the main type of cerebrovascular disease prevalent in Japan since the majority of cerebral infarction in Japan is of lacunar type in contrast to that in the United States and Europe. For patients without any episode of stroke, it is important to differentiate from Alzheimer's disease. As in the United States and Europe, mixed dementia exists in Japan with Alzheimer's disease and vascular dementia together and poses problems in clinical diagnosis because many patients may not have any episode of stroke, but they have neuroimaging characteristics compatible with both. The number of patients with atherosclerosis in large cervical and cerebral arteries is said to be increasing in Japan, and vascular dementia in Japan may present with different clinical pictures in the future.

Increased Blood-Brain Barrier Permeability in White Matter Lesions of Binswanger’s Disease Evaluated by Contrast-Enhanced MRI

We investigated blood-brain barrier (BBB) permeability in white matter lesions of Binswanger’s disease (BD) with contrast-enhanced MRI. Three subject groups were studied: 17 patients with BD and periventricular hyperintensities (PVH) on MRI, 10 patients with ischemic cerebrovascular events and with PVH but no dementia, and 14 age-matched control subjects without PVH. BBB permeability was quantified by calculation of T₁ change defined as [(T_1post – T_1pre)/T_1pre] ×100, where T_1pre and T_1post represent the T₁ relaxation times before and after Gd-DTPA administration. T₁ change in PVH of BD patients significantly decreased in comparison with that observed in PVH of the nondemented patients and in normal white matter of the control subjects, but no significant T₁ change was observed between the PVH of the nondemented patients and normal white matter of the controls. There was a significant correlation between the Mini-Mental State Examination score and T₁ change for areas of PVH in BD. These results suggest that BBB permeability increases in areas of PVH in BD and that a BBB dysfunction is related to a progression of cognitive impairment.

White matter changes in normal pressure hydrocephalus and Binswanger disease: specificity, predictive value and correlations to axonal degeneration and demyelination.

To analyse the diagnostic and prognostic value of periventricular hyperintensity (PVH) and deep white matter hyperintensity (DWMH) magnetic resonance imaging (MRI) changes and their relation to symptoms and cerebrospinal fluid (CSF) markers of demyelination (sulphatide) and axonal degeneration [neurofilament triplet protein (NFL)] in a large series of patients with normal pressure hydrocephalus (NPH) and Binswanger disease (BD). PVH and DWMH were determined by a semi-automatic segmentation method on T2-weighted images in 29 patients with NPH and 17 patients with BD. CSF analyses, psychometric testing and quantification of balance, gait and continence were performed in all patients and also postoperatively in NPH patients. No MRI variable could identify NPH or BD patients. Abundant PVH and DWMH preoperatively correlated with improvement in gait, balance and psychometric performance after shunt surgery (P < 0.05). CSF sulphatide correlated positively with the amount of DWMH (P < 0.05) while NFL was correlated to both PVH and DWMH (P < 0.05). Abundant PVH correlated with poor psychometric performance while DWMH correlated with gait disturbance (P < 0.05). Postoperative reduction in PVH correlated with improvement in gait, balance and psychometric performance. In spite of a refined quantification method, NPH and BD patients exhibited similar MRI changes. MRI had a predictive value in NPH patients. DWMH might relate to demyelination and PVH to neuronal axonal dysfunction. NPH and BD share the major part of symptoms and MRI changes, indicating a common pathophysiological pattern, and we raise the question of how to treat BD patients.

Vascular dementias

Cerebrovascular disorders are the second most frequent cause of dementia in late life next to Alzheimer's disease. A recent community-based autopsy study has demonstrated that relevant cerebrovascular changes are much more prevalent in individuals aged 70+ years than previously assumed. Furthermore, the combination between cerebrovascular lesions and Alzheimer-type pathology is the most common neuropathological finding in elderly patients with dementia. There is still some uncertainty about which types of cerebrovascular changes are most likely to cause cognitive impairment including dementia and which pathogenetic mechanisms are involved. Without doubt, however, the vascular dementias are a heterogeneous group of diseases in terms of etiology, histopathology, and clinical appearance. According to the vessel calibres and perfusion territories that are preferentially affected a distinction is commonly made between the frequent subcortical small-vessel disease and the rare cortical large-vessel disease. With these morphological subtypes three major clinical variants are associated: dementia due to subcortical lacunes and white matter changes including Binswanger's disease, multi-infarct-dementia, and dementia due to singular strategic infarcts. In most cases of dementia of cerebrovascular origin the pattern of intellectual impairment is frontal or subcortical, in contrast to the typical cortical presentation of Alzheimer's disease. Deterioration of executive function and attention as well as changes in personality, rather than memory loss, are the predominant symptoms. Therefore the current diagnostic criteria for dementia are poorly suited for the detection of vascular dementias. None of the criteria that have been specifically proposed for the diagnosis of vascular dementias provide clear guidelines for evaluating the causal relationship between cerebrovascular lesions and psychopathological findings. Further research will reveal whether clinical diagnosis can be improved by taking into account the heterogeneity of cerebrovascular diseases. A large proportion of dementias of cerebrovascular origin may be preventable by treating the risk-factors for stroke. Once significant cognitive impairment has occurred, however, there is no established pharmacological treatment for the vascular dementias to date. Only recently results of placebo-controlled clinical trials have become available showing that cholinergic treatment strategies are effective in vascular dementia and in dementia due to combined vascular and neurodegenerative pathologies.

¿Enfermedad de Binswanger o demencia multiinfarto? Claves diagnósticas en la demencia vascular

To develop a model that assists in the classification of patients with vascular dementia in two of its most relevant subtypes: multi-infarct dementia (cortical involvement) and Binswanger's disease (subcortical involvement). Retrospective analysis of 50 consecutive patients with Binswanger's disease and 50 patients with multi-infarct dementia studied throughout a 12-year period (1986-1998) in a tertiary university hospital. The statistical model was obtained by multivariant analysis (logit model) and its accuracy was estimated by means of ROC curve analysis. The variables included in the regression model were: arterial hypertension (p < 0.03), cardioembolic disease (p < 0.05), and presence of cortical (p < 0.01) and lacunar (p < 0.01) infarctions in CAT. The specificity of the model was 90%, the sensitivity near 60%, and the positive likelihood ratio 5.8. The area under the ROC curve was 0.80 (0.73-0.87). Despite the availability of consensus diagnostic criteria for vascular dementia, their use is very commonly restricted to the research field. We have developed a classification model for patients with vascular dementia in two relevant subgroups: multi-infarct dementia and Binswanger's disease. This model can contribute to make identification of these patients in the daily clinical practice easier.