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Biomedical subjects

D C Hesdorffer

Publications and source records attributed to D C Hesdorffer.

13 recordsLinked to original sources

Gaze deviation from contralateral pseudoperiodic lateralized epileptiform discharges (PLEDs).

Pseudoperiodic lateralized epileptiform discharges (PLEDs) usually produce "negative" neurologic findings. This contrasts with seizures which typically induce cortical activation with "positive" clinical manifestations. Gaze preference may arise from ipsilateral frontal eye fields (FEFs) damage because of the unopposed action of an intact contralateral FEF. Epileptic nystagmus (EN) and gaze deviation (GD) can also occur with focal temporo-parieto-occipital or hemispheric seizures in awake or obtunded patients. A patient with old right frontal and parieto-temporal cerebral infarctions manifested leftward gaze preference and deviation (without nystagmus) while alert and talking. Digitized EEG demonstrated PLEDs at approximately 1 Hz over the right fronto-central region, without electrographic seizures. This report illustrates that PLEDs without seizures may excite frontal regions proximate to the FEFs to produce contraversive gaze preference in an awake patient, and discusses putative mechanisms. Gaze deviation, in this case, was the principal clinical feature of PLEDs.

Aged↗

Long-term mortality after a first episode of status epilepticus.

OBJECTIVE: To evaluate long-term mortality among people with status epilepticus (SE). METHODS: The authors performed a population-based retrospective cohort study to determine long-term mortality after SE. Between January 1, 1965, and December 31, 1984, all first episodes of SE receiving medical attention were ascertained through the Rochester Epidemiology Project Records-Linkage System. Cases surviving the first 30 days (n = 145) were followed until death or study termination (February 1996). RESULTS: At 10 years, cumulative mortality among 30-day survivors was 43%. The standardized mortality ratio (SMR) at 10 years was 2.8 (95% CI, 2.1-3.5). The mortality rate of those with idiopathic/cryptogenic SE was not increased (SMR = 1.1; 95% CI, 0.5-2.3). The following characteristics of SE increased long-term risk for mortality: SE > or = 24 hours in duration vs. SE < 2 hours (relative risk [RR] = 2.3; 95% CI, 1.1-5.1); acute symptomatic etiology vs idiopathic/cryptogenic etiology (RR = 2.2; 95% CI, 1.0-5.1) SE; myoclonic SE vs generalized convulsive SE (RR = 4.0; 95% CI, 1.3-13). CONCLUSION: Forty percent of subjects who survived the first 30 days after an incident episode of SE die within the next 10 years. The long-term mortality rate was threefold that of the general population over the same time period. The long-term mortality rate at 10 years was worse for those with myoclonic SE, for those who presented with SE lasting more than 24 hours, and for those with acute symptomatic SE. The long-term mortality rate was not altered in those with idiopathic/cryptogenic SE. We conclude that SE alone does not modify long-term mortality.

Adolescent↗

Are certain diuretics also anticonvulsants?

A history of diuretic use has been shown to be protective for first unprovoked seizure in adult patients. Recent animal studies suggest that certain diuretics have anticonvulsant activity. We evaluated the potential for the anticonvulsant activity of current diuretic use in a population-based, case-control study in older adults. We also tested chlorthiazide and furosemide for seizure protection in animal models of epilepsy. Concurrent medical prescription of any diuretic was protective for the development of epilepsy [odds ratio (OR) = 0.62, 95% confidence interval (CI) = 0.39-0.99]. A protective effect for current thiazide use was observed (OR = 0.53, CI = 0.31-0.90), and a protective effect for furosemide was suggested (OR = 0.44, CI = 0.1-1.9). In mice, both chlorthiazide and furosemide suppressed the occurrence of maximal electroshock-induced seizures in a dose-dependent manner. Chlorthiazide's toxic dose for 50% of animals tested (TD50) could not be achieved even with dosing as high as 1,500 mg/kg for furosemide; TD50 was 549 mg/kg. Results were similar in rats. Furosemide and chlorthiazide are protective for unprovoked seizures in an epidemiological study and in animal models. Given the potential therapeutic value for seizure control, low toxicity, and low cost, therapeutic efficacy should be explored in clinical studies.

Aged↗

Status epilepticus and tiagabine therapy: review of safety data and epidemiologic comparisons.

