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PubMedDate not supplied

A congenital syndrome of mental deficiency, gait disturbance, sensorineural deafness and pigmentary retinopathy associated with premature atherosclerosis.

Many neurological disorders have been described in combination with sensorineural hearing loss and pigmentary retinopathy. We present the clinicopathological case of such a combination, associated with premature atherosclerosis of large cerebral arteries. In the literature dealing with the combination of deafness and pigmentary retinopathy, none of the many described syndromes was associated with premature atherosclerosis. The mitochondrial myopathy, encephalopathy, lactic acidosis, early atherosclerosis and stroke-like episodes (MELAS) syndrome can include deafness and blindness. In this syndrome small cerebral arteries are affected. In our case we did not find electron microscopic evidence of mitochondrial myopathy. Also the syndrome with encephalopathy, deafness, blindness and ataxia in young women is attributed to microangiopathy with small brain infarcts and retinal infarcts. In contrast, in our case, large cerebral arteries are affected. In the reverse order, none of the conditions with early atherosclerosis has been reported in combination with sensorineural deafness and pigmentary retinopathy. There is some similarity of our case to cases of Usher syndrome, type II. In the Usher syndrome, plasma lipid disturbances have been described and neuroradiological evidence of decreased circulation in the posterior cerebral circulation has been published. We suggest that in cases of congenital or acquired oto-ophthalmo-neurological disease the cerebral circulation and the lipid metabolism should be analyzed.

Arteriosclerosis↗
PubMed2004

The prostacyclin analogue beraprost sodium prevents development of arterial stiffness in elderly patients with cerebral infarction.

Prostacyclin (PGI(2)) inhibits platelet aggregation, smooth muscle cell proliferation, and vasoconstriction. Arterial stiffness assessed by pulse wave velocity (PWV) predicts mortality in various cardiovascular diseases. To study the preventive effects of a prostacyclin analogue, beraprost sodium, on arterial PWV values in elderly patients with cerebral infarction. Forty-four patients with a history of cerebral infarction received beraprost sodium (120 microg/day p.o.) or no beraprost sodium (control) for 3 months. Arterial PWV and ankle brachial indices (ABI) were determined prior to starting the medication and after 3 months of medication. Initially, there were no differences in age, blood pressure, and body mass index. Further, PWV or ABI did not differ between the beraprost sodium group (n = 22) and the control group (n = 22). After 3 months, PWV in beraprost sodium group was significantly reduced (-123 +/- 282) when compared with the control group (147 +/- 274)(P = 0.006). ABI was not significantly different when comparing the two groups at 3 months. Long-term administration of beraprost sodium prevents the decline in arterial biomechanics in elderly patients with cerebral infarction.

Administration, Oral↗
PubMed1984

[Staged or bilateral malacias in the area of the middle cerebral or posterior cerebral arteries. Comparative study of the risk of multifocal stroke in 120 patients].

We studied and compared 120 cases with an infarction in the superficial area of the middle cerebral artery (MCA) or the posterior cerebral artery (PCA). Among the patients with an infarction of the MCA area, 8% had a capsular involvement and 3% a delayed contralateral sylvian infarction. Among the patients with an infarction of the PCA area, 35% had a thalamo-mesencephalic involvement and 23% a delayed contralateral occipital infarction. Thus, multifocal infarction was significantly more frequent in the PCA area than in the MCA area. No particular vascular risk factor could explain this difference, which may be related to general constitutional factors, such as the type of collateral supply or the vascular anatomy itself. In the PCA area only, we found a significant association between the severity of risk factors and occurrence of multifocal infarction.

Aged↗
PubMed1995

Apolipoprotein(a) deposition in atherosclerotic plaques of cerebral vessels. A potential role for endothelial cells in lesion formation.

