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Query: UMLS:C0020473 (hyperlipidemia)
 15,891 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We reported a rare case of marked dilatation of the bilateral common carotid artery (CCA) associated with stenosis of the left middle cerebral artery (MCA). A 64-year-old female was admitted with right hemiparesis and dysarthria. She was hospitalized 2 years ago for cholecystitis. For 5 years, she has been under medical treatment for hypertension, diabetes mellitus, hyperlipidemia, cardiac failure associated with hypertrophic cardiomyopathy, and atrial fibrillation. Brain CT scan showed infarction of the left corona radiata. Angiography revealed marked dilatation of the bilateral CCA and the internal carotid artery (ICA), moderate dilatation of the innominate artery and the right subclavian artery, kinking of the right CCA, diverticular outpouching of the left ICA, and stenosis of the right external carotid artery and the left MCA. Breast CT scan revealed moderate dilatation and marked calcification of the ascending aorta and the aortic arch. Laboratory examination did not show any sign of inflammation, rheumatoid factor (RA), antistreptolysis-O (ASLO) and antinucleotic antibody. Based on the clinical course, radiological findings and laboratory data, possible diagnosis of the dilatation of the bilateral CCA was discussed with particular emphasis on arteriosclerotic aneurysm and aortitis syndrome.
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PMID:[Marked dilatation of the bilateral common carotid artery: a case report]. 773 79

Familial hyperlipidemia has received little attention as a possible cause of stroke in young patients. Some recent studies have demonstrated that lipoprotein (a) is a key factor for atherogenesis in familial hypercholesterolemia. Hypogonadism may also contribute to the elevation of serum lipids, but their influence as a risk factor for stroke is still less understood. A 34-year-old patient with heterozygous familial hypercholesterolemia presented with a left pure motor hemiparesis secondary to a right striatocapsular infarction. Arteriography showed atherosclerotic lesions in both internal carotid arteries. High levels of cholesterol, cLDL, apo B, and lipoprotein (a) were found. Clinical signs of hypogonadism were present and the karyotype led to the diagnosis of Klinefelter's syndrome (47,XXY). The early clinical course was excellent, and the levels of serum lipids were normalized with diet, lipid-lowering drugs and androgens. The importance of hyperlipidemia as a risk factor for stroke in the young, specially when it occurs in the context of familial hypercholesterolemia with elevated lipoprotein (a) levels, as well as the possible contribution of hypogonadism to the development of accelerated atherosclerosis in young patients, are discussed upon.
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PMID:[Striatocapsular infarct in a young patient with heterozygous familial hypercholesterolemia and Klinefelter's syndrome]. 828 24

We attempted to clarify the temporal profile and the predisposing factors for progressing neurological disorders in the patients with acute cerebral infarction in the territory of the deep perforators of the carotid system. The subjects were 19 patients with mild hemiparesis admitted to our hospital within 24 hours of stoke onset, and their mean age was 59.9 +/- 9.1. Six of those patients (about 32%) had gradual neurological deterioration after admission (progressive cases), and they had poor outcome compared with non-progressing patients. The mean progressing period was 3.7 +/- 1.0 days. Our examination suggest that both the changes in systemic hemodynamics and the risk factors for cerebrovascular disease (hypertension, diabetes mellitus, hyperlipidemia) do not always provide a correlation with the development of progressing stroke. However, we speculate that the impairment of the microcirculation plays a major role in progressing stroke in the territory of penetrating arteries because of the result that the mean infarct size of progressive patients had a tendency to be larger than that of non-progressive patients in the chronic stage.
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PMID:[Clinical course of acute deep infarcts in carotid system--pathogenesis of progressing stroke]. 1065 39

A 15-year-old woman with a history of transient dysarthria two years before, suddenly developed weakness of right upper extremity, right facial palsy, and dysarthria. She was admitted to our hospital on the third day. She had no hypertension, heart murmur and oedema. On neurological examination, she had mild right hemiparesis including face muscles and mild dysarthria. The right knee jerk was brisk with no Babinski's sign. Ataxia and sensory disturbance were not present. T2-weighted MRI showed a hyperintensity at the posterior limb of the left internal capsule. Cerebral angiography was unremarkable. Ultracardiography and 24-hour electrocardiography were normal. Laboratory data revealed no inflammatory findings, liver dysfunction, hyperglycemia and hyperlipidemia. Antinuclear and anticardiolipin antibodies were negative. Prothrombin time was normal, but activated partial thromboplastin time was slightly prolonged (35.4 sec, normal 25.2-34.4). Protein C, protein S and antithrombin III were normal. Heparin cofactor II (HC II) activity was decreased (44%) with normal HC II antigen (79%) and so she was diagnosed as heparin cofactor II deficiency type II (heparin cofactor II abnormality). Her father manifesting thromboangitis obliterans also had low HC II activity with normal HC II antigen. However, on her genetic analysis, we didn't detect any mutations in the coding region of HC II gene. Until now she has no recurrence of cerebrovascular attacks. On the basis of these results, we suspect that HC II deficiency was a possible risk factor of cerebral infarction in this case because she was so young and had no general risk factors except for HC II. No stroke associated with HC II deficiency type II has been reported up to date. This case is worth considering etiologies of juvenile cerebral infarction.
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PMID:[Juvenile cerebral infarction associated with heparin cofactor II abnormality. A case report]. 1096 62

