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W A Hauser

Publications and source records attributed to W A Hauser.

At least 37 records · Page 2Linked to original sources

Cause-specific mortality in adults with unprovoked seizures. A population-based incidence cohort study.

PURPOSE: To determine the cause-specific mortality relative to that expected in a population-based incidence cohort of people with unprovoked seizures. METHODS: The cohort comprises 224 inhabitants of Iceland first diagnosed as suffering from unprovoked seizures during a 5-year period from 1960 to 1964. The expected number of deaths was calculated by multiplying person-years of observation within 5-year age categories for each year from diagnosis through 1995 by cause-specific and sex-specific national death rates for those aged 20 years and above. The standardized mortality ratio (SMR) and 95% confidence intervals (95% CI) were calculated. RESULTS: All-cause mortality was increased among men (SMR 2.25, 95% CI 1.56-3.14) but not women (SMR 0.79, 95% CI 0.38-1.46). Among men, there were 8 deaths from accidents, poisoning and violence observed versus 2.82 expected (SMR 2.84, 95% CI 1.22-5.59) and 4 deaths from suicide versus 0.69 expected (SMR 5.80, 95% CI 1.56-14.84). All-cause mortality for men was still elevated after restriction of analysis to those with seizures of unknown etiology (SMR 1.73, 95% CI 1.05-2.67) with the excess deaths attributable to suicide (SMR 5.26, 95% CI 1.06-15.38). Both males and females with remote symptomatic unprovoked seizures had an increase in all-cause mortality due to excess mortality from all cancers, cerebrovascular disease and accidents. CONCLUSION: When compared with the age-, time-period- and gender-specific mortality in the general population, there is excess mortality in men but not women. The increased mortality for men is partly attributable to excess mortality from accidents and suicides.

Accidents↗

Race-ethnic disparities in the impact of stroke risk factors: the northern Manhattan stroke study.

BACKGROUND AND PURPOSE: Stroke risk factors have been determined in large part through epidemiological studies in white cohorts; as a result, race-ethnic disparities in stroke incidence and mortality rates remained unexplained. The aim in the present study was to compare the prevalence, OR, and etiological fraction (EF) of stroke risk factors among white, blacks, and Caribbean Hispanics living in the same urban community of northern Manhattan. METHODS: In this population-based incident case-control study, cases (n=688) of first ischemic stroke were prospectively matched 1:2 by age, sex, and race-ethnicity with community controls (n=1156). Risk factors were determined through in-person assessment. Conditional logistic regression was used to calculate adjusted ORs in each race-ethnic group. Prevalence and multivariate EFs were determined in each race-ethnic group. RESULTS: Hypertension was an independent risk factor for whites (OR 1.8, EF 25%), blacks (OR 2.0, EF 37%), and Caribbean Hispanics (OR 2.1, EF 32%), but greater prevalence led to elevated EFs among blacks and Caribbean Hispanics. Greater prevalence rates of diabetes increased stroke risk in blacks (OR 1.8, EF 14%) and Caribbean Hispanics (OR 2.1 P<0.05, EF 10%) compared with whites (OR 1.0, EF 0%), whereas atrial fibrillation had a greater prevalence and EF for whites (OR 4.4, EF 20%) compared with blacks (OR 1.7, EF 3%) and Caribbean Hispanics (OR 3.0, EF 2%). Coronary artery disease was most important for whites (OR 1.3, EF 16%), followed by Caribbean Hispanics (OR 1.5, EF 6%) and then blacks (OR 1.1, EF 2%). Prevalence of physical inactivity was greater in Caribbean Hispanics, but an elevated EF was found in all groups. CONCLUSIONS: The prevalence, OR, and EF for stroke risk factors vary by race-ethnicity. These differences are crucial to the etiology of stroke, as well as to the design and implementation of stroke prevention programs.

Aged↗

Treatment of nonfebrile status epilepticus in Rochester, Minn, from 1965 through 1984.