Atherosclerosis is the leading cause of death and serious morbidity in economically developed societies through its sequelae of coronary artery and cerebrovascular disease. The causes and mechanisms of atherosclerosis are still largely unknown. Serum levels of a lipoprotein, Lp(a), have been shown, in retrospective and some prospective clinical studies, to be associated with increased risk of myocardial and cerebral infarction. The active part of Lp(a), apo(a), has > 80% homology with plasminogen; thus it may competitively inhibit the thrombolytic action of plasminogen and enhance thrombogenesis. Lp(a) has been shown to be deposited in the vascular wall of the aorta and coronary vessels, but its presence in the cerebral vessels has not yet been shown. Autopsy specimens of vessels of the circle of Willis from 23 patients were examined for degree of atherosclerosis and deposition of apo(a) by immunohistochemistry with apo(a)-specific monoclonal antibodies. The amount of apo(a) deposition in cerebral vessels correlated well with the degree of cerebral atherosclerosis. Arterial deposition of apo(a) was found entirely within the endothelial cell and subendothelial cell layers. There was no staining within the media and adventitia, with the exception of staining within the endothelial cells of the vasa vasorum. Correlation between the morphology of apo(a) deposition and plaque stage was found suggesting that detection of apo(a) in endothelial cells is an early event in the development of the atherosclerotic plaque of cerebral vessels.

Adult↗
PubMed1993

Associations of serum total cholesterol, different types of stroke, and stenosis distribution of cerebral arteries. The Akita Pathology Study.

BACKGROUND AND PURPOSE: The relation between serum total cholesterol levels and stroke is controversial. The Akita Pathology Study provides data on the association of serum total cholesterol, different types of stroke, and distribution of stenosis in cerebral arteries. METHODS: The data are based on 750 autopsied men aged 30 years and older who were admitted to a local hospital in northeast Japan between 1966 and 1984. The overall autopsy rate was 88%. The grade of stenosis in the cerebral arteries was determined blindly by one pathologist using Baker's method for basal cerebral arteries (atherosclerosis scores) and using microscopic examination of a single basal ganglion slide for the intracerebral penetrating arteries (arteriolosclerosis scores). RESULTS: The age-adjusted mean value of serum total cholesterol concentration was 164 mg/dL for cerebral hemorrhage, 177 mg/dL for infarction in penetrating artery regions, and 200 mg/dL for infarction in cortical artery regions. Mean serum cholesterol was lower in deaths caused by cerebral hemorrhage than in those caused by myocardial infarction and other cardiovascular disease. Mean atherosclerosis score of basal cerebral arteries was low for cerebral hemorrhage, intermediate for penetrating artery infarction, and high for cortical artery infarction. Stenosis of both basal and penetrating arteries was minimum or absent in cases of cerebral hemorrhage. Only the basal arteries were stenotic in cases of cortical artery infarction, whereas both basal and penetrating arteries were stenosed in cases of penetrating artery infarction. There were positive associations of serum cholesterol with stenosis of basal and penetrating arteries. Among cases of cerebral hemorrhage, serum total cholesterol levels were even lower in men with no significant stenosis in either basal or penetrating arteries than in men with stenosis in either type of artery. CONCLUSIONS: The association of serum cholesterol with pathogenesis varies among stroke types. Elevated serum cholesterol levels were associated with the presence of cortical artery infarction, while low serum cholesterol levels were associated with cerebral hemorrhage.

Adult↗
PubMed1975

[Participation of smooth muscle cells in the formation of atherosclerotic plaques].

A study of the participation of the smooth muscle cells in the formation of atherosclerotic lesions was made on the autopsy material with the use of specific antiserum to the smooth muscle actomyosin and of indirect Coons' method. Typical forms of atherosclerotic lesions in the aorta, cerebral vessels and coronary arteries were studied. Smooth muscle cells were detected in the thickened intima alongside the atherosclerotic lesions, in fatty streaks, in the fibrous tissue of the atherosclerotic plaque, but they were not found in the atheromatous masses. The proliferation and migration of the smooth muscle cells is regarded as an essential factor in the pathogenetic mechanisms of atherosclersis.

Aorta↗