(Stroke. 1995;26:1-6.)
© 1995 American Heart Association, Inc.
Articles |
Improved Survival of Stroke PatientsDuring the 1980s
The Minnesota Stroke Survey
From the Division of Epidemiology, School of Public Health, University of Minnesota, Minneapolis.
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Abstract |
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Background and Purpose The underlying reasons for the decline in stroke mortality in the United States are not well understood and have been the subject of ongoing debate. This study was undertaken to determine whether survival of hospitalized stroke patients has changed during the 1980s, thereby contributing to the decline in stroke mortality during that period.
Methods For the years 1980, 1985, and 1990, we obtained listings of discharge diagnoses from hospitals in the Minneapolis-St Paul metropolitan area and identified all hospitalizations with a discharge diagnosis code of acute cerebrovascular disease according to the International Classification of Diseases, 9th Revision. A 50% random sample of men and women aged 30 to 74 years was selected in each survey for detailed medical record abstraction. Standardized sets of criteria for stroke were then used to validate acute stroke events throughout the 1980s. Each of the three period cohorts of hospitalized stroke patients (1980, 1985, and 1990) was followed for at least 2 years for all-cause mortality end point.
Results A total of 1853 patients met minimal criteria for acute stroke: 564 patients in 1980, 598 patients in 1985, and 691 patients in 1990. Controlling for age, the odds of death within 2 years after stroke were approximately 40% lower in 1990 than in 1980. The relative odds of 2-year death in 1990 (versus 1980) were 0.65 (95% confidence interval, 0.47 to 0.89) and 0.60 (95% confidence interval, 0.42 to 0.85) for men and women, respectively. The improved survival was evident in the short term (28 days) as well as for stroke patients who survived that period. Analysis according to stroke subtype revealed that improved survival of ischemic stroke and specifically of stroke with no apparent cardioembolic source largely accounted for the overall trend. The prognosis of stroke patients who were admitted in a comatose state has not changed during that decade.
Conclusions Despite the absence of any clear major advances in acute stroke therapy, survival of stroke patients substantially improved during the 1980s. The underlying reasons for this unexpected yet remarkable trend remain uncertain but may include improved supportive and rehabilitative care of stroke victims as well as a change in the natural history of the disease.
Key Words: epidemiology • mortality • prognosis
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Introduction |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Stroke mortality has declined in the United States for several decades, although the rate of the decline has not been constant.1 A relatively slow rate of decline during the 1960s was followed by an accelerated phase during the 1970s,2 3 which coincided with the introduction of the National High Blood Pressure Education Program4 and paralleled improvements in population levels of cardiovascular risk factors.5 6 However, both regional3 and national1 data indicate a substantial deceleration in the rate of the decline in stroke mortality during the 1980s. Stroke is still the third leading cause of death in the United States.7
The reasons for the overall favorable trend in stroke mortality are not well understood and have been the subject of ongoing debate.8 9 10 11 12 13 14 The observed trend could have resulted from declining stroke incidence, improved survival of stroke patients, or both. There is little doubt, however, that the trend is real and does not reflect artifactual changes in the assigned cause of death on death certificates.8
Attempts to elucidate causes of the decline in stroke mortality have encountered at least two major methodological challenges: the rapid increase in the use of neuroimaging technology and improvements in hospital record keeping. Computed tomography, which was introduced in the 1970s, quickly became a common diagnostic tool in patients with neurological disorders and has dramatically improved the diagnosis of stroke and its classification into subtypes. It has been suggested that greater use of this technology over time may have resulted in the detection of milder stroke cases that would otherwise not have been diagnosed.15 In a similar fashion, better recording of stroke symptoms and signs in medical records may have operated to increase the pool of verified (and milder) events in more recent years.14 From the surveillance perspective, these forces could increase case ascertainment over time, mask a true decline in stroke incidence, and lead to an artifactual decline in case-fatality rate.
Despite these methodological difficulties, several studies, including ours, have concluded that survival of stroke patients improved during the 1970s, thereby contributing to the decline in stroke mortality during that period.16 17 18 Little is known, however, about more recent trends. This report examines trends in stroke survival between 1980 and 1990 in a large and well-defined community, the Minneapolis-St Paul metropolitan area.
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Subjects and Methods |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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Survey Design
The Minnesota Heart Survey is a long-term, population-based surveillance investigation of the two main cardiovascular diseases (coronary heart disease and stroke) in Minneapolis and St Paul (the Twin Cities). The target population is composed of residents of the seven-county metropolitan area aged 30 to 74 years (1.1 million in 1990). Stroke surveillance was carried out for 1970, 1980, 1985, and most recently for 1990. Findings from the 1970s and early 1980s have been published.14 18 19 This report focuses on trends during the 1980s.
