Biomedical subjects

J F Annegers

Publications and source records attributed to J F Annegers.

At least 55 records · Page 3Linked to original sources

PubMed1996

Population-based study of seizure disorders after cerebral infarction.

We performed the first population-based study that determined the magnitude of the risk and identified the factors predictive of developing seizure disorders after cerebral infarction. Five hundred thirty-five consecutive persons without prior unprovoked seizures were followed from their first cerebral infarctions until death or migration out of Rochester, Minnesota. Thirty-three patients (6%) developed early seizures (within 1 week), 78% of which occurred within the first 24 hours after infarction. Using multivariate analysis, the only factor predictive of early seizure occurrence was anterior hemisphere location of infarct (odds ratio 4.0; 95% CI 1.2 to 13.7). Twenty-seven patients developed an initial late seizure (past 1 week), whereas 18 developed epilepsy (recurrent late seizures). Compared with the population in the community, the risk during the first year was 23 times higher for initial late seizures and 17 times higher for epilepsy. The cumulative probability of developing initial late seizures was 3.0% by 1 year, 4.7% by 2 years, 7.4% by 5 years, and 8.9% by 10 years. Independent predictive factors on multivariate analysis for initial late seizures were early seizure occurrence (hazard ratio of 7.8 [95% CI 2.8 to 21.7]) and stroke recurrence (3.1 [1.2 to 8.3]). Both early seizure occurrence (16.4 [5.5 to 49.2]) and stroke recurrence (3.5 [1.2 to 10.5]) independently predicted the development of epilepsy as well. We also found that early seizure occurrence predisposed those with initial late seizures to develop epilepsy.

Adolescent↗

PubMed1996

Dementia and adult-onset unprovoked seizures.

OBJECTIVE: We tested the hypothesis that dementia increases the risk of unprovoked seizure among adults. Partial- and generalized-onset seizures were considered together and separately. Additionally, we explored whether the increased risk was restricted to Alzheimer's disease (AD), as previously shown. DESIGN: Subjects in this population-based case-control study were 145 incident cases of first unprovoked seizure (without prior stroke, CNS infection, brain tumor, head trauma, mental retardation, or cerebral palsy) aged 55 years or older and 290 controls matched to cases on age, gender, and duration of medical follow-up. Using the records-linkage system of the Rochester Epidemiology Project, we obtained, for both cases and matched controls, information on dementia prior to onset of unprovoked seizure. Subjects were classified as having dementia if they met ad hoc criteria equivalent to those in the DSM-III. AD was distinguished from other dementias. RESULTS: Both a diagnosis of AD and a diagnosis of other dementia were associated with at least a six-fold increased risk of unprovoked seizure when controlling for age, sex, and length of medical follow-up in Rochester. There was no difference in risk when comparing generalized-onset seizures with partial-onset seizures. CONCLUSIONS: In the absence of other prior neurologic insult, both AD and other dementias increase the risk of generalized- and partial-onset unprovoked seizures.

Age of Onset↗

PubMed1996

Month-of-birth and incidence of acute lymphoblastic leukemia in children.

As a means of examining the virus-relatedness of acute lymphoblastic leukemia (ALL) in children, we investigated the association between month-of-birth and the occurrence of ALL in 1487 children aged 0-15 years at the time of diagnosis. Our hypothesis being that evidence of seasonal variation in births of ALL cases would suggest exposure to a transmissible etiologic agent during the perinatal period. The data were obtained from the Surveillance, Epidemiology, and End Results (SEER) Program and consisted of children diagnosed during the years 1973-1986. Aggregate monthly incidence rates of ALL stratified by month-of-birth, for each SEER site, all sites combined, and for broad geographic regions were calculated. No evidence for an association between month-of-birth and childhood ALL was found.

Adolescent↗

PubMed1996

Causes of epilepsy: contributions of the Rochester epidemiology project.

