Biomedical subjects

W A Hauser

Publications and source records attributed to W A Hauser.

At least 73 records · Page 4Linked to original sources

PubMed1997

Race-ethnicity and determinants of carotid atherosclerosis in a multiethnic population. The Northern Manhattan Stroke Study.

BACKGROUND AND PURPOSE: Risk factors for carotid atherosclerosis have been studied in white populations but infrequently in multiethnic cohorts. The aim of this study was to determine the importance of race-ethnicity and other factors associated with carotid atherosclerosis in a mixed population of Hispanics, blacks, and whites. METHODS: As part of the Northern Manhattan Stroke Study, 526 stroke-free community residents (aged > or = 40 years; 41% men, 59% women; 46% Hispanic, 31% black, 23% white) were recruited through random-digit dialing and had vascular risk factor evaluations. Maximum internal carotid artery plaque thickness (MICPT) was measured with B-mode ultrasound. The frequency distribution of MICPT was examined in the three race-ethnic groups, and multivariate regression was performed to identify factors that were independently associated with MICPT. RESULTS: Mean MICPT in the entire sample was 1.5 +/- 1.4 mm, increased directly with age, and was greater in whites and blacks than Hispanics. Other independent determinants of MICPT included smoking, glucose, LDL cholesterol, and hypertension. After we controlled for these covariates, Hispanic (versus non-Hispanic) race-ethnicity was still an independent determinant of less carotid plaque. There was a significant interaction between race-ethnicity and LDL cholesterol, with a greater effect of increasing LDL cholesterol among Hispanics. CONCLUSIONS: Atherosclerotic risk factors were predictive of MICPT in this mixed-ethnic cohort. Hispanics had significantly less carotid plaque after adjustment for other known risk factors, but they also had a greater impact of increasing LDL cholesterol.

Adult↗

PubMed1997

A population-based study of prognosis of ruptured cerebral aneurysm: mortality and recurrence of subarachnoid hemorrhage.

OBJECTIVE: To determine the risk of recurrent subarachnoid hemorrhage (SAH), mortality, and relative survivorship following SAH caused by ruptured cerebral aneurysm (RCA). DESIGN/METHODS: The 86 individuals with a first diagnosis of SAH caused by RCA in Iceland from 1958 through 1968 were followed a minimum of 24 years (range, 24 to 32.5 years) or until death to determine mortality and to identify those with recurrent SAH. RESULTS: Thirty-eight patients (44%) died within 30 days of the index event. Two additional (both comatose from onset of ictus) died in the following month. There were no deaths between 3 and 6 months after onset. Based upon the age/gender-specific person years of observation for the population of Iceland, the Standardized Mortality Ratio for the 44 surgically treated patients surviving 6 months was 1.3. Those neurologically normal or with only mild impairment at 6 months had no identified increase in mortality. Excess mortality that was limited to individuals with severe neurologic deficit at 6 months could be identified through the first 10 years after onset. Two 6-month survivors experienced recurrent SAH. CONCLUSIONS: Early mortality is high (47%) in patients with RCA. In patients operated on for RCA and surviving 6 months, recurrent SAH occurred in 5%. Survivorship among patients surgically treated and neurologically normal or with mild residual neurologic impairment at 6 months following presentation was similar to that expected in the general population. Survivorship among patients surgically treated who had severe residual neurologic impairment at 6 months was significantly reduced.

Adult↗

PubMed1997

Segregation analysis of cryptogenic epilepsy and an empirical test of the validity of the results.

We used POINTER to perform segregation analysis of cryptogenic epilepsy in 1,557 three-generation families (probands and their parents, siblings, and offspring) ascertained from voluntary organizations. Analysis of the full data set indicated that the data were most consistent with an autosomal dominant (AD) model with 61% penetrance of the susceptibility gene. However, subsequent analyses revealed that the patterns of familial aggregation differed markedly between siblings and offspring of the probands. Risks in siblings were consistent with an autosomal recessive (AR) model and inconsistent with an AD model, whereas risks in offspring were inconsistent with an AR model and more consistent with an AD model. As a further test of the validity of the AD model, we used sequential ascertainment to extend the family history information in the subset of families judged likely to carry the putative susceptibility gene because they contained at least three affected individuals. Prevalence of idiopathic/cryptogenic epilepsy was only 3.7% in newly identified relatives expected to have a 50% probability of carrying the susceptibility gene under an AD model. Approximately 30% (i.e., 50% x 61%) were expected to be affected under the AD model resulting from the segregation analysis. These results suggest that the familial distribution of cryptogenic epilepsy is inconsistent with any conventional genetic model. The differences between siblings and offspring in the patterns of familial risk are intriguing and should be investigated further.

