Abstracts of Literature
Management of Patients With Ruptured Cerebral Aneurysms in Hospital Population of Lithuania—Tamasauskas A (Dept of Neurosurgery, Kaunas Medical Univ Hospital, Eiveniu 2, Kaunas 3007, Lithuania), Tamasauskas J, Bernotas G, Inao S, Yoshida J—Acta Neurochir. 2000;142:51–59. Copyright © Springer-Verlag 2000.
A retrospective analysis of ruptured cerebral aneurysms among the hospital population of Lithuania was performed. A total of 507 patients were enrolled in the study during a 5 year period. The unadjusted annual incidence of ruptured cerebral aneurysms was found to be 2.7/100,000 in the hospital population of Lithuania and 3.9/100,000 in the hospital population of the defined area of the city of Kaunas. Overall management results showed a 45.6% good recovery and 31.6% death rate in this group of patients. Surgical results showed a 52.1% good outcome and 20.9% death rate. Despite the fact that the death rate according to the timing of surgery after the initial subarachnoid haemorrhage did not differ significantly (p>0.05) among early (0–3 days post SAH), moderate (4–7 days post SAH) and late (more than 7 days post SAH) surgery groups, it was found that 75 (14.8%) patients deteriorated while awaiting surgery. Initial bleeding together with rebleeding, medical complications and vasospasm were the main causes of death, constituting 61.3%, 18.1% and 9.4% of all deaths, respectively.
The results of this study showed that the annual incidence of ruptured cerebral aneurysms in Lithuania is similar to that in other European countries except for Finland. Overall management results in the Lithuanian hospital population indicated only a slight improvement compared to management results of previous population-based studies in other countries.
Key Words: cerebral aneurysm, stroke management
Effects of Graded Hyperventilation on Cerebral Blood Flow Autoregulation in Experimental Subarachnoid Hemorrhage—Ma X (The Neurobiology Research Unit, Afsnit 9302, Dept of Neurosurgery, Rigshospitalet, Juliane Maries vej 20, DK-2100 Copenhagen ⊘ Denmark), Willumsen L, Hauerberg J, Pedersen DB, Juhler M—J Cereb Blood Flow Metab. 2000;20:718–725. Copyright © 2000 The International Society for Cerebral Blood Flow and Metabolism. Published by Lippincott Williams & Wilkins, Inc.
An impaired CBF autoregulation can be restored by hyperventilation at a Paco2 level of about 2.9 to 4.1 kPa (22 to 31 mm Hg). However, it is uncertain whether the restoring effect can take place at lesser degrees of hypocapnia. In the current study, CBF autoregulation was studied at four Paco2 levels; 5.33 kPa (40 mm Hg, normoventilation), 4.67 kPa (35 mm Hg, slight hyperventilation), 4.00 kPa (30 mm Hg, moderate hyperventilation), and 3.33 kPa (25 mm Hg, profound hyperventilation). At each Paco2 level, eight rats 2 days after experimental subarachnoid hemorrhage (SAH) and eight sham-operated controls were studied. The CBF was measured by the intracarotid 133Xe method. The CBF autoregulation was found to be intact in all controls but completely disturbed in the normoventilated SAH rats. However, by slight hyperventilation, CBF autoregulation was restored in seven of eight SAH rats with a decline in CBF of 10%. The CBF autoregulation was found intact in all of the moderately or profoundly hyperventilated SAH rats, whereas the decline in CBF was 21% and 28%, respectively. In conclusion, hyperventilation to a Paco2 level between 4.00 and 4.67 kPa (30 to 35 mm Hg) appears to be sufficient for reestablishing an impaired autoregulation after SAH.
Key Words: subarachnoid hemorrhage, vasomotor reactivity
High Incidence of Hyponatremia in Patients With Ruptured Anterior Communicating Artery Aneurysms—Sayama T, Inamura T (Dept of Neurosurgery, Neurological Institute, Faculty of Medicine, Kyushu Univ, 3-1-1 Maidashi, Higashi-ku, Fukuoka 812-8582, Japan), Matsushima T, Inoha S, Inoue T, Fukui M—Neurol Res. 2000;22:151–155. Copyright © 2000 Forefront Publishing Group.
We studied the incidence and timing of hyponatremia (Na<135 mEq l−1) after subarachnoid hemorrhage (SAH) with special reference to ruptured anterior communicating artery (A-com) aneurysms. Hunt and Kosnik (HK) grading, symptomatic vasospasm in A-com aneurysm, and hydrocephalus were analyzed for connections to hyponatremia in 55 patients with ruptured A-com aneurysms, 65 with ruptured internal cerebral artery (ICA) aneurysms, and 49 with ruptured middle cerebral artery (MCA) aneurysms. Hyponatremia occurred in 28 (51%) of 55 patients with A-com aneurysms and in nine (18%) of 49 patients with MCA aneurysms. Severe hyponatremia (Na<130 mEq l−1) occurred in 16 patients (29%) in the A-com group, four patients (6%) in the ICA group, and three patients (6%) in the MCA group. The A-com aneurysm group had a significantly higher incidence of mild hyponatremia (p<0.01) and severe hyponatremia (p<0.001) than other groups. Among A-com cases, hyponatremia occurred significantly more often in HK grade III and IV cases (p<0.05), in cases with vasospasm (p<0.001), and in cases with hydrocephalus (p<0.01). Respective days of onset for symptomatic vasospasm and for hyponatremia were day 7.6±4.4 and day 10.6±5.8 following SAH, representing a 3-day delay for hyponatremia (p<0.05). In most patients hyponatremia resolved within 28 days following SAH. Hyponatremia occurred more often with A-com aneurysms, possibly because of vasospasm around the A-com or hydrocephalus causing hypothalamic dysfunction. Since hypervolemic therapy can cause hyponatremia, particularly careful observation is required during such therapy in patients with A-com aneurysm.
Key Words: subarachnoid hemorrhage, hyponatremia
Chronic Hydrocephalus in Elderly Patients Following Subarachnoid Hemorrhage—Yoshioka H (Dept of Neurosurgery, Shimane Prefectural Central Hospital, 116 Imaichi-cho, Izumo, Shimane 693, Japan), Inagawa T, Tokuda Y, Inokuchi F—Surg Neurol. 2000;53:119–125. Copyright © 2000 by Elsevier Science Inc.
BACKGROUND With the aging of the population, surgery for ruptured intracranial aneurysms is increasing among the elderly. We sought to clarify the characteristics of chronic hydrocephalus following aneurysmal subarachnoid hemorrhage (SAH) in elderly patients.
