Citations

Background and Purpose Despite growing concern over the large numbers of specialists in the United States, little information is available on how stroke treatment varies by the specialty of the attending physician. This study compares the costs and outcomes of acute stroke patients by physician specialty, especially between neurologists and other specialists. Methods We selected a random sample of Medicare patients aged 65 years and older admitted with cerebral infarction between January 1 and September 30, 1991, identified from the principal diagnosis on Medicare Provider Analysis and Review records. All Medicare claims for these patients were extracted from the date of admission through 90 days. The attending physician was identified as that physician billing for routine hospital visits during the first 7 days of the stay. Results Neurologists treating stroke patients were significantly more expensive than other physicians but obtained better outcomes. Ninety-day mortality rates for patients treated by neurologists were significantly lower than those for other specialists. These cost and outcome differences persisted even after adjustment for patient age, comorbidity, hospital teaching status, and other characteristics. Compared with other attending physicians, neurologists were significantly more likely to order diagnostic cerebrovascular tests (especially brain MRI scans), more likely to prescribe warfarin, and more likely to discharge patients to inpatient rehabilitation facilities. Conclusions Systematic triaging to neurologists based on clinical characteristics unmeasured by administrative data might explain these observed differences between neurologists and other physicians. Alternatively, these specialists may have been better able to identify the mechanism of stroke, information that then affected the course of treatment. Given current pressures to substitute generalists for specialists, however, more research is needed on these stroke treatment differences.

Atrial myxoma is uncommon and may be associated with brief isolated ischemic events. We describe a patient with atrial myxoma and an incompletely evaluated ischemic stroke followed 1 year later with almost complete brain necrosis. A 63-year-old woman presented with a rapidly progressive illness resulting in coma within 24 hours from multiple myxomatous emboli. Cranial computed tomographic scan demonstrated multiple hypodensities in both cerebellar and cerebral hemispheres. Postmortem examination revealed virtually complete brain necrosis, multiple peripheral artery embolizations, embolization in the coronary arteries with acute myocardial infarction, and tumor emboli in the spleen and kidneys. Although uncommon, atrial myxoma may present as a fatal multiple organ embolization that includes both anterior and posterior circulation territories of the brain.

Corticotropin releasing factor is an endogenous neuropeptide released by the hypothalamus that activates the pituitary-adrenocortical system in response to stressful stimuli. It has been demonstrated that corticotropin releasing factor increases the excitability of hippocampal neurons in both in vitro and in vivo studies, which may contribute to neurological injury during hypoxia. The purpose of this study was to determine the effects of corticotropin releasing factor and its synthetic competitive antagonist, alpha-CRF, on neuronal synaptic recovery after a hypoxic insult using the hippocampal slice. Wistar rat hippocampal brain slices (n = 120) were treated with various concentrations (10(-6) to 10(-11)) of corticotropin releasing factor or its synthetic antagonist during a 10-minute hypoxic episode. Extracellular recording of population spikes was used during and after the hypoxic insult to assess neuronal recovery. Corticotropin releasing factor provided dose-dependent neuronal protection with maximum recovery (37.95 +/- 8.71%) occurring at 10(-9) concentrations. The competitive antagonist alpha-CRF provided a similar degree of recovery at 10(-6) concentration, whereas 10(-9) molar concentration of competitive antagonist resulted in 16.84 +/- 7.68% recovery. Corticotropin releasing factor provides moderate protection to hypoxic hippocampal neurons in the brain slice preparation. The mechanism of action is unknown but appears to be a direct neuronal effect. These results support the hypothesis that corticotropin releasing factor may act as an endogenous neuroprotective hormone during hypoxia.