The contributions of the Rochester (Minnesota) Epidemiology Project and Mayo Clinic studies in the evaluation of the causes of epilepsy are summarized. The development of the unique population-based medical records-linkage resource is chronicled, and the measures of occurrence and association used in epidemiologic study designs to assess the causes of epilepsy are presented. The historical cohort design is optimal for the study of the relationship between common central nervous system insults and seizures, and case-control studies are best used for analysis of relatively rare seizure disorders. The major findings about the etiologic roles of traumatic brain injuries, central nervous system infections, cerebrovascular disease, brain tumors, neurodegenerative diseases, developmental disabilities, perinatal insults, and familial factors are discussed. The role of genetic factors in epilepsy has been controversial, perhaps because of the numerous causes of seizures and their episodic nature. Both potential environmental and genetic causes will continue to be assessed.

Epidemiologic Methods↗

PubMed1996

Descriptive epidemiology of epilepsy: contributions of population-based studies from Rochester, Minnesota.

Studies based on the Rochester Epidemiology Project medical records-linkage system have provided important insights into the epidemiology of epilepsy. The incidence of all convulsive disorders in Rochester, Minnesota, during a 50-year period exceeded 130 per 100,000 person-years. The age-adjusted incidence of epilepsy was 44 per 100,000 person-years; of a first unprovoked seizure, 61; and of acute symptomatic seizures excluding febrile convulsions, 31. In addition, 2% of the population experienced a febrile convulsion before the age of 5 years. The cumulative incidence of epilepsy through age 74 years was 3.0%, of all unprovoked seizures was 4.1%, and of any convulsive disorder approached 10%. For epilepsy, single unprovoked seizures, and acute symptomatic seizures, the incidence was significantly higher in males than in females, and it was high in the first year of life but highest in those age 75 years or older. For epilepsy alone, approximately 60% of incidence cases experienced partial seizures, and two-thirds had no clearly identified antecedent. Cerebrovascular disease was the most commonly identified antecedent of epilepsy, accounting for 11% of cases. Over time, the incidence of epilepsy and of unprovoked seizures decreased in children and increased in the elderly population. The age-adjusted prevalence of active epilepsy on Jan. 1, 1980, was 6.8 per 1,000 residents. Prevalence was low in the first decade of life, increased to a plateau in the adult years, and further increased in the elderly population. Almost 1.5% of the population older than 75 years of age had active epilepsy. About 25% of prevalence cases had an identified cause; 60% experienced partial epilepsy.

Age Distribution↗

PubMed1995

Case-control study of the risk factors for eclampsia.

A case-control study was conducted to investigate risk factors for eclampsia. A total of 66 cases of eclampsia were ascertained from deliveries between 1977 and 1992 at two hospitals in Houston, Texas, based on the criteria defined by the American College of Obstetrics and Gynecology. Cases were matched to nonpreeclamptic controls on a 4:1 ratio on the basis of hospital and month of delivery. The ratio of eclampsia cases to number of deliveries over the study period was 0.63 per 1,000. In a logistic regression model, risk factors for eclampsia included 1) two or fewer prenatal care visits (odds ratio (OR) = 6.10, 95% confidence interval (CI) 2.26-16.41), 2) urinary tract infection (OR = 4.23, 95% CI 1.27-14.06), 3) primigravidity (OR = 2.87, 95% CI 0.97-8.44), 4) obesity (OR = 2.49, 95% CI 0.78-7.96), 5) black ethnicity (OR = 2.25, 95% CI 0.88-5.78), 6) history of diabetes (OR = 2.07, 95% CI 0.45-9.62), and 7) age < or = 20 years (OR = 1.55, 95% CI 0.47-5.10). Nulliparity was not shown to be a risk factor for eclampsia when controlled for primigravidity, and neither were previous history of abortion or previous history of pregnancy-induced hypertension. Thus, prior pregnancy itself, independent of outcome and preeclamptic/eclamptic complications, appears to be the protective factor against eclampsia in a subsequent pregnancy.

Abortion, Induced↗

PubMed1995

Cigarette smoking and alcohol consumption as risk factors for colorectal adenomatous polyps.

