Biomedical subjects

R A Solomon

Publications and source records attributed to R A Solomon.

At least 37 records · Page 2Linked to original sources

PubMed1998

Diagnosis and monitoring of cerebral hyperfusion after carotid endarterectomy with single photon emission computed tomography: case report.

OBJECTIVE AND IMPORTANCE: Focal neurological deficits after carotid endarterectomy may result from ischemia or hyperperfusion. The usefulness of single photon emission computed tomography (SPECT) for differentiating between these two mechanisms has not been previously emphasized. CLINICAL PRESENTATION: An 83-year-old man experienced dysarthria and left-sided weakness immediately after undergoing endarterectomy of the right internal carotid artery. The results of computed tomography of the head were normal, and transcranial Doppler sonography showed symmetrically elevated velocities in both middle cerebral arteries. On the 1st postoperative day, the patient's deficits worsened in parallel with spontaneous increases in blood pressure, and blood pressure reduction with labetalol resulted in clinical improvement. INTERVENTION: On the 2nd postoperative day, technetium-99-hexametazime SPECT demonstrated markedly increased flow in the right basal ganglia and inferior frontal cortex, confirming the diagnosis of cerebral hyperperfusion. The patient's deficits continued to improve with antihypertensive therapy, and SPECT performed 7 and 48 days after surgery showed gradual normalization of the focal hyperemia. CONCLUSION: SPECT can be used to diagnose and monitor cerebral hyperperfusion after carotid endarterectomy and may be of particular value for differentiating hyperperfusion from ischemia when characteristic computed tomographic and transcranial Doppler sonographic findings are absent.

Aged↗

PubMed1998

Complex intracranial aneurysms: combined operative and endovascular approaches.

OBJECTIVE: Endovascular management of complex intracranial aneurysms is increasingly being considered as an alternative to standard surgical clipping. However, little attention has been paid to the complementary nature of surgery and endovascular therapy. METHODS: Between September 1992 and May 1997, 12 patients with complex intracranial aneurysms were treated with combined operative and endovascular methods. Seven patients demonstrated subarachnoid hemorrhage (two of Grade II, two of Grade III, and three of Grade IV). Five patients demonstrated unruptured aneurysms, i.e., three giant aneurysms (one vertebrobasilar junction aneurysm, one middle cerebral artery bifurcation aneurysm, and one internal carotid artery-ophthalmic artery aneurysm), one large internal carotid artery-ophthalmic artery aneurysm, and one middle cerebral artery serpentine aneurysm. Management strategies involved either surgery followed by endovascular therapy (S-E; n = 5) or endovascular therapy followed by surgery (E-S; n = 7). S-E paradigms included aneurysm exploration followed by endovascular treatment (S-E1; n = 3), partial aneurysm clipping followed by endovascular aneurysm packing (S-E2; n = 1), and extracranial-to-intracranial bypass followed by endovascular parent vessel occlusion (S-E3; n = 1). E-S paradigms included superselective angiography followed by surgical clipping (E-S1; n = 2), Guglielmi detachable coil partial dome packing followed by delayed surgical clipping (E-S2; n = 2), proximal temporary vessel balloon occlusion followed by aneurysm clipping (E-S3; n = 2), and proximal permanent vessel occlusion followed by surgical aneurysm decompression for mass effect treatment (E-S4; n = 1). RESULTS: Eleven aneurysms (92%) were completely eliminated. The remaining aneurysm was 90% obliterated and remained quiescent at the 34-month follow-up examination, despite presenting with subarachnoid hemorrhage. No patient experienced repeat bleeding (follow-up period, 23+/-28 mo). There were no deaths. One patient achieved a fair outcome (Glasgow Outcome Scale score of III); all other patients experienced excellent outcomes (Glasgow Outcome Scale score of I). In all cases, the aneurysm management paradigm chosen had a positive effect on definitive therapy. CONCLUSION: Several factors can contribute to the complexity of intracranial aneurysms. Management strategies that combine operative and endovascular techniques in a complementary way, for the best possible outcomes for these patients, can be designed accordingly.

Adult↗

PubMed1998

Neuropsychometric changes in patients after carotid endarterectomy.