Adolescent↗

PubMed1997

Regulations prohibiting blood donation by individuals with seizures or epilepsy are not necessary.

Throughout the world people who have epilepsy and seizures are prohibited from donating blood. These restrictions are based on the assumption that they are prone to adverse donor reactions, specifically, syncope and convulsions. We describe a study evaluating whether that concern is warranted. During a two year period beginning in 1987, blood donors with a history of seizures were actively recruited by the American Red Cross in the state of Maryland, USA. According to accepted standards, adverse reactions were classified as "slight", for dizziness and nausea without loss of consciousness; "moderate", denoting syncope; and "severe", indicating convulsive syncope. We reviewed a total of 329,143 satisfactory blood donations, and 613 individuals reporting a history of seizures donated blood 723 times. Among donors with seizures, 186 (25.7%) were taking antiepileptic medication, and 61 (8.4%) had one or more seizures in the preceding year. Individuals with seizures had a low incidence of adverse reactions (3.34%). Although slightly higher than the entire population (2.24%), this difference was not statistically significant. In particular, the risk of syncope with or without convulsive activity was low for people with seizures (.21%) and not significantly increased as compared to other donors (.28%). Our study supports the view that individuals with seizures or epilepsy are not at greater risk for adverse reactions after blood donation. Major restrictions on individuals with epilepsy and seizures as blood donors are not warranted.

Adolescent↗

PubMed1996

Relations of genetic and environmental factors in the etiology of epilepsy.

We assessed the relations of genetic and environmental factors in the etiology of epilepsy. The study population comprised 9,705 first-degree relatives of 1,951 adults with epilepsy ascertained from voluntary organizations. We calculated standardized morbidity ratios for specific etiologies of epilepsy in the relatives of probands with the same etiologies, using population incidence rates from Rochester, MN, as the reference. Relatives of probands with idiopathic/cryptogenic epilepsy had increased risk for idiopathic/cryptogenic epilepsy and for epilepsy associated with neurological deficit presumed present at birth (cerebral palsy or mental retardation) but not for symptomatic epilepsy associated with postnatal central nervous system insults. Relatives of probands with neurodeficits had increased risks for idiopathic/cryptogenic epilepsy. Risk for epilepsy was not increased among relatives of probands with postnatal symptomatic epilepsy. The degree of increased risk of idiopathic/cryptogenic epilepsy in relatives of probands with idiopathic/cryptogenic epilepsy diminished with increasing age of the relatives; risk was not increased at age 35 or older. These findings support the possibility of shared genetic susceptibility to epilepsy and cerebral palsy, and suggest that the genetic contributions to postnatal symptomatic epilepsy are minimal.

Adolescent↗

PubMed1996

Prevalence of epilepsy in the elderly: the Rotterdam Study.

We assessed the prevalence of epilepsy in an elderly population in The Netherlands. The study was conducted from 1991 to 1993 as part of the Rotterdam Study, a population-based door-to-door study of all elderly people living in Ommoord, a suburb of Rotterdam, and included 5,559 persons aged 55-95 years. All subjects were screened for epilepsy through direct questions regarding the existence of epilepsy and antiepileptic drug (AED) use, in addition to relevant questions from the World Health Organization (WHO) protocol for epidemiologic studies of neurologic diseases. Further evaluation of screen positives was made by a panel of 1 study physician and 4 epileptologists, who also classified all confirmed cases of epilepsy according to the classifications of the International League Against Epilepsy (ILAE). The overall prevalence of active epilepsy in our study population was 0.9% including special syndromes and 0.8% excluding special syndromes. The prevalence increased with age from 0.7% for those aged 55-64 years to 1.2% for those aged 85-94 years. The increase with age was detected among men and women both. Our study confirms other findings showing that the prevalence of active epilepsy increases with age in the elderly. The prevalence figures in our study were high as compared with those of other population-based studies. Epilepsy appears to be a major cause of morbidity in the elderly.

Age Distribution↗

PubMed1996

Incidence of epilepsy in rural Iceland: a population-based study.

