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Query: UMLS:C0038454 (stroke)
 147,016 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Twenty-three elderly patients were found to have a consistent pattern of leukoencephalopathy by computed tomography and nuclear magnetic resonance imaging. Eight patients presented with vague, nonspecific symptoms and had no neurologic deficits. The other 15 patients had neurologic deficits that presented in one of three ways: stroke, seven patients; slowly progressive dementia and gait disturbance, five patients; or slowly progressive dementia alone, three patients. Risk factors for arteriosclerosis (hypertension, diabetes) were present in 18 patients (78%). The necropsy of one patient revealed arteriosclerotic vasculopathy characteristic of subcortical arteriosclerotic encephalopathy (SAE) or Binswanger's disease. Subcortical arteriosclerotic encephalopathy may be a relatively common affliction of elderly patients, most of whom have risk factors for arteriosclerosis. The modes of presentation and associated clinical signs are variable, and more than one third may have no neurologic deficit. In some cases SAE overlaps with normal pressure hydrocephalus by clinical and neuroimaging criteria. Some patients with normal pressure hydrocephalus who do not respond to ventricular shunting may actually have SAE.
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PMID:Subcortical arteriosclerotic encephalopathy (Binswanger's disease). Computed tomographic, nuclear magnetic resonance, and clinical correlations. 403 2

Because the arterial baroreceptor reflex function that modulates the variability of blood pressure decline with advancing age, blood pressure in the elderly is more variable than in young patients. Recent advances in ambulatory blood pressure monitoring devices clarified the changes in the blood pressures in daily life which had been never observed by the office blood pressure measurement. 1. White coat hypertension: Temporary elevation of blood pressure in the clinic is referred as a white coat hypertension and there is much recent evidence indicating that it is common in the elderly. Our recent data indicated that left ventricular mass in patients with white coat hypertension is higher than that in the normotensive groups, although it is lower than that in the true persistent hypertensive group. This suggests that white coat hypertension is never innocent and should be treated by a mild antihypertensive drug. 2. Morning surge: Many reports indicate that cardiovascular events occur more frequently in the early morning, suggesting a morning rise in blood pressure might be associated with this catastrophe. Using an activetrace that assesses physical activity objectively, we recently clarified that morning surge can be divided into two types. One is morning rise which begins in accordance with awakening and arising. The other is a rise during sleep before awakening. 3. Although blood pressure rises during the daytime and decreases at nighttime in healthy individuals, recent reports indicate that there are many conditions in which blood pressure does not fall at night. Individuals with this condition have been called non-dippers and tend to be associated with hypertensive target-organ damage such as silent stroke or Binswanger's dementia.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Ambulatory blood pressure in the elderly with hypertension]. 769 38

The pathogenic mechanism underlying the vascular changes in Binswanger's encephalopathy (BE) is unknown. To test whether alterations of the humoral immunity may lead to endothelium damage, we analyzed serum levels of anti-brain endothelium antibodies (ABEA) (IgG and IgM) in 16 BE patients, 19 subjects with ischemic vascular disease without mental deterioration and 18 normal healthy subjects. ABEA IgM were found elevated in 1/16 (6%) BE patients and in 4/19 (21%) patients with cerebrovascular diseases; an increase in ABEA IgG was found in 6/16 (38%) BE patients and in 7/19 (37%) cerebrovascular patients. Association with anti-cardiolipin antibodies (IgG and/or IgM) was found in 50% of BE patients with elevated ABEA and only 10% of those with no increase, whereas high titres of anti-neurofilament antibodies (1:10,000) were detected in 40% and 71% respectively. In BE, ABEA IgG but not IgM showed a trend, although not significant, towards a correlation with the duration of the disease (rs = 0.47; p = 0.07) and significantly correlated with the cognitive function as assessed by the Mini mental state (MMS) score (rs = 0.56; p = 0.02). Higher mean values of the MMS score were found in BE patients with elevated ABEA than in those without (p = 0.04). This difference was not due to language disorders neither to an association with stroke risk factors or anti-neurofilament antibodies. However, there were no significant differences in MMS scores between cerebrovascular patients with ABEA and those without. A "neuro-protective" role is hypothesized for the ABEA in the development of dementia in BE.
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PMID:Serum anti-brain endothelium antibodies and cognitive assessment in patients with Binswanger's encephalopathy. 772 40