BACKGROUND AND PURPOSE: One hundred twelve patients undergoing elective carotid endarterectomy for symptomatic and asymptomatic carotid artery stenosis were enrolled in a prospective study to evaluate the incidence of change in postoperative cerebral function. METHODS: Patients were evaluated preoperatively and postoperatively before hospital discharge and at follow-up 1 and 5 months later with a battery of neuropsychometric tests. The results were analyzed by both event-rate and group-rate analyses. For event-rate analysis, change was defined as either a decline or improvement in postoperative neuropsychometric performance by 25% or more compared with a preoperative baseline. RESULTS: Approximately 80% of patients showed decline in one or more test scores, and 60% had one or more improved test scores at the first follow-up examination. The percentage of declined test scores decreased and the percentage of improved test scores increased with subsequent follow-up examinations. Group-rate analysis was similar for group performance on individual tests. However, a decline in performance was seen most commonly on verbal memory tests, and improved performance was seen most commonly on executive and motor tests. CONCLUSIONS: Neuropsychometric evaluation of patients undergoing carotid endarterectomy for significant carotid artery stenosis demonstrates both declines and improvements in neuropsychometric performance. The test changes that showed decreased performance may be associated with ischemia from global hypoperfusion or embolic phenomena, and the improvement seen may be related to increased cerebral blood flow from removal of stenosis.

Aged↗

PubMed1998

Management of symptomatic and asymptomatic unruptured aneurysms.

Intradural unruptured saccular aneurysms are being diagnosed with increasing frequency. Left untreated, these lesions usually progress, and the cumulative risk from bleeding usually outweighs the risk of treatment. Exceptions include patients with limited life expectancy and patients over the age of 70 with small asymptomatic or giant posterior circulation lesions associated with few symptoms. Therapeutic intervention offers little over the natural history for these patients, and therapy should be considered only if symptoms progress or growth is documented. Treatment options should be coordinated by an experienced cerebrovascular surgeon with access to interventional adjuncts; EC-IC bypass, and circulatory arrest. GDC coiling should be reserved for non-surgical cases, as the durability of this treatment is still being evaluated.

Aneurysm, Ruptured↗

PubMed1998

Hypothermic cardiac standstill for cerebral aneurysm surgery.

Surgical management of giant cerebral aneurysms remains a major technical challenge for modern neurosurgeons. Endovascular approaches for giant aneurysms does not provide an acceptable alternative to direct surgical approaches. The use of deep hypothermic circulatory arrest as an adjunct during clipping of complex giant aneurysms shows promise as a treatment for otherwise incurable lesions. Patient selection and techniques of circulatory arrest surgery are discussed.

Brain↗

PubMed1997

The safety of intraoperative lumbar subarachnoid drainage for acutely ruptured intracranial aneurysm: technical note.

Recently, some concern has arisen regarding the safety of intraoperative spinal drainage for brain relaxation in aneurysm surgery, due to anecdotal association with both aneurysmal rebleeding and increases in symptomatic vasospasm. To address these concerns, we reviewed our experience with frequent spinal drainage and early surgery in 432 consecutive cases of surgically treated aneurysmal subarachnoid hemorrhage. Unless contraindicated by mass effect or associated pathology, all grade I-III patients referred within 14 days were treated with spinal drainage at surgery. In this cohort (n = 314), there were no cases of meningitis or nerve root injury. Only one case of intraoperative rebleeding could be associated with spinal drain placement (0.3%). In grade IV-V patients, 47% required preoperative ventriculostomy, and 11% were ineligible for spinal drainage due to mass effect. There were, however, no complications related to spinal drainage in the remaining 23 patients. Permanently-shunted hydrocephalus (8%) and symptomatic vasospasm (19%) were infrequent overall. When analyzed by grade, spinal drains were generally associated with equal or reduced incidence of these developments when compared to patients without spinal drainage. We conclude that brain relaxation can be safely and effectively obtained using intraoperative spinal drains during early aneurysm surgery.

Acute Disease↗

PubMed1997

Elastin degradation in the superficial temporal arteries of patients with intracranial aneurysms reflects changes in plasma elastase.

