PubMed Health⌕ Search

Biomedical subjects

Joseph Broderick

Publications and source records attributed to Joseph Broderick.

At least 19 recordsLinked to original sources

Association of serial biochemical markers with acute ischemic stroke: the National Institute of Neurological Disorders and Stroke recombinant tissue plasminogen activator Stroke Study.

BACKGROUND AND PURPOSE: Biochemical markers of acute neuronal injury may aid in the diagnosis and management of acute ischemic stroke. Serum samples from the National Institute for Neurological Disorders and Stroke (NINDS) recombinant tissue plasminogen activator Stroke Study were analyzed for the presence of 4 biochemical markers of neuronal, glial, and endothelial cell injury. These biochemical markers, myelin basic protein (MBP), neuron-specific enolase (NSE), S100beta, and soluble thrombomodulin, were studied for an association with initial stroke severity, infarct volume, and functional outcome. METHODS: In the original NINDS study, serum samples were drawn from all patients on presentation to the Emergency Department and at approximately 2 and 24 hours after initiation of study therapy. In this analysis, stored serum samples were available for 359 patients; 107 patients had samples for all 3 time points. Serum marker concentrations were measured by ELISA techniques. We examined the relation between serum concentrations of each marker and the degree of baseline neurological deficit, functional outcome, and infarct size on computed tomography at 24 hours and the effect of fibrinolytic therapy. RESULTS: Higher 24-hour peak concentrations of MBP, NSE, and S100beta were associated with higher National Institutes of Health Stroke Scale baseline scores (r=0.186, P<0.0001; r=0.117, P=0.032; and r=0.263, P<0.0001, respectively). Higher peak concentrations of MBP and S100beta (r=0.209, P<0.0001; r=0.239, P<0.0001) were associated with larger computed tomography lesion volumes. Patients with favorable outcomes had smaller changes in MBP and S100beta (P<0.05) concentrations in the first 24 hours. Soluble thrombomodulin was not associated with any severity or outcome measure. CONCLUSIONS: This study corroborates previous work demonstrating correlations of MBP, NSE, and S100beta with clinical and radiographic features in acute stroke. Despite significantly better outcomes in the tissue plasminogen activator-treated group, we found no difference in the early release of the 4 biomarkers between treatment groups. Further study will define the role of biomarkers in acute stroke management and prognostication.

Acute Disease↗

The unchanging incidence and case-fatality of stroke in the 1990s: a population-based study.

BACKGROUND AND PURPOSE: Many advances were made in stroke prevention strategies during the 1990s, and yet temporal trends in stroke incidence and case-fatality have not been reported in the United States. Blacks have a 2-fold higher risk of stroke; however, there are no data over time showing if any progress has been made in reducing racial disparity in stroke incidence. The objective of this study was to examine temporal trends in stroke incidence and case-fatality within a large, biracial population during the 1990s. METHODS: Within a biracial population of 1.3 million, all strokes were ascertained at all local hospitals using International Classification of Diseases, 9th Revision codes during July 1993 to June 1994 and again in 1999. A sampling scheme was used to ascertain cases in the out-of-hospital setting. Race-specific incidence and case-fatality rates were calculated and standardized to the 2000 US Census population. A population-based telephone survey regarding stroke risk factor prevalence and medication use was performed in 1995 and 2000. RESULTS: There were 1954 first-ever strokes in 1993-1994 and 2063 first-ever strokes in 1999. The annual incidence of first-ever hospitalized stroke did not significantly change between study periods: 158 per 100,000 in both 1993-1994 and 1999 (P=0.97). Blacks continue to have higher stroke incidence than whites, especially in the young; however, case-fatality rates continue to be similar between races and are not changing over time. Medication use for treatment of stroke risk factors significantly increased in the general population between study periods. CONCLUSIONS: Despite advances in stroke prevention treatments during the 1990s, the incidence of hospitalized stroke did not decrease within our population. Case-fatality also did not change between study periods. Excess stroke mortality rates seen in blacks nationally are likely the result of excess stroke incidence and not case-fatality, and the racial disparity in stroke incidence did not change over time.

