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Query: UMLS:C0004153 (atherosclerosis)
 77,401 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The diagnosis of occlusion of the intradural vertebrobasilar artery (OIDVBA) was made by means of cerebral angiography in 22 patients. The clinical presentation, course and followup were studied in conjunction with the angiographic findings in each case and the following conclusions made. OIDVBA is not rare. It occurs one-fourth as often as occlusion of the carotid artery. The correct diagnosis is not made clinically before angiography in the majority of patients. Complete visualization of the neck and intracranial vasculature is necessary to document the occlusion. Atherosclerotic thrombosis is the most common type of occlusive lesion. The most common predisposing factors are atherosclerosis, hypertensive cardiovascular disease, diabetes mellitus, and developmental vertebrobasilar hypoplasia. Most patients with occlusion are in the 7th and 8th decades of life and transient attacks of vertebrobasilar ischemia precede the occlusion in one-half of the cases. Emboli usually lodge in the terminal portion of the basilar artery whereas thrombotic occlusions tend not to be located in a characteristic segment. A majority of patients diagnosed angiographically survive their OIDVBA, but most distal occlusions result in death, often following several weeks of coma. In the surviving majority, disturbance of gait, impairment of vision, and symptoms of transient vertebrobasilar ischemia are the most common sequelae.
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PMID:Occlusion of the intradural vertebrobasilar artery. 63 67

A 44-year-old trained marathon runner collapsed after completing 24 miles of the 1973 Boston Marathon. He was resuscitated from ventricular fibrillation. Death occurred after 50 days of coma. Extensive transmural anterior myocardial infarction was documented on electrocardiogram and proved at autopsy, yet the coronary arteries were free of significant atherosclerosis. We believe this report to be the first documentation of a myocardial infarction in a trained athlete while participating in a marathon. We emphasize that the relation between exertion and infarction is unknown. Advocates of long distance running for prevention of, or rehabilitation from, ischemic heart disease should be aware of this possible complication.
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PMID:Fatal myocardial infarction in marathon racing. 93 83

The victim, 52 year old man, was thrust down and hit his left occiput against the concrete floor. He was hospitalised and his comatose state continued to the death. On admission, blood pressure was 212/110 mmHg and the computed tomography scan of the head showed only an extensive right subdural hematoma. But the intracerebral hemorrhages in the right frontal, temporal and parietal lobes were recognized 10.5 hours after the trauma. A subdural hematoma was evacuated by operation on the second hospital day. The intracerebellar hemorrhage also appeared 16 hours after the trauma. Blood pressure fluctuated between 160/80 and 200/110 mmHg. The photo of CT scan at 38.5 hours after the trauma showed little subdural hematoma and new intracerebral hemorrhage located in the left temporal lobe. On the third hospital day, he was equipped with a respirator and blood pressure was between 132/84 and 242/100 mmHg. The reaction of the pupils to light disappeared on the 8th hospital day. Blood pressure gradually decreased on the 9th and 10th hospital days and he died on the 11th day. Autopsy revealed a bruise in the left occiput, a linear fracture in the frontal and left parietal bones and a small amount of subdural hematoma on the surface of the right cerebral hemisphere. Cortical contusions were found in the right frontal, the both temporal and the left parietal lobes. Intracerebral hemorrhages were found in the right frontal, the both temporal and the right parietal lobes. Intracerebellar hemorrhage was also found. Cardiac hypertrophy and atherosclerosis of the aorta were recognized. We thought that small hemorrhages which were not clearly detectable by CT scan immediately after injury may have developed into massive intracerebral and intracerebellar hemorrhages due to high blood pressure after a hospitalization.
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PMID:[Traumatic intracerebral hemorrhage developing in the apparent course]. 192 Sep 31

Intraluminal clot of the internal cervical carotid artery is commonly thought to require emergency surgery: 7 intraluminal clots specially threatening (6 of whom had a long defect--15 mm and more) are demonstrated by intraarterial digital angiography--4 patients experienced mild stroke, 3 major stroke. 3 of whom had previous recurrent T.I.A. (3 transient blindness, 1 hemispheric TIA). Carotid angiography identified 3 severe atherosclerotic stenosis, 3 ulcerated plaques and 1 dissection. One patient with coma carus died quickly. Anticoagulation therapy (6 cases) was made, 4 weeks along, without neurologic complications. Follow-up angiograms showed total resolution (4 cases), partial lysis (1 case) and mild extension (1 case). Delayed endarterectomy was made only for severe carotid atherosclerosis (5 cases). In our experience, intraluminal clot of the carotid artery may not be a surgical emergency but require anticoagulant therapy and delayed surgery if major underlying lesions.
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PMID:[Intraluminal thrombosis of the cervical internal carotid artery]. 207 76

Duplication or fenestration of the basilar artery, a result of an embryologic malformation, has an incidence of up to 5.3% in the general population. The most common complication of this anomaly is the formation of aneurysms. Thrombosis of a partially duplicated basilar artery developed in a 43-year-old man who complained of visual disturbances followed by seizures and coma, and who eventually died. Autopsy showed a partially organized thrombus occluding both halves of a duplicated portion of the basilar artery, old infarcts in the calcarine cortices, and a recent large infarct in the basis pontis. There was only minimal atherosclerosis of other intracranial arteries, including the vertebral arteries. Hemodynamic disturbances and turbulent blood flow at the site of fenestration may be the cause of the thrombosis that occurred in this artery.
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PMID:Segmental duplication of the basilar artery with thrombosis. 334 42