OBJECTIVE: alpha 1-Antitrypsin (AAT) and alpha 2-macroglobulin (AMG) are elastase inhibitors that bind the enzyme and reduce measured levels of free elastase. It was recently demonstrated that some patients with intracranial aneurysms have significantly elevated plasma elastase (PE) levels. Although this elevation is unrelated to plasma AAT, it is unknown whether abnormal AAT phenotypes or reduced AMG levels play a role. Moreover, the pathological significance of this elevation is not understood. METHODS: Plasma from 24 patients with aneurysms (ruptured, n = 15; unruptured, n = 9) and 10 age-matched patients who comprised a control group was analyzed for PE and AMG levels by enzyme-linked immunosorbent assay and for AAT phenotype by isoelectric focusing. Sections of superficial temporal temporal artery obtained from these patients at the time of surgery were examined for evidence of elastin degradation by using a van Gieson stain, with scoring on a nine-point quantitative scale. RESULTS: Patients with aneurysms showed significantly elevated PE levels (119 +/- 28 versus 17 +/- 7 micrograms/ml, P < 0.05), but AMG levels were not decreased. AAT phenotypic abnormalities were observed in 10% (2 of 20) of the patients with aneurysms, but this was not different from the expected population incidence (7%). Elastin degradation scores were significantly higher in patients with aneurysms than in patients control group (4.26 +/- 0.54 versus 1.21 +/- 0.43, P < 0.05). In addition, patients with higher elastase levels (> 80 micrograms/ml) demonstrated 55% higher degradation scores than did those with lower elastase levels (< 80 micrograms/ml). CONCLUSION: These data suggest that high PE levels may play a role in systemic arterial elastin degradation seen in patients with intracranial aneurysms. These data also support the contention that elevated elastase levels are not the result of decreased protease inhibitor levels. Although PE levels were significantly higher for the entire group of patients with aneurysms, this assay has relatively low sensitivity for predicting the presence of unruptured aneurysms. Additional study is necessary to determine whether serum elastase levels greater than 80 micrograms/ml, in the setting of other risk factors, are useful in identifying asymptomatic patients for additional screening.

Adult↗

PubMed1997

Direct intraoperative measurement of human brain temperature.

OBJECTIVE: Because hypothermia enhances human tolerance for cerebral ischemia, profound hypothermia is induced in many centers so that the circulation can be arrested while clips are applied to high-risk giant cerebral aneurysms. Brain temperature is measured directly with an intracerebral probe that avoids the uncertainty of surrogate monitoring. However, when there is a large thermal gradient between brain temperature and that of the operating room, even direct measurements can sometimes be misleading. This study was undertaken to determine how deeply a thermal sensor must be embedded in the cerebral parenchyma to ensure that the ambient environment does not distort the measurement of brain temperature. METHODS: Each of 39 normothermic patients had a thermocouple sensor inserted into a temporal lobe seizure focus just before its resection. Brain temperature was measured as the sensor was withdrawn in stages. RESULTS: At both 3 and 2 cm beneath the cortical surface, the temperature of the brain was essentially the same. However, when the sensor was withdrawn to 1 cm, recorded temperature decreased from 35.7 +/- 0.9 to 34.3 +/- 1.4 degrees C (P < 0.001) and irrigation in the vicinity caused major thermal change. At shallower depths, even lower brain temperatures were recorded. No morbidity was attributable to the temperature measurements. CONCLUSION: Direct intraoperative measurement of human brain temperature is feasible and safe, but accuracy requires that the temperature sensor be inserted at least 2 cm into the cerebral cortex.

Body Temperature Regulation↗

PubMed1997

Matrix metalloproteinase-9 in cerebral aneurysms.

OBJECTIVE: Generalized disruption of arterial wall morphological changes in patients harboring cerebral aneurysms has been documented; however, little is known regarding the pathogenesis of these changes. To explore the role of the elastolytic gelatinase, matrix metalloproteinase-9 (MMP-9), levels of this enzyme in the wall of intracranial aneurysms were compared with those in both intracranial and extracranial arteries. The tissue levels of its major inhibitor, tissue inhibitor of metalloproteinase (TIMP), were measured in these tissues as well. The activity of MMP-9 in plasma was also evaluated. METHODS: The aneurysm wall was excised from three of six patients undergoing craniotomies for aneurysm clipping. A 1-cm segment of superficial temporal artery (STA) was obtained from each of six patients. Additional STAs were obtained from six patients in the control group who were undergoing craniotomies for nonvascular disease. An intracranial artery was also obtained from the anterior temporal neocortical resection of a patient undergoing a craniotomy for mesial temporal sclerosis. MMP-9 and TIMP levels were determined via Western blot analysis. Using substrate gel Zymography, MMP-9 plasma activity was determined for a separate cohort of patients with aneurysms (n = 6) and patients in the control group (n = 6). RESULTS: MMP-9 and TIMP levels in the aneurysm wall were markedly increased beyond levels in both extracranial arteries (STAs from patients with aneurysms and patients in the control group) and the intracranial artery. There were no differences in the levels of MMP-9 in the STAs of patients harboring aneurysms when compared with patients in the control group. Also, no differences were noted in plasma MMP-9 activity. CONCLUSION: Local rather than systemic perturbations in MMP-9 levels may contribute to the matrix disruption associated with cerebral aneurysms. This local up-regulation is not the result of TIMP down-regulation. The lack of increased systemic metalloproteinase activity precludes the use of plasma MMP-9 activity as a screening tool for presymptomatic aneurysms. However, local therapeutic modulation of MMP-9 activity may help arrest aneurysm progression.

