Abstracts of Literature
CT Angiography: Source Images and Postprocessing Techniques in the Detection of Cerebral Aneurysms—Velthuis BK (Dept of Radiology, RM, E01.132, University Hospital Utrecht, Heidelberglaan 100, 3584 CX Utrecht, Netherlands), van Leeuwen MS, Witkamp TD, Boomstra S, Ramos LMP, Rinkel GJE—AJR Am J Roentgenol. 1997;169:1411–1417.
Objective. The purpose of this study was to evaluate CT angiography source images and to assess various postprocessing techniques for cerebral aneurysm detection in daily practice.
Materials and Methods. We retrospectively studied 17 patients who underwent digital subtraction angiography and CT angiography for possible cerebral aneurysms. Four observers assessed CT angiography data for aneurysms, first after viewing source images in cine mode and again after consecutively adding postprocessing techniques in the following order: maximum intensity projection (MIP) of a 2-cm slab without bone editing (slab-MIP), taking 3 min of operator time; MIP with bone editing (edited-MIP), taking 20 min; shaded-surface display (SSD) without bone editing (3 min); and SSD with bone editing (20 min). In addition, the observers stated which postprocessing method they preferred.
Results. In nine patients, we found 13 aneurysms, 10 of which were larger than 5 mm in size. Sensitivity for detection of aneurysms on CT angiography was 92% for three observers and 77% for one observer. Specificity was 100% for two observers and 78% for two observers. Using four observers in a pooled analysis, the maximum of positive readings was 52. CT angiography was positive in 46 of these 52 instances: 41 positive readings after source image viewing, five additional positive readings after adding MIP, and no additional positive readings after adding SSD. Overall, MIP was judged superior to SSD and slab-MIP was judged to be better than edited-MIP.
Conclusion. In this study interactive source image viewing detected most cerebral aneurysms. Additional slab-MIP is an efficient postprocessing technique for display much like that of angiography, for verification of aneurysms found, and for detection of additional aneurysms. These conclusions need to be verified in a larger study group.
Key Words: aneurysm, image processing, computer-assisted
Reversal and Prevention of Cerebral Vasospasm by Intracarotid Infusions of Nitric Oxide Donors in a Primate Model of Subarachnoid Hemorrhage—Pluta RM, Oldfield EH (Surgical Neurology Branch, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bldg 10, Rm 5D-37, 9000 Rockville Pike, Bethesda, MD 20892), Boock RJ—J Neurosurg. 1997;87:746–751.
Decreased endothelium-derived relaxing factor, nitric oxide (NO), in the arterial wall has been hypothesized to be a potential cause of cerebral vasospasm following subarachnoid hemorrhage (SAH). The authors sought to determine whether intracarotid infusions of newly developed NO-donating compounds (NONOates) could reverse vasospasm or prevent the occurrence of cerebral vasospasm in a primate model of SAH. Twenty-one cynomolgus monkeys were studied in two experimental settings. In an acute infusion experiment, saline or NONOate was infused intracarotidly in four normal monkeys and in four monkeys after onset of SAH. During the infusions regional cerebral blood flow (rCBF) was measured in eight animals and CBF velocity in two. In a chronic infusion experiment, saline (four animals) or NONOate (diethy-lamine-NO [three animals] or proli-NO [six animals]) was infused intracarotidly in monkeys for 7 days after SAH. In acute infusion experiments, 3-minute intracarotid diethylamine-NO infusions reversed arteriographically confirmed vasospasm of the right middle cerebral artery (MCA) (as viewed on anteroposterior projection, the decrease in area was 8.4±4.3% in the treatment group compared with 35±12% in the control group; p<0.004), increased rCBF by 31±1.9% (p<0.002), and decreased the mean systolic CBF velocity in the right MCA. In a long-term infusion experiment, the area of the right MCA in control animals decreased by 63±5%. In animals undergoing a 7-day continuous glucantime-NO intracarotid infusion, the area of the right MCA decreased by 15±6.2%, and in animals undergoing a 7-day proli-NO infusion, the area of the right MCA decreased by 11±2.9% (p<0.05). The mean arterial blood pressure decreased in the glucan-time-NO group from 75±12 mm Hg (during saline infusion) to 57±10 mm Hg (during glucantime-NO infusion; p<0.05), but it was unchanged in animals undergoing proli-NO infusion (76±12 mm Hg vs. 78±12 mm Hg). Results of these experiments show that cerebral vasospasm is both reversed and completely prevented by NO replacement. However, only the use of regional infusion of the NONOate with an extremely short half-life avoided a concomitant decrease in arterial blood pressure, which could produce cerebral ischemia in patients with impaired autoregulation of CBF after the rupture of an intracranial aneurysm.
Key Words: vasospasm, nitric oxide
Intracranial Aneurysm: Anatomic Factors That Predict the Usefulness of Intraoperative Angiography—Derdeyn CP (Neuroradiology, Mallinckrodt Institute of Radiology, Washington University School of Medicine, 510 S Kingshighway Blvd, St Louis, MO 63110), Moran CJ, Cross DT III, Sherburn EW, Dacey RG Jr—Radiology. 1997;205:335–339.
Purpose: To correlate the size and location of intracranial aneurysm with the need to reposition the aneurysm clip after intraoperative angiography.
Materials and Methods: In 199 consecutive patients with 234 clipped intracranial aneurysms, 273 intraoperative angiographic studies were retrospectively reviewed. Aneurysm size and location, determined with preoperative angiographic and surgical reports, were correlated with the frequency of clip repositioning because of parent- or branch-vessel compromise or unexpected residual aneurysm.
Results: Findings from intraoperative angiograms resulted in clip repositioning in 46 of 273 (16.8%) studies. Clip repositioning was statistically significantly less frequent with aneurysms of the posterior communicating (three of 52 [5.7%] studies) and anterior choroidal (none of 12 studies) arteries. High rates of clip repositioning were found in aneurysms of the superior hypophyseal artery (seven of 18 [38.9%] studies), superior cerebellar artery (three of five [60.0%] studies), and bifurcation of the internal carotid artery (three of nine [33.3%] aneurysms). In 98 conventional follow-up angiographic studies, seven (7%) false-negative cases with unsuspected aneurysm neck remnant were found.
Conclusion: The rate of clip repositioning in aneurysms of the posterior communicating or anterior choroidal arteries was less than that at other locations (P<.05). Intraoperative angiography may not be necessary when aneurysms are at these two locations.
Key Words: aneurysm, angiography
Frequency of Deep Vein Thrombosis in Patients With Patent Foramen Ovale and Ischemic Stroke or Transient Ischemic Attack—Lethen H (Dept of Cardiology, University Hospital of Aachen, Pauwelsstrasse, 52072 Aachen, Germany), Flachskampf FA, Schneider R, Sliwka U, Köhn G, Noth J, Hanrath P—Am J Cardiol. 1997;80:1066–1069.