OBJECTIVE: To investigate the adequacy and efficacy of antiepileptic drug (AED) treatment of nonfebrile status epilepticus (SE). PATIENTS AND METHODS: We performed a population-based retrospective cohort study to evaluate the medical management of SE. Participants included 184 residents of Rochester, Minn, who experienced a first episode of nonfebrile SE between 1965 and 1984. RESULTS: Of the 184 patients, 133 (72.2%) received appropriate, prompt medical treatment for SE, i.e., intravenous diazepam, phenytoin, or phenobarbital. In 100 patients (75.8%), the dose of the first AED administered was less than that currently recommended. The first treatment was effective in terminating SE in 41 (31.1%) of 132 patients. The adequacy of treatment was highly predictive of drug efficacy (P = .002). The dose of the second AED treatment was inadequate in 52 (80%) of 65 patients treated. CONCLUSION: Based on this retrospective study, the treatment of SE is remarkable for both inadequacy and ineffectiveness. The inappropriate use of therapeutic regimens in the management of SE may be an important cause of ineffective medical treatment.

Adolescent↗

Autosomal dominant partial epilepsy with auditory features: defining the phenotype.

The authors previously reported linkage to chromosome 10q22-24 for autosomal dominant partial epilepsy with auditory features. This study describes seizure semiology in the original linkage family in further detail. Auditory hallucinations were most common, but other sensory symptoms (visual, olfactory, vertiginous, and cephalic) were also reported. Autonomic, psychic, and motor symptoms were less common. The clinical semiology points to a lateral temporal seizure origin. Auditory hallucinations, the most striking clinical feature, are useful for identifying new families with this synome.

Epilepsy, Partial, Sensory↗

Frequency and clinical determinants of dementia after ischemic stroke.

OBJECTIVE: To investigate the frequency and clinical determinants of dementia after ischemic stroke. METHODS: The authors administered neurologic, neuropsychological, and functional assessments to 453 patients (age 72.0 +/- 8.3 years) 3 months after ischemic stroke. They diagnosed dementia using modified Diagnostic and Statistical Manual of Mental Disorders, 3rd ed., revised criteria requiring deficits in memory and two or more additional cognitive domains as well as functional impairment. RESULTS: The authors diagnosed dementia in 119 of the 453 patients (26.3%). Regarding dementia subtypes, 68 of the 119 patients (57.1%) were diagnosed with vascular dementia, 46 patients (38.7%) were diagnosed with AD with concomitant stroke, and 5 patients (4.2%) had dementia for other reasons. Logistic regression suggested that dementia was associated with a major hemispheral stroke syndrome (OR 3.0), left hemisphere (OR 2.1) and right hemisphere (OR 1.8) infarct locations versus brainstem/cerebellar locations, infarcts in the pooled anterior and posterior cerebral artery territories versus infarcts in other vascular territories (OR 1.7), diabetes mellitus (OR 1.8), prior stroke (OR 1.7), age 80 years or older (OR 12.7) and 70 to 79 years (OR 3.9) versus 60 to 69 years, 8 or fewer years of education (OR 4.1) and 9 to 12 years of education (OR 3.0) versus 13 or more years of education, black race (OR 2.6) and Hispanic ethnicity (OR 3.1) versus white race, and northern Manhattan residence (OR 1.6). CONCLUSIONS: Dementia is frequent after ischemic stroke, occurring in one-fourth of the elderly patients in the authors' cohort. The clinical determinants of dementia include the location and severity of the presenting stroke, vascular risk factors such as diabetes mellitus and prior stroke, and host characteristics such as older age, fewer years of education, and nonwhite race/ethnicity. The results also suggest that concomitant AD plays an etiologic role in approximately one-third of cases of dementia after stroke.

Aged↗

Epilepsy, vagal nerve stimulation by the NCP system, all-cause mortality, and sudden, unexpected, unexplained death.