Aneurysm, Ruptured↗

PubMed1997

Treatment of inoperable carotid aneurysms with endovascular carotid occlusion after extracranial-intracranial bypass surgery.

OBJECTIVE: Hunterian ligation of the internal carotid artery (ICA) is an accepted treatment for inoperable carotid aneurysms. Preliminary extracranial-intracranial (EC-IC) bypass surgery is required in some patients. The reported incidence of thromboembolic and ischemic complications remains significant for these patients, despite a variety of advocated management strategies. We present our treatment paradigm. METHODS: Between April 1992 and March 1997, nine patients with inoperable ICA aneurysms were treated using EC-IC bypass surgery and then permanent endovascular ICA occlusion. All of the patients except one had been selected for bypass surgery on the basis of failing results of the ICA test occlusion with hypotensive challenge. ICA occlusion was performed by endovascular means and was delayed after bypass surgery was performed by a mean of 6 days (range, 2-20 d). All patients were managed in the intensive care unit after ICA occlusion. RESULTS: Clinical improvement was noted in all patients (mean follow-up, 21 mo; range, 3-42 mo). There were no major complications. Aneurysmal thrombosis was confirmed in all patients. Although ICA occlusion was delayed after bypass surgery, only one bypass was noted to be occluded. The occluded bypass occurred in a patient who subsequently underwent successful ICA occlusion. This patient was thought to have been improperly selected for bypass surgery. CONCLUSION: Certain carotid aneurysms can be effectively managed with hunterian ICA ligation. After preliminary identification of patients with borderline cerebrovascular reserve as candidates for EC-IC bypass surgery, close attention to the following points may help enhance clinical outcome: 1) excellence in surgical technique for EC-IC bypass surgery, 2) occlusion of the parent vessel as close to the aneurysm neck as possible by endovascular means, and 3) judicious postoperative combination of anticoagulation, fluid, and pressure management.

Adult↗

PubMed1997

Exacerbation of cerebral injury in mice that express the P-selectin gene: identification of P-selectin blockade as a new target for the treatment of stroke.

There is currently a stark therapeutic void in the treatment of evolving stroke. Although P-selectin is rapidly expressed by hypoxic endothelial cells in vitro, the functional significance of P-selectin expression in stroke remains unexplored. In order to identify the pathophysiological consequences of P-selectin expression and to identify P-selectin blockade as a potential new approach for the treatment of stroke, experiments were performed using a murine model of focal cerebral ischemia and reperfusion. Early P-selectin expression in the postischemic cerebral cortex was demonstrated by the specific accumulation of radiolabeled anti-murine P-selectin IgG, with the increased P-selectin expression localized to the ipsilateral cerebral microvascular endothelial cells by immunohistochemistry. In experiments designed to test the functional significance of increased P-selectin expression in stroke, neutrophil accumulation in the ischemic cortex of mice expressing the P-selectin gene (PS +/+) was demonstrated to be significantly greater than that in homozygous P-selectin-null mice (PS -/-). Reduced neutrophil influx was accompanied by greater postischemic cerebral reflow (measured by laser Doppler) in the PS -/- mice. In addition, PS -/- mice demonstrated smaller infarct volumes (5-fold reduction, P<.05) and improved survival compared with PS +/+ mice (88% versus 44%, P<.05). Functional blockade of P-selectin in PS +/+ mice using a monoclonal antibody directed against murine P-selectin also improved early reflow and stroke outcome compared with control mice, with reduced cerebral infarction volumes noted even when the blocking antibody was administered after occlusion of the middle cerebral artery. These data are the first to demonstrate a pathophysiological role for P-selectin in stroke and suggest that P-selectin blockade may represent a new therapeutic target in the treatment of stroke.