To evaluate the additional value of transesophageal (TEE) compared with transthoracic (TTE) echocardiography and the role of patent foramen ovale (PFO) and deep vein thrombosis in the work-up of embolic events, patients with presumed cardiac embolic stroke or transient ischemic attack (neurovascular etiology was excluded) were prospectively studied by transthoracic and transesophageal contrast echocardiography. If PFO was detected echocardiographically, PFO size was assessed semiquantitatively and phlebography of both legs was performed. Two hundred forty-two consecutive patients (153 men, 60±15 years) were studied. In 197 patients, neuroimaging showed evidence of embolic infarction. TEE identified 138 potential cardiac sources of embolism in 111 patients, compared with 69 by TTE (p<0.01) in 59 patients. TEE detected potential cardiac sources in 52 patients with negative TTE examination and was significantly superior compared with TTE for identifying left atrial thrombi, spontaneous echo contrast, PFO, atrial septal aneurysm, and atheroma of the ascending aorta. In patients with a positive TTE, additional diagnostic information by TEE was found in only 6 patients and did not change therapy. Phlebography was performed in 53 patients with PFO and revealed deep vein thrombosis in 5 patients (9.5%); all had medium or large PFOs. Thus, in patients with cerebral ischemia of suspected cardiogenic origin and a normal TTE examination, TEE detects potential causes of embolism in 31% of patients and is therefore of diagnostic relevance. Conversely, in the presence of a diagnostic TTE an additional TEE confers only marginal diagnostic benefit. Deep venous thrombosis was detected in nearly 10% of patients with PFO as the sole identifiable cardiac risk factor. Given that in 4 of 5 patients deep vein thrombosis was clinically silent, phlebography should be performed in patients with medium or large interatrial shunts if paradoxical embolism is suspected.
Key Words: thrombosis, foramen ovale, patent
Hyperhomocyst(e)inemia is a Risk Factor for Arterial Endothelial Dysfunction in Humans—Woo KS (Prince of Wales Hospital, Dept of Medicine, Shatin, Hong Kong), Chook P, Lolin YI, Cheung ASP, Chan LT, Sun YY, Sanderson JE, Metreweli C, Celermajer DS—Circulation. 1997;96:2542–2544.
Background Hyperhomocyst(e)inemia is associated with premature peripheral vascular, cerebrovascular, and coronary artery disease. Because homocysteine has been found to be damaging to endothelial cells in animal and cell culture studies, we evaluated the association between hyperhomocysteinemia and arterial endothelial dysfunction (a marker of early atherosclerosis) in asymptomatic adult subjects.
Methods and Results Using high-resolution ultrasound, we measured endothelium-dependent flow-mediated dilation (EDD) and endothelium-independent nitroglycerin-induced dilation (GTN) of the brachial artery in 14 prospectively defined hyperhomocysteinemic (mean plasma homocysteine, 34.8±8.5 μmol/L), nonsmoking, healthy subjects aged 53±9 years and 14 control subjects with low plasma homocysteine levels (9.9±3.2 μmol/L). The two groups were well matched for age; sex; body mass index; blood pressure, blood cholesterol, folate, and vitamin B12 levels; and vessel diameter. EDD was significantly lower in hyperhomocysteinemic subjects (6.5±1.7%) than in subjects with low homocysteine levels (10.8±1.7%) (P<.001). GTN responses were similar in the two subject groups (P=.90). Multivariate analysis confirmed homocysteine level as the strongest predictor for impaired EDD, independent of age, sex, body mass index, or blood pressure, folate, vitamin B12, and cholesterol levels.
Conclusions Hyperhomocysteinemia is an independent risk factor for arterial endothelial dysfunction in healthy middle-aged adults.
Key Words homocyst(e)ine, endothelium, vascular
Mechanisms of Infarction in the Superficial Posterior Cerebral Artery Territory—Steinke W (Dept of Neurology, Marien-Hospital Düsseldorf, Rochusstrasse 2, D-40479 Düsseldorf, Germany), Mangold J, Schwartz A, Hennerici M—J Neurol. 1997;244:571–578.
Numerous reports have described a variety of clinical syndromes resulting from posterior cerebral artery (PCA) infarction, whereas only a few pathoanatomical and retrospective clinical studies have investigated the underlying mechanisms. Therefore we attempted to determine the causes of infarction in the superficial posterior cerebral artery (PCA) territory by means of a more comprehensive, modern vascular and cardiac study. During a 4-year period 74 consecutive patients (49 men, 25 women) with acute PCA infarction documented on CT (n=74) and MRI (n=41) were included in the study. Patients had a neurological examination, vascular studies [extra- and transcranial Doppler (n=74), magnetic resonance (n=31) or intra-arterial (n=22) angiography], cardiac evaluation [ECG (n=74), transthoracic (n=74) and transoesophageal echocardiography (n=30)], and coagulation tests. A cardiac source of embolism was established in 31%, significant vertebrobasilar artery disease in 22%, and PCA stenosis or occlusion in 8% of the patients. Rare causes, such as hypercoagulopathy or paradoxical embolism via a patent foramen ovale, were present in 15%. However, in spite of the comprehensive diagnostic evaluation, the cause of the stroke remained undetermined in 24% of the cases. Apart from complete infarcts of the posterior branches of the PCA, which occurred more frequently in cardioembolic strokes (18%, P<0.05), the topographical patterns of infarct extension and the coincidence of infarction in the deep territories of the PCA, the cerebellum and brainstem were not significantly different among the causal subgroups. The frequency of haemorrhagic transformation (18%) was highest among cardioembolic strokes (44%, P<0.001). This prospective study of PCA infarction demonstrated embolism from cardiac and vascular sources as the predominant cause. In contrast to previous studies, we found no evidence of migraine as a cause of PCA infarction, whereas paradoxical embolism was the presumed cause in a considerable number of cases. Whereas the cause of stroke could not reliably be derived from infarct topography, haemorrhagic transformation indicated there had been cardioembolism in most cases.
Key Words: cerebral arteries, stroke classification
Mass Effect and Death From Severe Acute Stroke—Pullicino PM (Stroke Program, Dept of Neurology, Buffalo General Hospital, 100 High St, Buffalo, NY 14203), Alexandrov AV, Shelton JA, Alexandrova NA, Smurawska LT, Norris JW—Neurology. 1997;47:1090–1095.