PURPOSE: This report concerns the 2-year extension of the study of mortality and sudden, unexpected, unexplained death in epilepsy (SUDEP) in the cohort of patients receiving vagal nerve stimulation by the NCP System for the treatment of epilepsy. METHODS: A cohort of 1,819 individuals was followed 3,176.3 person-years from implantation. The 25 deaths that occurred during NCP System activation were reviewed for SUDEP by a panel. RESULTS: The mortality rates were lower [standardized mortality ratio (SMR = 3.6)] with the extended follow-up compared to the previous finding (SMR = 5.3). The SUDEP rates (4.1 vs. 4.5 per 1,000 person-years) were similar to those in the previous study of this cohort. When the vagal nerve stimulation experience is stratified by duration of use, the rate of SUDEP was 5.5 per 1,000 over the first 2 years, but only 1.7 per 1,000 thereafter. CONCLUSIONS: The mortality and SUDEP rates are similar to those reported from clinical trials of new drugs and cohorts of severe epilepsy. The lower SUDEP rates after 2 years of follow-up are intriguing, but require further investigation.

Adolescent↗

Risk of epilepsy in long-term survivors of surgery for aneurysmal subarachnoid hemorrhage: a population-based study in Iceland.

PURPOSE: Epilepsy is known to result from aneurysmal subarachnoid hemorrhage (SAH). There are no population-based estimates of the absolute risk or the duration for which this risk is elevated. We have conducted a population-based study in Iceland of the risk of epilepsy after a ruptured cerebral aneurysm to address these questions. METHODS: The index patients are all of the patients who presented with SAH caused by ruptured cerebral aneurysm in Iceland during an 11-year period (1958 to 1968) and survived more than 6 months. We determined the number of index patients who developed epilepsy. The observed number of cases of epilepsy was compared with that expected based on the incidence of epilepsy in Iceland. RESULTS: There were 44 index patients; 11 (25%) developed epilepsy, all within 4 years of the insult. Seven (70%) of 10 patients with acute symptomatic seizures (defined as seizures during the first 2 weeks after the hemorrhage) developed epilepsy (relative risk, 7.0; 95% confidence interval, 2.3-21.6). Epilepsy was more frequent in patients with severe neurological residua (48%) compared with patients without (20%) (relative risk, 2.5; 95% confidence interval, 0.9-6.3). CONCLUSIONS: The risk for epilepsy among survivors of SAH caused by ruptured cerebral aneurysm is substantially increased. Both acute symptomatic seizure and persistent neurological impairment are associated with a further increase in the risk of epilepsy.

Epilepsy↗

Major depression is a risk factor for seizures in older adults.

We tested the hypothesis that major depression meeting DSM-III-R criteria or medical therapies for depression increase the risk for unprovoked seizures. Major depression was associated with a sixfold increased risk for unprovoked seizures (95% CI, 1.56-22). The risk remained increased even when controlling for age, sex, length of medical follow-up, and medical therapies for depression. In the absence of known prior neurological insult, major depression is associated with an increased risk for unprovoked seizures.

Aging↗

Predictors of multiple seizures in a cohort of children prospectively followed from the time of their first unprovoked seizure.

The objective of this study was to assess the risk of multiple recurrences after an initial seizure recurrence in childhood. In a prospective study, 407 children were followed for a mean of 9.6 years from the time of their first unprovoked seizure. Data regarding each seizure recurrence were obtained and analyzed using statistical methods for survival analysis. The cumulative risk of a second seizure was 29%, 37%, 43%, and 46% at 1, 2, 5, and 10 years, respectively. Of the 182 children who experienced a second seizure, 131 (72%) experienced a third seizure, 105 (58%) have had 4 or more seizures, and 52 (29%) have experienced 10 or more seizures. The cumulative risk of a third seizure was 57%, 63%, and 71% at 1, 2, and 5 years, respectively, after the second seizure. After a third seizure, the cumulative risk of another seizure was 69%, 72%, and 81% at 1, 2, and 5 years, respectively. After a second seizure, factors associated with an increased risk of additional recurrences included a remote symptomatic etiology (rate ratio = 1.7) and the occurrence of a second seizure within 6 months of the first seizure (rate ratio = 1.7). After a second seizure, the risk of subsequent seizures was greater than 50% even in the lowest risk group. With the exception of etiology, factors associated with an increased risk of multiple recurrences after the initial seizure were different than those associated with multiple recurrences after a second seizure. Factors associated with multiple recurrent seizures may be different than those associated with an initial recurrence. As most patients who experience a second seizure experience further seizures, these data suggest that two seizures are a sufficient epidemiological criterion for the definition of epilepsy.