PURPOSE: To determine whether an increased risk of status epilepticus (SE) and complex partial status epilepticus (CPSE) is associated with tiagabine (TGB) therapy. METHODS: Thirteen cases in which an EEG, performed on patients with altered mental status taking TGB, was reported to demonstrate spike-and-wave discharges (SWDs) were reviewed by a panel of experts. In addition, all cases of suspected SE from TGB clinical trials were reviewed. The occurrence of SE in four epidemiologic cohorts from Rochester, Minnesota, Turku, Finland, Bronx, New York, and New Haven, Connecticut was analyzed as an external comparison. RESULTS: Review of the 13 cases with reported SWDs found that the majority had had prior EEGs with similar findings, and only three were thought to have electrographic evidence of SE. There was no difference in the frequency of SE or CPSE in the placebo-controlled clinical trials between the TGB-treated (1.0% SE, 0.8% CPSE) and placebo-treated (1.5% SE, 1.5% CPSE) groups. The 5% frequency of SE and 3% frequency of CPSE in the TGB-treated patients in the long-term safety studies, which included 2,248 patients, were very similar to the rates of occurrence of SE and CPSE in the four external cohorts. The major risk factor for the occurrence of SE and CPSE in all groups was a prior episode of SE (p < 0.0001). CONCLUSIONS: Over a 3-year period, SE will occur in 5-10% of patients with epilepsy not in remission. At highest risk are those who have had a prior episode of SE. Treatment with TGB in recommended doses does not increase the risk of SE in patients with partial seizures.

Adolescent↗

Time trends in incidence, mortality, and case-fatality after first episode of status epilepticus.

PURPOSE: Status epilepticus (SE) is a medical emergency associated with a high mortality. Clinical series have suggested that mortality after SE has decreased. No studies have systematically examined trends in incidence, mortality, and case fatality after SE in a well-defined population. METHODS: All first episodes of SE receiving medical attention between January 1, 1935, and December 31, 1984, were ascertained through the Rochester Epidemiology Project Records-Linkage System and followed up until death or study termination (February 1, 1996). We calculated incidence rates in the 50-year period (1935-1984), while we considered mortality and case-fatality in the last 30-year period (1955-1984). RESULTS: Incidence of SE increased over time to 18.1/100,000 (1975 through 1984). The increase was related to an increased incidence in the elderly and to the advent of myoclonic SE after cardiac arrest, a condition not seen in the early decades. In the last decade, approximately 16% of the incidence was due to myoclonic SE. The mortality rates increased from 3.6 per year in the decade 1955-1965 to 4.0/100,000 per year between 1975 and 1984. The 30-day case-fatality (CF) was unchanged, although a trend toward improvement was shown after excluding myoclonic SE. CONCLUSIONS: Incidence and mortality rates of SE have increased in the last 30 years. Case fatality remained the same. The increased incidence and mortality are due to the occurrence in the last decade of myoclonic SE after cardiac arrest. The mortality in the elderly was twice that of the youngest age group, across all study periods. Changes in the age and cause distribution of SE over time are responsible for the stable survivorship. There is improvement in survivorship in the last decade when myoclonic SE is excluded.

Age Distribution↗

Long-term fracture risk among infertile women: a population-based cohort study.

Nulliparity has been linked to bone loss and fractures, but the contribution of infertility is unclear. The purpose of this study was to assess the long-term risk of fractures among infertile women. In a population-based retrospective cohort study, all 658 Olmsted County, Minnesota, women with infertility (failure to conceive after 1 year despite intercourse without contraception) first diagnosed at Mayo Clinic in 1935-1964 were followed for fractures. Risk was assessed by comparing new fractures of each type to the number expected from sex-specific and age-specific fracture rates in the general population (standardized incidence ratios [SIR]). During 18,130 person-years of follow-up, 184 women experienced at least one fracture when 291 would have been expected on the basis of fracture incidence rates in the general population (SIR 0.6, 95% CI 0.5-0.7). There was no increase in proximal femur fractures (SIR 1.0, 95% CI 0.6-1.6) and a statistically significant decrease in the risk of distal forearm fractures (SIR 0.7, 95% CI 0.5-0.97), two of the three sites traditionally associated with osteoporosis. By contrast, there was a significant increase in subsequent vertebral fractures (SIR 1.9, 95% CI 1.4-2.4) that was consistent across divergent causes of infertility and reported menstrual patterns. Although an apparent increase in the risk of vertebral fractures requires further investigation, we saw no indication of an increase in limb fractures, suggesting that infertility does not have long-term adverse skeletal effects like those reported for athletes and dieters with irregular menses.