Adolescent↗

Lack of evidence for an association between hemodynamic variables and hematoma growth in spontaneous intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Early hematoma expansion in spontaneous intracerebral hemorrhage (ICH) is associated with worse clinical outcome. We hypothesized that hemodynamic parameters are associated with the increase in hematoma volume owing to their relationship to blood vessel wall stresses. METHODS: We performed a post hoc analysis of clinical and computed tomography (CT) data from patients enrolled in a prospective observational study of ICH patients presenting within 3 hours from symptom onset. Hematoma volumes were measured at hospital arrival and at 1 and 20 hours from presentation. Blood pressure and heart rate, recorded at 19 time points between presentation and 20 hours, were used to derive hemodynamic variables. Multivariable logistic-regression models were constructed to assess the relation between hemodynamic parameters and hematoma growth, adjusted for clinical covariates. RESULTS: From the original study, 98 patients underwent baseline and 1-hour CT scans; of these, 65 had 20-hour CT scans. Substantial hematoma growth was observed in 28% within the first hour. Of the 65 patients not undergoing surgery within 20 hours, 37% experienced hematoma growth by 20 hours. Neither baseline or peak hemodynamic parameters nor changes in hemodynamic parameters were significantly associated with hematoma growth at either 1 or 20 hours. CONCLUSIONS: We found no blood pressure or heart rate parameters, individually or in combination, that were associated with hematoma growth. Our data suggest the influence of hemodynamic parameters on vessel wall stress to be an unlikely target for intervention in reducing the risk of early hematoma growth in ICH.

Cerebral Hemorrhage↗

The use of standardized patients for mock oral board exams in neurology: a pilot study.

BACKGROUND: Mock oral board exams, fashioned after the live patient hour of the American Board of Psychiatry and Neurology exam, are commonly part of resident assessment during residency training. Exams using real patients selected from clinics or hospitals are not standardized and do not allow comparisons of resident performance across the residency program. We sought to create a standardized patient mock oral board exam that would allow comparison of residents' clinical performance. METHODS: Three cases were created and then used for this mock oral boards exercise utilizing trained standardized patients. Residents from the University of Cincinnati and Indiana University participated in the exam. Residents were scored by attending physician examiners who directly observed the encounter with the standardized patient. The standardized patient also assessed each resident. A post-test survey was administered to ascertain participant's satisfaction with the examination process. RESULTS: Resident scores were grouped within one standard deviation of the mean, with the exception of one resident who was also subjectively felt to "fail" the exam. In exams with two faculty "evaluators", scores were highly correlated. The survey showed satisfaction with the examination process in general. CONCLUSION: Standardized patients can be used for mock oral boards in the live patient format. Our initial experience with this examination process was positive. Further testing is needed to determine if this examination format is more reliable and valid than traditional methods of assessing resident competency.

Attitude of Health Personnel↗

Dynamics of intraventricular hemorrhage in patients with spontaneous intracerebral hemorrhage: risk factors, clinical impact, and effect of hemostatic therapy with recombinant activated factor VII.

OBJECTIVE: To evaluate predictors of intraventricular hemorrhage (IVH) and IVH growth, impact of IVH growth on outcome, and impact of recombinant activated factor VII (rFVIIa) in patients with intracerebral hemorrhage (ICH). METHODS: We analyzed 374 patients out of 399 who were randomized to rFVIIa (40, 80, or 160 mug/kg) or placebo for ICH (diagnosed within 3 h of symptoms). Risk factors for IVH growth (>2 ml increase in IVH volume at 24 h), and death or severe disability (modified Rankin scale score 4-6) at 3 months were identified (logistic regression). RESULTS: IVH was present in 38% (n = 141) of patients at baseline and 45% (n = 169) by 24 hours. IVH growth, by 24 hours, occurred in 17 and 10% of placebo- and rFVIIa-treated patients, respectively (P = 0.037). Risk factors for IVH growth included baseline mean arterial pressure greater than 120 mmHg, larger baseline ICH volume, IVH present at baseline, shorter time from symptom onset to baseline computed tomographic scan, and treatment (rFVIIa versus placebo) (all, P < or = 0.037). Predictors of death or severe disability included older age, lower baseline Glasgow Coma Score, larger baseline ICH volume, IVH growth greater than 2 ml, IVH present at baseline or 24 hours, and treatment (rFVIIa versus placebo) (all, P < or = 0.0405). CONCLUSION: Presence of IVH at any time and early IVH growth worsen clinical outcome and increase mortality. Elevated mean arterial pressure at baseline may be a modifiable risk factor for IVH growth. Beneficial effects of rFVIIa on ICH outcome may be mediated, at least in part, by reducing IVH growth.