Background: In severe acute stroke, the degree of midline cerebral displacement is related to level of consciousness but not to survival. Early identification of patients at high risk of death from mass effect would assist patient management decisions. Methods: We measured lesion volume, horizontal pineal displacement (PD), and horizontal septum pellucidum displacement (SD) on axial CT of consecutive patients with severe (Canadian Neurological Scale score ≤5) acute hemispheric stroke. We correlated CT measurements with the probability of 14-day survival. Results: Forty-six (39%) of 118 patients died within 14 days and 72 (61%) died within 1 year following stroke. Crude risk factors for 14-day mortality were as follows: lesion volume ≥400 ml, SD ≥9 mm, PD ≥4 mm, intraventricular hemorrhage, and coma on admission. Only SD (p=0.001) and coma on admission (p=0.019) remained significant in multivariate analysis, but PD was highly correlated with SD (r=0.82). PD of ≥4 mm on a scan performed within 48 hours of stroke onset identified patients with a low probability of 14-day survival (0.16; CI 0 to 0.32) with a specificity of 89% and a sensitivity of 46%. Conclusions: The degree of horizontal midline cerebral displacement correlates with the likelihood of death following stroke. Patients with ≥4 mm PD on CT performed within 48 hours of stroke onset are at high risk for early death.
Key Words: stroke, acute, death
Basilar Artery Embolism: Clinical Syndrome and Neuroradiologic Patterns in Patients Without Permanent Occlusion of the Basilar Artery—Schwarz S (Dept of Neurology, University of Heidelberg, 400 Im Neuenheimer Feld, Heidelberg 69120, Germany), Egelhof T, Schwab S, Hacke W. Neurology. 1997;49:1346–1352.
The objective of this study was to clarify the clinical and radiologic features, risk factors, and prognosis of basilar embolism without permanent basilar artery occlusion. Forty-five patients (mean age, 59 years) with basilar artery embolism participated in the study. Patients with basilar artery occlusion were excluded. The Glasgow Coma Scale (GCS) score on admission was <7 in five patients, 7 to 12 in 11 patients, and >12 in 29 patients. Etiologic factors were cardiac arrhythmia (17 patients), vertebral artery occlusion (12 patients), cervical spine trauma (4 patients), embolism following angiography (2 patients), and surgery (1 patient). MRI was performed in 17 patients and CT in 39 patients. Radiologic examinations were initially normal in 14 patients and remained normal in three patients. Final infarct localization was the thalamus (36 patients), cerebellum (20 patients), posterior cerebral artery territory (21 patients), midbrain (12 patients), and pons (8 patients). Eight to 12 weeks after stroke 12 patients were without clinical signs (Glasgow Outcome Scale [GOS] 1), 15 patients had minor neurologic deficits (GOS 2), 10 were severely disabled (GOS 3), and eight patients had died (GOS 5). Outcome correlated with GCS on admission (p<0.0001) and with the number of ischemic lesions (p=0.0001). The typical syndrome is an acute loss of consciousness followed by multiple brainstem symptoms. Usually, clinical symptoms improve rapidly and, in some patients, completely. Compared with basilar occlusion, basilar embolism has a relatively low mortality and outcome is frequently excellent.
Key Words: basilar artery, embolism
Use of Low-Dose Oral Contraceptives and Stroke in Young Women—Schwartz SM (Cardiovascular Health Research Unit, 1730 Minor Ave, Suite 1360, Seattle, WA 98101), Siscovick DS, Longstreth WT Jr, Psaty BM, Beverly RK, Raghunathan TE, Lin D, Koepsell TD—Ann Intern Med. 1997;127:596–603.
Background: Low-dose oral contraceptives are widely used, but there are limited data on the cerebrovascular risks associated with these medications.
Objective: To determine whether use of low-dose oral contraceptives influences the risk for stroke.
Design: Population-based case–control study.
Setting: Women 18 to 44 years of age who resided in western Washington State between 1991 and 1995.
Participants: Patients with ischemic stroke (n=60), hemorrhagic stroke (n=102), and other types of stroke (n=11) and controls identified through random-digit dialing (n=485).
Measurements: Details about oral contraceptive use and other risk factors for stroke were obtained through in-person interviews.
Results: The estimated incidences of hemorrhagic stroke and ischemic stroke were 6.4 and 4.3 per 100 000 women-years, respectively. Compared with women who had never used oral contraceptives (after adjustment for risk factors for stroke), current users of low-dose oral contraceptives had estimated odds ratios of 0.93 (95% CI, 0.37 to 2.31) for hemorrhagic stroke and 0.89 (CI, 0.27 to 2.94) for ischemic stroke. Compared with past users of oral contraceptives, current users had odds ratios of 1.41 (CI, 0.67 to 2.96) for hemorrhagic stroke and 1.37 (CI, 0.49 to 3.81) for ischemic stroke. For past users compared with never users, the odds ratios were 0.59 (CI, 0.30 to 1.18) for hemorrhagic stroke and 0.57 (CI, 0.25 to 1.32) for ischemic stroke. The odds ratio for hemorrhagic stroke in current users of low-dose oral contraceptives containing norgestrel or levonorgestrel was elevated (3.23 [CI, 1.24 to 8.41]). Among patients with hemorrhagic stroke, the odds ratio for aneurysmal bleeding associated with current use of low-dose oral contraceptives containing norgestrel or levonorgestrel was 4.46 (CI, 1.58 to 12.53).
Conclusions: The overall risk for stroke and type of stroke was not increased among current users of low-dose oral contraceptives in the study population. Larger studies are needed to clarify both the relation of risk for stroke to past use of oral contraceptives and the possible association between current use of norgestrel-containing oral contraceptives and hemorrhagic stroke.
Key Words: contraceptives, oral, young adults
Risk Factors for Microangiopathy-Related Cerebral Damage in the Austrian Stroke Prevention Study—Schmidt R (Dept of Neurology, Karl-Franzens University Graz, Auenbruggerplatz 22, A-8036 Graz, Austria), Fazekas F, Hayn M, Schmidt H, Kapeller P, Roob G, Offenbacher H, Schumacher M, Eber B, Weinrauch V, Kostner GM, Esterbauer H—J Neurol Sci. 1997;152:15–21.
Microangiopathy-related cerebral damage (MARCD) represents a common incidental MRI observation in the elderly. The risk factors of such findings are widely unknown. We therefore performed MRI in 349 randomly selected volunteers (ages 50 to 70 years) without neuropsychiatric disease, and evaluated the association of MARCD with conventional and recently suggested cerebrovascular risk factors such as apolipoprotein E genotypes, plasma concentrations of essential antioxidants and anticardiolip in antibody titres. MARCD was defined as evidence of early confluent and confluent deep white matter hyperintensities and lacunes. It was present in 71 (20.3%) subjects. Individuals with MARCD were older than those without such findings (62.7 years vs 59.6 years; P=0.0001). They had a higher rate of arterial hypertension (45.1% vs 28.1%; P=0.006) and cardiac disease (50.7% vs 37.1%; P=0.04), higher systolic blood pressure readings at exam (144.4 mmHg vs 136.7 mmHg; P=0.004), and higher serum fibrinogen concentrations (327.1 mg/dl vs 292.5 mg/dl; P=0.001). Their levels of total cholesterol (217.6 mg/dl vs 231.2; P=0.009), apolipoprotein A-I (167.3 mg/dl vs 177.4 mg/dl, P=0.02), lycopene (0.17 μmol/l vs 0.24 μmol/l; P=0.003), retinol (1.91 μmol/l vs 2.10 μmol/l; P=0.02) and alpha-tocopherol (27.55 μmol/l vs 31.14 μmol/l; P=0.001) were significantly lower. Forward stepwise regression analysis created a model of independent predictors of MARCD with age entering first (odds ratio 2.01/10 years), fibrinogen second (odds ratio 2.45/100 mg/dl), alpha-tocopherol third (odds ratio 0.55/10 μmol/l), and arterial hypertension fourth (odds ratio 1.96). The association of MARCD with various treatable clinical conditions may have preventive implications.