Adult↗

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↗

Hip fractures among infertile women.

A retrospective cohort study was conducted in a population-based inception cohort of 1,157 Olmsted County, Minnesota, women with infertility (failure to conceive after 1 year despite intercourse without contraception) that was first diagnosed at the Mayo Clinic (Rochester, Minnesota) between 1935 and 1964. In this relatively young cohort, 31 hip fractures were observed during 35,849 person-years of follow-up; 36.5 had been expected (standardized incidence ratio = 0.85, 95% confidence interval 0.58-1.20). Standardized incidence ratios did not differ by type or cause of infertility. The data suggested that women with consistently irregular menses may have a greater risk of hip fracture. This finding should be confirmed by additional studies with longer follow-up periods and with assessment of other fracture outcomes.

Adult↗

Risk of unprovoked seizure after acute symptomatic seizure: effect of status epilepticus.

We asked whether acute symptomatic status epilepticus (SE) increases the risk for subsequent unprovoked seizure compared with less prolonged acute symptomatic seizure. We also explored whether the risk of unprovoked seizure differs by cause. We ascertained all first episodes of acute symptomatic seizure among residents of Rochester, Minnesota, through the Rochester Project's records-linkage system. Information was collected on seizure duration, age, sex, cause, and subsequent unprovoked seizure. At 10 years of follow-up, the risk of unprovoked seizure was 41% for those with acute symptomatic seizure with SE and 13% for those without SE. Controlling for age, sex, and cause, SE increased the risk for subsequent unprovoked seizure 3.3-fold (95% confidence interval, 1.8-6.1) compared with brief acute symptomatic seizures. Among patients with SE, the risk of unprovoked seizure was increased 18.8-fold for patients with anoxic encephalopathy, 7.1-fold for patients with a structural cause, 3.6-fold for patients with a metabolic cause. The increased risk for unprovoked seizure after SE compared with shorter seizures may be due to SE being a marker for severity of injury, damage caused by SE, or a biological substrate associated with the tendency to experience SE.

Acute Disease↗

Incidence of status epilepticus in Rochester, Minnesota, 1965-1984.

We determined the incidence of status epilepticus (SE) by ascertaining all first episodes of SE in Rochester, Minnesota through the Rochester Epidemiology Project's records-linkage system between January 1, 1965 and December 31, 1984. Information was collected on age, gender, duration, seizure type, and etiology. The age-adjusted incidence of SE was 18.3 per 100,000 population. SE incidence was U-shaped, peaking under 1 year and over 60 years of age. The incidence of SE was greater for males than for females, for acute symptomatic etiology than any other etiology, and for partial SE that did not generalize than any other seizure type. Status of long duration (at least 2 hours) occurred more frequently among infants and the elderly than among persons aged 1 to 65 years. Cumulative incidence was 4 per 1,000 to age 75 and showed the greatest increase after age 60. Given the aging of the population, SE will become an increasingly important public health problem.

Adolescent↗

Short-term mortality after a first episode of status epilepticus.

PURPOSE: Studies evaluating short-term mortality among people who experience status epilepticus (SE) have produced conflicting results. Most studies are derived from clinical series with results affected by unspecified follow-up period and select referral of cases. This study was planned to evaluate short-term mortality after a first episode of SE. METHODS: We performed a population-based retrospective cohort study to determine the short-term mortality following a first episode of SE. Between January 1, 1965 and December 31, 1984, we studied all first episodes of afebrile SE who received medical attention in Rochester, Minnesota. Cases were followed until death or end of the study (February 1996). RESULTS: Mortality within the first 30 days was 19% (38 deaths out of 201 incident SE). Thirty-four deaths (89%) occurred among those with nonfebrile acute symptomatic SE, while 4 deaths (11%) occurred among those with unprovoked SE. Within the acute symptomatic group, after adjusting for age, there was a decreased risk of death in women (RR = 0.4; 95% CI: 0.2-0.9). No effect of duration or seizure type was shown after adjusting for other risk factors. CONCLUSIONS: One out of 5 subjects with SE died within the first 30 days. Short-term mortality is associated with the presence of an underlying acute etiology. Among acute symptomatic cases, women had a decreased risk of dying.

Adolescent↗

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↗

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↗