We present the clinical manifestations of 4 male patients with acute stroke-like symptoms and polyneuropathy after long-term exposure to carbon disulfide (CS2) in a viscose rayon plant. The ages of onset of polyneuropathy ranged from 42 to 45 years with a duration of CS2 exposure between 6 and 21 years. The ages of onset of stroke were from 42 to 48 years. The risk factors for stroke including heart disease and diabetes were denied, except for smoking in 4, hyperlipidemia in 2 and hypertension in 1. At the initial visit in 1992, only 2 patients developed sudden onset of hemiparesis suggesting a lacunar stroke before the diagnosis of CS2 intoxication. Brain computed tomography (CT) scans showed low-density lesions in the basal ganglia in 2 patients, cortical atrophy in 1 and normal in 1. Brain magnetic resonance image (MRI) study disclosed multiple lesions in the corona radiata and basal ganglia on T(2)-weighted images in 3 patients and cortical atrophy in 1. After the diagnosis, they left their jobs for a CS2-free environment, and improvement of the working conditions was noted. During 5 years follow-up period, another 2 patients also developed an acute episode of stroke with hemiparesis. Brain CT and/or MRI follow-up studies in these 2 patients revealed new lesions in the basal ganglia and corona radiata. Intriguingly, a patient with previous stroke also developed new lesions in the bilateral thalami and brainstem. Carotid Doppler scan, transcranial Doppler scan and/or cerebral angiography did not show any prominent stenosis or occlusion in the major intracranial large arteries. We conclude that encephalopathy may occur in patients after long-term CS2 exposure, probably due to impaired cerebral perfusion. The lesions tend to occur in the basal ganglia, corona radiata and even brainstem, particularly involving the small-sized vessels. In addition, the cerebral lesions may progress even after cessation of CS2 exposure. Therefore, we suggest that CS2 exposure may be a risk factor for stroke.
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PMID:Carbon disulfide vasculopathy: a small vessel disease. 1130 75

Progressing stroke with neurological deterioration (PSND), i.e., neurological deterioration of patients during the first days following a stroke, although not an infrequent event, has hitherto been addressed only by few studies. This is the first investigation conducted in Israel with the aim to determine its prevalence and characteristics. Data regarding 140 patients with first ever stroke were collected prospectively between May 1999 and October 2000. All patients underwent a thorough daily neurological examination over the first 7 days, using the Canadian Neurological Scale. Most (90%), patients had hemiparesis, with dysarthria, aphasia and dysphagia being the most frequent associated neurological deficits. Thirty percent of the patients were on anti-aggregant therapy prior to the stroke. The prevalence of PSND was 23%. The 1-month in-hospital death rate of these PSND patients was 31%. Univariate analysis showed that previous anti-aggregant therapy, Parkinson's disease (PD), obesity, hyperlipidemia, and presence of aphasia were significantly more frequent in the PSND group. In addition, these patients arrived earlier to the emergency room. However, logistic regression analysis showed that only PD and obesity could possibly be considered as predictors for development of PSND. The prevalence as well as the death rate of PSND in this group of Israeli elderly is within the range reported in the literature. However, prior anti-aggregant treatment and PD, are here reported for the first time as associated conditions. Future research will possibly clarify the links between these entities and PSND.
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PMID:Progressing stroke with neurological deterioration in a group of Israeli elderly. 1591 Oct 42