Key Words: risk factors, small-vessel disease
Hormone Replacement Therapy and Risk of Non-fatal Stroke—Pedersen AT (Dept of Obstetrics and Gynaecology 537, Hvidovre Hospital, University of Copenhagen, Kettegårds Alle 30, DK-2650 Hvidovre, Denmark), Lidegaard Ø, Kreiner S, Ottesen B—Lancet. 1997;350:1277–1283.
Background The effect of postmenopausal hormone replacement therapy (HRT) on the risk of subtypes of stroke is as yet unclear. To investigate the effect of oestrogen and combined oestrogen-progestagen therapy on the risk of non-fatal haemorrhagic and thromboembolic stroke, we carried out a case-control study.
Methods From the Danish National Patient Register we identified all Danish women aged 45–64 years who had a non-fatal, first-ever cerebrovascular attack during 1990–92. Two age-matched controls were randomly selected for each case from the Danish National Person Register. Important correlates of hormone use and stroke, on which information was obtained from postal questionnaires, were controlled for by multivariate analyses based on log-linear graphical models. The analyses included data on 1422 cases classified in four subtypes of stroke (160 subarachnoid haemorrhage, 95 intracerebral haemorrhage, 846 thromboembolic infarction, 321 transient ischaemic attack) and 3171 controls.
Findings After adjustment for confounding variables and correction for the trend in sales of HRT preparations, no significant associations were detected between current use of unopposed oestrogen replacement therapy and non-fatal subarachnoid haemorrhage (odds ratio 0.52 [95% CI 0.23–1.22]), intracerebral haemorrhage (0.15 [0.02–1.09]), or thromboembolic infarction (1.16 [0.86–1.58]), respectively, compared with never use. Current use of combined oestrogen-progestagen replacement therapy had no significant influence on the risk of subarachnoid haemorrhage (1.22 [0.79–1.89]), intracerebral haemorrhage (1.17 [0.64–2.13]), or thromboembolic infarction (1.17 [0.92–1.47]). A significantly increased incidence of transient ischaemic attacks among former users of HRT and among current users of unopposed oestrogen may to some extent be explained by selection—HRT users being more aware of symptoms than non-users.
Interpretation Unopposed oestrogen and combined oestrogen-progestagen replacement therapy have no influence on the risk of non-fatal thromboembolic or haemorrhagic stroke in women aged 45–64 years.
Key Words: hormones, risk factors
High Dose Baclofen Is Neuroprotective but Also Causes Intracerebral Hemorrhage: A Quantal Bioassay Study Using the Intraluminal Suture Occlusion Method—Jackson-Friedman C (Dept of Neurosciences, School of Medicine, University of California, San Diego, CA 92161), Lyden PD, Nunez S, Jin A, Zweifler R—Exp Neurol. 1997;147:346–352.
Agonists of the GABA-A receptor are neuroprotective after experimental stroke, but studies of GABA-B agonists have contradicted each other. To further investigate whether GABA-B agonists may be neuroprotective, we devised a quantal bioassay using the intraluminal occlusion method of inducing reversible cerebral ischemia. Subjects underwent middle cerebral artery occlusion for varying amounts of time, ranging from 5 to 90 min. Behavioral outcome was measured 48 h later with a quantal observational scale: score of abnormal given for any one of asymmetric forepaw flexion on tail lift, asymmetric grip, circling, reduced exploration, seizures, or death. To the grouped response data the logistic equation was used to find the ED50, the duration of occlusion that caused one-half of the subjects to be abnormal. To find the potency ratio for each drug, we divided the ED50 for treatment by that for vehicle. We administered baclofen, a GABA-B agonist, intraperitoneally 5 min after the onset of ischemia. Baclofen (20 mg/kg) was neuroprotective (potency ratio of 3.0, P<0.05), but a lower dose (10 mg/kg) was not. However, both doses of baclofen caused significantly more intracerebral hemorrhages than control. In awake animals, both baclofen doses caused significant increases in mean arterial pressure, but no changes in other cardiorespiratory variables. The glutamate antagonist MK-801, the GABA-A agonist muscimol, and hypothermia were all protective using the bioassay (potency ratios ranging from 1.5 to 3.0). We conclude that although baclofen (20 mg/kg) may be neuroprotective, its utility is complicated by postischemic hypertension and cerebral hemorrhages.
Key Words: stroke, experimental, neuroprotection
Effects of Chronic Nitric Oxide Synthase Inhibition on Cerebral Arterioles in Rats—Chillon J-M, Ghoneim S, Baumbach GL (Dept of Pathology, 105 Medical Laboratories, University of Iowa College of Medicine, Iowa City, IA 52242)—Hypertension. 1997;30:1097–1104.
We examined the effects of nitric oxide (NO) synthase inhibition on the structure and mechanics of cerebral arterioles. We measured pressure, diameter, and cross-sectional area of the vessel wall (histologically) in maximally dilated cerebral arterioles in Sprague-Dawley rats that were untreated or treated for 3 months with the NO synthase inhibitor NG-nitro-l-arginine methyl ester (L-NAME; 10 mg/kg per day). Treatment with L-NAME increased cerebral arteriolar mean (87±6 versus 42±2 mm Hg, P<.05) and pulse (25±2 versus 13±2 mm Hg, P<.05) pressures, as well as cross-sectional area of the vessel wall (1839±70 versus 1019±58 μm2, P<.05) and external diameter (101±4 versus 87±2 μm, P<.05). These findings suggest that hypertension induced by NO synthase inhibition is accompanied by hypertrophy of the vessel wall and enlargement of cerebral arterioles in rats. To determine the role of cerebral arteriolar pulse pressure in hypertrophy of cerebral arterioles during inhibition of NO synthase, we measured the cross-sectional area of the vessel wall in rats treated with L-NAME that underwent unilateral carotid clipping. Unilateral carotid clipping failed to prevent increases in cross-sectional area of the vessel wall (1507±173 and 1613±148 μm2 in the clip and sham sides, respectively) in rats treated with L-NAME, even though increases in pulse pressure were prevented (16±1 and 27±1 mm Hg in the clip and sham sides, respectively, P<.05). These findings suggest that inhibition of NO synthase may promote hypertrophy of cerebral arterioles independently of increases in arteriolar pulse pressure.