Aging↗

Recombinant activated factor VII for acute intracerebral hemorrhage: US phase IIA trial.

BACKGROUND AND PURPOSE: Ultra-early hemostatic therapy may improve outcome after intracerebral hemorrhage (ICH) by preventing rebleeding and hematoma expansion. We conducted this trial to evaluate the safety of activated recombinant factor VII (rFVIIa; NovoSeven) for preventing early hematoma growth in acute ICH. METHODS: In this multicenter, randomized, double-blind, placebo-controlled, dose-escalation trial, 40 patients diagnosed with ICH by computed tomography within 3 hours of onset were treated with placebo or 5, 20, 40, or 80 microg/kg of rFVIIa ( n = 8 per group). Patients with any history of thromboembolic or vaso-occlusive disease were excluded. The primary endpoint was the frequency of adverse events (AEs). RESULTS: Mean age was 65 years (range 34 - 91) and the median admission Glasgow Coma Scale score was 14.5 (range 6 to 15). Mean ICH volume was 17 +/- 19 mL; nearly three-quarters were located in the basal ganglia ( n = 29). The mean interval from onset to treatment was 178 +/- 41 minutes. Thirty-three patients experienced 186 AEs, which occurred with similar frequency in the five groups. There were 10 thromboembolic AEs, including one case of deep vein thrombosis (20 microg g/kg group); one case of cerebral infarction (placebo); two cases of pulmonary embolism (20 and 40 microg g/kg groups); and six instances of ischemic ECG changes or cardiac enzyme elevation (placebo [ n = 2], 20 microg g/kg [ n = 1], 40 microg g/kg [ n = 1], and 80 microg g/kg [ n = 2] groups). No consumption coagulopathy or dose-related increase in edema-to-ICH volume ratio occurred. CONCLUSIONS: Ultra-early rFVIIa treatment for ICH was associated with a reasonable safety profile in this preliminary study across a wide range of dosages. Further research is warranted to investigate the safety and potential efficacy of rFVIIa for minimizing ICH growth.

Adult↗

Association of Phosphodiesterase 4D with ischemic stroke: a population-based case-control study.

BACKGROUND AND PURPOSE: The Phosphodiesterase 4D (PDE4D) gene was reported recently to be associated with ischemic stroke in an Icelandic population. The association was found predominately with large vessel and cardioembolic stroke. However, 2 recent reports were unable to confirm this association, although a trend toward association with cardioembolic stroke was reported. None of the reports included significant proportions of blacks. We tested for genotype and haplotype association of polymorphisms of the PDE4D gene with ischemic stroke in a population-based, biracial, case-control study. METHODS: A total of 357 cases of ischemic stroke and 482 stroke-free controls from the same community were examined. Single nucleotide polymorphisms (SNPs) were chosen based on significant associations reported previously. Linkage disequilibrium (LD), SNP, and haplotype association analysis was performed using PHASE 2.0 and Haploview 3.2. RESULTS: Although several univariate associations were identified, only 1 SNP (rs2910829) was found to be significantly associated with cardioembolic stroke among both whites and blacks. The rs152312 SNP was associated with cardioembolic stroke among whites after multiple comparison corrections. The same SNP was not associated with cardioembolic stroke among blacks. However, significant haplotype association was identified for both whites and blacks for all ischemic stroke, cardioembolic stroke, and stroke of unknown origin. Haplotype association was identified for small vessel stroke among whites. CONCLUSIONS: PDE4D is a risk factor for ischemic stroke and, in particular, for cardioembolic stroke, among whites and blacks. Further study of this gene is warranted.

3',5'-Cyclic-AMP Phosphodiesterases↗

NIHSS training and certification using a new digital video disk is reliable.

