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Query: UMLS:C0042373 (vascular disease)
 17,070 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The most important morphological findings in dementia of Alzheimer type (DAT) are Alzheimer neurofibrillary tangles, senile plaques, amyloid angiopathy, granulovacuolar degeneration and Hirano bodies. The morphological and immunocytochemical findings in these changes are described, in particular those related to the pathological cytoskeleton. Their possible relationship to the disturbed synthesis of neurotransmitters recently demonstrated is considered, and their relevance for the clinical syndrome of dementia is discussed. Hypothetical etiologies (ageing per se, genetics, infection and chronic intoxication) are briefly mentioned.
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PMID:Dementia of Alzheimer type (DAT)--a review of its morbid anatomy. 300 58

We studied cerebral amyloid deposits in the hippocampal area immunohistochemically, using antiserum to synthetic beta peptide (1-28) in 66 patients with or without dementia and aged 17 to 91 years old. Senile plaques (SP) and amyloid angiopathy (AA) were detected in 36 (55%) and 19 (29%) patients, respectively. Also, cerebral amyloid deposits from the brains of seven patients with dementia and five patients without were studied in serial sections stained with Bodian, modified Bielschowsky, Congo red, and beta protein immunostain. In the patients with Alzheimer-type dementia (ATD) diffuse plaques, typical of this group, were stained with beta protein antiserum but not with Bodian stain, because the plaques were devoid of abnormally swollen neuritic processes. The diffuse plaques often contained one or more neuronal cell bodies. As well as primitive and classic plaques and AA, the beta protein immunostain demonstrated small deposits among the SP, small stellate deposits of layer 1, subpial fibrillar deposits, and focal cribriform deposits of parasubiculum, which may be new types of amyloid deposits. Amyloid plaques within the subcortical white matter were only found in ATD brains. In the non-demented patients various kinds of SP, including diffuse and compact ones, were immunostained. They tended to be small and few. beta protein immunostain with formic acid pretreatment is a useful method for the identification of a variety of senile cerebral amyloid deposits.
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PMID:A variety of cerebral amyloid deposits in the brains of the Alzheimer-type dementia demonstrated by beta protein immunostaining. 305 48

We investigated amyloid deposition in the brain and other organs in 105 consecutive autopsy cases, aged 59 to 101 years. They consisted of two groups; 15 patients with dementia of Alzheimer type (DAT) and 90 patients without DAT. Amyloid deposition was found in 93% of all cases. The incidence of amyloid deposition increased with age. The number of organs affected with amyloid deposition in each case also increased with age. The incidence of amyloid deposition in each organ was as follows; 88% in pituitary gland, 66% in brain [amyloid of senile plaque (SP) (61%) and/or cerebral amyloid angiopathy (CAA) (56%)], 33% in pancreas, 3% in heart, and less in others. In immunohistochemical studies using the antisera to the various kinds of amyloid or related proteins, amyloid beta protein was demonstrated in brain amyloids including SP and CAA, but not in others. Cardiac amyloid was positive for prealbumin. Pituitary amyloid and CAA were positive for amyloid P-component. The incidence of brain amyloids in DAT were significantly higher than that in non-DAT. There was no significant difference in the incidence of pituitary and pancreatic amyloid between DAT and non-DAT. In the non-DAT patients, there were significant positive correlations in amyloid deposition between the brain and pituitary gland and between the brain and pancreas. Acceleration of amyloid deposition would be a process confined to the brain in the patients with DAT. The pathogenesis of the accelerated deposition of brain amyloids is discussed from the point of view of amyloidosis.
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PMID:Systemic amyloid deposition in old age and dementia of Alzheimer type: the relationship of brain amyloid to other amyloid. 306 4