Key Words: nitric oxide synthase, cerebral arteries
In Vivo Uptake of [3H]Nimodipine in Focal Cerebral Ischemia: Modulation by Hyperglycemia—Osuga S, Hogan MJ (Neuroscience Research Institute, University of Ottawa, 451 Smyth Rd, Ottawa, ON, Canada K1H 8M5)—J Cereb Blood Flow Metab. 1997;17:1057–1065.
Cell membrane depolarization and tissue acidosis occur rapidly in severely ischemic brain. Preischemic hyperglycemia is recognized to increase ischemic tissue acidosis and the present studies were undertaken to correlate depolarization and tissue acidosis during acute focal cerebral ischemia and hyperglycemia. We used a dual-label autoradiography method to simultaneously measure the in vivo distribution of [3H]nimodipine and [14C]DMO (5,5-dimethyl-2,4-oxazolidinedione) in brain to identify regions of ischemic depolarization and measure regional net tissue pH. Regional cerebral blood flow (CBF) was measured in separate studies. Measurements were made 30 minutes after combined middle cerebral artery and ipsilateral common carotid artery occlusion in normoglycemic and hyperglycemic rats. Tissue pH in the ischemic cortex was depressed to 6.76±0.11 in normoglycemic rats (n=12) and 6.57±0.13 in hyperglycemic rats (n=12), with significantly greater acidosis in the hyperglycemic group (P<0.001). In contrast the ratio of [3H]nimodipine uptake in the ischemic cortex relative to the contralateral nonischemic cortex was significantly greater in normoglycemic (1.83±0.45) than hyperglycemic (1.40±0.50) rats (P<0.05). Within this region of ischemic cortex CBF was 31±22 mL/100 g in normoglycemic rats (n=8) and 33±22 mL/100 g/min in hyperglycemic rats (n=9). Cerebral blood flow did not differ between these two groups in any region. Thus hyperglycemia reduced the extent of ischemic depolarization within the cortex during the first 30 minutes of focal cerebral ischemia. This effect may be related to the increased tissue acidosis or to other factors that may lessen calcium influx and preserve cellular energy stores in the ischemic cortex of the hyperglycemic rats.
Key Words: hyperglycemia, nimodipine
A Mouse Model of Embolic Focal Cerebral Ischemia—Zhang Z, Chopp M (Henry Ford Hospital, Neurology Dept, 2799 W Grand Blvd, Detroit, MI 48202), Zhang RL, Goussev A—J Cereb Blood Flow Metab. 1997;17:1081–1088.
We developed a mouse model of embolic focal cerebral ischemia, in which a fibrin-rich clot was placed at the origin of the middle cerebral artery (MCA) in C57BL/6J mice (n=31) and B6C3 mice (n=10). An additional three nonembolized C57BL/6J mice were used as a control. Embolus induction, cerebral vascular perfusion deficit, and consequent ischemic cell damage were confirmed by histopathology, immunohistochemistry, laser confocal microscopy, and regional cerebral blood flow (rCBF) measurements. Reduction in rCBF and cerebral infarct were not detected in the control animals. An embolus was found in all C57BL/6J and B6C3 mice at 24 hours after injection of a clot. Regional CBF in the ipsilateral parietal cortex decreased to 23% (P<0.05) and 17% (P<0.05) of preembolization levels immediately and persisted for at least 1 hour in C57BL/6J mice (n=6) and in B6C3 mice (n=3), respectively. A significant decrease of rCBF was accompanied by a corresponding reduction of plasma perfusion in the ipsilateral MCA territory. Neurons exhibited marked reduction in microtubule-associated protein-2 immunostaining coincident with the area of perfusion deficit. The percent infarct volume was 30.3%±13.4% for C57BL/6J mice (n=17), and 38.3%±15.3% for B6C3 mice (n=7) at 24 hours after embolization. This model of embolic ischemia is relevant to thromboembolic stroke in humans and may be useful to investigate embolic cerebral ischemia in the genetically altered mouse and for evaluation of antiembolic therapies.
Key Words: embolism, stroke, experimental
Cathepsin B and Middle Cerebral Artery Occlusion in the Rat—Seyfried D (Dept of Neurosurgery, Henry Ford Hospital, 2799 W Grand Blvd, Detroit, MI 48202), Han Y, Zheng Z, Day N, Moin K, Rempel S, Sloane B, Chopp M—J Neurosurg. 1997;87:716–723.
Lysosomal proteases, although tightly regulated under physiological conditions, are known to contribute to cell injury after various forms of tissue ischemia have occurred. Because cathepsin B is a prominent lysosomal protease found in brain parenchyma, the authors hypothesized that it may contribute to neuronal cell death after focal cerebral ischemia. The authors measured the expression and spatial distribution of cathepsin B within the ischemic brain in 43 animals by means of immunohistochemical analysis in a rat model of transient middle cerebral artery (MCA) occlusion. Cathepsin B activity was also measured within specific ischemic brain regions by using an in vitro assay (22 animals). In addition, the authors tested the therapeutic effect of preischemic intraventricular administration of stefin A, a cysteine protease inhibitor, on the volume of cerebral infarction after transient MCA occlusion (15 animals). Increased cathepsin B immunoreactivity was detected exclusively within the ischemic neurons after 2 hours of reperfusion following a 2-hour MCA occlusion. Cathepsin B immunolocalization in the ischemic region decreased by 24 hours of reperfusion, but then increased by 48 hours of reperfusion because the infarct was infiltrated by inflammatory cells. Increased immunolocalization of cathepsin B in the inflammatory cells located in the necrotic infarct core continued through 7 days of reperfusion. Cathepsin B enzymatic activity was significantly increased in the ischemic tissue at 2, 8, and 48 hours, but not at 24 hours of reperfusion after 2 hours of MCA occlusion. Continuous intraventricular infusion of stefin A, before 2 hours of MCA occlusion (15 animals), significantly reduced infarct volume compared with control animals (12 animals): the percentage of hemispheric infarct volume was 20±3.9 compared with 33±3.5 (standard error of the mean; p=0.025). These data indicate that neuronal cathepsin B undergoes increased expression and activation within 2 hours of reperfusion after a 2-hour MCA occlusion and may be a mechanism contributing to neuronal cell death. Intraventricular infusion of stefin A, an inhibitor of cathepsin B, significantly reduces cerebral infarct volume in rats.
Key Words: cerebral ischemia, focal, neuronal death
Juxtalumenal Location of Plaque Necrosis and Neoformation in Symptomatic Carotid Stenosis—Bassiouny HS (University of Chicago, 5841 S Maryland Ave, MC 5028, Chicago, IL 60637), Sakaguchi Y, Mikucki SA, McKinsey JF, Piano G, Gewertz BL, Glagov S—J Vasc Surg. 1997;26:585–594.
