A centralized administrative structure for curriculum integration and management.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to B A Sandok.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
This study is a prospective analysis of the predictive value of diffuse and localized carotid bruit. Patients with asymptomatic carotid bruits are compared with a population-based age- and sex-matched control group known not to have carotid bruit, in regard to subsequent transient ischemic attack, stroke, and death. Each person was followed until death or for 5 years. Among the 566 patients with asymptomatic carotid bruit, the annual stroke rate given survival was 1.5%/yr or 7.5% at 5 years by actuarial analysis. The annual stroke rate given survival for the 428 patients in the population-based cohort was 0.5%/yr or 2.4% at 5 years. Patients with localized carotid bruit were not significantly different from those with diffuse carotid bruits in regard to subsequent cerebral ischemic events (p = 0.11). These data indicate that patients with asymptomatic diffuse or localized carotid bruit are approximately three times more likely to have ischemic stroke than an age- and sex-matched population sample known not to have carotid bruit.
Clinical and angiographic features and outcome in 25 patients with spontaneous dissections of the vertebral arteries are described. Most patients were in their fourth or fifth decade of life, and women predominated. Forty-eight percent of the patients were hypertensive. Angiographic evidence of fibromuscular dysplasia was noted in one only. Brainstem ischemic symptoms (usually a lateral medullary syndrome) and ipsilateral occipital headache and neck pain (often preceding but sometimes associated with or following the brainstem ischemic event) were the most common clinical findings. The angiographic features in decreasing order of frequency were luminal stenosis (often irregular and tapered), aneurysm, occlusion, and intimal flap. On follow-up, most of the patients (88%) made complete or very good recoveries. Angiographic abnormalities either subsided or improved in 76%. Multivessel dissection (involvement of both vertebral arteries or one or both vertebral arteries and one or both internal carotid arteries) was noted in about two-thirds of the patients. This tendency of vertebral artery dissections to involve multiple cervicocephalic vessels concurrently, if not simultaneously, implies that four-vessel angiography should be attempted if a vertebral artery dissection is visualized. It also raises the possibility of an underlying arteriopathy that predisposes the vessel to dissection.
Thirty-one patients with vascular malformations of the posterior fossa were studied to determine their clinical presentation and radiologic diagnosis. The most common clinical presentations were acute hemorrhage (68%, 21/31) and progressive or fluctuating focal neurologic deficits resembling those found in other pathologic processes (19%, 6/31). Trigeminal neuralgia and hemifacial spasm occurred in these patients, but they were rarely initial presenting symptoms. Computed tomography, after infusion of contrast medium, was abnormal in 95% (20/21) of the patients. Angiography established or confirmed the diagnosis in most of the patients; however, a negative angiogram, especially in cases with recent hemorrhage, does not exclude the diagnosis.
A 19-year-old woman had severe focal inflammatory encephalitis. Six years previously, she had had classic untreated Lyme disease characterized by erythema chronicum migrans, bilateral facial palsies, and lymphocytic meningitis. During her recent encephalitic illness, Lyme disease serologic tests were positive by indirect immunofluorescence microscopy, enzyme-linked immunosorbent assay, and western blot (immunoblot technique) testing. We hypothesize that the patient's focal inflammatory encephalitis was a result of a persistent spirochetal infection of the central nervous system.
Emergency revascularization procedures for patients with acute stroke are controversial. Thirty-four patients with acute internal carotid artery occlusion documented at the time of emergency endarterectomy were analyzed. Before operation, all these patients had profound neurological deficits including hemiplegia and aphasia. There was a 94% success rate in restoring patency. In follow-up, nine patients (26.5%) had a normal neurological exam, four (11.8%) had a minimal deficit, 10 (29.4%) had a moderate hemiparesis, which was improved over their preoperative deficit, 4 (11.8%) remained hemiplegic, and seven (20.6%) died. The natural history of patients with acute carotid occlusion and profound neurological deficits is dismal. In comparison, 13 patients (38%) made a dramatic recovery. The surgical mortality rate compares favorably with the natural history. Good collateral flow was a good prognostic factor, while a simultaneous middle cerebral artery embolus was associated with a poorer prognosis. An emergency carotid endarterectomy may be indicated in selected patients with acute internal carotid artery occlusion with profound neurological deficits. Full preoperative angiography may identify those patients who would benefit from surgical intervention and reduce the operative mortality rate.
A prospective study of 1,517 consecutive cerebral angiographic examinations is reported. The incidence of all complications was 8.5%, and the incidence of all neurologic complications was 2.6%. The overall incidence of permanent neurologic deficit was 0.33%. The incidence of permanent neurologic deficit in patients referred for evaluation of symptomatic cerebrovascular disease was 0.63%. Older age, increased serum creatinine concentration, and the use of more than one catheter all were significantly associated with serious neurologic complications. Although patients with a recent stroke or frequent transient ischemic attacks had a higher incidence of serious neurologic complications, this increase was not statistically significant for this sample.
Carotid artery fibromuscular dysplasia is uncommon. Most patients have a benign clinical course so caution should be used in treating these. Treatment for asymptomatic patients is not advised; symptomatic patients with evidence of progressive cerebral ischemia should be treated with medical or surgical therapy based on the presumed responsible pathophysiologic mechanism.