For each surveillance year, listings of discharge diagnoses were obtained from acute-care hospitals serving the metropolitan area. For 1980 and 1985, 30 of the 31 metropolitan hospitals provided data, with the single nonparticipating hospital having a low patient volume. For 1990, all 25 operating hospitals collaborated in this research. With these listings, a sampling frame was constructed for each survey to include Twin Cities residents aged 30 to 74 years who had been discharged with one or more of the following acute cerebrovascular disease codes (International Classification of Diseases, 9th Revision [ICD-9]) listed in any position: 431 (intracerebral hemorrhage); 432 (other and unspecified intracranial hemorrhage); 434 (occlusion of cerebral arteries); 436 (acute but ill-defined cerebrovascular disease); and 437 (other and ill-defined cerebrovascular disease). This wide range of codes was chosen to capture nearly all hospitalized events (high sensitivity) at the cost of reviewing non–stroke-related hospitalizations (low specificity). Patients discharged with a diagnosis of subarachnoid hemorrhage (ICD-9 430) and transient cerebral ischemia (ICD-9 435) were not targeted, nor were patients discharged with a diagnosis of ICD-9 433 (occlusion and stenosis of precerebral arteries). The latter ICD-9 rubric is rarely used exclusively to indicate acute stroke. For each surveillance year, a 50% random sample was selected from the sampling frame for hospital record abstraction and mortality follow-up. The study was approved by the institutional review board of the University of Minnesota.
Hospitalized Stroke Data Collection
Using standardized data collection forms and a detailed
protocol, trained nurses abstracted a wide range of clinical data from
the medical record. Abstracted information included neurological
symptoms and signs, diagnostic and therapeutic procedures, and autopsy
reports whenever available. Ambiguous clinical data were resolved in
periodic meetings with study physicians. Neuroimaging reports were
photocopied and later abstracted in a standardized fashion by study
physicians, independent of clinical data. Reliability studies indicated
a high level of agreement on key items between nurse abstractors as
well as between physicians.
Stroke Validation and Classification
Considerable variation in diagnostic and coding practices among
physicians, across hospitals, and particularly over time has undermined
attempts to monitor disease trends through hospital discharge codes
alone.20 21 To permit valid inference about time trends,
surveillance studies typically apply a standard set of criteria (ie, a
diagnostic algorithm) to a defined sample of discharge
codes.21 22 23 Such algorithms minimize subjective judgement,
maintain high levels of specificity (ie, identify only definite
events), and, most importantly, allow selection of comparable events
from different time periods.
Following concepts described in the National Survey of Stroke24 and in other sources,25 26 we developed two computerized diagnostic algorithms to validate stroke diagnosis consistently during the 1980s. We used two algorithms to ensure that findings were internally consistent and not attributable to differential case ascertainment over time. The first algorithm, labeled here "World Health Organization (WHO) criteria," used the basic WHO definition of acute stroke,27 namely, a new neurological deficit of presumably vascular origin that lasted at least 24 hours (or until death if the patient died within 24 hours). The second algorithm, labeled here the "Minnesota Stroke Survey (MSS) criteria," required, in addition, documentation of either one "major" or two "minor" specific neurological deficits. A major deficit was defined as aphasia, two of three body parts (face, arm, leg) affected unilaterally, visual field deficit, or coma. Minor deficits included dysarthria, apraxia, unsteady gait, one affected body part (face, arm, or leg), or abnormal plantar reflex. Both algorithms excluded events with a nonstroke etiology (eg, brain tumor, subdural hematoma) and used autopsy results whenever available. The autopsy rate, however, did not exceed 6% in any survey year.
Events meeting the criteria of either algorithm were classified as brain infarction or brain hemorrhage when neuroimaging studies were available or as "undetermined type" in their absence. Brain infarction was further classified as "possibly embolic" if one of the following was documented in the chart: atrial fibrillation, mitral stenosis, intracardiac thrombus, systemic embolus, recent myocardial infarction, or cerebral or cardiac angiography that closely preceded the stroke. All other brain infarctions were labeled "thrombotic."
To enhance the specificity of the MSS criteria, we excluded (for that algorithm only) events with nonsupportive neuroimaging more than 48 hours after symptom onset. In terms of specificity for stroke, both the WHO and the MSS criteria are more specific than the sample of unvalidated cerebrovascular disease discharges; of the two algorithms, the MSS criteria are less sensitive but more specific. Events that met the MSS criteria were, by definition, a subset of those that met the WHO criteria.