Central white matter lucencies are commonly seen in CT scans of elderly patients. Reports in the literature have implicated demyelination due to subcortical vascular disease (Binswanger disease) as the cause of these lucencies. Binswanger disease, however, is thought to be rare. Because of this apparent discrepancy we decided to determine the incidence and to attempt to define the clinical significance of the CT white-matter changes in a study population at New York University Medical Center. The studies of 275 normal and demented subjects, ages 23 to 85 years, were reviewed. All subjects received neurologic, psychiatric, and medical evaluation, formal psychometric evaluation of their cognitive status, and a CT scan. CT scans were evaluated for the presence and severity of white-matter changes (leukoencephalopathy). The incidence and severity of white-matter changes increased significantly with age (p less than 0.01). Leukoencephalopathy was consistently more common in demented patients than in normal subjects, but the difference was not statistically significant, and the severity of the leukoencephalopathy was not related to the severity of dementia (p less than 0.05). Five patients (ages 74 to 95 years) with a clinical diagnosis of Alzheimer disease who had CT evidence of lucencies were examined at autopsy. Neuropathology demonstrated extensive changes of Alzheimer disease in one brain and mild-to-moderate changes in the other four brains; areas of white-matter rarefaction were present in all brains, with microscopic evidence of arteriolar hyalinization. This study demonstrates that leukoencephalopathy is strongly related to the aging process and is seen in both "normal" and cognitively impaired individuals who have no other evidence of vascular disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Leukoencephalopathy in normal and pathologic aging: 1. CT of brain lucencies. 308 33

Clinical and neuropathologic evidence points to the development of Alzheimer's disease (AD) in seven Down's syndrome patients above age 40. Dementia was observed in these patients over periods of 2.5 to 9.2 years. The first clinical sign of AD, visual memory loss, was succeeded by impaired learning capacity and decreased occupational and social functioning, and culminated in seizures and urinary incontinence. The morphometric observations of the brains of these seven patients with AD showed that the numbers of plaques and tangles exceeded 20 per 1.5 X 10(6) microns2 area, in both the prefrontal and hippocampal cortices. Plaques and tangles were also evident in the basal ganglia, thalamus, hypothalamus, and midbrain. In addition, we found that four of the seven brains showed small strokes, and five of the seven amyloid angiopathy. This study also indicates that by longitudinal neuropsychological evaluations and lab tests, which exclude other causes of dementia, the diagnosis of AD can be made even in severely and profoundly retarded patients.
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PMID:Alzheimer's disease in Down's syndrome: clinicopathologic studies. 315 74

With immunohistoperoxidase techniques the presence of plasma (serum) proteins was investigated in senile plaques, congophilic angiopathy, neurons and glial cells in brains of patients with Alzheimer's dementia. Other investigators have found plasma proteins in brain parenchyma and suggested that blood-brain barrier dysfunction might be a primary factor in the pathogenesis of Alzheimer's dementia. These studies were performed on formol-fixed brains of patients with Alzheimer's dementia. In the present study we investigated both frozen and formol-fixed brain tissues. The influence of post-mortem delay, prolonged formol fixation and differences in clinical course on detection of plasma proteins by immunocytochemical techniques was also studied. Findings in cases with Alzheimer's dementia were compared with findings in nondemented controls with or without neurological disorders. Plasma proteins could not be demonstrated in the neuropil of a number of patients with Alzheimer's dementia. Moreover, plasma proteins were also found in neuronal cells and astrocytes in brains of nondemented controls. We discussed whether or not cytochemical detection of plasma proteins in the neuropil of post-mortem obtained brains is a reliable technique to investigate blood-brain barrier dysfunction. In our opinion there are, at the moment, no convincing arguments for blood-brain barrier dysfunction in Alzheimer's dementia.
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PMID:Lack of evidence for dysfunction of the blood-brain barrier in Alzheimer's disease: an immunohistochemical study. 318 57

