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

Serum lipoproteins were determined 8-12 weeks after the onset of ischemic cerebro-vascular disease (ICD) in 61 patients, 38 males and 23 females, before the age of 55. The results were compared with those of a matched control material. The diagnosis was based on clinical findings, CSF spectrophotometry, computer tomography, and angiography. Hyperlipoproteinemia was no common finding in these young and middle-aged patients with ICD. The normal mean total serum cholesterol concentration was the result of a slight increase in VLDL cholesterol and a concomitant HDL cholesterol reduction. In men, the HDL cholesterol concentration was lower than expected for any VLDL-TG concentration. The mean value of the HDL cholesterol concentration in the patients was 18% lower than in the control group. On agarose electrophoresis the lipoprotein variants "late prebeta", "sinking prebeta" and "rapid beta" lipoproteins could be demonstrated in the same frequency as in controls. There was no significant correlation between the degree of atherosclerosis, estimated by angiography, and any serum lipoprotein fraction. Several recent studies have stressed the importance of a low HDL concentration as an independent risk factor for atherosclerosis. The decreased HDL cholesterol levels found in the present material require further attention to the possible beneficial role of HDL in ICD.
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PMID:Dyslipoproteinemia in patients with ischemic cerebro-vascular disease: a study of stroke before the age of 55. 20 3

In a large autopsy series of elderly individuals, organic dementia was attributed to (pre-) senile atrophy in 52.8%, to cerebrovascular disease in 22.5%, while 13.6% were of mixed senile and vascular origin, and 1.3% showed communicating hydrocephalus with meningopathies or were of undetermined origin. A survey is given of the morphological criteria of dementia resulting from disorders of cerebral blood supply and CSF circulation. The anatomic basis of vascular dementias are: atherosclerotic encephalopathy with lacunar state or multiple infarcts; granular cortical atrophy resulting from local microcirculation disorders; hypertensive cerebrovascular disease with the common "mixed" cortico-subcortical type, and the rare Binswanger's subcortical type. Atypical cerebral hemorrhage in old individuals rather results from congophilic (amyloid) angiopathy than from hypertensive arteriosclerosis. Multiple infarct dementia may also result from thrombotic microangiopathy, thromboembolic disease or cerebral vasculitides. The anatomical features of dementia associated with communicating "normal-pressure" hydrocephalus (NPH) are meningopathy at the basis or on the convexity, and fibrosis of the choroid plexus and/or arachnoid villi of post-inflammatory or undetermined origin, and other non-specific changes (periventricular gliosis). This condition is also associated with hypertensive cerebrovascular disease and Alzheimer's disease. Cerebral biopsies in NPH as well as in other types of hydrocephalus show enlarged extracellular spaces with otherwise normal neuropil probably resulting from increased transcapillary filtration. In some cases of "idiopathic" NPH no causative anatomical changes are found. The relationship between cerebral tissue changes, abnormal blood and CSF dynamics in these conditions remains to be clarified.
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PMID:Neuropathological aspects of dementias resulting from abnormal blood and cerebrospinal fluid dynamics. 96 75

The clinical manifestations of 20 cases of insular cistern hematoma were characterized by sudden onset violent headache, vomiting, bloody CSF, and subhyaloid hemorrhage (1/3 cases). CT scan showed semilunar high density image centering on the insular cistern with serrate internal edge. The average volume of the hematoma was 20 ml. By means of cerebral angiography, operation and/or autopsy, 7 cases were identified as aneurysm of middle cerebral artery, 6 as aneurysm of posterior communicating artery, and 2 as amyloid angiopathy. In the other 5 cases, the etiology was unknown.
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PMID:Insular cistern hematoma. A special type of subarachnoid hemorrhage. 128 72

A 49-year-old male was admitted to our hospital because of severe headache and dizziness which had occurred suddenly one day before admission. There was no past history contributory to cerebral hemorrhage but was family history of cerebrovascular accidents in his father and brother. Neurological examination revealed left homonymous hemianopsia, mild left hemiparesis, and left side hemi-neglect in simultaneous stimuli on bilateral extremities. Laboratory data including peripheral blood cells, coagulation tests, and serum chemistry were unremarkable. Brain CT and MRI demonstrated large lobar hematoma in the right parieto-occipito-temporal region. Cystatin C level in the CSF samples taken on the 39th and 59 th days (38 and 27 ng/ml respectively) were low, compared with the normal value (greater than 100 ng/ml). These findings suggest that the lobar cerebral hemorrhage of the present case might have been caused by cerebral amyloid angiopathy with cystatin C deposits.
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PMID:[A case of lobar cerebral hemorrhage with low concentration of CSF cystatin C]. 191 34

12 pathologically verified cases of cerebrovascular leptospirosis were analysed of its clinical characteristics and types. Formation and development of cerebral panarteritis and infarctions were also discussed. It occurred in rural areas among children and adolescents after infection by leptospira pomona, especially following latent infection. Multiple occlusive vascular disorder presenting as a late manifestation of pomona infection occurred in 9 cases, intracranial hemorrhage in 2, and intracranial hypertension in 1 case. Cerebral panarteritis involved the main trunks of larger arteries at the base of the brain. Owing to invariable narrowing of intracranial portions of internal carotid arteries, infarcts always appeared in areas supplied by the middle cerebral artery, often accompanied by marginal infarction at watershed areas. It was suggested that cerebrovascular leptospirosis could be ascribed to residual infection of cerebral arteries soaked in CSF during the septicemic stage of pomona infection.
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PMID:[A clinicopathological analysis of 12 cases of cerebrovascular leptospirosis]. 225 11