Mortality Follow-Up
Vital status on hospital discharge was ascertained from
the hospital record. Vital status after discharge was ascertained
through linkage with the Minnesota Death Index (MINNDEX), a statewide
registry system shown to identify more than 98% of deaths found by the
National Death Index.28 Follow-up of the 1990 cohort has
been completed through 1992, allowing for assessment of time trends in
2-year survival of stroke patients.
Statistical Methods
Five percent to 10% of the samples of cerebrovascular disease
discharges included two hospitalizations per person in a given survey
year. If both events met the WHO criteria, one was randomly selected;
if only one event met the criteria, that event was selected.
Characteristics of the period cohorts of hospitalized stroke patients
(ie, 1980, 1985, 1990) were compared by the 
2
test for categorical variables, allowing for a value of "missing"
(ie, not recorded in the chart). Hence, the statistical test checked
the quality of record keeping over time as well as differences in the
prevalence of the characteristic. One-way ANOVA was used to compare
means of continuous variables.
Age-adjusted, sex-specific survival curves were plotted for each period cohort. Survival differences between two period cohorts were assessed by logistic regression models with an indicator variable for the survey year and age included in the model. Cox regression was considered unsuitable because the proportional hazards assumption was not satisfied. Survival differences between men and women within a given year were assessed after age adjustment. Pooled analyses for both sexes were performed after verifying that there was no statistical evidence for an interaction with sex. Computations were performed with SAS.29
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Results |
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Approximately 1000 person-based discharges were sampled for each survey year, with somewhat fewer discharges occurring in 1985 (Table 1
). Of these, 50% to 70% qualified as validated events
by the WHO criteria (moderately specific) and 37% to 47% by the MSS
criteria (highly specific). Subtype classification was limited for 1980
because neuroimaging studies were less frequently used than in 1985 or
1990 (57%, 75%, and 82% of the discharges, respectively). In 1985
and 1990, the vast majority of strokes were brain infarction, with
brain hemorrhage accounting for only about 10% of the events.
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Table 2 shows characteristics of validated stroke
patients (according to WHO criteria) in each survey. There was little
change over time in the sex or age distribution. Approximately 15% of
the patients in each survey were admitted in a comatose state, and more
than 75% had a documented major neurological deficit. The prevalence
of many clinical attributes increased over time, but the trend was
confounded by parallel improvement in hospital record keeping (ie,
decreasing frequency of missing data). Inference on time trends in
stroke severity is therefore limited.
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For both men (Fig 1) and women (Fig 2), age-adjusted survival curves demonstrated
substantial improvements in 2-year survival between 1980 and 1990.
Results were similar by either the WHO criteria or the MSS criteria.
The curves diverged as of the first few days after stroke, indicating
improvement in short- as well as long-term survival. The survival curve
of the 1985 cohort showed different patterns in the two sexes. In men
it was intermediate between the 1980 and 1990 curves and clearly more
similar to the 1980 curve (Fig 1), whereas in women it essentially
overlapped the 1990 curve (Fig 2). There was no evidence, however, of
survival differences between men and women in any survey year
(P>.1 for age-adjusted comparisons).
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As shown in Table 3, the age-adjusted odds of death
within 2 years after stroke were approximately 40% lower in 1990 than
in 1980. This trend, which was consistent by either set of stroke
criteria, reflected both short-term (28-day) survival gains as well as
gains for those who had survived that period. Improved survival was
also evident in subgroup analysis of patients with specific
neurological deficits. For example, the age- and sex-adjusted relative
odds of 2-year death (1990 versus 1980), for patients who were
validated by the WHO criteria and had two body parts affected, were
0.53 (95% confidence interval [CI], 0.38 to 0.73); the
corresponding relative odds for aphasic patients were 0.59 (95% CI,
0.37 to 0.95). Stratified analysis according to the consciousness
level of the patients revealed that survival gains were entirely
restricted to patients who were conscious on admission (data not
shown).
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Trend analysis by subtype indicated that most of the improved
survival could be attributed to improved odds of surviving an ischemic
stroke, primarily among patients classified as having a thrombotic
stroke (Table 4). There was no evidence of improved
survival over time for patients with hemorrhagic stroke. However, the
small number of patients having this stroke subtype precludes an
unequivocal conclusion about survival trends.
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Discussion |
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TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
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This large, population-based study of hospitalized stroke found substantial gains in 2-year survival of stroke patients during the 1980s. Survival improvements were evident both within the first 28 days after the event as well as for the subsequent 2 years among those surviving the short-term period. In both men and women, the odds of dying within 2 years after stroke were approximately 40% lower in 1990 than in 1980. These findings were consistent for cases identified through two diagnostic algorithms, which permitted a standardized diagnosis of events occurring 10 years apart.