PURPOSE: We wished to determine the incidence of epilepsy in the population of rural Iceland. METHODS: Cases were identified through review of records of primary care facilities for the study population, supplemented by review of referrals to EEG facilities and neurologic specialists. RESULTS: The incidence of epilepsy (recurrent unprovoked seizures) was 47 in 100,000. Age-specific incidence was bimodal, highest in the youngest and oldest age groups. About one third of the patients had an identifiable etiology, and one third had partial seizures. Integration of imaging and neurophysiologic data did little to modify the distribution of etiology or seizure type. CONCLUSIONS: The present study confirms findings of other recent studies of incidence in Western Countries.

Adolescent↗

PubMed1996

Clinical indicators of genetic susceptibility to epilepsy.

We evaluated clinical indicators of genetic susceptibility to epilepsy in the families of 1,957 adults with epilepsy (probands) ascertained from voluntary organizations. Very few of the probands in this series had idiopathic epilepsy syndromes. Among relatives of probands with postnatal CNS insults, risks of epilepsy were no higher than in the general population. Risk was increased in relatives of probands without identified CNS insults (i.e., those with idiopathic/cryptogenic epilepsy) or with neurological deficit presumed present at birth, compared with relatives of probands with postnatal CNS insults. Among relatives of probands with idiopathic/cryptogenic epilepsy, risks were higher in parents and siblings, but not in offspring, of probands with generalized onset as compared with partial onset seizures. Risks in offspring were higher if the probands had onset of idiopathic/cryptogenic epilepsy before age 10 as compared with age > or = 10 years, but risks in parents and siblings were not associated with the probands's age at onset. These results suggest that genetic susceptibility increases risk of some forms of cryptogenic epilepsy and of epilepsy associated with neurological deficit presumed present at birth, but not of postnatal symptomatic epilepsy. The influences on risk in offspring may differ from those in parents and siblings.

Adolescent↗

PubMed1996

Severe, uncontrolled hypertension and adult-onset seizures: a case-control study in Rochester, Minnesota.

PURPOSE: Hypertension is an established risk factor for clinically detected stroke, which is in turn a risk factor for epilepsy. This relation suggested that hypertension, particularly severe and uncontrolled, might increase the risk of epilepsy in the absence of prior clinically detected stroke. METHODS: Subjects in this population-based case-control study were the 145 incident cases of first unprovoked seizure 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, all blood pressure readings before each case's first seizure came to medical attention. Subjects were classified as hypertensive if they had at least two readings of > or = 160/95 mm Hg or if there was electrocardiographic evidence for left ventricular hypertrophy. RESULTS: Severe uncontrolled hypertension increased the risk of unprovoked seizure. Left ventricular hypertrophy without diuretic treatment was associated with an 11-fold increased risk of unprovoked seizure: left ventricular hypertrophy treated with diuretics did not increase the risk. CONCLUSIONS: In the absence of clinically detected stroke, left ventricular hypertrophy without diuretic use may increase the risk of unprovoked seizures, and diuretic treatment may protect against this increased risk.

Adolescent↗

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

A prospective, population-based epidemiologic study of status epilepticus in Richmond, Virginia.

This report presents the initial analysis of a prospective, population-based study of status epilepticus (SE) in the city of Richmond, Virginia. The incidence of SE was 41 patients per year per 100,000 population. The frequency of total SE episodes was 50 per year per 100,000 population. The mortality rate for the population was 22%, 3% for children and 26% for adults. Evaluation of the seizure types for adult and pediatric patients demonstrated that both partial and generalized SE occur with a high frequency in these populations. Based on the incidence of SE actually determined in Richmond, Virginia, we project 126,000 to 195,000 SE events with 22,200 to 42,000 deaths per year in the United States. The majority of SE patients had no history of epilepsy. These results indicate that SE is a common neurologic emergency.

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↗

PubMed1996

The risk of seizure recurrence after a first unprovoked afebrile seizure in childhood: an extended follow-up.