This study involved 151 consecutive patients who had transient focal cerebral ischemia (TIA) in one carotid arterial system and who had carotid endarterectomy on the side corresponding to the ischemic symptoms. Each patient was examined preoperatively by a neurologist, who also judged the postoperative morbidity and mortality. All patients were operated on by one surgeon. A major or minor ischemic stroke occurred in 3% of patients during operation or within 30 days thereafter. The mortality was less than 1% at 1 month. After the first month, ischemic stroke occurred at a rate of 2% per year, and two-thirds of the strokes were ipsilateral to the endarterectomy. Long-term mortality was 3% per year. Long-term stroke morbidity was less than would have been expected for a comparable group of patients with TIA, and the percentage of deaths due to a cardiac cause was greater than expected, owing to a relative shift from stroke mortality to cardiac mortality. No patient who had a cerebral blood flow of 40 ml or greater per 100 g of brain per minute during occlusion for endarterectomy had a stroke during operation or during 4 1/2 years of follow-up.
From a 10% sampling of the Olmsted County, Minnesota, population, persons of age 45 years and older were selected randomly in predetermined age and sex groupings and examined for cervical murmurs. Five hundred nine persons representing approximately 1% of all persons in the population between 45 and 54 years old, 2.5% of those 55 to 64 years old, and 3.5% of those more than 65 years old were included in the study. A cervical murmur of some type was heard in 64 persons (12.6%). Localized, midcarotid bifurcation bruits were noted in 22 persons (4.3%). Of this last group, 15 persons (2.9%) were asymptomatic. The prevalence of localized, asymptomatic carotid arterial bruits increased with age: 0.9% at 45 to 54 years, 2.1% at 55 to 64 years, 3.8% at 65 to 74 years, and 5% at 75 years and older; it was higher in females (4.4%) than in males (1.6%).
From 1962 through 1979, 13,955 cerebral angiograms were made at our institution. Fibromuscular dysplasia (FMD) was identified in 82 (0.6%) patients. Follow-up information with specific reference to subsequent cerebral ischemic events (CIEs) was obtained in 79 (96%) patients and forms the basis for this study. The patients ranged in age from 18 to 76 years (mean, 58 years). Seventy-four of the patients were women. During an average follow-up of 60 months, three patients suffered subsequent CIEs (50, 136, and 216 months after the initial diagnosis). Fibromuscular dysplasia of the carotid artery is often an incidental angiographic finding, which may be manifested with focal CIEs. Most patients had no subsequent cerebrovascular symptoms related to the FMD. Therefore, we suggest that medical or surgical therapy be reserved for selected patients who have evidence of progressive cerebral ischemia.
To assess the use of two-dimensional (2D) echocardiography in demonstrating a cardiac source for cerebral embolization, we studied 138 patients with one or more recent episodes of focal cerebral ischemia, in whom either a cardiac mechanism was suspected or no probable mechanism of ischemia was identified. Intracardiac thrombus was found in nine patients (6.5%); 32 (23.2%) had other cardiac disorders possibly related to the ischemia; and the remaining 97 (70.3%) had study results that were normal or added nothing to the clinical findings. Thus, 2D echocardiography was of limited value in patients with no clinical cardiac disease or hypertension only, and of greater value in patients with known cardiac disease, especially atrial fibrillation. Although 2D echocardiography can demonstrate a wide range of disorders that may be associated with ischemia, the overall low yield does not warrant routine use of this study in all patients with unexplained cerebral ischemic events.
The records of 40 patients with pathologically verified atrial myxoma identified during the period 1957 to 1977 were studied. The patients ranged in age from 17 to 77 years; women predominated by a ratio of 3:1. Thirty-five patients had left atrial myxoma, three patients had right atrial myxoma, one patient had bilateral myxomas, and one patient had a right atrial myxoma and subsequent removal of a left atrial myxoma. Ten of the 37 patients (27%) with left atrial myxoma had at least one neurologic event suggesting ischemia secondary to embolization. Transient or permanent ischemic events were noted in the cerebral hemispheres, brainstem, cerebellum, retina, and spinal cord. Although some patients were seen at the initial evaluation with primarily neurologic events, cardiac and constitutional symptoms dominated the clinical picture. Echocardiography and sector scanning provide a practical method for early clinical diagnosis.
Review of 35 patients from the Mayo Clinic with histologically proved atrial myxomas (7 with prior neurological events) who were followed for 12 to 235 months revealed that none had subsequent delayed neurological events attributable to their atrial myxomas.
On the basis of a review of the literature on anticoagulant, antiplatelet, and surgical treatment, supplemented by our personal experience, we have developed guidelines for the management of patients with transient ischemic attacks (TIA). 1. The majority of patients with vertebral-basilar TIA are treated medically. 2. If a skilled surgeon and an experienced angiographer are available, patients with typical carotid TIA who are suitable medical risks should have angiography followed by carotid endarterectomy if an appropriate lesion is found. 3. Nonoperated patients with TIA of less than 2 months' duration are treated with 3 months of warfarin therapy (unless contraindicated) before treatment with aspirin is begun. 4. Nonoperated patients with continuing TIA of 2 or more months' duration are treated with aspirin unless there has been a recent increase in the frequency, duration, or severity of TIA. Under these circumstances, warfarin therapy is advised for 3 months before aspirin is started. Aspirin therapy should be continued until the patient has been free of TIA for 1 year. 5. No treatment is advised for nonoperated patients whose last episode of TIA was longer than 12 months ago.
Explore the source record for details and available documents.
Explore the source record for details and available documents.