In the absence of apparent major advances in stroke therapy in the 1980s,30 the observed trends are remarkable, unexpected, and not well understood. At least two explanations can be suggested. First, better supportive and rehabilitative care of acute stroke may have played a role since stroke survival may be affected by the setting and characteristics of that care.31 Death after stroke is frequently attributed to sequelae such as pulmonary embolism and bronchopneumonia or is due to coexisting cardiac disease.32 These conditions were probably better prevented or managed in 1990 than in 1980. Unfortunately, our abstraction forms did not target them specifically.
A second potential explanation is a change in the natural history of stroke, with stroke becoming a less severe disease. Improved levels of cardiovascular disease risk factors,3 although primarily thought to decrease stroke incidence, may have also resulted in better prognosis for those suffering a stroke.33 Data from the Framingham Study cohort suggested that stroke severity declined between the 1950s and 1970s.34 We found improved survival as early as the first few days after the stroke, a time period when medical care is perhaps less likely to affect the outcome. In our data, improvements in hospital record keeping over time limit inference on trends in stroke severity. Regardless, improved survival was restricted to patients who were conscious on admission and cannot be attributed to a gross change in the case mix, such as a smaller proportion of comatose patients. Therefore, any decrease in stroke severity must have been more subtle.
It may be argued that the results are in part artifactual,
attributable to improved detection of milder events over time because
of increased use of neuroimaging and better record keeping. Several
counterarguments can be made, however. First, both algorithms yielded
similar odds ratio estimates. If indeed the results reflect artifactual
selection of milder events in 1990 than 1980, one would have expected
greater survival gains with the WHO criteria, which included milder
events. Second, improved survival was observed among patients with
specific notable deficits (eg, two affected body parts or aphasia) that
were probably as likely to be detected by clinicians in 1980 as in
1990, regardless of neuroimaging studies. Finally, at least for men,
stroke survival also improved from 1985 to 1990, a period characterized
by an already widespread use of neuroimaging technology and a
relatively stable quality of hospital records (Table 2
).
Changes in hospital reimbursement rules, such as the introduction of diagnosis-related groups in the early 1980s or greater public awareness of stroke symptoms, could have affected the case mix of hospitalized stroke patients with increased representation of milder cases over time. These speculative trends, however, do not explain notable and consistent improvement in subgroups of patients with substantial neurological deficits. It is unlikely that stroke patients with aphasia or hemiparesis were differentially hospitalized in 1980 and 1990.
We are uncertain regarding the interpretation of the sex differences found in the mid-decade results. Since the difference was not statistically significant, it is possible that random variation has accounted for the 1985 results and that the year did not represent the survival experience of stroke patients in adjacent years (1984, 1986). Alternatively, it may be that stroke survival improved similarly in both sexes during the full decade, but it began improving earlier in the decade among women and later among men. It is worth noting that in Rochester, Minnesota, the decline in stroke incidence that was observed until the end of the 1970s did not coincide for men and women, beginning earlier among women than among men.8
Although a substantial number of stroke cases in 1980 could not be definitively classified into subtypes, it appears that improvements in the odds of surviving ischemic stroke and, more specifically, of strokes with no apparent cardioembolic source have made by far the largest contribution to the overall trend. Hemorrhagic stroke constituted a small fraction of the case mix, and any potential improvement in that subtype was unlikely to have had an important impact on the overall trend.
This study adds to a growing body of evidence that improved survival after stroke has played a prominent role in the decline of stroke mortality in the United States.16 17 18 While declining incidence probably contributed to the decline in stroke mortality during the 1970s and before,15 35 there is little or no evidence for a decline in stroke incidence during the 1980s.15 Indeed, the slowing of the decline in stroke mortality during the last decade3 suggests that while both declining incidence and improved survival accounted for the mortality trend during the 1970s, improved survival primarily contributed thereafter.
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Acknowledgments |
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This study was supported by a grant (RO1-HL-23727) from the National Heart, Lung, and Blood Institute. We are indebted to Drs Gregory Burke, Richard Crow, Aaron Folsom, Richard Gillum, Linda Goldman, and David Jacobs for their contributions to the design and conduct of this study; to Mary Porter, Elise Brodin, Kristine Bisgard, and Tracy Stites for programming assistance; to the dedicated nurse abstractors who participated in this project; and to Sherrie Weller for assistance with the manuscript preparation.
