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To determine the risk of seizure recurrence after a first seizure due to neurocysticercosis (NC) and to evaluate risk factors for seizure recurrence, including the influence of antihelminthic treatment.

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.

Status epilepticus (SE) will occur in 50,000 to 60,000 individuals in the United States annually: one third as the presenting symptom in patients with a 1st unprovoked seizure or with epilepsy, one third in patients with established epilepsy, and one third in individuals with no history of epilepsy. The greatest number of cases will occur in children, although the risk is equally high in the over-60 population. In patients with epilepsy, SE is more likely to occur in those with partial seizures and in those with remote symptomatic epilepsy. The presence of a preexisting neurologic abnormality is associated with an increased risk of SE in those with acute systemic insults. There is a high mortality reported, but this is related predominantly to the underlying condition. The 1 to 2 mortality attributed to SE probably reflects an overestimation of the risk. There is an increased risk of seizures and of intellectual dysfunction following the occurrence of an episode of SE, although the causal association is not clear. Individuals with epilepsy who experience an episode of SE probably have a lower likelihood of remission of epilepsy.

The psychologic and social aspects of epilepsy have rarely been assessed in community-based samples. We administered the Washington Psychosocial Seizure Inventory in 1985-1986 to 125 nonretarded adults, 18 to 59 years of age, who in 1980 had active epilepsy and resided in Rochester, Minnesota. Individuals having seizures or taking anticonvulsant medications within the past 12 months had somewhat poorer adjustment than those without recent seizures or medications, but even this more severely affected group appeared relatively well adjusted.

Short-latency components of median nerve somatosensory evoked potentials are generally assumed to be unaffected by sleep and level of arousal. We found that sleep prolongs the latency and alters the morphology of the N20 component in normal subjects. These changes may represent differential effects of sleep on various elements contributing to generation of the N20. Failure to control for patient state may degrade the reliability of clinical somatosensory evoked potential testing.

We identified 217 patients with status epilepticus (SE), including all seizure types from all etiologies, over a 3-year period. There was a significant interaction between organic brain disease and a history of epilepsy in the development of SE. The majority of patients (59) had no history of epilepsy. These patients were more likely to have acute precipitants associated with SE and less likely to have had prior brain disease. They were older, were more likely to have generalized convulsive seizures, and had a high proportionate mortality. Among the 88 patients with a history of epilepsy, a higher proportion had prior brain insults, but fewer had acute precipitants. These patients were younger and their mortality was low, but they often had recurrent SE before and after the identified episode. Significant acute or prior brain disease is an important factor in the development of SE, even in patients with a history of epilepsy.

Although an association between migraine and epilepsy has long been discussed, it has rarely been studied systematically. According to the evidence from the large epidemiologic study reviewed in this article, individuals with epilepsy are 2.4 times more likely to develop migraine than their relatives without epilepsy. Risk of migraine is elevated in patients with partial-onset and generalized-onset seizures. The comorbidity of migraine and epilepsy may be explained by a state of neuronal hyperexcitability that increases the risk of both disorders. Clinical and EEG features useful in the differential diagnosis of migraine and epilepsy as well as in the diagnosis of both conditions when they occur concurrently are reviewed. When migraine and epilepsy occur together, therapy with agents effective for both conditions should be considered.

Sixty-three patients with isolated global anoxic-ischemic injury were prospectively evaluated after cardiopulmonary arrest (CPA); 25 (40) survived, 16 to an excellent recovery, 8 to a good recovery, and 1 with severe deficits. Forty-six percent of the patients achieved full alertness, and only patients who did so survived. Seventy-five percent of patients arousable or initially alert (level of consciousness [LOC] ≥ 4) survived, all but two with excellent outcomes. Twenty-eight percent of patients initially in deep coma (LOC ≤ 3) survived, all with excellent or good outcomes. Ninety percent of patients who became fully alert did so within 72 hours. The likelihood of alerting is correlated with the LOC at given intervals after CPA. Reliable predictions of survival and outcome can often be based upon LOC alone within 2 days after CPA.

A cohort of 666 children who had convulsions with fever were followed to determine the risks of subsequent epilepsy High risks were found in children with preexisting cerebral palsy or mental retardation. Other major risk factors were atypical features of the febrile convulsions (such as focal seizures) and duration of febrile seizures for 10 minutes or more. The risk of developing epilepsy by age 20 was about 6 percent for all children who had experienced febrile convulsions. However, this risk figure consisted of a combination of 2.5 percent of children without prior neurologic disorder or atypical or prolonged seizures, and 17 percent of those with such complications.

We followed 208 patients identified on the day of their 1st unprovoked seizure for a mean duration of 4 years. Seizures recurred in 64. Recurrence risks were estimated to be 14, 29, and 34 at 1, 3, and 5 years following the 1st episode. A history of previous neurologic insult (remote symptomatic) was associated with a 2.5-fold increased risk of recurrence. Among idiopathic cases, a sibling with epilepsy, a generalized spike and wave EEG, or a history of acute symptomatic seizure increased risk for recurrence. Among remote symptomatic cases, status epilepticus, a prior acute symptomatic seizure, or Todd's paresis increased risk. Depending upon clinical features, recurrence risk at 5 years following a 1st seizure ranged from 23 to 80. Treatment with anticonvulsant medication was not associated with a decrease in recurrence risks.