BACKGROUND: Results of epidemiologic studies suggest that there is limited evidence for the association between cigarette smoking and risk of colorectal cancer. Cigarette smoking has been shown to increase the risk of colorectal adenomatous polyps, which are recognized as precursors of colorectal cancer, while few studies have examined the association between alcohol consumption and the development of adenomatous polyps. PURPOSE: We examined the association between cigarette smoking, alcohol consumption, and the presence of colorectal adenomatous polyps. METHODS: Analyses were based on data from a case-control study of dietary and other lifestyle factors for colorectal adenomatous polyps. We assessed the risk of adenomatous polyps associated with total number of years of smoking, number of cigarettes smoked per day, and pack-years of smoking for past and current smokers separately. We also assessed the joint association between cigarette smoking and alcohol consumption on the risk of adenomatous polyps. RESULTS: Current smokers who smoked more than 20 pack-years were at significantly higher risk of adenomatous polyps compared with never smokers (odds ratio [OR] = 2.56; 95% confidence interval [CI] = 1.28-5.14). Past smokers also had an increased risk of having adenomatous polyps, but no clear trend was observed for pack-years of smoking. Alcohol consumption was positively associated with risk of adenomatous polyps. Compared with nondrinkers, the strongest risk was observed for individuals who consumed 2.31-9.46 g alcohol per day (OR = 2.23; 95% CI = 1.29-3.83), and a decrease in risk was observed for individuals who consumed 9.47-67.36 g alcohol per day (OR = 1.63; 95% CI = 0.92-2.88). Among current smokers, a joint effect was observed for individuals who smoked and drank compared with those who never smoked and were not current drinkers (OR = 4.21; 95% CI = 1.88-9.41). For past smokers, a significant joint effect of smoking and current alcohol consumption was also observed, but the risk was not as strong as that for current smokers (OR = 2.61; 95% CI = 1.40-4.87). CONCLUSIONS: These data provide further evidence of the positive association between cigarette smoking and the development of colorectal adenomatous polyps. The combination of cigarette smoking and alcohol consumption increased the risk of adenomatous polyps. IMPLICATIONS: Future research should focus on the understanding of the role of cigarette smoking and alcohol consumption as these two factors relate to the evolution of colorectal adenomatous polyps and subsequent carcinogenesis.

Adenomatous Polyposis Coli↗

PubMed1995

A case-control study of nonrandom distribution of bleomycin-induced chromatid breaks in lymphocytes of lung cancer cases.

We used a case-control study design to determine the association between bleomycin-induced chromatid breaks and the risk of lung cancer in general and by specific histopathological types. Lymphocytes from primary blood cultures of 78 controls and 75 cases with 4 histopathological types of lung cancer were treated with 0.03 unit/ml bleomycin for 5 h, and the frequency of induced chromatid breakage and the locations of the breaks were determined in Q-banded preparations. After adjustment for their length, the larger chromosomes had more breaks than the smaller chromosomes in both cases and controls. The cases had significantly more breaks on chromosomes 4 and 5 than the controls did, with odds ratios (ORs) of 4.9 [95% confidence limits (CL), 2.0, 11.7] and 3.9 (95% CL, 1.6, 9.3), respectively. When the lung cancers were classified by histopathological type, adenocarcinomas had significantly more breaks on chromosomes 4 and 5, with ORs of 3.0 (95% CL, 1.0, 8.7) and 3.5 (95% CL, 1.2, 10.7), respectively. For squamous cell carcinoma, the ORs were significantly elevated for breaks on chromosomes 2, 4, and 5 with ORs of 3.5 (95% CL, 1.0, 11.7), 10.2 (95% CL, 2.5, 41.9), and 7.9 (95% CL, 1.9, 32.8). For small cell carcinoma, breaks on chromosomes 2 and 4 showed significantly increased ORs of 33.2 (95% CL, 2.2, 513.3) and 20.4 (95% CL, 1.7, 250.1), respectively. However, no specific chromatid breaks were detected in cases with large cell carcinoma. When the frequency of chromatid breaks at specific regions was calculated, breaks at 4p14, 4q27, 4q31, 5q21-q22, 5q31, and 5q33 were significantly more common in lung cancer cases than in controls. Lung cancer risk had a dose-response relationship with breaks on chromosomes 4 and 5. Cigarette smoking had a strong interaction with breaks on chromosomes 2, 4, and 5. The findings suggest that the susceptibility of particular chromosome loci to mutagenic damage may be a risk factor for specific types of lung cancer.