The aim of this experiment was to study the serial changes in brain intracellular pH, cerebral blood flow, and the oxidation/reduction level of intramitochondrial nicotinamide adenine dinucleotide fluorescence across the cortical surface during severe incomplete global ischemia. Reduced nicotinamide adenine dinucleotide fluorescence and brain intracellular pH using the pH-sensitive indicator umbelliferone were measured with in vivo panoramic fluorescence imaging of the cortical surface. Cerebral blood flow was measured with the clearance of both umbelliferone and xenon-133. Fifteen minutes of severe incomplete global ischemia was produced by temporary occlusion of the innominate, left carotid, and subclavian arteries in five fasted New Zealand White rabbits. Baseline brain intracellular pH was homogeneous over the exposed cortex, measuring 7.00 +/- 0.02, while cerebral blood flow was 48.0 +/- 2.6 ml/100 g/min. During 15 minutes of ischemia, cerebral blood flow measured 6.3 +/- 1.8 ml/100 g/min and brain pH declined to 6.61 +/- 0.02 (p < 0.005); in addition, there were acidotic foci with pH measuring 6.40 +/- 0.10. During reperfusion, there was an initial normalization of brain intracellular pH without an alkaline shift followed by a recurrent cortical acidosis of pH 6.88 +/- 0.06. There was a heterogeneous pattern of fluorescence that increased significantly following 60 minutes of reperfusion, coinciding with a postischemic hypoperfusion. The hypoperfusion was a uniform reduction in cerebral blood flow over the brain's surface, with reductions of 42.5% and 44.2% at 30 and 45 minutes, respectively. During incomplete global ischemia there is a heterogeneous pattern of brain intracellular pH and reduced nicotinamide adenine dinucleotide changes that do not correlate with changes in cortical blood flow. The acidotic foci that were approximately 0.2 pH units more acidotic than the surrounding cortex may be the result of continued glucose delivery under anaerobic conditions. The degree of reduced nicotinamide adenine dinucleotide fluorescence suggests that the cortex is most vulnerable to metabolic failure after 60 minutes of reperfusion following severe incomplete global ischemia. The heterogeneous pattern of brain intracellular pH and reduced nicotinamide adenine dinucleotide changes suggest that there may be a selective vulnerability of cortical tissue to an ischemic challenge.

Experiments were designed to determine the effect of subarachnoid hemorrhage on endothelium-dependent relaxations in small arteries of the brain stem. A "double-hemorrhage" canine model of the disease was used, and the presence of vasospasm in the basilar artery was confirmed by angiography. Secondary branches of both untreated basilar arteries (inner diameter, 324 +/- 11 microns; n = 12) and arteries exposed to subarachnoid hemorrhage for 7 days (inner diameter, 328 +/- 12 microns; n = 12) were dissected and mounted on glass microcannulas in organ chambers. Changes in the intraluminal diameter of pressurized arteries were measured using a video dimension analyzer. In untreated arteries, 10(-11) to 10(-7) M vasopressin, 10(-10) to 10(-6) M bradykinin, and 10(-9) to 10(-6) M calcium ionophore A23187 caused endothelium-dependent relaxations. At 10(-6) and 3 x 10(-4) M the nitric oxide synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME) abolished relaxations to vasopressin and produced small but significant rightward shifts of the concentration-response curves to bradykinin and A23187. At 10(-3) M L-arginine prevented the inhibitory effect of L-NAME. Subarachnoid hemorrhage abolished relaxations to vasopressin but did not affect relaxations to bradykinin or A23187. These studies suggest that in small arteries of the brain stem vasopressin causes relaxations by activation of the endothelial L-arginine pathway. This mechanism of relaxation is selectively inhibited by subarachnoid hemorrhage. Preservation of endothelium-dependent relaxations to bradykinin and A23187 is consistent with the concept that small arteries are resistant to vasospasm after subarachnoid hemorrhage.

Cervical internal carotid artery dissections are diagnosed with an increasing frequency, but reliable epidemiologic data are not available. The aim of this study was to determine the incidence rate of spontaneous cervical internal carotid artery dissection in a defined population. Using the medical record linkage system used for epidemiologic studies in Rochester, Minn, all patients diagnosed with spontaneous cervical ICA dissection for 1987 through 1992 were identified. A total of 10 patients with spontaneous cervical internal carotid artery dissection (6 women and 4 men; mean age, 44 years) were identified. For the period 1987 through 1992, the average annual incidence rate for all ages was 2.6 per 100,000 (95% confidence intervals, 0.9 to 4.2). This study, for the first time, provides incidence rates for spontaneous cervical internal carotid artery dissections. No diagnoses were made before 1987, probably reflecting an increased awareness of the disorder among physicians.