BACKGROUND AND PURPOSE: NIH Stroke Scale certification is required for participation in modern stroke clinical trials and as part of good clinical care in stroke centers. The existing training and certification videotapes, however, are more than 10 years old and do not contain an adequate balance of patient findings. METHODS: After producing a new NIHSS training and demonstration DVD, we selected 18 patients representing all possible scores on 15 scale items for a new certification DVD. Patients were divided into 3 certification groups of 6 patients each, balanced for lesion side, distribution of scale item findings, and total score. We sought to measure interrater reliability of the certification DVD using methodology previously published for the original videotapes. Raters were recruited from 3 experienced stroke centers. Each rater watched the new training DVD and then evaluated one of the 3 certification groups. RESULTS: Responses were received from 112 raters: 26.2% of all responses came from stroke nurses, 34.1% from emergency departments/other physicians, and 39.6% from neurologists. One half (50%) of raters were previously NIHSS-certified. Item responses were tabulated, scoring performed as previously published, and agreement measured with unweighted kappa coefficients for individual items and an intraclass correlation coefficient for the overall score. kappa ranged from 0.21+/-0.05 (ataxia) to 0.92+/-0.09 (LOC-C questions). Of 15 items, 2 showed poor, 11 moderate, and 2 excellent agreement based on kappa scores. The intraclass correlation coefficient for total score was 0.94 (95% confidence interval, 0.84 to 1.00). Reliability scores were similar among specialists and centers, and there were no differences between nurses and physicians. kappa scores trended higher among raters previously certified. CONCLUSIONS: These certification DVDs are reliable for NIHSS certification, and scoring sheets have been posted on a web site for real-time, online certification.

Cerebrovascular Disorders↗

Association of apolipoprotein E4 and haplotypes of the apolipoprotein E gene with lobar intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Conflicting reports in the literature exist with regard to the association of apolipoprotein E (apo E) alleles and lobar intracerebral hemorrhage (ICH). We genotyped 12 single-nucleotide polymorphisms in the 5' upstream regulatory, exonic, and intronic regions of the apo E gene and performed genotype and haplotype association analyses. METHODS: We prospectively enrolled subjects with hemorrhagic stroke and matched them with 2 controls based on age, race, and sex. Each case was reviewed by a physician to determine case status and location of the ICH. Multivariate logistic-regression modeling with backward elimination was used to determine significant risk factors for lobar ICH. Associations at the genotype and haplotype levels and linkage disequilibrium were conducted according to standard statistical methods. RESULTS: Between May 1997 and December 2002, 315 cases of ICH were recruited, of whom 107 were lobar ICH cases matched to 205 controls. No association was found for apo E2, E3, or E4 with nonlobar ICH. Independent, significant risk factors for lobar ICH included apo E4, untreated hypertension, anticoagulant use, a first-degree relative with ICH, and < or =high school education (compared with >high school education). Treated hypercholesterolemia compared with "no history of hypercholesterolemia" was associated with a decreased risk of lobar ICH. Haplotype association analysis demonstrated a significant association of the apo E gene with lobar ICH among whites (P<0.0001) and blacks (P=0.0024). CONCLUSIONS: Apo E4 is independently associated with lobar ICH but not nonlobar ICH. Haplotypes of the apo E gene are associated with lobar ICH. Untreated hypertension is a risk factor for lobar ICH.

Alleles↗

Recombinant activated factor VII for acute intracerebral hemorrhage.

BACKGROUND: Intracerebral hemorrhage is the least treatable form of stroke and is associated with high mortality. Among patients who undergo computed tomography (CT) within three hours after the onset of intracerebral hemorrhage, one third have an increase in the volume of the hematoma related to subsequent bleeding. We sought to determine whether recombinant activated factor VII (rFVIIa) can reduce hematoma growth after intracerebral hemorrhage. METHODS: We randomly assigned 399 patients with intracerebral hemorrhage diagnosed by CT within three hours after onset to receive placebo (96 patients) or 40 microg of rFVIIa per kilogram of body weight (108 patients), 80 microg per kilogram (92 patients), or 160 microg per kilogram (103 patients) within one hour after the baseline scan. The primary outcome measure was the percent change in the volume of the intracerebral hemorrhage at 24 hours. Clinical outcomes were assessed at 90 days. RESULTS: Hematoma volume increased more in the placebo group than in the rFVIIa groups. The mean increase was 29 percent in the placebo group, as compared with 16 percent, 14 percent, and 11 percent in the groups given 40 microg, 80 microg, and 160 microg of rFVIIa per kilogram, respectively (P=0.01 for the comparison of the three rFVIIa groups with the placebo group). Growth in the volume of intracerebral hemorrhage was reduced by 3.3 ml, 4.5 ml, and 5.8 ml in the three treatment groups, as compared with that in the placebo group (P=0.01). Sixty-nine percent of placebo-treated patients died or were severely disabled (as defined by a modified Rankin Scale score of 4 to 6), as compared with 55 percent, 49 percent, and 54 percent of the patients who were given 40, 80, and 160 microg of rFVIIa, respectively (P=0.004 for the comparison of the three rFVIIa groups with the placebo group). Mortality at 90 days was 29 percent for patients who received placebo, as compared with 18 percent in the three rFVIIa groups combined (P=0.02). Serious thromboembolic adverse events, mainly myocardial or cerebral infarction, occurred in 7 percent of rFVIIa-treated patients, as compared with 2 percent of those given placebo (P=0.12). CONCLUSIONS: Treatment with rFVIIa within four hours after the onset of intracerebral hemorrhage limits the growth of the hematoma, reduces mortality, and improves functional outcomes at 90 days, despite a small increase in the frequency of thromboembolic adverse events.