Adenocarcinoma↗

PubMed1995

Prognosis of amyotrophic lateral sclerosis and the effect of referral selection.

We followed two cohorts of Amyotrophic Lateral Sclerosis (ALS) patients to examine the survival and prognostic factors of ALS and the impact of selective referral on prognosis of ALS. The first cohort consisted of population-based incident ALS cases from Harris County, Texas, first diagnosed between 1985 and 1988. The second was a clinical series from a tertiary care center in Houston, Texas, diagnosed between 1977 and 1989. The overall 3-year survival was 29% in the incidence cohort and 32% in the referral cohort; however, the 5-year survival was much lower for the incidence cohort than the referral cohort (4% vs 21%). The large difference in 5-year survival was not explained by the distributions of prognostic factors in the two cohorts but due to stronger unfavorable effects of prognostic factors in the incidence cohort than the referral cohort. In both cohorts, older age at diagnosis, bulbar onset, and positive family history of ALS were unfavorable prognostic factors while blacks had better survival than whites or hispanics. We confirmed that longer duration from onset to diagnosis was a favorable prognostic factor in both cohorts but the effect was more pronounced in the referral series.

Adult↗

PubMed1995

Incidence of acute symptomatic seizures in Rochester, Minnesota, 1935-1984.

We determined the incidence of seizures due to acute CNS insults for residents of Rochester, Minnesota, U.S.A., from 1935 through 1984. The age-adjusted incidence rates for 1955-1984, the period of most complete case ascertainment, was 39.0/100,000 person-years (United States 1970 population as standard). The age-adjusted incidence was considerably higher in men: 52.0 as compared with 29.5 in women. The 3.6% risk of experiencing an acute symptomatic seizure in an 80-year lifespan approaches that of developing epilepsy. The major causes of acute symptomatic seizures were traumatic brain injury, cerebrovascular disease, drug withdrawal, and CNS infections. Each type of acute symptomatic seizure has age, gender, and time period patterns that reflect the occurrence of the underlying cause.

Adolescent↗

PubMed1995

Cohort study of incidence of sudden unexplained death in persons with seizure disorder treated with antiepileptic drugs in Saskatchewan, Canada.

To measure the incidence of sudden unexplained death in treated persons with epilepsy (SUDEP) and to identify risk factors for SUDEP, a cohort of 6,044 persons aged 15-49 years with more than four prescriptions for antiepileptic drugs (AEDs) was identified from the Saskatchewan Health prscription drug file. To exclude subjects whose sudden deaths (SUDs) might be misattributed to another chronic underlying disease, subjects with hospitalizations for cancer or heart problems were excluded. To exclude subjects without epilepsy, subjects with > 2-year AED treatment followed by AED-free time and subjects receiving < 1 U/day were excluded. The final cohort consisted of 3,688 subjects. Follow-up was started at the first AED prescription listed in the prescription drug file and ended at the earliest of the following: age 50 years, death, or last registration in the Saskatchewan Health. For 153 of 163 deaths occurring in the cohort, copies of anonymized death certificates were obtained and copies of anonymized autopsy reports of potential SUDEP cases were examined. There were 18 definite/probable SUDs and 21 possible SUDEPs, yielding a minimum incidence of 0.54 SUDEP per 1,000 person-years and a maximum of 1.35 SUDEP per 1,000 person-years. SUDEP incidence increased with male sex, number of AEDs ever prescribed, and prescription of psychotropic drugs and was highest in males with a history of treatment with three or more AEDs and four or more psychotropic drug prescriptions. Poisson regression showed a 1.7-fold increase in risk of SUDEP for each increment in maximum number of AEDs administered, a likely surrogate for severity and persistence of seizures.