METHODS Of the 576 surgically treated patients, 289 were aged 59 years or younger, 169 were 60 to 69, and 118 were 70 years or older. The relationship between chronic hydrocephalus and the causative factors was analyzed for each age group.
RESULTS Of the 576 patients, chronic hydrocephalus was observed in 215 (37%), with the incidence increasing significantly with age (p<0.001) and being the highest in the oldest age group. In elderly patients, the incidence of chronic hydrocephalus was relatively high, even after mild SAH. The incidence of chronic hydrocephalus was high regardless of age in patients with severe SAH, such as in those with H&H grades III–IV, SAH grades III–IV, acute hydrocephalus, symptomatic vasospasm, and intraventricular hemorrhage, and in those with vertebro-basilar artery aneurysms.
CONCLUSION In the elderly, the incidence of chronic hydrocephalus following SAH was significantly higher than in younger patients, even after mild SAH. In elderly patients, careful observation and individualized treatment are necessary even if SAH is mild.
Key Words: subarachnoid hemorrhage, hydrocephalus
Motor Strokes Sparing the Leg: Different Lesions and Causes—de Freitas GR, Devuyst G, van Melle G, Bogousslavsky J (Dept of Neurology, Centre Hospitalier Universitaire Vaudois, CH-1011 Lausanne, Switzerland)—Arch Neurol. 2000;57:513–518.
Background: A considerable number of patients develop stroke without involvement of the lower limb. However, there are few reports about the motor syndrome when the leg is spared.
Objective: To study clinical findings, causative factors, and lesion topography in stroke patients with a motor deficit sparing the leg.
Patients and Methods: We studied 895 patients with paresis sparing the leg from the 3901 patients enrolled in the Lausanne Stroke Registry. They were compared with 1644 stroke patients with paresis involving the leg, by means of univariate and multivariate analysis.
Results: Eight hundred forty-four infarcts (94.3%) and 51 hemorrhages (5.7%) led to weakness sparing the leg. Different sites of lesion were found, but the majority were caused by superficial infarcts. Almost half of the lesions were confined to superficial branches of the middle cerebral artery territory, with 276 (30.8%) in the anterior (superior) and 138 (15.4%) in the posterior (inferior) middle cerebral artery. More than half of the infarcts had a presumed embolic source from large-artery disease or from the heart. In comparison with patients with paresis involving the leg, patients without leg involvement had a lower prevalence of small-artery disease (P<.001), but a higher prevalence of migraine (P<.001), transient ischemic attack (P=.001), atherosclerosis without stenosis (P=.005), large-artery disease (P<.001), and left hemispheric strokes (P<.001). They also had a lower frequency of hemorrhagic stroke.
Conclusions: Patients without leg involvement had different stroke lesions and causes and were characterized by more superficial infarcts mainly caused by emboli from large-artery disease and atherosclerosis without stenosis.
Key Words: stroke, acute, motor activity
Impaired Cerebral Vasoreactivity and Risk of Stroke in Patients With Asymptomatic Carotid Artery Stenosis—Silvestrini M (Clinica Neurologica, Università di Roma “Tor Vergata,” Ospedale S. Eugenio, P le dell’Umanesimo 10, 00144 Rome, Italy), Vernieri F, Pasqualetti P, Matteis M, Passarelli F, Troisi E, Caltagirone C—JAMA. 2000;283:2122–2127.
Context Standards for treating patients with asymptomatic carotid artery stenosis have been difficult to establish because of the lack of evidence for factors influencing these patients’ prognoses. However, preliminary evidence suggests that an alteration in cerebral hemodynamic function may play a relevant role in the occurrence of stroke in patients with carotid artery disease.
Objective To investigate the relationship between cerebrovascular reactivity to hypercapnia and cerebrovascular events in patients with severe unilateral asymptomatic carotid artery stenosis.
Design and Setting Prospective, blinded longitudinal study conducted in an outpatient neurovascular department in Italy between June 1996 and April 1998, with a median follow-up of 28.5 months.
Patients Ninety-four patients with asymptomatic carotid artery stenosis of at least 70% (74 men; mean age, 71 years).
Main Outcome Measures Subsequent occurrence of cerebral ischemic events (transient ischemic attack or stroke) or death, analyzed by cerebrovascular reactivity to hypercapnia (measured by transcranial Doppler ultrasonography and calculated by the breath-holding index values in the middle cerebral arteries).
Results The overall annual rate for all ischemic events was 7.9%. Seventeen patients (18%) had ischemic events, all but 1 of which were ipsilateral to the carotid artery stenosis. Among factors considered, only lower breath-holding index values in the middle cerebral artery ipsilateral to carotid artery stenosis were significantly associated with the risk of an event (hazard ratio, 0.09; 95% confidence interval, 0.02–0.38; P=.001, by multivariate analysis). Based on data from previously studied healthy subjects, the cutoff of the breath-holding index for distinguishing between impaired and normal cerebrovascular reactivity was determined to be 0.69. Using this cutoff, the annual ipsilateral ischemic event risk was 4.1% in patients with normal and 13.9% in those with impaired breath-holding index values.
Conclusions These results suggest a link between impaired cerebrovascular reactivity and the risk of ischemic events ipsilateral to severe asymptomatic carotid stenosis.
Key Words: vasomotor activity, carotid artery diseases
Body Iron Stores and Early Neurologic Deterioration in Acute Cerebral Infarction—Dávalos A (Section of Neurology, Hospital Universitari Doctor Josep Trueta, Avda Francia s/n, 17007 Girona, Spain), Castillo J, Marrugat J, Fernandez-Real JM, Armengou A, Cacabelos P, Rama R—Neurology. 2000;54:1568–1574. Copyright © 2000 by the American Academy of Neurology.