Adolescent↗

The protective effect of moderate alcohol consumption on ischemic stroke.

CONTEXT: Moderate alcohol consumption has been shown to be protective for coronary heart disease, but the relationship between moderate alcohol consumption and ischemic stroke is more controversial. OBJECTIVE: To determine the association between alcohol consumption and risk of ischemic stroke. DESIGN: Population-based case-control study conducted between July 1993 and June 1997. SETTING: Multiethnic population in northern Manhattan, New York, NY, aged 40 years or older. PATIENTS AND OTHER PARTICIPANTS: Cases (n = 677) had first ischemic stroke and were matched to community controls (n = 1139) derived through random digit dialing by age, sex, and race/ethnicity. Mean +/- SD age of cases was 70.0+/-12.7 years; 55.8% were women; 19.5% were white, 28.4% black, and 50.7% Hispanic. MAIN OUTCOME MEASURE: First ischemic stroke (fatal or nonfatal). RESULTS: Moderate alcohol consumption, up to 2 drinks per day, was significantly protective for ischemic stroke after adjustment for cardiac disease, hypertension, diabetes, current smoking, body mass index, and education (odds ratio [OR], 0.51; 95% confidence interval [CI], 0.39-0.67). This protective effect of alcohol consumption was detected in both younger and older groups, in men and women, and in whites, blacks, and Hispanics. In a quadratic model of stroke risk, increased risk of ischemic stroke was statistically significant among those consuming 7 or more drinks per day (OR, 2.96; 95% CI, 1.05-8.29). CONCLUSIONS: Moderate alcohol consumption was independently associated with a decreased risk of ischemic stroke in our elderly, multiethnic, urban subjects, while heavy alcohol consumption had deleterious effects. Our data support the National Stroke Association Stroke Prevention Guidelines regarding the beneficial effects of moderate alcohol consumption.

Adult↗

Risk of epilepsy in patients with multiple sclerosis: a population-based study in Iceland.

PURPOSE: Several clinical series reported an association between multiple sclerosis (MS) and epilepsy. We conducted a total population study in Iceland to determine the risk for developing epilepsy in patients with MS compared with that expected in the general population. METHODS: Medical records of the 188 incidence cases of clinically definite MS first diagnosed in Iceland during the 25-year study period (1965-1989) were reviewed. The cases were followed up through 1994 or until death to identify those developing seizures or epilepsy. The expected number of cases with epilepsy in the MS-incidence cohort were calculated based on the age-specific incidence for epilepsy in Iceland and the age-specific person years of follow-up in the MS cohort. RESULTS: During the 2,771 person years of observation after diagnosis of clinically definite MS, three MS patients developed epilepsy. One additional case developed epilepsy after onset of MS symptoms but before diagnosis of MS. The cumulative incidence of epilepsy by 10 years after diagnosis of MS was 1.9%. Given the age-specific person years of follow-up after diagnosis of MS, only one case of epilepsy would have been expected; standardized incidence ratio (SIR), 3.0 (95% confidence interval (CI), 0.6-8.8). CONCLUSIONS: MS is a risk factor for developing epilepsy. Patients with MS have a threefold increase in risk for developing epilepsy when compared with that expected in the general population. The reason for this increased risk is unclear and needs further investigation.

Adult↗

Incidence of epileptic syndromes in Rochester, Minnesota: 1980-1984.