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Footnotes |
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Reprint requests to Eyal Shahar, MD, Division of Epidemiology, School of Public Health, University of Minnesota, 1300 S Second St, Suite 300, Minneapolis, MN 55454-1015.
Received September 7, 1994; revision received October 17, 1994; accepted October 17, 1994.
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C. A. Derby, K. L. Lapane, H. A. Feldman, and R. A. Carleton Trends in Validated Cases of Fatal and Nonfatal Stroke, Stroke Classification, and Risk Factors in Southeastern New England, 1980 to 1991 : Data From the Pawtucket Heart Health Program Stroke, April 1, 2000; 31(4): 875 - 881. [Abstract] [Full Text] [PDF]
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H. Numminen, M. Kaste, K. Aho, O. Waltimo, and M. Kotila Decreased Severity of Brain Infarct Can in Part Explain the Decreasing Case Fatality Rate of Stroke Stroke, March 1, 2000; 31(3): 651 - 655. [Abstract] [Full Text] [PDF]
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 L. B. Morgenstern, R. F. Frankowski, P. Shedden, W. Pasteur, and J. C. Grotta Surgical treatment for intracerebral hemorrhage (STICH): A single-center, randomized clinical trial Neurology, November 1, 1998; 51(5): 1359 - 1363. [Abstract] [Full Text] [PDF]
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S. J. Teipel, H. Hampel, G. E. Alexander, M. B. Schapiro, B. Horwitz, D. Teichberg, E. Daley, H. Hippius, H.-J. Moller, and S. I. Rapoport Dissociation between corpus callosum atrophy and white matter pathology in Alzheimer's disease Neurology, November 1, 1998; 51(5): 1381 - 1385. [Abstract] [Full Text] [PDF]
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A. Demchuk and D. Krieger Large middle cerebral artery infarction Neurology, November 1, 1998; 51(5): 1514 - 1514. [Full Text] [PDF]
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T. Heinsius and J. Bogousslavsky Large middle cerebral artery infarction Neurology, November 1, 1998; 51(5): 1514 - 1515. [Full Text] [PDF]
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R. G. Hart, D. G. Sherman, J. D. Easton, and J. A. Cairns Prevention of stroke in patients with nonvalvular atrial fibrillation Neurology, September 1, 1998; 51(3): 674 - 681. [Abstract] [Full Text] [PDF]
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S. M. Greenberg Cerebral amyloid angiopathy: Prospects for clinical diagnosis and treatment Neurology, September 1, 1998; 51(3): 690 - 694. [Abstract] [Full Text] [PDF]
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H. Ay, K. L. Furie, K. Yamada, and W. J. Koroshetz Diffusion-weighted MRI characterizes the ischemic lesion in transient global amnesia Neurology, September 1, 1998; 51(3): 901 - 903. [Abstract] [Full Text] [PDF]
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J. van Gijn Leukoaraiosis and vascular dementia Neurology, September 1, 1998; 51(3_Suppl_3): S3 - S8. [Abstract] [Full Text] [PDF]
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T. J. DeGraba The role of inflammation after acute stroke: Utility of pursuing anti-adhesion molecule therapy Neurology, September 1, 1998; 51(3_Suppl_3): S62 - S68. [Abstract] [Full Text] [PDF]
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K. Ikeda, Y. Iwasaki, M. Kinoshita, H. Kishikawa, T. Suzuki, M. Ichijo, K. Arima, Y. Matsuoka, and S. Irimajiri Medial medullary infarctions Neurology, August 1, 1998; 51(2): 643 - 643. [Full Text] [PDF]
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C. Bassetti, J. Bogousslavsky, H. Mattle, and A. Bernasconi Medial medullary infarctions Neurology, August 1, 1998; 51(2): 643 - 643. [Full Text] [PDF]
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A. I. Qureshi, W. H. Giles, and J. B. Croft Impaired Glucose Tolerance and the Likelihood of Nonfatal Stroke and Myocardial Infarction : The Third National Health and Nutrition Examination Survey Stroke, July 1, 1998; 29(7): 1329 - 1332. [Abstract] [Full Text] [PDF]
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M. Peltonen, B. Stegmayr, and K. Asplund Time Trends in Long-term Survival After Stroke : The Northern Sweden Multinational Monitoring of Trends and Determinants in Cardiovascular Disease (MONICA) Study, 1985–1994 Stroke, July 1, 1998; 29(7): 1358 - 1365. [Abstract] [Full Text] [PDF]