Animals↗

PubMed1997

Use of a spectrophotometric hemoglobin assay to objectively quantify intracerebral hemorrhage in mice.

BACKGROUND AND PURPOSE: There is great interest in developing novel anticoagulant or thrombolytic strategies to treat ischemic stroke. However, at present there are limited means to accurately assess the hemorrhagic potential of these agents. The present studies were designed to develop and validate a method to accurately quantify the degree of intracerebral hemorrhage (ICH) in murine models. METHODS: In a murine model, ICH was induced by stereotaxic intraparenchymal infusion of collagenase B alone (6 x 10(-6) U; n = 5) or collagenase B followed by intravenous recombinant tissue plasminogen activator (rt-PA) (0.1 mg/kg; n = 6). Controls consisted of either sham surgery with stereotaxic infusion of saline (n = 5) or untreated animals (n = 5). ICH was (1) graded by a scale based on maximal hemorrhage diameter on coronal sections and (2) quantified by a spectrophotometric assay measuring cyanomethemoglobin in chemically reduced extracts of homogenized murine brain. This spectrophotometric assay was validated with the use of known quantities of hemoglobin or autologous blood added to a separate cohort of homogenized brains. With this assay, the degree of hemorrhage after focal middle cerebral artery occlusion/reperfusion was quantified in mice treated with postocclusion high-dose intravenous rt-PA (10 mg/kg; n = 11) and control mice subjected to stroke but treated with physiological saline solution (n = 9). RESULTS: Known quantities of hemoglobin or autologous blood added to fresh whole brain tissue homogenates showed a linear relationship between the amount added and optical density (OD) at the absorbance peak of cyanomethemoglobin (r = 1.00 and .98, respectively). When in vivo studies were performed to quantify experimentally induced ICH, animals receiving intracerebral infusion of collagenase B had significantly higher ODs than saline-infused controls (2.1-fold, increase; P = .05). In a middle cerebral artery occlusion and reperfusion model of stroke, administration of rt-PA after reperfusion increased the OD by 1.8-fold compared with animals that received physiological saline solution (P < .001). When the two methods of measuring ICH (visual score and OD) were compared, there was a linear correlation (r = .88). Additional experiments demonstrated that triphenyltetrazolium staining, which is commonly used to stain viable brain tissue, does not interfere with the spectrophotometric quantification of ICH. CONCLUSIONS: These data demonstrate that the spectrophotometric assay accurately and reliably quantifies murine ICH. This new method should aid objective assessment of the hemorrhagic risks of novel anticoagulant or thrombolytic strategies to treat stroke and can facilitate quantification of other forms of ICH.

Animals↗

PubMed1996

Cerebral protection in homozygous null ICAM-1 mice after middle cerebral artery occlusion. Role of neutrophil adhesion in the pathogenesis of stroke.

Acute neutrophil (PMN) recruitment to postischemic cardiac or pulmonary tissue has deleterious effects in the early reperfusion period, but the mechanisms and effects of neutrophil influx in the pathogenesis of evolving stroke remain controversial. To investigate whether PMNs contribute to adverse neurologic sequelae and mortality after stroke, and to study the potential role of the leukocyte adhesion molecule intercellular adhesion molecule-1 (ICAM-1) in the pathogenesis of stroke, we used a murine model of transient focal cerebral ischemia consisting of intraluminal middle cerebral artery occlusion for 45 min followed by 22 h of reperfusion. PMN accumulation, monitored by deposition of 111In-labeled PMNs in postischemic cerebral tissue, was increased 2.5-fold in the ipsilateral (infarcted) hemisphere compared with the contralateral (noninfarcted) hemisphere (P < 0.01). Mice immunodepleted of neutrophils before surgery demonstrated a 3.0-fold reduction in infarct volumes (P < 0.001), based on triphenyltetrazolium chloride staining of serial cerebral sections, improved ipsilateral cortical cerebral blood flow (measured by laser Doppler), and reduced neurological deficit compared with controls. In wild-type mice subjected to 45 min of ischemia followed by 22 h of reperfusion, ICAM-1 mRNA was increased in the ipsilateral hemisphere, with immunohistochemistry localizing increased ICAM-1 expression on cerebral microvascular endothelium. The role of ICAM-1 expression in stroke was investigated in homozygous null ICAM-1 mice (ICAM-1 -/-) in comparison with wild-type controls (ICAM-1 +/+). ICAM-1 -/- mice demonstrated a 3.7-fold reduction in infarct volume (P < 0.005), a 35% increase in survival (P < 0.05), and reduced neurologic deficit compared with ICAM-1 +/+ controls. Cerebral blood flow to the infarcted hemisphere was 3.1-fold greater in ICAM-1 -/- mice compared with ICAM-1 +/+ controls (P < 0.01), suggesting an important role for ICAM-1 in the genesis of postischemic cerebral no-reflow. Because PMN-depleted and ICAM-1-deficient mice are relatively resistant to cerebral ischemia-reperfusion injury, these studies suggest an important role for ICAM-1-mediated PMN adhesion in the pathophysiology of evolving stroke.