Purpose: The structural features that underlie carotid plaque disruption and symptoms are largely unknown. We have previously shown that the chemical composition and structural complexity of critical carotid stenoses are related to plaque size regardless of symptoms. To further determine whether the spatial distribution of individual plaque components in relation to the lumen corresponds to symptomatic outcome, we evaluated 99 carotid endarterectomy plaques.
Methods: Indications for operation were symptomatic disease in 59 instances (including hemispheric transient ischemic attack in 29, stroke in 19, and amaurosis fugax in 11) and angiographic asymptomatic stenosis >75% in 40. Plaques removed after remote symptoms beyond 6 months were excluded. Histologic sections from the most stenotic region of the plaque were examined using computer-assisted morphometric analysis. The percent area of plaque cross-section occupied by necrotic lipid core with or without associated plaque hematoma, by calcification, as well as the distance from the lumen or fibrous cap of each of these features, were determined. The presence of foam cells, macrophages, and inflammatory cell collections within, on, or just beneath the fibrous cap was taken as an additional indication of plaque neoformation.
Results: The mean percent angiographic stenosis was 82%±11% and 79%±13% for the asymptomatic and symptomatic groups, respectively (p>0.05). The necrotic core was twice as close to the lumen in symptomatic plaques when compared with asymptomatic plaques (0.27±0.3 mm vs 0.5±0.5 mm; p<0.01). The percent area of necrotic core or calcification was similar for both groups (22% vs 26% and 7% vs 6%, respectively). There was no significant relationship to symptom production of either the distance of calcification from the lumen or of the percent area occupied by the lipid necrotic core or calcification. The number of macrophages infiltrating the region of the fibrous cap was three times greater in the symptomatic plaques compared with the asymptomatic plaques (1114±1104 vs 385±622, respectiely, p<0.009). Regions of fibrous cap disruption or ulceration were more commonly observed in the symptomatic plaques than in the asymptomatic plaques (32% vs 20%). None of the demographic or clinical atherosclerosis risk factors distinguished between symptomatic and asymptomatic plaques.
Conclusions: These findings indicate that proximity of plaque necrotic core to the lumen and cellular indicators of plaque neoformation or inflammatory reaction about the fibrous cap are associated with clinical ischemic events. The morphologic complexity of carotid stenoses does not appear to determine symptomatic outcome but rather the topography of individual plaque components in relation to the fibrous cap and the lumen. Imaging techniques that precisely resolve the position of the necrotic core and evidence of inflammatory reactions within carotid plaques should help identify high-risk stenoses before disruption and symptomatic carotid disease.
Key Words: atherosclerosis, carotid stenosis
Mass Effect Caused by Clinically Unruptured Cerebral Arteriovenous Malformations—Miyasaka Y (Dept of Neurosurgery, Kitasato University School of Medicine, 1-15-1 Kitasato, Sagamihara, Kanagawa 228, Japan), Kurata A, Tanaka R, Nagai S, Yamad M, Irikura K, Fujii K—Neurosurgery. 1997;41:1060–1064.
Objective: It is generally considered that mass effect caused by arteriovenous malformations (AVMs) is evidence of ruptures. In the present study, the incidence of mass effect in clinically unruptured AVMs was evaluated, and the underlying causative factors and pathophysiological mechanisms were studied.
Methods: Twenty-seven patients with clinically unruptured supratentorial pial AVMs were examined. The majority were suffering from epilepsy, and frontal lobe involvement was revealed in approximately half of the patients. Angiographic studies, computed tomographic scans, and magnetic resonance images were obtained for all patients. Twenty-one patients underwent removal of AVMs. In 10 of the surgically treated patients, intraoperative vascular pressure measurements were obtained before removal of the AVMs.
Results: Mass effect was detected in 12 (44%) of the 27 patients. Cortical sulci obliteration (eight patients) and lateral ventricle displacement (seven patients) were frequently noted. The volume of AVMs was significantly larger in patients with mass effect than in those without mass effect (P<0.001). Large dilated venous sacs or ectatic veins were observed to be associated with mass effect (P<0.001). In only one patient was gross displacement related to a surrounding massive brain edema. Draining vein pressure in patients with mass effect was significantly elevated as compared to the average value in patients without mass effect (22±5 versus 12±3 mm Hg) (P<0.01).
Conclusion: The present study suggests that mass effect is not infrequent in clinically unruptured AVMs. Furthermore, multiple causative factors were detected, including the large size of AVMs, marked draining vein dilatation, and brain edema around the AVMs. Findings also indicated that a pathophysiologically high pressure in the venous drainage system may contribute to mass effect.
Key Words: cerebral arteriovenous malformations, magnetic resonance imaging
Acute Stroke: Usefulness of Early CT Findings Before Thrombolytic Therapy—von Kummer R (Dept of Neuroradiology, Technische Universität, Fetscherstrasse 74, D-01307 Dresden, Germany), Allen KL, Holle R, Bozzao L, Bastianello S, Manelfe C, Bluhmki E, Ringleb P, Meier DH, Hacke W—Radiology. 1997;205:327–333.
Purpose: To determine whether the extent of subtle parenchymal hypoattenuation detected on computed tomographic (CT) scans obtained within 6 hours of ischemic stroke is a factor in predicting patients’ response to thrombolytic treatment.
Materials and Methods: The baseline CT scans of 620 patients, who received either recombinant tissue plasminogen activator (rt-PA) or a placebo, in a double-blind, randomized multicenter trial were prospectively evaluated and assigned to one of three categories according to the extent of parenchymal hypoattenuation: none, 33% or less (small), or more than 33% (large) of the middle cerebral artery territory. The association between the extent of hypoattenuation on the baseline CT scans and the clinical outcome in the placebo-treated and the rt-PA–treated groups after 3 months was analyzed.
Results: In 215 patients with a small hypoattenuating area, treatment increased the chance of good outcome. In 336 patients with a normal CT scan and in 52 patients with a large hypoattenuating area, rt-PA had no beneficial effect but increased the risk for fatal brain hemorrhage.
Conclusion: The response to rt-PA in patients with ischemic stroke can be predicted on the basis of initial CT findings of the extent of parenchymal hypoattenuation in the territory of the middle cerebral artery.
Key Words: thrombolytic therapy, tomography, emission computed
Transtemporal Power- and Frequency-Based Color-Coded Duplex Sonography of Cerebral Veins and Sinuses—Bamugartner RW (St Elizabeth’s Medical Center, 736 Cambridge St, Boston, MA 02135), Gönner F, Arnold M, Müri RM—AJNR Am J Neuroradiol. 1997;18:1771–1781.