Binswanger's type encephalopathy is characterized by progressive dementia and diffuse subcortical ischemic lesions associated with arteriosclerosis. Hypertension is believed to be a major pathogenic factor in causing this encephalopathy but there are some cases of the encephalopathy not suffering from hypertension. In 1985, Yamamura et al. and Fukutake et al. reported familial cases of normotensive juvenile Binswanger's type encephalopathy with alopecia and lumbago, and considered it to be possibly a new clinical syndrome. We reported three cases of relatively young-onset (under the age of 40) Binswanger's type encephalopathy with persistent hypotension. All three patients suffered from neither alopecia nor lumbago. Patient (male aged 40) had repeated episodes of ischemic stroke and had progressive dementia. Patients 2 (male aged 41) and 3 (male aged 34) were not in a state of dementia, but had a history of transient ischemic attacks, and at present are completely symptom-free. Though there were no risk factors for cerebrovascular disease in these cases, the repeated episodes of ischemic stroke and the existence of small multiple lacunes in the basal ganglia on CT and MRI suggest that the white matter damage was principally due to a vascular disorder. In these cases, persistent hypotension was characteristic and might be a factor for the induction and exacerbation of this encephalopathy. These three cases are different from the classic form of Binswanger's type encephalopathy based on hypertension. Normotensive cases have been described before, but our cases do not seem to fall into this category because the blood pressure constantly remained hypotensive.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Binswanger's type encephalopathy without alopecia and lumbago in young hypotensive patients]. 772 96

White matter changes, which are noted in Binswanger's disease and which may be due to ischemia, have previously been explained mainly on the basis of the hemodynamic mechanism. To elucidate the etiopathophysiology of Binswanger's disease from the hemorheology viewpoint, platelet activation in the cerebral circulation was studied in 30 patients with Binswanger's disease, who satisfied the diagnostic criteria of Binswanger's disease proposed by Bennett et al. Plasma beta-thromboglobulin concentration gradients (delta BTG) between the jugular vein and the antecubital vein, as indicators of platelet activation in the cerebral circulation, were determined in these patients (Binswanger's disease group) compared with those of different stroke subtypes groups (lacunar, atherothrombotic, cardioembolic) in the chronic phase and 25 patients with various diseases other than stroke (non-stroke group). Among these groups, the elevation of delta BTG levels in the Binswanger's disease group (4.55 +/- 6.95) were so frequent and prominent that differences were significant, especially in comparison to those of the cardioembolic group, and the non-stroke group. The enhanced platelet activation in the cerebral circulation observed in Binswanger's disease indicated not only the widespread development of underlying vascular lesions, but also accelerated release reaction of vasoactive substances from platelets into the blood stream, which could biochemically injure the vascular wall and neurons downstream, resulting in Binswanger's disease.
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PMID:[The role of platelet in the etiology of Binswanger's disease]. 782 2

To elucidate platelet activation in cerebral circulation and its significance in ischemic stroke, the plasma beta-thromboglobulin (BTG) concentration gradients between the internal jugular vein and the antecubital vein were investigated in 164 patients with ischemic stroke. They consisted of cases of lacunar, atherothrombotic, cardioembolic stroke, and Binswanger's disease. The diagnosis of each stroke category was based on both computed tomographic (CT) and clinical findings. In particular, Binswanger's disease was diagnosed by the diagnostic criteria proposed by Bennett et al. Blood was withdrawn simultaneously from the internal jugular vein (A) and the antecubital vein (B) followed by determination of the BTG-A level and the BTG-B level, respectively. The BTG levels of 184 paired blood samples, thus, were obtained and the ratio (delta BTG) of BTG-A/BTG-B was calculated as an indicator for platelet activation in the cerebral circulation. According to the timing of the examination, these values of the acute phase less than 7 days after the event were separated from those of the chronic phase more than 28 days after the event. The delta BTG levels were also determined in 25 of controls with diseases other than stroke and considered to reflect platelet activation in the cerebral circulation. The mean delta BTG values of each stroke subtype without ticlopidine treatment, compared with those of controls (0.96 +/- 0.42), were significantly higher except those during the chronic phase of cardioembolic stroke and pronounced variability of delta BTG was noted in most subtypes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Clinical study of platelet activation in cerebral circulation--comparison between ischemic stroke subtypes and Binswanger's disease]. 799 86