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K. Herholz, T. Holzer, B. Bauer, R. Schroder, J. Voges, R. I. Ernestus, G. Mendoza, G. Weber-Luxenburger, J. Lottgen, A. Thiel, et al. 11C-methionine PET for differential diagnosis of low-grade gliomas Neurology, May 1, 1998; 50(5): 1316 - 1322. [Abstract] [Full Text] [PDF]
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D. C. Tong, M. A. Yenari, G. W. Albers, M. O'Brien, M. P. Marks, and M. E. Moseley Correlation of perfusion- and diffusion-weighted MRI with NIHSS score in acute (<6.5 hour) ischemic stroke Neurology, April 1, 1998; 50(4): 864 - 869. [Abstract] [Full Text] [PDF]
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S. J. Kittner, B. J. Stern, M. Wozniak, D. W. Buchholz, C. J. Earley, B. R. Feeser, C. J. Johnson, R. F. Macko, R. J. McCarter, T. R. Price, et al. Cerebral infarction in young adults: The Baltimore-Washington Cooperative Young Stroke Study Neurology, April 1, 1998; 50(4): 890 - 894. [Abstract] [Full Text] [PDF]
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H.F.K. Chiu, L.C.W. Lam, I. Chi, T. Leung, S. W. Li, W. T. Law, D.W.S. Chung, H.H.L. Fung, P. S. Kan, C. M. Lum, et al. Prevalence of dementia in Chinese elderly in Hong Kong Neurology, April 1, 1998; 50(4): 1002 - 1009. [Abstract] [Full Text] [PDF]
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W. I. Schievink, E.F.M. Wijdicks, V. V. Michels, J. Vockley, and M. Godfrey Heritable connective tissue disorders in cervical artery dissections: A prospective study Neurology, April 1, 1998; 50(4): 1166 - 1169. [Abstract] [Full Text] [PDF]
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J. Poirier Lacunes due to dilatations of perivascular spaces Neurology, April 1, 1998; 50(4): 1194 - 1195. [Full Text] [PDF]
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K. S. Wong, Y. N. Huang, S. Gao, W.W.M. Lam, Y. L. Chan, and R. Kay Intracranial stenosis in Chinese patients with acute stroke Neurology, March 1, 1998; 50(3): 812 - 813. [Abstract] [Full Text] [PDF]
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D. MacGowan, M. Janal, C. Clark, R. Wharton, R. Lazar, R. L. Sacco, and J. P. Mohr Central poststroke pain associated with lateral medullary infarction Neurology, March 1, 1998; 50(3): 837 - 837. [Full Text] [PDF]
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I. E. Silverman Central poststroke pain associated with lateral medullary infarction Neurology, March 1, 1998; 50(3): 836 - 837. [Full Text] [PDF]
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A. J. Grau, F. Buggle, H. Becher, E. Zimmermann, M. Spiel, T. Fent, M. Maiwald, E. Werle, M. Zorn, H. Hengel, et al. Recent bacterial and viral infection is a risk factor for cerebrovascular ischemia: Clinical and biochemical studies Neurology, January 1, 1998; 50(1): 196 - 203. [Abstract] [Full Text] [PDF]
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J. M. Ferro, T. P. Melo, and M. Guerreiro Headaches in intracerebral hemorrhage survivors Neurology, January 1, 1998; 50(1): 203 - 207. [Abstract] [Full Text] [PDF]
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G. W. Petty, R. D. Brown Jr., J. P. Whisnant, J. D. Sicks, W. M. O'Fallon, and D. O. Wiebers Survival and recurrence after first cerebral infarction: A population-based study in Rochester, Minnesota, 1975 through 1989 Neurology, January 1, 1998; 50(1): 208 - 216. [Abstract] [Full Text] [PDF]
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C. Hills and R. S. Sohn Peripheral nerve sheath tumor presents as idiopathic intracranial hypertension Neurology, January 1, 1998; 50(1): 308 - 309. [Full Text] [PDF]
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F. Yoshii, M. Haida, and Y. Shinohara Heavy T2-weighted spin-echo inverted image of dilated perivascular space Neurology, January 1, 1998; 50(1): 310 - 311. [Full Text] [PDF]
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J. S. Kim, J. H. Lee, and M. C. Lee Patterns of sensory dysfunction in lateral medullary infarction: Clinical-MRI correlation Neurology, December 1, 1997; 49(6): 1557 - 1563. [Abstract] [Full Text] [PDF]
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H. Yamanouchi, T. Mizutani, S. Matsushita, and Y. Esaki Paroxysmal atrial fibrillation: High frequency of embolic brain infarction in elderly autopsy patients Neurology, December 1, 1997; 49(6): 1691 - 1694. [Abstract] [Full Text] [PDF]