This study, in biologically bred hyperglycemic diabetic rats, examined the effect of a intravenous insulin infusion (1.5 units.hr-1) on blood, plasma, and brain glucose concentrations to determine their relationship during decreasing blood and plasma glucose levels. The data were compared to saline-treated diabetic rats and saline-treated nondiabetic littermates. The volume and duration of the treatment infusion were similar in all groups. Insulin infusion in diabetic rats produced the expected reduction in blood and plasma glucose, and normoglycemia was produced within 78 +/- 37 minutes (mean +/- SD). However, once normoglycemia was achieved, brain glucose was still significantly greater by 44% than in nondiabetic rats (p = 0.015). Moreover, the ratio of brain to plasma glucose was more than 50% greater in diabetic than nondiabetic rats, irrespective of whether or not they received insulin (p less than 0.01). We conclude that measurement of blood or plasma glucose in diabetic subjects will tend to underestimate the amount of glucose in the brain and that this relationship is not influenced by acute insulin therapy.

A combined autoradiographic and immunohistochemical method was used to correlate the extent of focal cerebral ischemia and morphologic ischemic damage following unilateral carotid occlusion in 16 gerbils for 5-30 minutes. Immunohistochemical lesions detectable by the reaction for microtubule-associated proteins 1 and 2 were visible in the subiculum-CA1 and CA2 regions of the hippocampus and layer III/IV of the cerebral cortex after 5 minutes of ischemia (n = 4). Local blood flow was promptly reduced but still heterogeneous after 10 minutes of ischemia (n = 4); local blood flow in immunohistochemical lesions was less than 5 ml/100 g/min except in highly vulnerable regions, where flow values of 5-15 ml/100 g/min were observed. After 15 minutes of ischemia (n = 4) local blood flow in less vulnerable regions including the thalamus and caudoputamen also declined to less than 5 ml/100 g/min, and immunohistochemical lesions became visible in those regions after 30 minutes of ischemia (n = 4). On the other hand, many brain regions tolerated local blood flow of less than 5 ml/100 g/min without ischemic damage. The present study demonstrates that selective tissue vulnerability during progressive cerebral ischemia depends on the degree of hypoperfusion and on factors inherent to neurons in various brain regions.

This is a study of 45 patients who underwent angiography and surgery of one or both carotid arteries (56 surgical procedures). All patients had detailed neuro-ophthalmological evaluations including determination of retinal artery pressure (RAP) and scrutiny for emboli in small vessels. Preoperatively, the absolute RAP value has a high correlation with the degree of stenosis of the ipsilateral carotid artery when that stenosis exceeds 80%. The asymmetry of RAP values is greatest when the stenosis is much more severe in one artery than in the other. Both RAP values may show an absolute decrease when the stenosis is severe bilaterally. In these patients, postoperatively there usually is not only an increase in the RAP on the side operated on but also on the side contralateral to the initial procedure. Almost without exception, RAP should be normal after carotid artery surgery. The finding of a subnormal RAP after operation demands immediate investigation.

Acetazolamide was given to five of ten cats for 48 to 54 hours after extradural occlusion of a middle cerebral artery (MCA). At seven to eight days later, measurements of regional cerebral blood flow (CBF) and estimates of the sizes of the ischemic and infarcted areas of the brains were made. Neurological deficits were more severe and the ischemic and infarcted regions were larger in the cats given acetazolamide. Cerebral edema (brain swelling) was present and reactive hyperemia was common in the treated cats, even one week after MCA occlusion. The hypercapnia and decreases of pH of nonischemic brain tissue that are caused by acetazolamide are harmful for ischemic brain tissue, presumably because of vasodilatation in nonischemic brain tissue with resultant increases of intracranial pressure and decreases of CBF of ischemic regions.