Adolescent↗

PubMed1995

Secular trends and birth cohort effects in unprovoked seizures: Rochester, Minnesota 1935-1984.

The incidence of idiopathic/cryptogenic epilepsy and isolated unprovoked seizures has been relatively stable in the population of Rochester, Minnesota, for the 50-year period 1935 through 1984. In each decade, the age-specific rates exhibited a consistent U-shaped pattern of decreasing rates from infancy to age 40-49 and a progressive increase thereafter to a second peak at age 70 years. Males had a 15% higher incidence of cryptogenic unprovoked seizures than females. The most pronounced secular trend was a decrease in the incidence in children aged < 10 years for the first 4 decades of the study; however, this trend was interrupted by a slight rebound in the decade 1975-1984. There has been a progressive decrease in the incidence of cryptogenic unprovoked seizures in individuals aged > or = 50 from 1965 through 1984. This decrease paralleled the decrease in cerebrovascular disease in the community. The decrease in idiopathic unprovoked seizures may be related to a concurrent trend in "silent stroke." Plots and Poisson regression analysis did not show patterns in the incidence of idiopathic unprovoked seizures related to successive birth cohorts. However, significantly lower incidence rates were observed for the 1930-1934 birth cohort, about half that of all others, between the ages of 5 and 54 years.

Adult↗

PubMed1995

Risk of stroke with mitral valve prolapse in population-based cohort study.

BACKGROUND AND PURPOSE: The purpose of this study was to clarify whether mitral valve prolapse increases the subsequent risk of stroke. METHODS: A historical cohort study was conducted on 1079 residents of Olmsted County, Minnesota, who had an initial echocardiographic diagnosis of mitral valve prolapse between 1975 and 1989 without prior stroke or transient ischemic attack and who were followed up for first stroke occurrence. RESULTS: There was an overall twofold increase in the incidence of stroke among individuals with mitral valve prolapse relative to the reference population (standardized morbidity ratio, 2.1; 95% confidence interval, 1.3 to 3.2). Sex, duration of follow-up from the diagnosis of mitral valve prolapse, or calendar year of initial diagnosis did not modify the association. Within the cohort of patients who were at least 35 years old at diagnosis of mitral valve prolapse, a time-dependent proportional-hazards multivariate model and a person-years analysis revealed that age, ischemic heart disease, congestive heart failure, and diabetes mellitus were important determinants for stroke when person-years of observation after mitral valve replacement were excluded. Among seven persons with mitral valve replacement, three strokes occurred in 24 person-years of follow-up. For those with an auscultatory diagnosis of mitral valve prolapse only as the indication for echocardiography (44%), the risk of stroke relative to the population was 1.0 (95% confidence interval, 0.2 to 2.9); for those with another cardiac diagnosis, the standardized morbidity ratio was 2.5 (95% confidence interval, 1.5 to 4.0). CONCLUSIONS: Individuals with uncomplicated mitral valve prolapse did not have an increased risk of stroke, although a small increase in the risk may not have been detected.

Adult↗

PubMed1995

Survival time and season-of-treatment initiation in children with acute lymphoblastic leukemia.

We examined survival in childhood acute lymphoblastic leukemia (ALL) as a function of season-of-treatment initiation. Survival for 1797 children aged 15 and under from the Surveillance, Epidemiology, and End Results (SEER) cancer registry, diagnosed and treated from 1973-1986 was obtained. There was no significant seasonal pattern for survival by season-of-treatment initiation. Neither age, gender, nor treatment type served as effect modifiers or confounders in this relationship. Female gender, age between one and ten years, and certain broad categories of treatment type were significant predictors of survival in separate univariate analyses, however. The nonsignificance of the results do not support the concept that season-of-treatment initiation is a prognostic factor in survival from ALL in children.

Adolescent↗

PubMed1995

A case-control study of wood dust exposure, mutagen sensitivity, and lung cancer risk.