Purpose: To determine the ability of transtemporal power- and frequency-based transcranial color-coded duplex sonography to aid in the assessment of cerebral veins and sinuses, as well as to provide reference data for flow direction and velocity. Methods: Using a color duplex device equipped with a 2.0/2.5-MHz sector scan, we insonated 120 healthy volunteers and three patients with cerebral venous thrombosis. Results: In subjects 20 to 59 years old, deep middle cerebral veins were identified in 88%, basal veins in 97%, straight sinuses in 60%, and transverse sinuses in 42%. The corresponding values for subjects 60 to 79 years old were 53%, 86%, 23%, and 20%, respectively. Velocities were highest in transverse and straight sinuses, slower in basal veins, and slowest in deep middle cerebral veins. Flow was directed lateromedially in the deep middle cerebral vein, rostrocaudally in the basal vein and straight sinus, and mediolaterally in the transverse sinus. Two patients with straight sinus thromboses showed reversed flow direction in the basal veins, and one patient with superior sagittal sinus thrombosis showed elevated velocities in a deep middle cerebral vein. Conclusion: Transtemporal power- and frequency-based color-coded duplex sonography enabled imaging and velocity measurements in deep cerebral veins in subjects 20 to 59 years old, but detection of the straight and transverse sinuses was low. In older subjects, only the basal vein was regularly assessed.
Key Words: cerebral veins, duplex scanning
Impaired Cerebrovascular Autoregulation After Hypoxic-Ischemic Injury in Extremely Low–Birth-Weight Neonates: Detection With Power and Pulsed Wave Doppler US—Blankenberg FG (Dept of Radiology, Stanford University School of Medicine, 300 Pasteur Dr, Stanford, CA 94305), Loh N-N, Norbash AM, Craychee JA, Spielman DM, Person BL, Berg CA, Enzmann DR—Radiology. 1997;205:563–568.
Purpose: To evaluate regional cerebral blood flow with power and pulsed wave Doppler ultrasound (US) in extremely low–birth-weight neonates with periventricular leukomalacia (PVL), germinal matrix hemorrhage (GMH), or both.
Materials and Methods: The lenticulostriate arteries of 17 preterm neonates (birth weight ≤1,100 g) were assessed daily with Doppler US during the first 5–6 days of life. The mean arterial pressure and bilateral peak velocity, resistive index, coronal vascular cross-sectional area, and product of the peak velocity and vascular cross-sectional area were measured.
Results: Five neonates developed PVL, GMH, or both; results of follow-up examinations in 11 patients were normal. One neonate with severe intrauterine growth retardation and renal tubular acidosis was excluded. Neonates with PVL, GMH, or both showed significantly greater mean values and more variable values of vascular cross-sectional area and product of peak velocity and cross-sectional area than neonates without PVL or GMH (P<.025). Mean resistive index was significantly lower in neonates with PVL, GMH, or both than in neonates without (P<.01). There were no significant differences between mean arterial pressure in neonates with and those without PVL, GMH, or both.
Conclusion: By enabling the detection of autoregulatory fluctuations in cerebral blood flow associated with hypoxic-ischemic injury, power and pulsed wave Doppler US may enable identification of preterm neonates who are at risk of developing PVL, GMH, or both during the 1st week of life.
Key Words: ultrasonography, autoregulation
Embolization of Cerebral Arteriovenous Malformations With Silk: Histopathologic Changes and Hemorrhagic Complications—Schmutz F, McAuliffe W, Anderson DM, Elliott JP, Eskridge JM (Dept of Neurological Surgery, University of Washington, Seattle, WA 98195), Winn HR—Am J Neuroradiol. 1997;18:1233–1237.
Purpose: To evaluate the safety of silk as an embolic agent for preoperative embolization of cerebral arteriovenous malformations (AVMs) by assessing the histopathologic changes and hemorrhagic complications associated with its use. Methods: Histopathologic specimens, medical records, and radiologic records of 73 patients with AVMs embolized with silk (alone or in combination with other agents) were reviewed retrospectively. Forty-eight histologic specimens obtained at surgery were analyzed for inflammatory responses and compared with the time interval between embolization and surgery. Postembolization angiograms were assessed for vasculitis and CT scans were reviewed for evidence of hemorrhage after embolization. Results: There was no angiographic evidence of vasculitis. Histologic evidence of vasculitis was absent or mild in 92% of cases and histologic evidence of perivascular inflammation was absent or mild in 73% of cases. The frequency of histologic changes associated with vasculitis, perivascular inflammation, and vessel necrosis varied with the time interval between embolization and AVM resection. Intracranial hemorrhage, as a direct complication of silk use, occurred in one patient. Another patient had subarachnoid hemorrhage 24 hours after embolization, caused by rupture of a posteroinferior cerebellar artery aneurysm. Intraventricular high-density material appeared on routine postembolization CT scans in two other patients who had intraventricular AVM extension. This high-density material was thought to be contrast extravasation from intrinsically leaky AVM nidus vessels and not frank hemorrhage. Conclusion: Embolization of AVMs with silk does not result in marked inflammation or increased hemorrhagic complications as compared with other agents.
Key Words: cerebral arteriovenous malformations, embolization, therapeutic
Intracranial Angioplasty: Experience and Complications—Takis C, Kwan ES, Pessin MS, Jacobs DH, Caplan LR (Dept of Neurology, New England Medical Center, 750 Washington St, Boston, MA 02111)—Am J Neuroradiol. 1997;18:1661–1668.
Purpose: To review our experience with intracranial angioplasty, including the complications we encountered. Methods: During a 3-year period, from 1993 to 1996, 10 patients had intracranial percutaneous transluminal angioplasty (PTA). The stenosed vessels included three internal carotid arteries, one middle cerebral artery, one basilar artery, and five vertebral arteries. Stenosis in all patients was 75%, or greater. PTA was technically successful in eight patients; in two patients it could not be performed owing to inability to traverse the stenosed area. Results: Two patients had successful and uneventful PTA. Five patients had vasospasm, which resolved with local vasodilators in two and with repeat PTA in one. Vasospasm led to stroke in two patients. Compromise of perforating vessels and arterial dissection were associated with stroke in two patients. Conclusion: Intracranial PTA is technically feasible but associated with risks related to vasospasm, arterial trauma, and compromise of perforating vessels.
Key Words: angioplasty, balloon, cerebral vessels
Does Daily Aspirin Diminish Severity of First-Ever Stroke?—Karepov V, Bornstein NM (Stroke Unit, Dept of Neurology, Tel Aviv Medical Center, 6 Weizmann St, Tel Aviv 64239, Israel), Hass Y, Korczyn AD—Arch Neurol. 1997;54:1369–1371.
Background: There are still uncertainties about aspirin efficacy in first-ever ischemic stroke prevention. Also it is unknown whether the severity of first ischemic stroke can be modified by aspirin pretreatment.
Objective: To analyze a series of patients who had their first ischemic stroke while taking aspirin to evaluate the ability of aspirin prophylaxis to diminish the severity of first-ever ischemic stroke.
Design: Case-control study.
Setting: Tertiary medical center to which patients were referred.
Patients: All consecutive patients admitted to the Tel Aviv Medical Center, Tel Aviv, Israel, from May 1988 through May 1994 because of first-ever ischemic stroke were divided into 2 groups according to aspirin use before stroke: aspirin-treated and non–aspirin-treated groups.