Background: Iron-dependent free radicals formation has been related to greater damage in cerebral ischemia. The authors analyzed whether increased body iron stores were associated with early neurologic worsening and excitatory amino acid release in patients with acute ischemic stroke. Methods: Ferritin, total iron, and glutamate concentrations in plasma and CSF were measured on admission in 100 consecutive patients with a cerebral infarction of <24 hours’ duration. The authors diagnosed progressing stroke when the Canadian Stroke Scale score decreased one or more points between admission and 48 hours. Cranial CT was performed on admission and repeated on days 4 to 7 of hospitalization. Results: Ferritin concentrations in plasma (median 391, range 119 to 500 versus 148, 21 to 399 ng/mL) and in CSF (17.4, 6.8 to 82, versus 4.8, 0.6 to 14 ng/mL) were significantly higher in the 45 patients with subsequent progressing stroke than in those with nonprogressing stroke (p<0.001). There was a positive correlation between ferritin and glutamate concentrations in plasma (r=0.81, p<0.001) and CSF (r=0.64, p<0.001). Plasma ferritin concentrations >275 ng/mL in plasma (OR, 33.5; 95% CI, 4.7 to 235) and >11 ng/mL in CSF (OR, 11.4; 95% CI, 3.1 to 41) were independently and significantly related to early neurologic worsening. The effect was reduced by >60% after controlling for glutamate concentrations, but remained significant. Conclusions: High plasma and CSF ferritin concentrations within the first 24 hours from the onset of ischemic stroke are associated with early neurologic deterioration. Increased body iron stores may contribute to stroke progression by enhancing the cytotoxic mechanisms in cerebral ischemia.
Key Words: stroke, acute, iron
Poststroke Depression and Emotional Incontinence: Correlation With Lesion Location—Kim JS (Dept of Neurology, Asan Medical Center, Song-pa, PO Box 145, Seoul 138-600, Korea), Choi-Kwon S—Neurology. 2000;54:1805–1810. Copyright © 2000 by the American Academy of Neurology.
Objective: To correlate the location of stroke with poststroke depression (PSD) and emotional incontinence (PSEI). Methods: The authors prospectively studied 148 patients (94 men and 54 women, mean age 62 years) with single, unilateral stroke (126 infarcts and 22 hemorrhages) at 2 to 4 months poststroke with regard to the presence of PSD (using Diagnostic and Statistical Manual of Mental Disorders IV criteria and Beck Depression Inventory) and PSEI. The lesion location was analyzed by CT or MRI. Results: Twenty-seven patients (18%) had PSD and 50 (34%) had PSEI. The presence of PSD and PSEI was not related to the nature, laterality, or size of the lesion. The frequency of PSEI, but not of PSD, was higher in women than in men and in ischemic rather than hemorrhagic stroke (p<0.05). Although both PSD and PSEI were related to motor dysfunction and location (anterior versus posterior cortex) of the lesion, location was a stronger determinant for PSD (p<0.05). The prevalence of PSD/PSEI in each location was 75%/100% in frontal lobe of anterior cerebral artery territory, 50%/0 in temporal lobe, 30%/40% in frontal—middle cerebral artery territory, 13%/0 in occipital lobe, 19%/45% in lenticulocapsular area, 11%/16% in thalamus, 16%/53% in pontine base, 36%/55% in medulla, and 0/22% in cerebellum. Parietal and dorsal pontine lesions were not associated with PSD or PSEI. PSEI was more closely associated with lenticulocapsular strokes than was PSD (p<0.01). Conclusion: Development of PSD and PSEI is strongly influenced by lesion location, probably associated with the chemical neuroanatomy related to the frontal/temporal lobe–basal ganglia–ventral brainstem circuitry. Although the lesion distribution is similar, PSEI is more closely related to lenticulocapsular strokes than is PSD.
Key Words: depression, stroke outcome
Carotid Wall Thickness Is Predictive of Incident Clinical Stroke: The Atherosclerosis Risk in Communities (ARIC) Study—Chambless LE (Dept of Biostatistics, School of Public Health, Univ of North Carolina, Chapel Hill, NC 27514), Folsom AR, Clegg LX, Sharrett AR, Shahar E, Nieto FJ, Rosamond WD, Evans G—Am J Epidemiol. 2000;151:478–487.
Few studies have determined whether carotid artery intima-media thickness (IMT) is associated prospectively with risk of first ischemic stroke. In the Atherosclerosis Risk in Communities Study, carotid IMT, an index of generalized atherosclerosis, was defined as the mean of IMT measured by B-mode ultrasonography at six sites of the carotid arteries. The authors assessed the relation of mean IMT to stroke incidence over 6–9 years’ follow-up (1987–1995) among 7,865 women and 6,349 men aged 45–64 years without prior stroke at baseline in four US communities. There were 90 incident ischemic stroke events for women and 109 for men. In sex-specific Cox proportional hazards models adjusting only for age, race, and community, the hazard rate ratios comparing extreme mean IMT values (>or=1 mm) to values less than 0.6 mm were 8.5 for women (95% confidence interval: 3.5, 20.7) and 3.6 for men (95% confidence interval: 1.5, 9.2). The relation was graded, and models with cubic splines indicated significant nonlinearity, with hazards increasing more rapidly at lower IMTs than at higher IMTs. Thus, models using linear IMT values substantially underestimate the strength of the association at lower IMTs. The strength of the association was reduced by the inclusion of putative stroke risk factors, but it remained elevated at higher IMTs. Hence, mean carotid IMT is a noninvasive predictor of future ischemic stroke incidence.
Key Words: carotid artery diseases, risk factors
Serum C-Reactive Protein and Self-Reported Stroke: Findings From the Third National Health and Nutrition Examination Survey—Ford ES (Div of Nutrition, National Center for Chronic Disease Prevention and Health Promotion, Centers for Disease Control and Prevention, 4770 Buford Hwy, MS K26, Atlanta, GA 30341), Giles WH—Arterioscler Thromb Vasc Biol. 2000;20:1052–1056. Copyright © 2000 American Heart Association, Inc.
C-reactive protein may predict the risk of coronary heart disease, but its association with stroke has not been well studied. We used data from the Third National Health and Nutrition Examination Survey, conducted from 1988 to 1994, to examine the association between serum C-reactive protein concentrations and self-reported past history of stroke among 8850 US men and women aged ≥40 years. The unadjusted geometric mean of C-reactive protein concentration was higher among participants with stroke than those without stroke (0.45±0.02 versus 0.32±0.01, P<0.001). After adjusting for age, sex, race or ethnicity, education, smoking status, systolic blood pressure, serum cholesterol, high density lipoprotein cholesterol, history of diabetes mellitus, body mass index, and physical activity, the odds ratio for stroke among participants with C-reactive protein concentrations ≥0.55 mg/dL compared with participants with concentrations ≤0.21 mg/dL was 1.71 (95% CI 1.11 to 2.64 [odds ratio per mg/dL 1.19, 95% CI 1.05 to 1.34]). These cross-sectional data support findings from other studies suggesting that C-reactive protein concentration may be a risk factor or marker for stroke in the US population.