We retrospectively analyzed the records of 63 consecutive patients with spontaneous intracerebral hemorrhage (ICH) who had been treated in our neurological intensive care unit from 1981 to 1985 (aged 17 to 84 years). In this sample, the prognostic value of initial clinical and laboratory findings was studied. The following factors were significantly correlated with mortality: concomitant cardiac failure, general atherosclerosis, and chronic obstructive pulmonary disease; coma or deranged brainstem reflexes on admission; concomitant intraventricular or subarachnoid hemorrhage, hydrocephalus and midline shift on CT scan. ICH location did not significantly correlate with outcome. Among lobar ICH occipital hematomas carried the best prognosis. No prognostic importance was detected for age and gender, initial blood pressure, time interval between ICH and admission, ECG or angiographic findings, or laboratory values.
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PMID:[Prognostic significance of initial clinical and instrumental parameters in spontaneous intracerebral hemorrhages]. 339 30

The use of insulin by diabetics has largely removed the threat of death from ketotic coma but cardiovascular dysfunction remains a major cause of death in patients with diabetes. Recent research has indicated a generalized membrane defect, which may cause abnormalities of calcium metabolism in nerves, cardiac and smooth muscle as well as endothelial cells and thus may lead respectively to the development of neuropathy, primary cardiomyopathy, microangiopathy and atherosclerosis in the diabetic population. Each of these pathogenic processes, which are associated with insulin deficiency, alone or in combination with others, may result in cardiac dysfunction in chronic diabetes. Activation of the sympathetic nervous system and abnormalities in catecholamine metabolism have been identified in diabetes; their involvement in the genesis of cardiac pump failure as well as large and small vessel disease is likely. The membrane defects as indicated by changes in both plasma membrane and glycocalyx in diabetic cardiomyopathy appear to be complex and may involve alterations in the metabolism of lipids and pyrimidine nucleotides. It seems that intracellular calcium overload is intimately involved in the development of diabetic cardiomyopathy; however, a concentrated research effort is required to understand the primary biochemical lesion in the pathogenesis of cardiac dysfunction in diabetes. In the meantime, a heightened awareness on the part of clinicians concerning the susceptibility of diabetic patients to cardiovascular problems may help in reducing mortality and morbidity in the diabetic population.
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PMID:Pathogenesis of cardiac dysfunction in diabetes mellitus. 385 Jul 73

Three labile diabetic patients had recurring episodes of altered sensorium. Each had severe cerebrovascular disease with superimposed metabolic derangements, including ketoacidosis, hyperglycemia without ketosis, mild uremia, and possibly cerebral edema. Two of the patients were examined postmortem. Severe leptomeningeal scarring, basal ganglial calcification and destruction of small intracerebral vessels without evidence of large vessel atherosclerosis were found unexpectedly in one patient, a rare occurrence in this country although recently reported from Europe. The other patient had large vessel atherosclerosis only. The clinical expression of the vascular disease was modified by concurrent abnormalities and reflected the sum total of the complexities which coexisted. The pathophysiology of the unconscious state necessarily depends on the inciting factors. Ketoacidotic coma is associated with depressed cerebral oxygen consumption. Spinal fluid pH is usually maintained during ketosis but is sometimes lowered inadvertently during bicarbonate therapy, with resultant coma. Other variables influencing the clinical expression, with or without ketosis, would include, among others, blood viscosity alterations, rapid decrements in blood sugar, and existing degrees of lactic acidosis. The increasing life-span of the juvenile diabetics, favorably influenced by improved management and recently by hemodialysis, may uncover vascular complications heretofore rarely seen and create additional diagnostic and therapeutic enigmas.
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PMID:Cerebral syndromes of diabetes mellitus. 579 97

A possible relation between parenteral Depo-Provera and the subsequent development of medullary infarction in a heavy smoker is reported. The patient, a 40-year old Chinese woman had smoked 30 cigarettes daily for many years. She received injections of 150 mg Depo-Provera in April and July 1979. 2 days after the 2nd injection she was admitted to the hospital for vomiting and vertigo of 2 days duration. Clinical examination showed a 12th nerve palsy with the tongue deviated to the right but no other neurological abnormalities. She was treated symptomatically with intravenous fluids and stemetil and improved. On the 5th day her vertigo and vomiting progressed and she developed more lower brain stem signs. The same day she had a grand mal fit and went into a coma. She died on the 7th hospital day. A partial autopsy limited to the skull revealed minimal atherosclerosis of the vertebral artery but no thrombosis or occlusion. Cut sections after perfusion revealed an area of softening associated with some hemorrhage involving the whole length of the right half of the medulla oblongata dorsal to the olivary nucleus. Histological examination revealed an infarct undergoing liquefaction necrosis. The possibility of a causative relationship is suggested by the development of tinnitis about 12 hours after injection of Depo-Provera.
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PMID:Medullary infarction--was it depo-provera? 645 93

Pure cortical arterial injury is defined as an acute subdural hematoma (ASDH) due to micro laceration of the cortical artery without cerebral contusion. We analyzed this peculiar ASDH in 14 cases. This ASDH has the following characteristics. 1) This disease develops in elderly persons after minor head trauma. 2) After a relatively long lucid interval, the consciousness level of these patients decreases rapidly to semicoma or deep coma. 3) Brain atrophy, atherosclerosis and a tendency to bleed (drugs, hemodialysis, thrombocytopenia, etc.) are involved in this hematoma. 4) The clinical outcome is generally poor because of systemic complications. The authors infer the mechanism of pure cortical arterial injury to be as follows. Minor hemorrhage occurs due to direct impact damage after trivial head trauma, but physiological hemostatic actions are set in motion. After a lucid interval, rebleeding from the injured cortical artery causes massive subdural hemorrhage.
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PMID:[Acute subdural hematoma due to pure cortical arterial injury: analysis of 14 cases]. 933 Mar 92


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