To investigate the association between withdrawal from antiepileptic drugs (AEDs) and status epilepticus (SE), we evaluated AED levels at the time of, and prior to, an episode of SE in 65 patients with epilepsy. At least one AED was therapeutic in 65 of patients at the time of SE, and all prescribed AEDs were therapeutic in 48. Ten patients had subtherapeutic AED levels before, and at the time of, SE. Sixteen patients with previously therapeutic levels (25) had one or more subtherapeutic AED level at the time of SE. Many of the patients had other acute or remote factors that could be associated with SE, and 46 had had previous episodes of SE. Low AED levels or withdrawal can explain only some cases of SE. Citing AED irregularity as the major cause of SE in patients with epilepsy oversimplifies a complex, poorly understood situation.

Nineteen (30) of 63 adult survivors of cardiopulmonary arrest had seizures after admission to the hospital. Eleven of 19 had more than one type of seizure. Myoclonic seizures began within 12 hours of the arrest in eight patients, and after 3 or more days in four patients. Only two (17) patients with myoclonic seizures survived. Partial seizures usually began within 12 hours of the arrest and were controllable with anticonvulsants; 4 of 12 patients survived. Two of four patients with generalized tonic-clonic seizures survived; one of four with “shivering” lived. Overall, patients with seizures had a survival rate of 32 (6 of 19), compared with 43 for patients without seizures. None of the survivors had recurrent seizures within 6 months after hospital admission.

We studied the risk for seizure disorders among relatives of probands with febrile convulsions. The risk for febrile convulsions was raised in siblings, offspring, and nieces and nephews of probands. Risks to siblings were higher if one or both parents also had febrile convulsions, or the proband had no identified neurologic abnormality before the febrile convulsion, if the proband had recurrent febrile convulsions, or the febrile convulsions were complex. The risk for epilepsy was raised in siblings of probands, but not in other relatives. If the proband had febrile convulsions followed by epilepsy, risk to siblings for febrile convulsions and for epilepsy was significantly higher than when probands had either condition alone.

We reviewed 81 patients with dementia and autopsy findings of Alzheimer's disease (AD) to identify patients with seizures or myoclonus after onset of dementia. Eight (10) had seizures, and eight others (10) had myoclonus. The incidence of seizures was 10 times more than expected in a reference population. Seizures occurred in any stage of AD, but myoclonus was often a late manifestation. Both seizures and myoclonus, individually or together, are manifestations of AD and may be seen at any time in the course of the illness.

To determine the risk of recurrent subarachnoid hemorrhage (SAH), mortality, and relative survivorship following SAH caused by ruptured cerebral aneurysm (RCA).

We tested the a priori hypothesis that hypertension can lead to seizures through vascular brain damage that might or might not involve manifest stroke. A case-control study with 227 patients admitted for a first unprovoked seizure and 294 acute surgical controls was carried out at Harlem Hospital Center, New York City, between 1981 and 1984. History of hypertension was significantly associated with unprovoked seizures, even after adjustment for antecedent stroke and other potential confounders (adjusted odds ratio [OR] 1.57; 95 confidence limit [CL], 1.0 to 2.44). There was marked synergism between history of stroke and history of hypertension; subjects with a history of both had a fourfold increase in seizure risk compared with subjects with neither (adjusted OR 4.07; 95 CL, 1.50 to 11.0). In these data, history of hypertension appears to be an independent risk factor for new-onset unprovoked seizures, especially, but not only, in conjunction with a history of stroke.

Lacunar infarcts (LACs) and deep intracerebral hemorrhages (DICHs) occur in the same structures and may result from the same pathology. It is unclear why one patient has an LAC while another has DICH. We compared LAC to DICH cases derived from a population-based incidence study. In multivariate analysis, LAC cases were significantly older, more likely to have diabetes, and had higher cholesterol than DICH cases.

Some investigators believe that patients with epilepsy are at increased risk of sudden death, perhaps because of cardiac arrhythmias. We studied 338 patients with epilepsy referred for simultaneous ambulatory EEG/ECG monitoring. High-risk cardiac arrhythmias were detected in 18 (5.3) patients while low-risk arrhythmias or negative studies were found in the others. Fifty-six electrographic seizures were seen in 17 patients, but no associated ventricular arrhythmias or conduction defects were identified. We conclude that the incidence of serious cardiac arrhythmias predisposing to sudden death is not increased in patients with epilepsy.

Incidence and time trends of Reye's syndrome have been determined in Olmsted County, MN, using the facilities of the Rochester Epidemiology Program Project at Mayo Clinic. Incidence rates in individuals under 18 years of age were 1.1 per 100,000 person-years in the 1970–75 time interval and 1.7 in the 1976–81 interval. Failure to identify any case in the earliest time interval yields a rate of zero, and an incidence higher than 0.6 per 100,000 can be excluded with 95 probability. This finding is consistent with an increasing incidence over time in this community and does not exclude the possibility that Reye's syndrome did not exist in Olmsted County before 1970.

Neurology1979;29:297–303