Vascular dementia (VD) and Alzheimer's type dementia are two main causes of dementia in the aged. Considering historical backgrounds and ethnic differences, a simplified classification of VD is suggested. First, poststroke dementia of acute onset associated with an infarct that is large enough to impair general cognitive functions, or strategically located. Second, multi-infarct dementia that develops incrementally with increasing numbers of infarcts, and which should be classified as multiple cortical infarct dementia and multiple small infarctor lacunar dementia. Third, vascular dementia of the Binswanger type (VDBT). We compared two types of white matter lesions, periventricular hyperintensity (PVH) and confluent centrum semiovale hyperintensity (CCSH) in lacunar stroke patients with regard to the cerebral blood flow (CBF). In patients with PVH, there was a significant positive correlation between the dementia scores and the CBF in the parietal and temporal areas but not in the frontal area. In CCSH patients, there was a significant positive correlation in the frontal area but not in the parieto-temporal areas. Therefore, dementia in most patients with PVH may not be primarily related to the PVH, but may possibly be due to coexisting Alzheimer's type dementia, and dementia in most CCSH patients may be related to cerebrovascular disease. VDBT is unique clinically in its slowly progressive intellectual deterioration and pathologically in diffuse, confluent, and almost symmetrical white matter lesions. For the pathogenesis of VDBT, our studies suggest that hypertension, short-term variations in blood pressure, and a sustained nighttime elevation of blood pressure promote small vessel disease and cause ischemia of the cerebral white matter that is located in the end-fields of penetrating arteries; this leads to an imparied integrity of the blood-brain barrier and free radical generation, both of which may have important roles in producing diffuse white matter degeneration.
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PMID:[Problems in vascular dementia]. 864 89

Since the late 1800s, when Alzheimer and Binswanger proposed the concept of "arteriosclerotic brain degeneration," there has been an evolution in thinking regarding cerebrovascular disease (CVD) as a basis for dementia. While later work recognized the importance of specific infarct characteristics including volume, multiplicity, and location, recent studies have found that many factors may work in combination with those characteristics to produce dementia, including white matter disease; vascular risk factors such as diabetes; comorbid illnesses, particularly those that might produce cerebral ischemia or hypoxia; genetic factors; and host characteristics such as older age and fewer years of education. Studies of the prevalence of vascular dementia (VaD) have suggested that CVD is second only to Alzheimer's disease as a basis for dementia in Western countries and the most common basis in certain Asian countries, but those studies may have underestimated the frequency of dementia associated with CVD due to a failure to perform brain imaging and decreased survival among patients with CVD. Few studies of the incidence of VaD have been performed, but they have also consistently demonstrated an elevated risk associated with CVD. While certain methodologic issues have contributed to the debate regarding the importance of CVD as a basis for dementia, including variability in the techniques that have been used to characterize brain lesions, assess cognitive function, and diagnose dementia; difficulties inherent in the determination of a causal role for CVD in dementia; and the potential confounding effects of aphasia and depression in patients with stroke, it is clear that VaD remains an important public health problem.
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PMID:Vascular dementia: a construct in evolution. 896 67

Vascular dementia (VAD) is currently considered to be the second most common cause of dementia in Europe and the USA, second to dementia of the Alzheimer's type (DAT). However, in Asia and many developing countries the incidence of VAD exceeds that of DAT. The positive clinical diagnostic workup for VAD requires six steps: (1) clear-cut quantitative assessment of cognitive deficits utilizing standard neuropsychological tests to establish and quantify the dementia syndrome and rule out pseudo-dementia OF depression; (2) ascertaining the presence of risk factors for stroke; (3) identifying cerebral vascular lesions by neuroimaging (MRI, Iodine or Xenon contrasted CT, PET and SPECT); (4) exclusion of other causes of dementia; (5) differential diagnosis of possible, probable or definite VAD versus DAT and ascertaining when there are mixtures of the two; and (6) temporal identification of causality between onset and progression of the dementia with identified cerebral vascular lesions. There are eight subtypes of VAD: (1) multi-infarct dementias. These are due to large cerebral emboli, and are usually readily identifiable; (2) strategically placed infarctions causing dementia; (3) multiple subcortical lacunar lesions. Patients with these develop VAD at least five to twenty-five times more frequently than those in age-matched general population samples; (4) Binswanger's disease (arteriosclerotic subcortical leuko-encephalopathy). This form is rare. Neuroimaging confirms the diagnosis during life but the diagnosis can not be made by neuroimaging alone; (5) mixtures of two or more of above VAD subtypes; (6) hemorrhagic lesions causing dementia; (7) subcortical dementias due to cerebral autosomally dominant arteriolopathy with subcortical infarcts and leuko-encephalopathy (CADASIL), or to familial amyloid angiopathies and coagulopathies all of which present with multiple subcortical lacunar lesions similar to Binswanger's disease; (8) mixtures of DAT and VAD. The clinical significance of leukoaraiosis and its suspected relationships to VAD remains to be better established. The presence of ischemic infarctions, single or multiple large or multiple small (lacunar) by neuroimaging are necessary for the diagnosis of VAD, but identifying their presence, by neuroimaging alone, does not permit the diagnosis of dementia which can only be established by neuropsychological assessments. VAD is a clinical entity, identifiable in at least 30-70% of patients after strokes but mechanisms responsible for the cognitive impairments are complex. Some of these mechanisms are incompletely understood but provide subjects for important future research.
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PMID:Vascular dementia: still a debatable entity? 898 Dec 95