Vascular dementia results from ischemic injury to the brain. Depression is a frequent complication of cerebrovascular dementia (CVD) occurring in 25 to 80% of patients during the course of their illness. Depression is unrelated to the severity of intellectual compromise or to the co-existence of delusions. The symptom profile of depression in CVD is indistinguishable from that of late-onset idiopathic major depressive episodes. The frequency of depression differs with the subtype of CVD and is most common in disorders with lesions of the frontal lobes, either cortical or subcortical. In addition to lesion site, other contributors to depression in CVD include vascular disease of other organs, drug therapy of co-existing medical conditions, and psychological reactions to disability. The depression of CVD responds to treatment with antidepressant agents.
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PMID:Depression in vascular dementia. 322 47

We report here two autopsied cases of patients who had been in a longstanding bedridden state from cerebrovascular dementia. They showed a clinical history of persistent hypertension, a history of acute strokes, a lengthy clinical course with long plateau periods and a gradual accumulation of focal neurological symptoms and signs, including dementia and prominent motor disturbances and pseudobulbar palsy. They had been in a bedridden state for the last several years and had to be fed. The pathology seemed to predominently affect the perforating vessels to the subcortical gray and white matter. Demyelination, loss of axons, patchy gliosis and infiltration by macrophages were noted in the involved regions. The long penetrating vessels of the white matter showed advanced arteriosclerotic changes. There was a relative sparing of the cortex. The low attenuation of the white matter with moderate to severe atrophy, and an infarction might well be significant features on a CT-scan of these conditions. One of the possible mechanisms on the pathogenesis of chronic vascular disease includes diffuse ischemia related to hypertensive vasculopathy.
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PMID:Diffuse white matter involvement seen in patients in longstanding bedridden state from cerebrovascular dementia. 324 76

Many disorders--including vascular disease, alcoholism, Huntington's disease, drug toxicity, metabolic disorders, brain tumors, depression, and other psychiatric disorders--can cause dementia. Moreover, 50% of all dementia patients have Alzheimer's disease. Guidelines have been established to define the types of dementia. A detailed history, which may note previous depression, and a physical examination are essential. Assessment of the patient's mental status and a neurological examination may help to distinguish other forms of dementia from Alzheimer's disease. Brain imaging and psychometric testing may also help to establish a diagnosis. Metabolic screening for reversible causes of dementia, such as thyroid disturbance or electrolyte-imbalance, is essential. Common features of Alzheimer's disease include memory loss; difficulty with problem solving, abstractions, and calculations; and language and visuospatial deficits. Delusions are common in the early phase of the disease. It is not yet possible to diagnose Alzheimer's disease with complete accuracy. Additional neurophysiological and biochemical markers for diagnosis must be developed.
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PMID:Dementia update: diagnosis and neuropsychiatric aspects. 328 27

The efficacy of magnetic resonance imaging (MRI) in the diagnosis of diseases of the central nervous system is reviewed. MRI, computed tomography (CT) and certain radionuclide studies are compared in the evaluation of intracranial tumours, cerebral vascular disease, multiple sclerosis and other white matter diseases, dementia, head injury, infection, epilepsy, spinal lesions and in paediatric central nervous system disorders. The measurement of cerebrospinal fluid volumes and dynamics by MRI is discussed. MRI most clearly has advantages where CT is degraded by bone hardening and streak artefacts (spine, skull base, posterior and temporal fossa, sella and parasellar regions) and in diseases in which the X-ray attenuation of the suspected lesion differs little from normal parenchyma (paediatric brain disorders, demyelination and dysmyelination, early oedema associated with infarction, infection or low-grade infiltrating neoplasm, subacute and chronic haemorrhage and lesions in the spinal subarachnoid space and cord). Elsewhere MRI and CT should be seen as complementary rather than competitive methods of imaging. In spite of an absence of information about the contribution of MRI to management decisions and a lack of rigorous, prospective controlled trials, MRI will play an increasing role in the diagnosis of diseases of the central nervous system.
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PMID:Magnetic resonance imaging of the brain and spine. 328 26


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