Adult↗

Derivation of transcranial Doppler criteria for rescue intra-arterial thrombolysis: multicenter experience from the Interventional Management of Stroke study.

BACKGROUND AND PURPOSE: Transcranial Doppler (TCD) has the potential to identify acute stroke patients with arterial occlusion when treatment with intravenous recombinant tissue plasminogen activator (rtPA) may fail to open the vessel. We examined clinical utility and prognostic value of TCD flow findings in patients enrolled in an intravenous/intra-arterial rtPA pilot trial (Interventional Management of Stroke [IMS] study). METHODS: Patients enrolled in the IMS trial who underwent urgent TCD performed before intra-arterial rtPA treatment were included. TCD findings were analyzed by a mean flow velocity (MFV) ratio using reciprocal middle carotid artery (MCA) depths bilaterally (affected MCA-to-contralateral MCA MFV ratio [aMCA/cMCA MFV ratio]). The clinical utility of TCD was determined by its ability to predict outcome and identify a proximal arterial occlusion that requires intra-arterial lysis per protocol. RESULTS: Twenty-nine of 80 patients enrolled in IMS trial had pre-intra-arterial lysis TCD (mean age, 61+/-11; men-to-women ratio: 17:12; median baseline National Institutes of Health Stroke Score, 17). No temporal window was found in 3 patients (10%). Cerebral angiography was performed at mean 174+/-36 minutes from stroke onset. TCD was performed at median 93.5 minutes from onset. The aMCA/cMCA MFV ratio <0.6 had a sensitivity of 94% (95% confidence interval [CI], 63% to 99%), specificity of 100% (97.5%; lower CI of 54%), positive predictive value of 100% (lower CI, 80%); and negative predictive value of 86% (CI, 42% to 99%) for identifying proximal occlusion in the anterior circulation that require intra-arterial lysis. All patients with absent MCA flow (n=6) had poor outcomes (modified Rankin Scale > or =3) (P=0.014). CONCLUSIONS: TCD is a useful modality for evaluating the arterial circulation in acute ischemic stroke patients; it may have significant potential as a screening tool for intravenous/intra-arterial lysis protocols.

Aged↗

Safety and feasibility of recombinant factor VIIa for acute intracerebral hemorrhage.

BACKGROUND AND PURPOSE: Hematoma growth occurs in 38% of intracerebral hemorrhage (ICH) patients scanned by computed tomography (CT) within 3 hours of onset. Activated recombinant factor VII (rFVIIa) promotes hemostasis at sites of vascular injury and may minimize hematoma growth after ICH. METHODS: In this randomized, double-blind, placebo-controlled, dose-escalation trial, 48 subjects with ICH diagnosed within 3 hours of onset were treated with placebo (n=12) or rFVIIa (10, 20, 40, 80, 120, or 160 microg/kg; n=6 per group). The primary endpoint was the frequency of adverse events (AEs). Safety assessments included serial electrocardiography (ECG), troponin I and coagulation testing, lower extremity Doppler ultrasonography, and calculation of edema:ICH volume ratios. RESULTS: Mean age was 61 years (range, 30 to 93) and 57% were male. At admission, mean National Institutes of Health Stroke Scale (NIHSS) score was 14 (range, 1 to 26), median Glasgow Coma Scale score was 14 (range, 6 to 15), and mean ICH volume was 21 mL (range, 1 to 151). Mean time from onset to treatment was 181 minutes (range, 120 to 265). Twelve serious AEs occurred, including 5 deaths (mortality 11%). Six AEs were considered possibly treatment-related, including rash, vomiting, fever, ECG T-wave inversion, and 2 cases of deep vein thrombosis (placebo and 20-microg/kg groups). No myocardial ischemia, consumption coagulopathy, or dose-related increase in edema:ICH volume occurred. CONCLUSIONS: This small phase II trial evaluated a wide range of rFVIIa doses in acute ICH and raised no major safety concerns. Larger studies are justified to determine whether rFVIIa can safely and effectively limit ICH growth.