Animals↗

PubMed1996

Consequences of electroencephalographic-suppressive doses of propofol in conjunction with deep hypothermic circulatory arrest.

BACKGROUND: Some patients who undergo cerebral aneurysm surgery require cardiopulmonary bypass and deep hypothermic circulatory arrest. During bypass, these patients often are given large doses of a supplemental anesthetic agent in the hope that additional cerebral protection will be provided. Pharmacologic brain protection, however, has been associated with undesirable side effects. These side effects were evaluated in patients who received large doses of propofol. METHODS: Thirteen neurosurgical patients underwent cardiopulmonary bypass and deep hypothermic circulatory arrest to facilitate clip application to a giant or otherwise high-risk cerebral aneurysm. Electroencephalographic burst suppression was established before bypass with an infusion of propofol, and the infusion was continued until the end of surgery. Hemodynamic and echocardiographic measurements were made before and during the prebypass propofol infusion and again after bypass. Emergence time also was determined. RESULTS: Prebypass propofol at 243 +/- 57 micrograms.kg-1.min-1 decreased vascular resistance from 34 +/- 8 to 27 +/- 8 units without changing heart rate, arterial or filling pressures, cardiac index, stroke volume, or ejection fraction. Propofol blood concentration was 8 +/- 2 micrograms/ml. Myocardial wall motion appeared hyperdynamic at the end of cardiopulmonary bypass, and all patients were weaned therefrom without inotropic support. After bypass, vascular resistance decreased further, and cardiovascular performance was improved compared to baseline values. Nine of the 13 patients emerged from anesthesia and were able to follow commands at 3.1 +/- 1.4 h. Three others had strokes and a fourth had cerebral swelling. CONCLUSIONS: Propofol infused at a rate sufficient to suppress the electroencephalogram does not depress the heart or excessively prolong emergence from anesthesia after cardiopulmonary bypass and deep hypothermic circulatory arrest.

Adolescent↗

PubMed1996

Procedural and strain-related variables significantly affect outcome in a murine model of focal cerebral ischemia.

The recent availability of transgenic mice has led to a burgeoning number of reports describing the effects of specific gene products on the pathophysiology of stroke. Although focal cerebral ischemia models in rats have been well described, descriptions of a murine model of middle cerebral artery occlusion are scant and sources of potential experimental variability remain undefined. We hypothesized that slight technical modifications would produce widely discrepant results in a murine model of stroke and that controlling surgical and procedural conditions could lead to reproducible physiological and anatomic stroke outcomes. To test this hypothesis, we established a murine model that would permit either permanent or transient focal cerebral ischemia by intraluminal occlusion of the middle cerebral artery. This study provides a detailed description of the surgical technique and reveals important differences among strains commonly used in the production of transgenic mice. In addition to strain-related differences, infarct volume, neurological outcome, and cerebral blood flow appear to be importantly affected by temperature during the ischemic and postischemic periods, mouse size, and the size of the suture that obstructs the vascular lumen. When these variables were kept constant, there was remarkable uniformity of stroke outcome. These data emphasize the protective effects of hypothermia in stroke and might help to standardize techniques among different laboratories to provide a cohesive framework for evaluating the results of future studies in transgenic animals.

Animals↗

PubMed1996

Mild hypothermia reduces penumbral glutamate levels in the rat permanent focal cerebral ischemia model.

