Showing papers on "Status epilepticus published in 1990"

Seizure recurrence after a 1st unprovoked seizure An extended follow‐up

Abstract: 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 Todd9s 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.

Status epilepticus: epidemiologic considerations.

Abstract: 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 biochemical basis and pathophysiology of status epilepticus.

Abstract: Status epilepticus (SE), both convulsive and nonconvulsive, can arise from diverse etiologies in either a normal brain or a previously epileptic brain. SE has a distinct natural history and unattended can lead to profound, life-threatening, systemic metabolic and physiologic disturbances. These factors may account for the poor prognosis associated with this disorder. However, there is mounting experimental evidence that SE itself, independent of metabolic and physiologic disturbances, leads to lasting brain dysfunction.

The significance of myoclonic status epilepticus in postanoxic coma.

Abstract: We report 11 adults who exhibited myoclonic status epilepticus (MSE) after cardiac arrest. Based on pathologic, electroencephalographic, and clinical evidence, we conclude that our patients died from the initial anoxic-ischemic insult rather than as a result of MSE. We suggest that the seizures in these nonsurvivors were self-limited events arising from lethal damage to neurons. Thus, in patients with bilaterally synchronous facial myoclonus, bilateral loss of pupillary or oculovestibular reflexes, and suppression and burst-suppression on EEG, it is not warranted to use anesthetic barbiturates to treat MSE.

Seizures in Human Immunodeficiency Virus Infection

Abstract: • Among 630 patients with human immunodeficiency virus infection, 70 patients with new-onset seizures were studied. Generalized seizures occurred in 66 patients (94%): they occurred as the initial seizure in 56 patients (80%) and during follow-up in another 10 patients (14%). Partial seizures (18 patients), status epilepticus (10 patients), and recurrent seizures (38 patients) were also noted. Identified processes included cerebral toxoplasmosis in 11 patients, cerebral lymphoma in 8, metabolic derangement in 8, cryptococcal meningitis in 7, and vascular infarction in 4. In 32 patients (46%) seizures were not associated with identifiable brain lesions and were believed to result from human immunodeficiency virus cerebral infection. Phenytoin treatment was associated with adverse drug reactions in 16 of 62 patients who received it. Our results suggest that the majority of patients with human immunodeficiency virus and seizures do not have secondary focal brain lesions as the cause of the seizures and that human immunodeficiency virus infection alone can, and often does, cause seizures.

The hippocampus in experimental chronic epilepsy: A morphometric analysis

Abstract: The effect of intermittent seizures on the pyramidal neurons of the hippocampus is largely unknown. To determine whether recurrent seizures centered in the hippocampus can produce neuronal loss in this region, a morphometric analysis was performed from standardized sections of hippocampus using 5 groups of animals: (1) surgical control subjects, (2) rats kindled by the rapidly recurring hippocampal seizure (RRHS) paradigm, (3) kindled rats with a few additional limbic seizures (528 +/- 66 seizures), (4) kindled rats with many limbic seizures (1,523 +/- 130 seizures), and (5) rats experiencing limbic status epilepticus (SE) induced by "continuous" hippocampal stimulation. The RRHS and SE protocols induced significant neuronal loss in the CA1 region, but no evidence was found for additional cell loss with increasing numbers of intermittent seizures. These intermittent seizures were, however, associated with a significant thickening of the basal and apical dendritic fields of the CA1 region. These findings indicate that intermittent seizures produce no significant hippocampal neuronal loss and may result in a hypertrophy of CA1 dendritic fields.

Febrile status epilepticus.