Key Words: risk factors, stroke prevention
C-Reactive Protein Is a Strong but Nonspecific Risk Factor of Fatal Stroke in Elderly Persons—Gussekloo J (Section of Gerontology and Geriatrics, Dept of General Internal Medicine, Leiden Univ Medical Centre, C-2-R, PO Box 9600, 2300 RC Leiden, Netherlands), Schaap MCL, Frölich M, Blauw GJ, Westendorp RGJ—Arterioscler Thromb Vasc Biol. 2000;20:1047–1051. Copyright © 2000 American Heart Association, Inc.
An elevated level of C-reactive protein is a strong predictor of cardiovascular events in elderly persons. Whether C-reactive protein has direct adverse vascular effects or is a marker of aspecific systemic inflammation remains to be determined. The aim of this study was to investigate the relation between C-reactive protein and the occurrence of fatal strokes in elderly persons. In the Leiden 85-Plus Study, a population-based prospective follow-up study, we studied the levels of C-reactive protein in 80 participants who died from stroke within the first 5 years of follow-up. Levels of C-reactive protein were determined in serum samples at baseline. Levels of C-reactive protein were also determined in 82 control subjects who survived for the first 5 years of follow-up and in 83 participants who died from noncardiovascular causes. Mortality risks were estimated with logistic regression and adjusted for differences in age, sex, smoking, medication, total cholesterol, history of diabetes or hypertension, and previous cardiovascular events. Levels of C-reactive protein at baseline were 2-fold higher in subjects who died from stroke than in control subjects (median 5.7 versus 2.7 mg/L. P<0.005). The levels of C-reactive protein in subjects who died from stroke or from noncardiovascular causes were similar (median 5.7 versus 4.9 mg/L, P=0.7). The risk of death from stroke as well as from noncardiovascular causes increased linearly up to 10-fold in subjects with the highest levels of C-reactive protein at baseline (P<0.001). The levels of C-reactive protein were lower when more time had elapsed between blood sampling and time of death during follow-up (P=0.01). C-reactive protein is a strong but nonspecific risk factor of fatal stroke in old persons. The data do not support the idea that C-reactive protein has direct vascular effects that underlie fatal cerebrovascular disease.
Key Words: risk factors, cerebral ischemia
C-Reactive Protein, Cardiovascular Risk Factors, and Mortality in a Prospective Study in the Elderly—Strandberg TE (Dept of Medicine, Univ of Helsinki, PO Box 340, FIN-00029 HYKS, Finland), Tilvis RS—Arterioscler Thromb Vasc Biol. 2000;20:1057–1060. Copyright © 2000 American Heart Association.
Serum C-reactive protein (CRP) reflects inflammation and predicts cardiovascular disease in middle-aged individuals. We investigated CRP, risk factors, and 10-year mortality in 3 elderly cohorts (aged 75, 80, and 85 years; n=455) of the population-based Helsinki Aging Study. Clinical and laboratory examinations were performed at baseline, and in 1998, CRP was measured by a sensitive method (sensitivity 0.3 mg/L) from frozen serum samples. Mortality data were retrieved from national registers. Serum CRP ranged from 0.18 to 170.0 mg/L (interquartile range 0.68 to 4.10 mg/L, median 1.60 mg/L). CRP correlated significantly with body mass index and plasma insulin and was associated with smoking at baseline. An inverse correlation was found with albumin and total and HDL cholesterol. CRP was not associated with diabetes or cardiovascular disease but was significantly (P=0.015) higher in persons with (n=70) than without (n=385) dementia. During the 10-year follow-up. 61% (n=278) of the cohort died: half of the deaths were due to cardiovascular diseases. Mean CRP in survivors and nonsurvivors was 3.16 and 5.22 mg/L (P=0.017), respectively. After controlling for age and sex, baseline CRP (per 10 mg/L) significantly predicted the 10-year total mortality (risk ratio 1.20, 95% CI 1.08 to 1.32) and cardiovascular mortality (risk ratio 1.22, 95% CI 1.10 to 1.35). Predictive value was found in the 75-year-old cohort, but it was clearly attenuated in the 80- and 85-year-old cohorts. The results indicate that CRP is associated with several cardiovascular risk factors in the elderly. CRP alone predicts overall and cardiovascular mortality, but the prediction was significant in only the 75-year-old cohort.
Key Words: risk factors, aging
Hyperhomocysteinemia Increases Risk of Death, Especially in Type 2 Diabetes: 5-Year Follow-Up of the Hoorn Study—Hoogeveen EK (Institute for Research in Extramural Medicine, Vrije Universiteit, van der Boechorststraat 7. 1081 BT Amsterdam, Netherlands), Kostense PJ, Jakobs C, Dekker JM, Nijpels G, Heine RJ, Bouter LM, Stehouwer CDA—Circulation. 2000;101:1506–1511. Copyright © 2000 American Heart Association, Inc.
Background—A high serum total homocysteine (tHcy) concentration is a risk factor for death, but the strength of the relation in patients with type 2 (non-insulin-dependent) diabetes mellitus compared with nondiabetic subjects is not known. A cross-sectional study suggested that the association between tHcy and cardiovascular disease is stronger in diabetic than in nondiabetic subjects. We therefore prospectively investigated the combined effect of hyperhomocysteinemia and type 2 diabetes on mortality.
Methods and Results—Between October 1, 1989, and December 31, 1991, serum was saved from 2484 men and women, 50 to 75 years of age, who were randomly selected from the town of Hoorn, The Netherlands. Fasting serum tHcy concentration was measured in 171 subjects who died (cases: 76 of cardiovascular disease) and in a stratified random sample of 640 survivors (control subjects). Mortality risks were calculated over 5 years of follow-up by means of logistic regression. The prevalence of hyperhomocysteinemia (tHcy>14 μmol/L) was 25.8%. After adjustment for major cardiovascular risk factors, serum albumin, and HbA1c, the odds ratio (95% CI) for 5-year mortality was 1.56 (1.07 to 2.30) for hyperhomocysteinemia and 1.26 (1.02 to 1.55) per 5-μmol/L increment of tHcy. The odds ratio for 5-year mortality for hyperhomocysteinemia was 1.34 (0.87 to 2.06) in nondiabetic subjects and 2.51 (1.07 to 5.91) in diabetic subjects (P=0.08 for interaction).
Conclusions—Hyperhomocysteinemia is related to 5-year mortality independent of other major risk factors and appears to be a stronger (1.9-fold) risk factor for mortality in type 2 diabetic patients than in nondiabetic subjects.