Although the cerebroprotective effects of hypothermia in focal models of ischemia are undisputed, the underlying mechanisms of this protection are still subject to much controversy. To analyze whether mild hypothermia attenuates glutamate levels in the penumbra surrounding permanent focal infarcts, extracellular glutamate concentration was analyzed bilaterally by microdialysis 20 minutes before to 120 minutes after a middle cerebral artery occlusion (MCAO) in rats. Normothermic animals (n = 11) had a baseline glutamate concentration of 1.14 +/- 0.40 mumol/ml (standard error of the mean) before the MCAO. Extracellular glutamate levels increased gradually after vessel occlusion to peak at 10.1 +/- 1.45 mumol/ml 80 minutes after the MCAO. This level gradually decreased to 5.72 +/- 1.67 mumol/ml by 120 minutes. Hypothermic animals (n = 11) had a baseline glutamate concentration of 1.73 +/- 0.83 mumol/ml before the MCAO. Extracellular glutamate levels increased after vessel occlusion but stabilized at 3.47 +/- 1.37 mumol/ml 30 minutes after the MCAO and remained stable until completion of the experiment. There were no significant differences in cortical blood flow between the normothermic and hypothermic groups at any time during the experiment. Infarct volumes, expressed as a percentage of the volume of the right (ipsilateral) hemisphere, were 19.8 +/- 2.16% in the normothermic group and 13.0 +/- 1.42% in the hypothermic group (P < 0.02). Although the normothermic penumbral glutamate levels began to increase immediately after the MCAO, they did not peak until 80 minutes after occlusion. In contrast, the normothermic core glutamate levels peaked within 30 minutes after the MCAO. Glutamate diffusion from the core region to the penumbra might account for this delay. Hypothermic cerebroprotection might involve a reduction in the pool of potentially diffusable glutamate in the core region but have little direct effect on glutamate release in the penumbra.

Animals↗

PubMed1996

Perimesencephalic nonaneurysmal subarachnoid hemorrhage: review of the literature.

OBJECTIVE: A critical review of the literature on the incidence, presentation, diagnosis, and prognosis of perimesencephalic nonaneurysmal subarachnoid hemorrhage. METHODS: Review of the relevant literature. CONCLUSION: The importance of early computed tomography (< 3 d), anatomy of the perimesencephalic and neighboring cisterns, and adequate four-vessel angiography are discussed. Treatment strategies, including the avoidance of repeated angiographic studies and surgical exploration, are presented.

Cerebral Angiography↗

PubMed1996

Relationship between the volume of craniotomies for cerebral aneurysm performed at New York state hospitals and in-hospital mortality.

BACKGROUND AND PURPOSE: After a craniotomy for cerebral aneurysm, postoperative mortality can be significant. Previous studies have shown that hospitals performing frequent high-risk procedures (such as coronary artery bypass) have a lower mortality than hospitals where these procedures are performed infrequently. METHODS: The Statewide Planning and Research Cooperative System of the New York State Department of Health reviewed all discharges in New York State from 1987 through 1993 for the diagnoses of subarachnoid hemorrhage and/or cerebral aneurysm and for patients with the procedure code for craniotomy for ruptured or unruptured cerebral aneurysm. In-hospital mortality and length of stay were examined in relation to the volume of craniotomies for aneurysm performed at each individual hospital. RESULTS: A total of 15,376 discharges for subarachnoid hemorrhage and 5638 craniotomies for aneurysm were tabulated in 208 hospitals. For all patients who underwent craniotomy for ruptured cerebral aneurysm (n = 4034), there was a 43% (95% confidence interval, 29% to 57%) reduction in mortality rate in hospitals performing more than 30 craniotomies per year for cerebral aneurysm compared with hospitals performing less surgery (8.8% versus 15.5%, P < .0001). For all patients who underwent craniotomy for unruptured cerebral aneurysm (n = 1604), there was an identical 43% (95% confidence interval, 14% to 73%) reduction in mortality in hospitals performing more than 30 craniotomies per year for cerebral aneurysm (4.6% versus 8.1%, P = .0087). CONCLUSIONS: Hospitals that frequently perform aneurysm operations have lower mortality rates for patients undergoing craniotomy for cerebral aneurysm than hospitals that perform fewer operations.

Aneurysm, Ruptured↗