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H. S. Jorgensen, H. Nakayama, H. O. Raaschou, and T. S. Olsen Acute stroke: Prognosis and a prediction of the effect of medical treatment on outcome and health care utilization: The Copenhagen Stroke Study Neurology, November 1, 1997; 49(5): 1335 - 1342. [Abstract] [Full Text] [PDF]
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D. S. Migita, M. W. Devereaux, and R. L. Tomsak Cocaine and pupillary-sparing oculomotor nerve paresis Neurology, November 1, 1997; 49(5): 1466 - 1467. [Full Text] [PDF]
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W. M. Clark Cytokines and reperfusion injury Neurology, November 1, 1997; 49(5_Suppl_4): S10 - S14. [Full Text] [PDF]
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M. M. Bednar, C. E. Gross, M. Balazy, and J. R. Falck Antineutrophil strategies Neurology, November 1, 1997; 49(5_Suppl_4): S20 - S22. [Full Text] [PDF]
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R. J. Winquist and S. Kerr Cerebral ischemia-reperfusion injury and adhesion Neurology, November 1, 1997; 49(5_Suppl_4): S23 - S26. [Full Text] [PDF]
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J. H. Garcia, J. A. Gutierrez, and K.-F. Liu Non-neuronal responses to short-term occlusion of the middle cerebral artery Neurology, November 1, 1997; 49(5_Suppl_4): S27 - S31. [Full Text] [PDF]
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W. M. Clark and J. A. Zivin Antileukocyte adhesion therapy: preclinical trials and combination therapy Neurology, November 1, 1997; 49(5_Suppl_4): S32 - S38. [Full Text] [PDF]
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R. L. Sacco Risk factors, outcomes, and stroke subtypes for ischemic stroke Neurology, November 1, 1997; 49(5_Suppl_4): S39 - S44. [Full Text] [PDF]
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N. M. Bornstein, I. Y. Bova, and A. D. Korczyn Infections as triggering factors for ischemic stroke Neurology, November 1, 1997; 49(5_Suppl_4): S45 - S46. [Full Text] [PDF]
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A. J. Grau Infection, inflammation, and cerebrovascular ischemia Neurology, November 1, 1997; 49(5_Suppl_4): S47 - S51. [Full Text] [PDF]
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K. R. Lees Cerestat and other NMDA antagonists in ischemic stroke Neurology, November 1, 1997; 49(5_Suppl_4): S66 - S69. [Abstract] [Full Text] [PDF]
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R. M. Lazar, R. S. Marshall, J. Pile-Spellman, L. Hacein-Bey, W. L. Young, J. P. Mohr, and B. M. Stein Anterior translocation of language in patients with left cerebral arteriovenous malformation Neurology, September 1, 1997; 49(3): 802 - 808. [Abstract] [Full Text] [PDF]
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J.-P. Neau, P. Ingrand, C. Couderq, M.-P. Rosier, M. Bailbe, P. Dumas, P. Vandermarcq, and R. Gil Recurrent intracerebral hemorrhage Neurology, July 1, 1997; 49(1): 106 - 113. [Abstract] [Full Text] [PDF]
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G. Schlaug, B. Siewert, A. Benfield, R. R. Edelman, and S. Warach Time course of the apparent diffusion coefficient (ADC) abnormality in human stroke Neurology, July 1, 1997; 49(1): 113 - 119. [Abstract] [Full Text] [PDF]
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M. Leone, E. Bottacchi, E. Beghi, E. Morgando, R. Mutani, G. Amedeo, R. Cremo, M. Gianelli, and L. R. Ceroni Alcohol use is a risk factor for a first generalized tonic-clonic seizure Neurology, March 1, 1997; 48(3): 614 - 620. [Abstract] [Full Text] [PDF]
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J. Chen and R. Simon Ischemic tolerance in the brain Neurology, February 1, 1997; 48(2): 306 - 311. [Full Text] [PDF]
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A. I. Qureshi, M. S. Akbar, E. Czander, K. Safdar, R. S. Janssen, and M. R. Frankel Crack cocaine use and stroke in young patients Neurology, February 1, 1997; 48(2): 341 - 345. [Abstract] [Full Text] [PDF]
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E. Shahar, P. G. McGovern, J. S. Pankow, K. M. Doliszny, M. A. Smith, H. Blackburn, and R. V. Luepker Stroke Rates During the 1980s: The Minnesota Stroke Survey Stroke, February 1, 1997; 28(2): 275 - 279. [Abstract] [Full Text]