Morphological study of the choroid plexuses of two patients with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS) revealed an enormously increased number of mitochondria with structural abnormalities in almost all of the choroidal epithelial cells. The majority of the cells also showed loss of microvilli and collapsed or attenuated apical cytoplasmic processes with increased electron density and lysosome-like dense bodies. The blood vessels of the choroid plexus showed the features of mitochondrial angiopathy previously described in the pial arteries of the same patients. These findings are interpreted as the morphological expression of a primary biochemical defect of the mitochondrial function in the choroid plexus, and as the probable explanation for increased CSF lactate and pyruvate levels in this disease.
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PMID:Involvement of choroid plexus in mitochondrial encephalomyopathy (MELAS). 343 8

We report here two cases of isolated angiitis of the central nervous system associated with congophilic angiopathy. The clinical history lasted 9 months in the first patient (65 years old) and 9 years in the second patient (59 years old). It was characterized by progressive intellectual deterioration, increased protein content of the CSF and evidence of focal brain lesions in the CT scan. One patient showed chronic intracranial hypertension. Vascular lesions were limited to the brain and were characterized by granulomatous and necrotizing angiitis of the small leptomeningeal and intracortical vessels. Amyloid deposits were present in large amounts along vascular segments showing vasculitis, in foreign body giant cells, in plaque-like structures surrounding diseased perforating arterioles, along cortical microvessels and in many neuritic plaques. Close proximity and topographic overlap of vasculitis and amyloid changes suggest a possible pathogenetic relationship.
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PMID:Amyloid angiopathy combined with granulomatous angiitis of the central nervous system: report on two patients. 407 38

The onset of multiple sclerosis (MS) after age 60 is uncommon. The clinical features of three such cases are described. Considerable diagnostic delay was seen in each case as symptoms were initially attributed to other conditions that more commonly afflict the elderly, including atypical facial pain, neuropathy, peripheral and cerebral vascular disease, arthritis, benign prostatic hypertrophy, and ischemic optic neuropathy. Although MS should be considered a diagnosis of exclusion in this age group, cerebral evoked potentials and CSF immunoglobulin studies can increase the diagnostic yield and may be helpful in the appropriate clinical context.
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PMID:Multiple sclerosis with onset after age 60. 619 35

Data from 11 observed patients with spontaneous pontine haemorrhages were compared to the findings in 235 cases reported in 9 studies. Causes of pontine haemorrhages which have an incidence of 2 to 4/100 000/year include hypertension, vascular malformations (a.v.-haemangioma, cavernous haemangioma, capillary teleangiectasies), anticoagulative treatment and inflammatory vascular disease. Diffusely spreading hypertensive haemorrhages are of apo-plectiform onset with fast developing coma, and show disturbance of vegetative function (disturbance of respiration, cardiac dysrhythmias, hyperthermia, hypertension), miosis and other neuroophthalmologic symptoms, flaccid tetraparalysis and blood-stained cerebrospinal fluid; mortality is high, reaching 50% after 24 hours and 90% after 3 weeks. Vascular malformations are the origin of circumscribed pontine haematomas with slowly progressing disturbance of consciousness and brain stem symptoms with variable course exhibiting multiple remissions and recurrences. In respect of symptomatology and clinical course, slight lateral hypertensive pontine haemorrhages must be placed between these two typical syndromes. Diagnosis of pontine haemorrhages is supported by x-ray computed tomography, but vascular malformations can be detected only by cerebral angiography. Treatment of patients with pontine haemorrhages must be based on intensive care with regular control via CT. Increased intracranial pressure and internal hydrocephalus caused by blockage of CSF passage necessitate ventricular drainage. While hypertensive pontine haemorrhages cannot be surgically treated, pontine haematomas and the causative vascular malformations can be removed.
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PMID:[Spontaneous pontine hemorrhage]. 647 27

Congenital errors of folate metabolism can be related either to defective transport of folate through various cells or to defective intracellular utilization of folate due to some enzyme deficiencies. Defective transport of folate across the intestine and the blood-brain barrier was reported in the condition 'Congenital Malabsorption of Folate'. This disease is characterized by a severe megaloblastic anaemia of early appearance associated with mental retardation. Anaemia is folate-responsive, but neurological symptoms are only poorly improved because of the inability to maintain adequate levels of folate in the CSF. A familial defect of cellular uptake was described in a family with a high frequency of aplastic anaemia or leukaemia. An isolated defect in folate transport into CSF was identified in a patient suffering from a cerebellar syndrome and pyramidal tract dysfunction. Among enzyme deficiencies, some are well documented, others still putative. Methylenetetrahydrofolate reductase deficiency is the most common. The main clinical findings are neurological signs (mental retardation, seizures, rarely schizophrenic syndromes) or vascular disease, without any haematological abnormality. Low levels of folate in serum, red blood cells and CSF associated with homocystinuria are constant. Methionine synthase deficiency is characterized by a megaloblastic anaemia occurring early in life that is more or less folate-responsive and associated with mental retardation. Glutamate formiminotransferase-cyclodeaminase deficiency is responsible for massive excretion of formiminoglutamic acid but megaloblastic anaemia is not constant. The clinical findings are a more or less severe mental or physical retardation. Dihydrofolate reductase deficiency was reported in three children presenting with a megaloblastic anaemia a few days or weeks after birth, which responded to folinic acid. The possible relationship between congenital disorders such as neural tube defects or dihydropteridine reductase deficiency and disturbances of folate metabolism are discussed. Neurological symptoms present in most of these congenital disorders highlight the role of folate in the central nervous system.
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PMID:Congenital errors of folate metabolism. 853 63


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