PURPOSE: To determine the incidence and the distribution of epileptic syndromes in a well-defined population. METHODS: By using the records-linkage system of the Rochester Epidemiology Project, we screened all the residents of Rochester, Minnesota, who received a diagnosis of seizures, convulsions, or epilepsy from 1980 through 1984. One hundred fifty-seven residents with incident epilepsy (recurrent unprovoked seizures) were classified by using the International League Against Epilepsy (ILAE) Classification of the Epilepsies and Epileptic Syndromes. Residents with special syndromes were excluded. With a pretested algorithm, patients were classified at three levels of specification: major syndromic groups (e.g., localization-related syndromes), syndromic subgroups (e.g., idiopathic epilepsy with age-related onset), and whenever possible, individual syndromes. RESULTS: All but one patient were classified into major syndromic groups and subgroups. The annual age-adjusted incidence per 100,000 population was 52.3 cases (34.9 for localization-related epilepsies; 7.7 for generalized epilepsies; 9.7 for undetermined epilepsies). Incidence was 0.2 for idiopathic, 17.2 for cryptogenic, 17.5 for symptomatic localization-related epilepsies, 3.7 for idiopathic, 1.7 for symptomatic or cryptogenic (age-related), and 2.3 for symptomatic (non age-related) generalized epilepsies. CONCLUSIONS: With the exception of idiopathic epilepsies, the incidence of the major syndromic categories in our study was higher than that provided by previous population-based studies.

Adolescent↗

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

PURPOSE: To determine the prevalence of epilepsy (recurrent unprovoked seizures) in the population of rural Iceland. METHODS: Review of records of primary-care facilities for the population of rural Iceland supplemented by review of referrals to electroencephalographic facilities and neurologic specialists to identify all individuals with unprovoked seizures or receiving treatment for epilepsy in the calendar year 1993. RESULTS: Crude prevalence was 4.8 per 1,000 and was 4.8/1,000 after age adjustment to the 1970 United States population. Age-adjusted prevalence was higher in male (5.1) than in female subjects (4.4) and increased with advancing age. Sixty-two percent of prevalence cases were of unknown cause. Sixty-three percent of cases had major motor seizures without aura or generalized epileptiform pattern on EEG. Sixty-four percent of patients had had seizures in the year of observation. Seizure control was inversely correlated with number of medications. Ten percent of the prevalence group was taking no medication, although the frequency of seizures was high in this medication-free group. CONCLUSIONS: Prevalence of epilepsy in rural Iceland is consistent with that reported in recent studies in other developed countries. The data provide insights into the approaches of treatment and use of specialized diagnostic testing in the country. The prevalence is similar to that in other European countries but lower than that reported from rural areas in Latin America.

Adolescent↗

Validity of telephone interview data for vascular disease risk factors in a racially mixed urban community: the Northern Manhattan Stroke Study.

The aims of our study were to assess the validity and reliability of a telephone survey instrument designed to measure vascular disease risk factors and to assess whether these measurements were influenced by age, gender, race/ethnicity, or other sociodemographic variables. Subjects were sampled and interviewed using random digit dialing methodology from the multiethnic community of northern Manhattan. For the validity study, 261 consecutive subjects were clinically assessed in-person within 60 days of the telephone interview. A retest reliability study of the telephone interview was conducted in 92 randomly selected subjects within 30 days of the initial interview. The telephone interview instrument had a sensitivity of more than 55% and a specificity of 74% or greater for various vascular disease risk factors. Sensitivity, specificity, and positive predictive value did not vary significantly or systematically among whites, blacks, and Hispanics, but subjects with access to health care were more likely to provide valid data. The reliability substudy indicated a good reliability for the telephone interview. These results support the validity of telephone interviews for estimating the prevalence of vascular risk factors in urban populations.

Age Factors↗

Spinal muscular atrophy. Incidence in Iceland.

Spinal muscular atrophy (SMA) is among the commonest degenerative disorders of the nervous system in childhood. This is an inherited autosomal recessive disease which results in premature death of anterior horn cells of the spinal cord and is manifested by progressive weakness and atrophy of skeletal muscles. Few studies have looked at the frequency of the disease in a defined population. We identified all patients diagnosed with SMA in Iceland during a 15-year period. The diagnosis is based on typical symptoms and supported by results of electromyography/nerve conduction studies and muscle biopsy. The average annual incidence was 13.7 per 100,000 live births for all types of SMA, which is similar to that reported in other population-based studies.

Adolescent↗

Dose-response effect of fetal cocaine exposure on newborn neurologic function.