We report a 91-year-old man who had a stroke and died of renal failure. He had been treated for hypertension since 20 years before the onset of the present illness. In addition, he was operated on a gastric cancer 17 years previously. Otherwise he was doing well until May 29, 1991 (when he was 87-year-old) when he had sudden onset of dysarthria and right facial weakness. He was admitted to our hospital. On admission, general physical examination was unremarkable, and neurologic examination revealed a mentally sound man with slight dysarthria, right facial weakness, orolingual dyskinesia, and dysequilibrium in which he showed difficulty in tandem gait; however, no cerebellar ataxia was noted. A cranial CT scan revealed leukoaraiosis with multiple low density areas in the cerebral white matter. His BUN was 37 mg/dl and Cr 2.2 mg/dl. His neurologic symptoms cleared within the next few weeks and he was discharged with ticlopidine 100 mg q.d.. He had been doing well after the discharge except for gradual worsening of his renal function; his BUN was 65 mg/dl and Cr 3.27 mg/dl in April of 1994. On March 10, 1995, he fell down and hit his back; he became unable to walk because of pain, and he was admitted again on March 16, 1995. On admission, his blood pressure was 170/80 mmHg. There was an 1 + pitting pretibial edema; otherwise general physical examination was unremarkable. Neurologic examination revealed an alert and oriented man, however, Hasegawa's dementia scale was 23/30. Higher cerebral functions as well as cranial nerves were intact. He showed some unsteadiness of gait, however, no motor weakness or ataxia was noted. Deep tendon reflexes were diminished, but Chaddock sign was positive bilaterally. Vibration was diminished in the feet, however, pain and touch sensations were intact. Laboratory examination revealed a compression fracture of the twelfth thoracic vertebra. Blood count and chemistries were as follows; Hb 7.6 g/dl, Hct 23.3%, TP 6.0 g/dl, Alb 3.6 g/dl, BUN 87 mg/dl, Cr 4.53 mg/dl, T-Chol 174 mg/dl, HDL-Chol 49 mg/dl, Glu 156 mg/dl, Na 142 mEq/L, K 5.4 mEq/L, Cl 115 mEq/L. A urine specimen contained 1 + protein and 1 + glucose, and the sediments contained hyaline casts. A cranial CT scan was essentially same as that taken four years ago. His hospital course was complicated with pneumonia, congestive heart failure, and progressive renal failure. He was treated with intravenous fluid, chemotherapy, and other supportive measures, however, he expired from respiratory failure on April 30, 1995. He was discussed in a neurologic CPC, and the chief discussant arrived at the conclusion that the patient had Binswanger's disease in the brain, benign nephrosclerosis from arteriolosclerosis due to hypertension, congestive heart failure, and pneumonia. Opinions were divided regarding the question as to whether or not this patient had Binswanger's disease. Although his cranial CT scan revealed leukoaraiosis, his dementia and gait disturbance was only mild until his fall on March, 1995. Clinical features did not conform to those of Binswanger's disease. Postmortem examination of the right hemisphere revealed wide spread atherosclerosis and arteriolosclerosis. The kidney showed benign nephrosclerosis due to arteriolosclerosis. Sclerotic changes were also seen in the coronary arteries and the left middle cerebral artery with 70% stenosis. Myelin stain showed diffuse myelin pallor of the cerebral white matters with scattered small infarcts. Arterioles in the white matter showed arteriolosclerosis. Small infarcts were also seen in the putamen and in the thalamus. This patient appeared to have had circulatory disturbance of the white matter which is the basic abnormality causing Binswanger's disease. However, white matter changes in this patient were not quite severe enough to make a pathologic diagnosis of Binswanger's disease.
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PMID:[A 91-year-old man with a stroke, hypertension, and renal failure]. 899 Apr 84


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