Key Words: risk factors, death
The Cytosolic Antioxidant Copper/Zinc–Superoxide Dismutase Prevents the Early Release of Mitochondrial Cytochrome c in Ischemic Brain After Transient Focal Cerebral Ischemia in Mice—Fujimura M, Morita-Fujimura Y, Noshita N, Sugawara T, Kawase M, Chan PH (Neurosurgical Laboratories, Stanford Univ, 701B Welch Rd, #148, Palo Alto, CA 94304)—J Neurosci. 2000;20:2817–2824. Copyright © 2000 Society for Neuroscience.
Release of mitochondrial cytochrome c into the cytosol is a critical step in apoptosis. We have reported that early release of cytochrome c in vivo occurs after permanent focal cerebral ischemia (FCI) and is mediated by the mitochondrial antioxidant manganese superoxide dismutase (SOD). However, the role of reactive oxygen species produced after ischemia-reperfusion in the mitochondrial apoptosis process is still unknown, although overexpression of copper/zinc-SOD (SOD1), a cytosolic isoenzyme, protects against ischemia–reperfusion. We now hypothesize that the overexpression of SOD1 also prevents apoptosis after FCI. To address this issue, we examined the subcellular distribution of the cytochrome c protein in both wild-type mice and in SOD1 transgenic (Tg) mice after transient FCI. Cytosolic cytochrome c was detected as early as 2 hr after reperfusion, and correspondingly, mitochondrial cytochrome c was significantly reduced after FCI. Cytosolic cytochrome c was significantly lower in the SOD1 Tg mice compared with wild types 2 (p<0.0001) and 4 (p<0.05) hr after FCI. Apaf-1, which interacts with cytochrome c and activates caspases, was constitutively expressed in both groups of animals, with no alteration after FCI. Double staining with cytochrome c immunohistochemistry and terminal deoxynucleotidyl transferase-mediated uridine 5′-triphosphate-biotin nick end labeling showed a spatial relationship between cytosolic cytochrome c expression and DNA fragmentation. A significant amount of DNA laddering was detected 24 hr after ischemia and was reduced in SOD1 Tg mice. These data suggest that SOD1 blocks cytosolic release of cytochrome c and could thereby reduce apoptosis after transient FCI.
Key Words: cerebral ischemia, apoptosis
Time Window for Clinical Effectiveness of Mass Evacuation in a Rat Balloon Model Mimicking an Intraparenchymatous Hematoma—Valdes EL, Lain AH, Calandre L (Dept of Neurology and Pathology and Research Center, 12 de Octubre Univ Hospital, Madrid, Spain), Grau M, Cabello A, Gomez-Escalonilla C—J Neurol Sci. 2000;174:40–46. Copyright © 2000 Elsevier Science BV.
The purpose of this study is to evaluate in a rat model if the early removal of an experimental intracerebral mass mimicking an extensive subcortical hematoma improves neurological outcome. Fifty six male Wistar rats were studied. A balloon was placed sterotactically at the level of the striatum. The balloon was inflated to 100 μl for periods of 10, 60 or 120 min (with 10 animals in each group). In 10 animals the balloon was not deflated and there were four sham operated cases. Neurological deficit was evaluated by a blinded observer by means of a clinical scale from 0 to 8 points at 24 and 72 h after inflation. Three additional animals at each inflation period were sacrificed after 6 h for pathological study with hematoxylin–eosin staining. Death rate was 9/10 animals who had permanent inflation, 4/10 in those with 2 h inflation, 2/10 for 1 h inflation and 0/10 for 10 min inflation (P<0.01 in chi square test). Many animals developed a particular clinical syndrome not previously described. Mean 72 h clinical scores (0–8 points) were 7.6 (S.D.: 1.2) for the permanent inflation group, 4.4 (S.D.: 3.2) for 2 h of inflation, 2.3 (S.D.: 3.2) for 1 h and 0.4 (0.9) for 10 min of inflation (P<0.01 in Kruskal Wallis test). In the pathological study the rate of damaged neurons was significantly higher in the permanent than in transient inflation groups. In conclusion, in this balloon model evacuation of an extensive acute expanding subcortical (hematoma-like) mass must be performed within a limited time window to prevent the development of irreversible neurological deficits or death.
Key Words: intracerebral hemorrhage, stroke, experimental
Amyloid β-Protein Length and Cerebral Amyloid Angiopathy-Related Haemorrhage—McCarron MO (Dept of Neurology and Neuropathology, Institute of Neurological Sciences, Southern General Hospital, Glasgow, G5I 4TF, UK), Nicoll JAR, Stewart J, Cole GM, Yang F, Ironside JW, Mann DMA, Love S, Graham DI—Neuroreport. 2000;11:937–940. Copyright © Lippincott Williams & Wilkins.
The relationship between amyloid β-protein (Aβ) length and the apolipoprotein E (APOE) ε2 allele, which is over-represented in cerebral amyloid angiopathy-related haemorrhage (CAAH), has not previously been examined. Of 57 CAA patients studied, 37 had CAAH. All patients, particularly those with CAAH had more blood vessels immunoreactive for Aβ40 than Aβ42 in both the leptomeninges and cerebral cortex. CAAH patients had more Aβ40-immunoreactive blood vessels in the leptomeninges (p<0.001) and cortex (p=0.027) than had non-haemorrhage patients. Cortical blood vessels, usual source of haemorrhage in CAAH, were more frequently Aβ42 immunoreactive in APOE ε2 carriers than in non-ε2 carriers (p=0.022). The APOE ε2 allele may predispose to CAAH by increasing the seeding of cortical blood vessels by Aβ42.
Key Words: intracerebral hemorrhage, amyloidosis
Pure Sensory Stroke Caused by a Cerebral Hemorrhage: Clinical-Radiologic Correlations in Seven Patients—Shintani S (Dept of Neurology, Toride Kyodo General Hospital, 2-1-1 Hongoh, Toride City, Ibaraki 302-0022, Japan), Tsuruoka S, Shiigai T—AJNR Am J Neuroradiol. 2000;21:515–520. Copyright © American Society of Neuroradiology.
BACKGROUND AND PURPOSE: Pure sensory stroke (PSS) usually is caused by a lacunar infarct; reports of PSS caused by cerebral hemorrhage have been rare. We correlated clinical and neuroradiologic findings in patients with PSS caused by cerebral hemorrhage.
METHODS: We retrospectively studied seven patients with appropriate clinical findings and lesions revealed by X-ray CT and MR imaging (five men, two women; age range, 46–64 years; mean age, 55.9 years).