BACKGROUND: Studies of fetal cocaine exposure and newborn neurologic function have obtained conflicting results. Although some studies identify abnormalities, others find no differences between cocaine-exposed and cocaine-unexposed infants. To determine the effects of prenatal cocaine exposure on intrauterine growth and neurologic function in infants, we prospectively evaluated 253 infants shortly after birth. METHODS: Women who delivered a live singleton >36 weeks by dates were eligible for enrollment. Maternal exclusionary criteria were known parenteral drug use, alcoholism, and acquired immunodeficiency syndrome; infant exclusionary criteria were Apgar scores </=4 at 5 minutes, obvious congenital malformations, seizures, or strokes. A total of 98% of infants were evaluated between 1 to 7 days of age. Newborns were assessed with the Neurological Examination for Children (NEC) by a pediatric neurologist (C.A.C.) who was blinded to exposure status. Gestational age was determined by Ballard's examination. Cocaine exposure was determined for the last trimester by radioimmunoassay of maternal hair (RIAH). Exposure values ranged from 2 to 4457 ng/10 mg hair. Infants were excluded if a maternal hair sample was missing (N = 13). The sample comprises 240 woman and infant pairs-104 cocaine-exposed and 136 cocaine-unexposed. RESULTS: Compared with unexposed controls, cocaine-exposed infants exhibited higher rates of intrauterine growth retardation (24% vs 8%), small head circumference ([HC] <10th% percentile) (20% vs 5%) and neurologic abnormalities: global hypertonia (32% vs 11%), coarse tremor (40% vs 15%), and extensor leg posture (20% vs 4%). We found increasing odds (odds ratio) of growth and neurologic impairment with increasing level of cocaine exposure in stratified analyses. The odds ratio associated with three levels of cocaine exposure (no exposure, low exposure = RIAH 2-66 ng/mg; and high exposure = RIAH 81-4457 ng/mg) respectively are: 1.0, 3.3, and 6.1 for small head size (chi2 for trend); 1.0, 3. 3, and 4.3 for global hypertonia (chi2 for trend); 1.0, 3.4, and 7.4 for extensor leg posturing (chi2 for trend); and 1.0, 3.8, and 3.8 for coarse tremor (chi2 for trend). Significant associations between cocaine exposure and neurologic signs were found in logistic regression equations that controlled for 20 or more variables. CONCLUSION: We conclude that adverse neonatal effects associated with fetal cocaine exposure follow a dose-response relationship: newborns with higher levels of prenatal cocaine exposure show higher rates of impairments in fetal head growth and abnormalities of muscle tone, movements, and posture. Significant relationships between cocaine exposure and these outcomes remain in controlled analyses.

Adult↗

Risk of recurrent seizures after two unprovoked seizures.

BACKGROUND: Patients with a single unprovoked seizure have about a 35 percent risk of recurrence in the subsequent five years. We studied the risk of recurrence after two unprovoked seizures. METHODS: We prospectively followed 204 patients with a first unprovoked seizure from the day of the initial seizure. Information was obtained from patients (and verified by a review of their medical records) about the dates and circumstances of any subsequent seizures. The risk of a second, third, and fourth seizure was estimated by the Kaplan-Meier method. RESULTS: Of the 204 patients, 63 had a second seizure, 41 a third seizure, and 26 a fourth seizure. The mean age of the patients was 36 years, 10 percent were less than 16 years of age, 70 percent were male, 71 percent had epilepsy of unknown cause, and 66 percent had generalized seizures. The risk of a second unprovoked seizure was 33 percent. Among those with a second seizure, the risk of a third unprovoked seizure was 73 percent; among those with a third unprovoked seizure, the risk of a fourth was 76 percent. Most recurrences occurred within one year of the second or third seizure. The risk of a third seizure was higher in those with a presumed cause of epilepsy (relative risk, 1.9; 95 percent confidence interval, 1.0 to 3.4). CONCLUSIONS: Although only about one third of patients with a first unprovoked seizure will have further seizures within five years, about three quarters of those with two or three unprovoked seizures have further seizures within four years.

Adolescent↗