We report 6 patients with Cheiro-oral syndrome (COS), with special reference to clinical features and responsible lesions. The time intervals from the onset of symptoms to arrival in our department were less than 24 hours in 3 patients, 2 days in 2, and 5 days in 1. All patients had subjective sensory disturbance involving the unilateral hand and ipsilateral perioral regions, and 4 patients presented with objective sensory disturbance. The body parts of tingling sensation tended to be larger than those of superficial sensory disturbance. Three patients developed motor disturbance including hemiparesis with or without ataxia, clumsiness of fine finger movements, and dysarthria. Magnetic resonance imaging revealed fresh infarctions around the thalamus, including lacunar infarctions in 5 patients and branch atheromatous disease in 1 patient. The lesion sites responsible for COS were ventral posterolateral (VPL) and ventral posteromedial (VPM) nuclei in the thalamus in 4 patients, thalamic pulvinar nucleus and medial geniculate body in 1, thalamic ventroposterior region-internal capsule-corona radiata in 1. Three patients had asymptomatic brain infarctions. Risk factors were hyperlipidemia, hypertension, diabetes mellitus, smoking, arteriosclerosis of the carotid artery, and polycythemia. In the convalescent stage, 5 patients suffered from residual sensory-motor disturbance, whereas 1 patient recovered from COS. COS has been attributed mainly to small infarctions in the thalamic ventroposterior nuclei. However, it is suggested that damage to ascending sensory fibers projecting to the thalamic VPL and VPM nuclei can cause COS. Because initial symptoms of COS are apt to be overlooked, early diagnosis and treatment are necessary to avoid residual sensory-motor disturbance.
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PMID:[A clinicoanatomical study of thalamic cheiro-oral syndrome]. 1652 19

A 41-year-old man with hypertension and hyperlipidemia who complained of left hemiparesis after a temporal headache was admitted to our hospital. A cervical MRI with gadolinium enhancement revealed an intramural hematoma is compatible with right extracranial internal carotid artery dissection. Two weeks later, he complained of sudden onset of pain in the right side of his neck. The right extracranial internal carotid artery dissection followed by the right extracranial vertebral artery dissection was diagnosed. Spontaneous cervical artery dissection (SCAD) is one of the causes of stroke in young adults. The pathogenesis of SCAD remains unknown. Minor trauma like an excessive sneeze, migraine, and connective tissue disorders such as fibromuscular dysplasia and Ehlers-Danlos syndrome are well-known as risk factors for SCAD. Pathologically skin collagen abnormalities have been seen in German patients with SCAD without clinical evidence for any specific connective tissue disorder. We examined the ultrastructural morphology of the Japanese patient's dermal connective tissue components by electron microscopy. The patient's collagen fibers contained fibrils with highly variable diameters, and there were other ultrastructural abnormalities, including flower-like fibrils and large-diameter composite fibrils. This is the first report of a case of ultrastructural abnormalities of dermal connective tissue in a Japanese patient with SCAD.
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PMID:[Skin collagen abnormalities in a Japanese patient with extracranial internal carotid artery dissection followed by extracranial vertebral artery dissection]. 1661 39

A retrospective cohort study was carried out of new referrals to transient ischaemic attack (TIA) clinics in Glasgow. The aims of the study were to describe the profile of referrals and to assess the odds ratios for TIA, minor stroke or amaurosis fugax of both cardiovascular risk factors and clinical features. In total, data were collected for 813 new referrals in a period of six months. Thirteen point eight percent of referrals were from other Health Boards. The overall referral rate among residents of Greater Glasgow NHS Board was 165.6 per 100,000 per year. About 20% of referrals were made by clinicians in secondary care. The specialties from which referrals were most commonly made were accident and emergency, general medicine, ophthalmology and geriatric assessment. The most common risk factors in patients referred were hypertension (52.9%), smoking (31.7%), ischaemic heart disease (22.7%) and former smokers (22.4%). The most common clinical features were hemiparesis (13.3%), weakness of an upper limb (8.7%), vertigo (7.9%) and dysphasia (7.3%). In 48.7% of cases, a non-cerebrovascular diagnosis was made. Separate multivariate models were established for risk factors and clinical features. In the model for risk factors, five factors were significant for risk of TIA, stroke or amaurosis fugax. These were hyperlipidaemia, age over 64 years, hypertension, smoking and ex-smoking. In the model for clinical features, five factors were also significant. These were visual field defect, speech defact, facial weakness and hemiparesis.
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PMID:Epidemiological aspects of referral to TIA clinics in Glasgow. 1737 16

We report a case of calcified aortic stenosis revealed by an ischemic stroke. An 81-year-old man with hyperlipidemia, hypertension and renal function impairment presented with acute onset of right-sided hemiparesis and aphasia. Head CT scan revealed a rounded calcified high-density mass within the distal segment of the left anterior cerebral artery, consistent with a calcified cerebral embolus, and an infarct in the left paracentral lobule. Transesophageal echocardiography demonstrated a sclerotic aortic valve. The patient was discharged from hospital on aspirin and atorvastatin, and the outcome was favorable. Calcified embolus remains a rare event and it has been not yet reported in the territory of anterior cerebral artery. It may be observed in aortic and mitral valve diseases, calcified plaques of the internal carotid artery and aortic arch. Renal failure promotes their development and is the cause of cardiovascular diseases. To date, aortic valve calcification is not considered as a marker of stroke risk, except when associated with severe stenosis or left ventricular hypertrophy.
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PMID:[Stroke due to spontaneous calcified cerebral embolus as presenting feature of calcified aortic stenosis]. 1845 37


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