RESULTS: Hemorrhages involved the thalamus, pons, internal capsule, or cerebral cortex. MR imaging revealed thalamic PSS was located in the ventral posterior lateral (VPL) or ventral posterior medial (VPM) nucleus; a lesion producing a thalamic cheiro-oral syndrome was situated on the border between the VPL and VPM. Pontine PSS involved the medial lemniscus together with the ventral trigeminothalamic tract, sparing the anterior and lateral spinothalamic tracts. Accordingly, pontine PSS, but not thalamic PSS, selectively affected vibration and position sense while leaving pinprick and temperature perception intact, and oral sensory involvement was bilateral when cheiro-oral syndrome had a pontine origin. MR imaging revealed hemorrhage in the postcentral gyrus in the cortical variety of PSS and in the posterior part of the posterior limb (thalamocortical sensory pathway) in PSS of internal capsular origin. The postcentral gyral lesion impaired stereognosis and graphesthesia.
CONCLUSION: Focal hemorrhages can lead to purely sensory stroke syndromes, and the clinical deficits are fairly well linked with the locations of the bleeds.
Key Words: intracerebral hemorrhage, stroke onset
Utility of Magnetic Resonance Imaging in Acute Intracerebral Hemorrhage—Dylewski DA, Morgenstern LB (Dept of Neurology, 6431 Fannin 7.044 MSB, Houston, TX 77030), Demchuk AM—J Neuroimaging. 2000;10:78–83. Copyright © 2000 by the American Society of Neuroimaging.
The authors determine whether magnetic resonance imaging (MRI) during acute hospitalization for spontaneous intracerebral hemorrhage (ICH) provides new diagnostic information. ICD-9 codes were used to identify consecutive patients with spontaneous ICH at Hermann Hospital, Houston, Texas, between January 1995 and August, 1997. Two investigators employed rigorous criteria to determine whether the MRI findings led to a specific new diagnosis. Two hundred ninety-one patients met inclusion and exclusion criteria. Sixty-seven (23%) patients underwent brain MRI during the acute hospitalization. MRI provided a new diagnosis in 15 of these 67 patients (22%). Amyloid angiopathy and vascular malformation (four each) were the most frequently identified etiologies. The yield of MRI was low in basal ganglia and thalamic hemorrhage. Two of 23 (9%) patients with deep ICH and 13 of 44 (30%) patients with lobar and infratentorial hemorrhage had etiology determined by MRI. Timing of MRI did not affect yield.
Key Words: intracerebral hemorrhage, magnetic resonance imaging
Contrast Enhanced Color Duplex for Diagnosis of Subtotal Stenosis or Occlusion of the Internal Carotid Artery—Hofstee DJ (Dept of Clinical Neurophysiology, Medical Centre Haaglanden, Westeinde Hospital, Postbus 432, 2501 CK The Hague, Netherlands), Hoogland PH, Schimsheimer RJ, de Weerd AW—Clin Neurol Neurosurg. 2000;102:9–12. Copyright © 2000 Elsevier Science B.V.
Background and purpose. We initiated this prospective study to investigate the usefulness of contrast enhancement in combination with color Doppler-assisted duplex imaging (CDDI) for the distinction of subtotal internal carotid artery (ICA) stenosis and ICA occlusion. Methods. During 1 year all patients with a previously unknown subtotal ICA stenosis (>90%) or ICA occlusion on routine CDDI were included in the study. These patients underwent a CDDI with and without intravenous contrast. Levovist® 300 mg/ml. Results. The study group consisted of 32 patients, 15 with subtotal stenosis and high velocity at the ICA stenosis, two with subtotal stenosis and minimal residual color flow and relative low velocity at the ICA stenosis and 15 with ICA occlusion. In all patients the diagnosis by CDDI without and with contrast were the same. Image quality was improved with contrast in 13 of the 17 patients at the subtotal ICA stenosis. There was no significant difference in mean velocities at the subtotal ICA stenoses without and with contrast. Conclusion. The usefulness of contrast enhancement with CDDI for differentiating subtotal ICA stenosis and ICA occlusion is limited. Possibly it is useful in patients with moderate image quality of the CCA and ICA and in patients with a subtotal stenosis with minimal residual color flow and relative low velocity at the ICA stenosis.
Key Words: ultrasonography, carotid artery diseases
Use of Ultrasound Contrast in the Diagnosis of Carotid Artery Occlusion—Ferrer JME (Vall d’Hebron Hospital, Vascular Surgery Staff, Calle/Laforja no. 26, atico 2a, Barcelona 08006, Spain), Samsó JJ, Serrando JR, Valenzuela VF, Montoya SB, Docampo MM—J Vasc Surg. 2000;31:736–741. Copyright © 2000 by The Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter.
Objective: The purpose of this study was to evaluate the use of an echo-enhancing agent in patients with carotid artery occlusion to improve the sensitivity and specificity of carotid color flow ultrasonography.
Method: Between January 1997 and December 1998, a prospective study involving 85 cases of carotid artery occlusion in 84 patients was carried out. After a baseline duplex ultrasonography (DU) diagnosis, a second (DU) along with an echo-enhancement agent (SHU-508-A [Levovist]) study was carried out (echo enhancement ultrasonography diagnosis [DUEE]). In 82 cases, a contrast angiography was performed to confirm the diagnosis, whereas in the other three cases the diagnoses were confirmed with surgery.
Results: From the 85 internal carotid artery occlusions diagnosed at the initial DU examination, seven came out to be false occlusions in the DUEE examination (8.2%). There was a 100% correlation of the cases between the DUEE examination and the contrast angiography in the 82 cases in which this had been done. In three of the cases, the diagnosis was confirmed surgically because these displayed severe stenoses according to the DUEE studies in symptomatic patients, and so they required urgent treatment.
Conclusions: The DUEE study is a potent diagnosis tool that allows the differentiation between true carotid artery occlusions and pseudo-occlusions.
Key Words: carotid artery diseases, ultrasonography
Evaluation of Posterior Cerebral Artery Flow Velocity by Transcranial Color-Coded Real-Time Sonography—Kimura K (Cerebrovascular Div, Dept of Medicine, National Cardiovascular Center, 5-7-1 Fujishirodai, Suita, Osaka 565-8565, Japan), Minematsu K, Yasaka M, Wada K, Yamaguchi T—Ultrasound Med Biol. 2000;26:195–199. Copyright © 2000 World Federation for Ultrasound in Medicine & Biology.