The associations between lung cancer risk, mutagen sensitivity (a marker of cancer susceptibility), and a putative lung carcinogen, wood dust, were assessed in a hospital-based case-control study. There were 113 African -American and 67 Mexican-American cases with newly diagnosed, previously untreated lung cancer and 270 controls, frequency-matched on age, ethnicity, and sex. Mutagen sensitivity ( 1 chromatid break/cell after short-term bleomycin treatment) was associated with statistically significant elevated risk for lung cancer [odds ration (OR) = 4.3; 95% confidence intervals (CI) = 2.3-7.9]. Wood dust exposure was also a significant predictor of risk (overall OR = 3.5; CI = 1.4-8.6) after controlling for smoking and mutagen sensitivity. When stratified by ethnicity, wood dust exposure was s significant risk factor for African-Americans (OR = 5.5; CI = 1.6-18.9) but not for Mexican-Americans (OR = 2.0; CI = 0.5-8.1). The ORs were 3.8 and 4.8 for non-small cell lung cancer in Mexican-Americans (CI = 1.2-18.5). Stratified analysis suggested evidence of strong interactions between wood dust exposure and both mutagen sensitivity and smoking in lung cancer risk.

Adult↗

PubMed1994

Risk factors for seizure recurrence in children with febrile seizures: a pooled analysis of individual patient data from five studies.

To reassess the relations between postulated risk factors and seizure recurrence after a first febrile seizure (FS), the individual data from five follow-up studies that used similar definitions of FSs and risk factors were pooled and reanalyzed. The risk of frequent recurrent seizures and of the occurrence of complex seizures in previously healthy, untreated children was studied. Seizure recurrence hazard was described as a function of the child's attained age. The influence of various risk factors on the recurrence hazard was assessed, with control for other factors. Of a total of 2496 children with 1410 episodes of recurrent seizures, 32% had one, 15% had two, and 7% had three or more recurrent seizures after a first FS; 7% had a complex seizure. The hazard of recurrent seizures was highest between the ages of 12 and 24 months. After a first and a second recurrence, the risk of further FSs was two and two and one-half times higher, respectively. A history of febrile or unprovoked seizures in a first-degree family member and a relatively low temperature at the time of the first seizure were also associated with an increased risk of subsequent recurrences. Young age at onset (< 12 months), a family history of unprovoked seizures, and a partial initial FS were all associated with an increased risk of complex seizures. A higher recurrence rate in clinic-based studies compared with population-based studies could not be explained by a difference in the presence of the risk factors studied. Thus other factors must influence seizure recurrence after an initial FS.

Age Factors↗

PubMed1994

Excess leukemia and multiple myeloma in a mining county in northeast Texas.

From 1950 to 1979, cancer mortality rates in Titus County, Texas, increased with a significant excess of deaths from leukemia, lymphoma, brain and liver cancers, and melanoma. County residents requested this study to verify the apparent excess of cancer. Newly diagnosed cases of cancer among white residents from 1977 to 1984 were ascertained from the Texas Cancer Registry, hospital records, and death certificates. Direct and indirect methods were used to calculate incidence rates and standardized incidence ratios (SIR). We identified 663 cancers for 148,470 person-years of observation. No overall excess of cancer was found. However, we found a significant excess of leukemia (SIR = 2.53, 95% confidence interval [CI] = 1.86, 3.30) and multiple myeloma (SIR = 1.87, 95% CI = 1.02, 3.14). The reasons for the increased SIRs are unknown. However, the excess of cancers in this mining community may be relevant to the ongoing debate on the health effects of the disposal of combustion wastes from mining and fossil fuel and on the need for stricter regulations. Other potential risk factors include the presence of petrochemical and poultry industries. regulations. Other potential risk factors include the presence of petrochemical and poultry industries.

Cause of Death↗

PubMed1994

Epidemiology and genetics of epilepsy.

The objectives of this article are to present the classification of seizure disorders in population studies and family studies, the basic measures of occurrence and association that are used in genetic and epidemiologic studies, the frequencies of seizures and epilepsy in populations, the major acquired causes of epilepsy and the epidemiologic evidence for causation, the prognosis of seizures and epilepsy, and the role of genetic factors in epilepsy.

Epilepsy↗