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I. Miyai, A. D. Blau, M. Reding, and B. T. Volpe Patients with Stroke Confined to Basal Ganglia Have Diminished Response to Rehabilitation Efforts Neurology, January 1, 1997; 48(1): 95 - 101. [Abstract] [Full Text] [PDF]
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J. Pujol, J. Kulisevsky, A. Moreno, J. Deus, J. Alonso, J. Balanzo, J. L. Marti-Vilalta, and A. Capdevila Expedited Publication: Neurospectroscopic alterations and globus pallidus hyperintensity as related magnetic resonance markers of reversible hepatic encephalopathy Neurology, December 1, 1996; 47(6): 1526 - 1530. [Abstract] [Full Text] [PDF]
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W. G. Tatton Modulation of gene expression rather than monoamine oxidase inhibition: (-)-Deprenyl-related compounds in controlling neurodegeneration Neurology, December 1, 1996; 47(6_Suppl_3): 171S - 183S. [Abstract] [Full Text] [PDF]
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K. Toyoda, T. Imamura, Y. Saku, J. Oita, S. Ibayashi, K. Minematsu, T. Yamaguchi, and M. Fujishima Medial medullary infarction: Analyses of eleven patients Neurology, November 1, 1996; 47(5): 1141 - 1147. [Abstract] [Full Text] [PDF]
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G. Devuyst, J. Bogousslavsky, P. Ruchat, X. Jeanrenaud, P.-A. Despland, F. Regli, N. Aebischer, H. M. Karpuz, V. Castillo, M. Guffi, et al. Prognosis after stroke followed by surgical closure of patent foramen ovale: A prospective follow-up study with brain MRI and simultaneous transesophageal and transcranial Doppler ultrasound Neurology, November 1, 1996; 47(5): 1162 - 1166. [Abstract] [Full Text] [PDF]
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J. E. Ween, M. P. Alexander, M. D'Esposito, and M. Roberts Factors predictive of stroke outcome in a rehabilitation setting Neurology, August 1, 1996; 47(2): 388 - 392. [Abstract] [Full Text] [PDF]
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J. van der Grond, L.M.P. Ramos, B. C. Eikelboom, and W. P.Th.M. Mali Cerebral metabolic differences between the severe and critical hypoperfused brain Neurology, August 1, 1996; 47(2): 399 - 404. [Abstract] [Full Text] [PDF]
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A. Bruno, S. Carter, C. Qualls, and K. B. Nolte Incidence of spontaneous intracerebral hemorrhage among Hispanics and non-Hispanic whites in New Mexico Neurology, August 1, 1996; 47(2): 405 - 408. [Abstract] [Full Text] [PDF]
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M. Comabella, J. Alvarez-Sabin, A. Rovira, and A. Codina Bromocriptine and postpartum cerebral angiopathy: A causal relationship? Neurology, June 1, 1996; 46(6): 1754 - 1756. [Abstract] [Full Text] [PDF]
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K. B. Nolte, L. M. Brass, and C. F. Fletterick Intracranial hemorrhage associated with cocaine abuse: A prospective autopsy study Neurology, May 1, 1996; 46(5): 1291 - 1291. [Abstract] [Full Text] [PDF]
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J. Bogousslavsky, S. Garazi, X. Jeanrenaud, N. Aebischer, G. Van Melle, and For the Lausanne Stroke with Paradoxal Embolism St Stroke recurrence in patients with patent foramen ovale: The Lausanne Study Neurology, May 1, 1996; 46(5): 1301 - 1301. [Abstract] [Full Text] [PDF]
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R. L. Zhang, M. Chopp, W. X. Tang, Z. G. Zhang, S. D. Putney, and R. M. Starzyk Synthetic peptide derived from the Bordetella pertussis bacterium reduces infarct volume after transient middle cerebral artery occlusion in the rat Neurology, May 1, 1996; 46(5): 1437 - 1437. [Abstract] [Full Text] [PDF]
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P. H. Davis, Clarke W.R. PhD, B.H. Bendixen, H.P. Adams Jr., R. F. Woolson, A. Culebras, and the TOAST investigators. Silent cerebral infarction in patients enrolled in the TOAST study Neurology, April 1, 1996; 46(4): 942 - 948. [Abstract] [Full Text] [PDF]
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M.I. Chimowitz, J. Kokkinos, J. Strong, M. B. Brown, S. R. Levine, S. Silliman, M. S. Pessin, E. Weichel, C. A. Sila, A. J. Furlan, et al. The Warfarin-Aspirin Symptomatic Intracranial Disease Study Neurology, August 1, 1995; 45(8): 1488 - 1493. [Abstract] [Full Text] [PDF]
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