Using transcranial color-coded real-time sonography (TCCS), we measured peak-systolic flow velocities (PSVs) in segment P2 of 102 posterior cerebral arteries (PCAs) in 61 patients, with angiography. We divided 102 PCAs into four groups: control group (n=70) with no significant stenotic lesions; PCS group (n=7) with stenosis ≥50% of P2 segment; Col (+) group (n=13) and Col (−) group (n=12) had occlusive lesions in the carotid system with or without collateral flow from PCA to the middle cerebral artery through the leptomeningeal anastomosis. In the PCS group, PSV (255.7±67.2 cm/s) was higher than in the other three groups (p<0.0001). PSV was higher in the Col (+) group (127.6±31.2) than in the Col (−) (86.6±20.1) and control (83.8±24.8) groups (p<0.001). The measurement of PSV in the P2 segment of PCA using TCCS may help to identify a significant stenosis in PCA.
Key Words: ultrasonography, posterior cerebral artery
Does Prior Use of Aspirin Affect Outcome in Ischemic Stroke?—Kalra L (Univ of London Kings College, Guys Kings and St Thomas School of Medicine, Dept of Medicine, Denmark Hill Campus, Bessemer Rd, London SE5 9PJ, England), Perez I, Smithard DG, Sulch D—Am J Med. 2000;108:205–209.
BACKGROUND: Large intervention studies suggest that aspirin may reduce mortality when given to patients who present with strokes or transient ischemic attacks. We sought to determine whether patients who were already using aspirin at the time of an ischemic stroke had a lower mortality than those who were not. METHODS: A prospective cohort study was undertaken in patients (mean age 76±15 years) with acute ischemic stroke. Detailed information on demography, stroke characteristics, and aspirin use prior to the stroke was collected from patients, medical records, and other sources. Patients were classified by cause and subtype of stroke using standard criteria. Mortality was measured 4 weeks after the initial episode. RESULTS: Of the 1,457 patients, 650 (45%) were using aspirin (median dose 75 mg; range 75 to 300 mg) prior to the stroke. Prior use of aspirin was associated with lower 4-week mortality (14% versus 20%, P<0.01). Beneficial effects of prior aspirin use on mortality were seen in patients with atherosclerotic strokes (15% versus 21%, P<0.05) and with cardioembolic strokes (21% versus 34%, P<0.05), but not among patients with strokes due to small vessel occlusion (10% versus 11%, P=0.8). Prior aspirin use was also associated with lower mortality in patients in whom the cause of ischemic stroke could not be determined (15% versus 22%, P<0.01). The effect of prior aspirin use on mortality was independent of age, gender, other risk factors, and use of other medication. Conclusions: Prior use of low-dose aspirin may be associated with a small but significant reduction in stroke mortality.
Key Words: aspirin, stroke outcome
Aspirin Use and the Prevention of Acute Ischemic Cranial Nerve Palsy—Johnson LN (Neuro-ophthalmology Unit, Mason Eye Institute, Univ of Missouri-Columbia, Columbia, MO 65212), Stetson SW, Krohel GB, Cipollo CL, Madsen RW—Am J Ophthalmol. 2000;129:367–371. Copyright © 2000 by Elsevier Science Inc.
PURPOSE: To assess the relationship of aspirin use and ischemic cranial nerve palsies among patients with diabetes mellitus and hypertension.
METHODS: This retrospective case-control study involved 100 patients with ischemic cranial nerve palsies in association with diabetes, hypertension, or both (palsy cases) and 163 age-matched and sex-matched patients with diabetes, hypertension, or both but without ischemic cranial nerve palsies (nonpalsy control subjects). Comparisons were made with respect to duration of diabetes, dose and duration of aspirin use, dose and duration of tobacco use, and presence of cardiac or cerebrovascular disease.
RESULTS: There were 20 oculomotor, 33 trochlear, 37 abducens, and 10 facial nerve palsy cases. The median duration of diabetes was 6 years for cases and 7 years for control subjects. There were 34 cases (34%) who had used aspirin for a mean duration of 5.5 years before the onset of the cranial nerve palsy and 49 control subjects (30.1%) who had used aspirin for a mean duration of 4.3 years. There were no significant differences between cases and control subjects for duration of diabetes (P=.94); aspirin use (P=.51), duration (P=.50), and dosage (P=.89); tobacco use (P=.73) and consumption (P=.45); and proportion of cardiac disease (P=.17). Cerebrovascular disease was significantly less common among palsy cases than nonpalsy control subjects (P<.001). There was no significant difference in the odds of a patient having cranial nerve palsy in the aspirin group compared with the nonaspirin group (odds ratio, 1.12; 95% confidence interval, 0.70–2.04).
CONCLUSION: Aspirin use was not associated with a reduced rate of ischemic third, fourth, sixth, and seventh nerve palsies among patients with diabetes mellitus and hypertension. Aspirin appears to be ineffective in preventing ischemic third, fourth, sixth, and seventh cranial nerve palsies. Patients with ischemic cranial nerve palsy have a significantly lower rate of strokes and transient ischemic attacks than patients who have diabetes or hypertension but who do not have a history of cranial nerve palsy.
Key Words: aspirin, cranial nerve palsies
Is Cerebral Perfusion Pressure a Major Determinant of Cerebral Blood Flow During Head Elevation in Comatose Patients With Severe Intracranial Lesions?—Moraine J-J, Berré J, Mélot C (Dept of Intensive Care, Erasme Univ Hospital, Lennik Rd, 808, B-1070 Brussels, Belgium)—J Neurosurg. 2000;92:606–614.
Object. Head elevation as a treatment for lower intracranial pressure (ICP) in patients with intracranial hypertension has been challenged in recent years. Therefore, the authors studied the effect of head position on cerebral hemodynamics in patients with severe head injury.
Methods. The effect of 0°, 15°, 30°, and 45° head elevation on ICP, cerebral blood flow (CBF), systemic arterial (PsaMonro) and jugular bulb (Pj) pressures calibrated to the level of the foramen of Monro, cerebral perfusion pressure (CPP), and the arteriovenous pressure gradient (PsaMonro–Pj) was studied in 37 patients who were comatose due to severe intracranial lesions. The CBF decreased gradually with head elevation from 0 to 45°, from 46.3±4.8 to 28.7±2.3 ml · min−1 · 100 g−1 (mean±standard error, p<0.01), and the PsaMonro–Pj from 80±3 to 73±3 mm Hg (p<0.01). The CPP remained stable between 0° and 30° of head elevation, at 62±3 mm Hg, and decreased from 62±3 to 57±4 mm Hg between 30° and 45° (p<0.05). A simulation showed that the 38% decrease in CBF between 0° and 45° resulted from PsaMonro–Pj changes for 19% of the decrease, from a diversion of the venous drainage from the internal jugular veins to vertebral venous plexus for 15%, and from CPP changes for 4%.