Main Outcome Measures: Stroke severity was defined according to activities of daily living within 24 hours after admission: (1) mild stroke, with independence in activities of daily living; (2) moderate stroke, with partial dependency; and (3) severe stroke, with complete dependency. Using χ2 test, stroke severity was compared between patients taking aspirin before their stroke and non–aspirin-treated patients.
Results: Among 2113 consecutive patients with first-ever ischemic stroke, 125 patients had already been taking 100 to 500 mg of aspirin daily. Aspirin-treated and non–aspirin-treated patients did not differ in stroke severity. Mortality was lower in aspirin-treated patients (7.9%) than in non-aspirin-treated patients (12%), but this difference was not statistically significant (P=.17).
Conclusions: We conclude that aspirin as primary prevention treatment has no significant protective effect on severity of first-ever ischemic stroke. The diminution of mortality after first ischemic stroke in patients who had used aspirin should be investigated further.
Key Words: aspirin, stroke outcome
Direct Microsurgery of Dural Arteriovenous Malformation Type Carotid-Cavernous Sinus Fistulas: Indications, Technique, and Results—Day JD (Lahey Hitchcock Medical Center, Dept of Neurosurgery, 41 Mall Rd, Burlington, MA 01805), Fukushima T—Neurosurgery. 1997;41:1119–1126.
Objective: There is a subgroup of patients with Barrow Type D carotid-cavernous sinus fistulas (CCFs) who have progressive neurological deficits despite endovascular attempts at obliteration. To effectively arrest the progression of neurological deficits, especially visual loss, these patients require direct operative intervention. We have used a direct approach to such lesions, which comprehensively occludes all fistulous connections of the CCF.
Methods: We present a series of nine patients with Type D CCFs for which attempts at endovascular embolization failed and that, because of persistent symptoms, required surgical intervention. These lesions characteristically had extensive multiple external carotid artery feeders, often bilateral, in addition to the internal carotid artery feeders. The operative approach used was a combined extra- and intradural full exposure of the cavernous sinus and its contents, with identification and direct obliteration of all arterial input and selective ablation of the venous outflow from the cavernous sinus.
Results: All nine patients experienced resolution of their symptoms, and complete ablation of the lesions, as demonstrated by postoperative angiography, was achieved. Transient diplopia and trigeminal hypesthesia was observed in all nine patients, which resolved by 6 months postoperatively. One patient suffered from a temporary hemiparesis and another from permanent hemiparesis. There were no deaths related to surgery in this series.
Conclusions: Patients with Type D CCFs who have persistent, progressive neurological deficits after failed endovascular attempts at obliteration may be treated by a direct surgical approach to ablate the fistulas. The pertinent anatomic concepts, indications for surgery, and operative techniques that are different from previously described methods are discussed.
Key Words: microsurgery, cerebral arteriovenous malformations
Items of Interest
Endovascular Electrocoagulation: Concept, Technique, and Experimental Results—Cheng J (Leo G. Rigler Center for Radiological Research, Dept of Radiological Sciences, University of California Medical Center, Los Angeles, CA 90095), Guglielmi G, Chen H—AJNR Am J Neuroradiol. 1997;18:1669–1678.
The Stroke Prevention Policy Model: Linking Evidence and Clinical Decisions—Matchar DB (Center for Clinical Health Policy Research, Duke University, First Union Tower, Suite 230, 2200 W Main St, Durham, NC 27705), Samsa GP, Matthews JR, Ancukiewicz M, Parmigiani G, Hasselblad V, Wolf PA, D’Agostino RB, Lipscomb J—Ann Intern Med. 1997;127:704–711.
Long-term Stroke Risk in Children With Sickle Cell Disease Screened With Transcranial Doppler—Adams RJ (Dept of Neurology, HB2060, Medical College of Georgia, Augusta, GA 30912), McKie VC, Carl EM, Nichols FT, Perry R, Brock K, McKie K, Figueroa R, Litaker M, Weiner S, Brambilla D—Ann Neurol. 1997;42:699–704.
Homocyst(e)ine and Risk of Cardiovascular Disease in the Multiple Risk Factor Intervention Trial—Evans RW (University of Pittsburgh, Graduate School of Public Health, Dept of Epidemiology, 503 Parran Hall, 130 DeSoto St, Pittsburgh, PA 15261), Shaten BJ, Hempel JD, Cutler JA, Kuller LH—Arterioscler Thromb Vasc Biol. 1997;17:1947–1953.
Animal Models of Cerebral β-Amyloid Angiopathy—Walker LC (Fax 313-996-7178; E-mail email@example.com)—Brain Res. 1997;25:70–84.
Gene Therapy for Arterial Thrombosis—Vassalli G, Dichek DA (Gladstone Institute of Cardiovascular Disease, PO Box 419100. San Francisco, CA 94141-9100)—Cardiovasc Res. 1997;35:459–469.
Evaluation of Thrombolytic Agents—Bell WR Jr (Division of Hematology, Dept of Medicine, The Johns Hopkins University School of Medicine, Blalock Bldg, Rm 1002, 600 N Wolfe St, Baltimore, MD 21287-4928—Drugs. 1997;54:11–17.
Management of Patients With Acute Ischaemic Stroke—Adams HP Jr (Division of Cerebrovascular Diseases, Dept of Neurology, University of Iowa, 200 Hawkins Dr, Iowa City, IA 52242)—Drugs. 1997;54:60–70.
Logistics in Acute Stroke Management—Broderick JP (Dept of Neurology, University of Cincinnati, 231 Bethesda Ave, PO Box 670525, Cincinnati, OH 45267-0525)—Drugs. 1997;54:109–117.
Aneurysm Clips: Magnetic Quantification and Magnetic Resonance Imaging Safety—Dujovny M (Dept of Neurosurgery [M/C 799], University of Illinois at Chicago, 912 S Wood St, Chicago, IL 60612), Alp S, Dujovny N, Zhao YJ, Gundamraj NR, Misra M, Dobben G—J Neurosurg. 1997;87:788–794.
Acute Stroke: Prognosis and a Prediction of the Effect of Medical Treatment on Outcome and Health Care Utilization: The Copenhagen Stroke Study—Jørgensen HS (Dept of Neurology, Bispebjerg Hospital, Bispebjerg Bakke 23, DK-2400 Copenhagen NV, Denmark), Nakayama H, Raaschou HO, Olsen TS—Neurology. 1997;49:1335–1342.
Color Duplex Ultrasonography in the Diagnosis of Temporal Arteritis—Schmidt WA (Clinic of Rheumatology, Zepernicker Str 1, 13125 Berlin, Germany), Kraft HE, Vorpahl K, Völker L, Gromnica-Ihle EJ—N Engl J Med. 1997;337:1336–1342.
The abstracts in this section have been typeset for consistency with journal format but otherwise appear as in the original articles.
- Copyright © 1998 by American Heart Association