OBJECTIVE: To assess the long-term recurrence risks after a first unprovoked seizure in childhood. METHODS: In a prospective study, 407 children who presented with a first unprovoked seizure were then followed for a mean of 6.3 years from the time of first seizure. RESULTS: One hundred seventy-one children (42%) experienced subsequent seizures. The cumulative risk of seizure recurrence was 29%, 37%, 42%, and 44% at 1, 2, 5, and 8 years, respectively. The median time to recurrence was 5.7 months, with 53% of recurrences occurring within 6 months, 69% within 1 year, and 88% within 2 years. Only 5 recurrences (3%) occurred after 5 years. On multivariable analysis, risk factors for seizure recurrence included a remote symptomatic etiology, an abnormal electroencephalogram (EEG), a seizure occurring while asleep, a history of prior febrile seizures, and Todd's paresis. In cryptogenic cases, the risk factors were an abnormal EEG and an initial seizure during sleep. In remote symptomatic cases, risk factors were a history of prior febrile seizures and age of onset younger than 3 years. Risk factors for late recurrences (after 2 years) were etiology, an abnormal EEG, and prior febrile seizures in the overall group and an abnormal EEG in the cryptogenic group. These are similar to the risk factors for early recurrence. CONCLUSIONS: The majority of children with a first unprovoked seizure will not have recurrences. Children with cryptogenic first seizures and a normal EEG whose initial seizure occurs while awake have a particularly favorable prognosis, with a 5-year recurrence risk of only 21%. Late recurrences do occur but are uncommon.

Child↗

PubMed1995

Is the course of neurocysticercosis modified by treatment with antihelminthic agents?

BACKGROUND: Neurocysticercosis, occasionally associated with long-term neurologic sequelae such as epilepsy or hydrocephalus, is more often a condition characterized by a benign course and spontaneous remission without permanent neurologic symptoms. This variability in outcome has led to difficulties in the interpretation of studies of the effectiveness of drugs used to treat this condition. OBJECTIVE: To evaluate the relative efficacy of two antihelminthic agents against each other and against symptomatic treatment alone. METHODS: Randomized clinical trial of treatment of patients with newly identified active neurocysticercosis with oral prednisolone alone (27 patients), praziquantel with prednisolone (54 patients), or albendazole with prednisolone (57 patients). RESULTS: At 6 months and at 1 year after treatment, there were no differences in the three treatment groups in terms of the proportion of patients who were free of cysts or the relative reduction of number of cysts. At 2 years, there was no difference in the proportion of patients free of seizures during the entire follow-up period. Early and late sequelae occurred in a higher proportion of patients treated with praziquantel and albendazole, compared with those receiving only prednisolone. CONCLUSIONS: Previous reports of favorable response to treatment of neurocysticercosis with either praziquantel or albendazole are by no means definitive and may be a reflection of the natural history of the condition. The present study, with randomized treatment assignment and including a control group, raises questions as to what extent and in whom treatment with these drugs is effective, and suggests that treatment with antihelminthic agents may be associated with an increased frequency of long-term sequelae.

Adult↗

PubMed1995

Birth cohort and familial risk of epilepsy: the effect of diminished recall in studies of lifetime prevalence.

This study separated the effects of age, birth cohort, and generation (parents, siblings, and offspring) on familial risk of epilepsy. The study population comprised 9,741 parents, siblings, and offspring of 1,957 adult probands with epilepsy ascertained from 10 voluntary organizations in New York, New Jersey, Connecticut, and Massachusetts between 1985 and 1988. Semistructured telephone interviews with probands and selected family members were used to collect data on the history of epilepsy in the relatives. The risk of epilepsy increased in successive generations (cumulative incidence to age 40: parents, 1.8%; siblings, 2.9%; offspring, 5.6%) but, with the exception of one subgroup (offspring of female probands), these differences disappeared after controlling for age and birth year of the relatives. With age and relationship controlled, the risk of epilepsy increased approximately 50% for each 20 advancing years of birth. Population-based data indicate that age-specific incidence rates of epilepsy have not increased during the age and time periods investigated here; thus, the most plausible explanation for the findings is that epilepsy is underreported in persons born in earlier time periods. These results illustrate a general phenomenon of underreporting in studies of lifetime prevalence, and they caution against interpreting apparent cohort effects in such studies as evidence of secular changes in incidence.

Adolescent↗

PubMed1995

Localization of a gene for partial epilepsy to chromosome 10q.

There is strong evidence for a genetic contribution to epilepsy, but it is commonly assumed that this genetic contribution is limited to 'generalized' epilepsies, and that most forms of 'partial' epilepsy are nongenetic. In a linkage analysis of a single family containing 11 affected individuals, we obtained strong evidence for localization of a gene for partial epilepsy. This susceptibility gene maps to chromosome 10q, with a maximum two-point lod score for D10S192 of 3.99 at theta = 0.0. All affected individuals share a single haplotype for seven tightly linked contiguous markers; the maximum lod score for this haplotype is 4.83 at theta = 0.0. Key recombinants place the susceptibility locus within a 10 centimorgan interval.

Adolescent↗