Conclusions. During head elevation the arteriovenous pressure gradient is the major determinant of CBF. The influence of CPP on CBF decreases from 0 to 45° of head elevation.
Key Words: cerebral blood flow, intracranial pressure
Extracranial Carotid Artery Aneurysms: Texas Heart Institute Experience—El-Sabrout R (Dept of Cardiovascular Surgery, Transplantation Services, MC 2-114, PO Box 20345, Houston, TX 77225), Cooley D—J Vasc Surg. 2000;31:702–712. Copyright © 2000 by The Society for Vascular Surgery and International Society for Cardiovascular Surgery, North American Chapter.
Background and Purpose: Aneurysms of the extracranial carotid artery (ECA) are rare. Large single-institution series are seldom reported and usually are not aneurysm type-specific. Thus, information about immediate and long-term results of surgical therapy is sparse. This review was conducted to elucidate etiology, presentation, and treatment for ECA aneurysms.
Methods: We retrospectively reviewed the case records of the Texas Heart Institute/St Luke’s Episcopal Hospital, Houston, and found 67 cases of ECA aneurysms treated surgically (the largest series to date) between 1960 and 1995: 38 pseudoaneurysms after previous carotid surgery and 29 atherosclerotic or traumatic aneurysms. All aneurysms were surgically explored, and all were repaired except two: a traumatic distal internal carotid artery aneurysm and an infected pseudoaneurysm in which the carotid artery was ligated.
Results: Four deaths (three fatal strokes and one myocardial infarction) and two nonfatal strokes were directly attributed to a repaired ECA aneurysm (overall mortality/major stroke incidence, 9%); there was one minor stroke (incidence, 1.5%). The incidence of cranial nerve injury was 6% (four cases). During long-term follow-up (1.5 months–30 years; mean, 5.9 years), 19 patients died, mainly of cardiac causes (11 myocardial infarctions).
Conclusion: The potential risks of cerebral ischemia and rupture as well as the satisfactory long-term results achieved with surgery strongly argue in favor of surgical treatment of ECA aneurysms.
Key Words: carotid artery diseases, aneurysm
Surgical Treatment of Extracranial Internal Carotid Artery Aneurysms—Rosset E, Albertini J-N, Magnan PE, Ede B, Thomassin JM, Branchereau A (Dept of Vascular Surgery, Hopital de La Timone, Bd Jean Moulin, 13385 Marseille, Cedex 5, France)—J Vasc Surg. 2000;31:713–723. Copyright © 2000 by The Society for Cardiovascular Surgery, North American Chapter.
Purpose: Extracranial internal carotid artery aneurysms (EICAs) can be treated by carotid ligation or surgical reconstruction. In the consideration of the risk of stroke after internal carotid artery (ICA) occlusion, the aim of this study was to report the results of reconstructive surgery for these aneurysms, including lesions located at the base of the skull.
Methods: From 1980 to 1997, 25 ICA reconstructions were performed for EICA: 22 male patients and 3 female patients (mean age, 54.4 years). The cause was atherosclerosis (n=nine patients), dysplasia (n=12 patients), trauma (n=three patients), and undetermined (n=one patient). The symptoms were focal in 15 cases (12 hemispheric, three ocular), nonfocal in three cases (trouble with balance and visual blurring), and glossopharyngeal nerve compression in one case. Six cases were asymptomatic, including three cases that were diagnosed during surveillance after ICA dissection. In nine cases, the upper limit of the EICA reached the base of the skull. A combined approach with an ear, nose, and throat surgeon allowed exposure and control of the ICA.
Results: After operation, there were no deaths, one temporary stroke, two transient ischemic attacks, and 11 cranial nerve palsies (one with sequelae). The ICA was patent on the postoperative angiogram in all but one case. During follow-up (mean, 66 months), there were two deaths (myocardial infarction), one occurrence of focal epileptic seizure at 2 months, and one transient ischemic attack at 2 years. In December 1998, duplex scanning showed patency of the reconstructed ICA in all but one surviving patient.
Conclusion: Surgical reconstruction is a satisfactory therapeutic choice for EICA, even when located at the base of the skull.
Key Words: carotid artery diseases, aneurysm
Items of Interest
New Magnetic Resonance Imaging Methods for Cerebrovascular Disease: Emerging Clinical Applications—Neumann-Haefelin T (Dept of Neurology, J.W. Goethe Univ, Theodor-Stern-Kai 7, 6090 Frankfurt, Germany), Moseley ME, Albers GW—Ann Neurol. 2000;47:559–570. Copyright © 2000 by the American Neurological Association.
Distribution of Cranial MRI Abnormalities in Patients With Symptomatic and Subclinical CADASIL—Coulthard A (Depart of Radiology, Royal Victoria Infirmary, Queen Victoria Rd, Newcastle upon Tyne NE1 4LP, UK), Blank SC, Bushby K, Kalaria RN, Burn DJ—Br J Radiol. 2000;73:256–265. Copyright © 2000 The British Institute of Radiology.
Estrogen as a Neuroprotectant in Stroke—Hurn PD (Johns Hopkins Medical Institute, Dept of Anesthesiology and Critical Care Medicine, 600 N Wolfe St, Blalock 1404, Baltimore, MD 21287), Macrae IM—J Cereb Blood Flow Metab. 2000;20:631–652.
Transcranial Doppler Ultrasonography: Year 2000 Update—Babikian VL (Dept of Neurology, Boston Univ School of Medicine and Boston Veterans Administration, Medical Center, 150 S Huntington Ave, Boston, MA 02130), Feldmann E, Wechsler LR, Newell DW, Gomez CR, Bogdahn U, Caplan LR, Spencer MP, Tegeler C, Ringelstein EB, Alexandrov AV—J Neuroimaging. 2000;10:101–115. Copyright © 2000 by the American Society of Neuroimaging.
Yield of Diffusion-Weighted MRI for Detection of Potentially Relevant Findings in Stroke Patients—Albers GW (Stanford Stroke Center, 701 Welch Rd, Bldg B, Suite 325, Palo Alto, CA 94304), Lansberg MG, Norbash AM, Tong DC, O’Brien MW, Woolfenden AR, Marks MP, Moseley ME—Neurology. 2000;54:1562–1567. Copyright © 2000 by the American Academy of Neurology.
The abstracts in this section have been typeset for consistency with journal format but otherwise appear as in the original articles.
- Copyright © 2000 by American Heart Association