Acute Disease↗

Ischemic stroke subtypes: a population-based study of incidence rates among blacks and whites.

BACKGROUND AND PURPOSE: Blacks have an excess burden of stroke compared with whites; however, data comparing ischemic stroke subtypes among the 2 groups are limited and typically involve relative frequencies. The objective of this study is to compare the incidence rates of ischemic stroke subtypes between blacks and whites within a large, representative, biracial population. METHODS: The Greater Cincinnati/Northern Kentucky Stroke Study is designed to measure incidence rates and trends of all strokes within a well-defined, large, biracial population. Hospitalized cases were ascertained by International Classification of Disease (9th revision; ICD-9) discharge codes. Out-of-hospital events were ascertained by prospective screening of emergency department admission logs, review of coroners' cases, and monitoring all public health and hospital-based primary care clinics. A sampling scheme was used to ascertain events from nursing homes and all other primary care physician offices. All potential cases underwent detailed chart abstraction and confirmed by physician review. Based on all available clinical, laboratory, and radiographic information, ischemic stroke cases were subtyped into the following categories: cardioembolic, large-vessel, small-vessel, other, and stroke of undetermined cause. Race-specific incidence rates were calculated and compared after adjusting for age and gender, and standardizing to the 1990 US population. RESULTS: Between July 1, 1993, and June 30, 1994, 1956 first-ever ischemic strokes occurred among blacks and whites in the study population. Small-vessel strokes and strokes of undetermined cause were nearly twice as common among blacks. Large-vessel strokes were 40% more common among blacks than whites, and there was a trend toward cardioembolic strokes being more common among blacks. CONCLUSIONS: The excess burden of ischemic strokes among blacks compared with whites is not uniformly spread across the different subtypes. Large-vessel strokes are more common and cardioembolic stroke are as common among blacks, traditionally thought to be more common among whites.

Aged↗

Effect of untreated hypertension on hemorrhagic stroke.

BACKGROUND AND PURPOSE: Stroke is the third leading cause of death and the leading cause of disability in the United States. Intracerebral hemorrhage and subarachnoid hemorrhage represent approximately 20% of all stroke cases and have a mortality rate of 40% to 50%. Hypertension is an important risk factor for these subtypes of stroke. We sought to determine whether untreated hypertension carries a different risk from treated hypertension for hemorrhagic stroke. METHODS: Cases of hemorrhagic stroke in the greater Cincinnati region were identified by screening all area hospital emergency rooms, radiology reports, and International Classification of Diseases 9 codes. Medical records were reviewed for risk factors and medication use. Cases of hemorrhagic stroke were approached for enrollment into the genetic sampling and interview arm. If subjects agreed, the case was matched by age, race, and gender to population-based controls. RESULTS: Between May 1997 and December 2002, we recruited 549 cases of hemorrhagic stroke, of which 322 were intracerebral hemorrhage and 227 were subarachnoid hemorrhage. Untreated hypertension was found to be a significant risk factor for hemorrhagic stroke (odds ratio [OR]=3.5 [2.3 to 5.2]; P<0.0001) as was treated hypertension (OR=1.4 [1.0 to 1.9]; P=0.03). Insurance status of "self-pay" or Medicaid was a significant risk factor for untreated hypertension (OR=2.7 [1.6 to 4.4]). We estimate that 17% to 28% of hemorrhagic strokes among hypertensive patients would have been prevented if they had been on hypertension treatment. CONCLUSIONS: Untreated hypertension is highly prevalent and an important risk factor for hemorrhagic stroke. We estimate that among hypertensive subjects, approximately one fourth of hemorrhagic strokes would be prevented if all hypertensive subjects received treatment.

Female↗

West Nile virus encephalitis in organ transplant recipients: another high-risk group for meningoencephalitis and death.

West Nile virus infection has been spreading westward across the continental United States since 1999. Although it often presents as a mild, self-limiting viral illness, it can result in a devastating meningoencephalitis in some patient populations, particularly the elderly. We report in this article on two immunosuppressed transplant patients who developed a severe meningoencephalitis caused by mosquito-borne West Nile virus infection. Suggestions for the prevention, diagnosis, and treatment of West Nile virus infection in this patient population are described.

Adult↗