Abstract: As part of a study of status epilepticus in children (Maytal J, Shinnar S, Moshe SL, Alvarez LA. Pediatrics. 1989; 83:323-331); 44 children with febrile convulsions lasting more than 30 minutes were followed for a mean of 28 months (range 4 to 72). Thirty children were followed prospectively. Children with prior afebrile seizures or evidence of acute central nervous system infection were excluded. Nine (20%) children had prior neurological deficits. The duration of the febrile seizure was 0.5 to 1 hour in 41 cases (85%), 1 to 2 hours in 5 (10%), and greater than 2 hours in 2 children (5%). No child died or developed new neurological deficits following the seizures. The risk of recurrent seizures was increased, but only in the group with prior neurological abnormality. Six (66%) of these children had subsequent febrile seizures compared with 12 (34%) of the normal children (P = .08). Three (33%) had recurrent febrile status epilepticus compared with only 1 (3%) normal child (P = .023). The 2 children in the prospective arm of the study with recurrent febrile status epilepticus were both neurologically abnormal (P = .035). All 3 of the children who subsequently had afebrile seizures (2 prospective) were neurologically abnormal (P = .006 overall, P = .035 for prospective only). It is concluded that the occurrence of febrile status epilepticus in a neurologically impaired child is a risk factor for subsequent febrile as well as afebrile seizures. The occurrence of febrile status epilepticus in an otherwise normal child does not significantly increase the risk for subsequent febrile (brief or prolonged) or afebrile seizures in the first few years following the episode.

Pentobarbital and EEG burst suppression in treatment of status epilepticus refractory to benzodiazepines and phenytoin.

Abstract: Seven patients with complex partial or secondarily generalized tonic-clonic status epilepticus (SE) refractory to benzodiazepines (BZDs) and phenytoin (PHT) were treated with pentobarbital (PTB) coma with an EEG burst suppression (BSP) pattern. PTB administered by continuous intravenous (i.v.) infusion pump at a loading dose of 6-8 mg/kg in 40-60 min was usually sufficient to produce BSP activity and seizure control. PTB was continued 0-24 h at 1-4 mg/kg/h, adjusted to maintain blood pressure (BP) and BSP. Infusion rate was decreased if systolic BP (SBP) was less than 90 mm Hg. Normal saline fluid challenge was occasionally used to elevate BP, but in no case was it necessary to discontinue PTB infusion or use pressors. Other antiepileptic drugs (AEDs) were maintained at therapeutic levels for chronic seizure protection. Seizures were stopped in all cases. Four patients attained premorbid neurologic status, two patients briefly survived in vegetative states with recurring seizures after PTB withdrawal, and one patient died of asystole after receiving PTB for 7 h. Patients who had poor outcomes had prolonged seizures (16 h to 3 weeks) before institution of PTB anesthesia, and all had significant underlying central nervous system (CNS) pathology. PTB-induced BSP appears to be safe and effective for refractory SE if it is started soon after failure of a BZD and PHT. Ultimate prognosis depends on SE etiology.

Prolonged confusion following convulsions due to generalized nonconvulsive status epilepticus

Abstract: Among patients with a prolonged confusional state after convulsive seizure, we diagnosed 8 cases as generalized nonconvulsive status epilepticus. Six had a history of seizures, and 2 had new onset. The convulsive seizures were generalized in 6 and focal in two. The postictal confusion lasted up to 36 hours in the most prolonged case, and a delayed response to anticonvulsant medications occurred in all cases. The clinical symptoms ranged from mild confusion to coma. Psychiatric manifestations or automatisms were rare. The presumed etiology was due to diverse causes, but a withdrawal state was the most common. EEG demonstrated continuous or nearly continuous generalized ictal discharges of variable morphology. These cases call attention to the fact that some prolonged confusional states following convulsive seizures are in fact due to persistent seizure activity that can be diagnosed by EEG.

Amnesia due to lesions confined to the hippocampus: A clinical-pathologic study

Abstract: Reported here is the case of a 65-year-old man who suffered a burst of severe, repetitive generalized seizures (status epilepticus). On recovery of consciousness he was left with a profound impairment of memory, which remained unchanged for the subsequent 30 months of his life. During this period the cognitive defect was fully documented. Careful neuropathologic examination disclosed the presence of remarkably discrete lesions, confined to the hippocampus on each side. Because of the rarity of well-documented instances of this type and their importance in the study of memory function, we are reporting our case in some detail.

Propofol infusion for control of status epilepticus

Abstract: Summary Two patients with status epilepticus who were resistant to conventional treatment but responded to propofol infusions are reported. An electroencephalogram confirmed the seizures and their successful treatment.

The role of benzodiazepines in the management of status epilepticus.

Abstract: Benzodiazepines are the most potent drugs used in the management of status epilepticus (SE). A number of presynaptic, postsynaptic, and nonsynaptic actions of benzodiazepines have been described. However, only the benzodiazepines' enhancement of gamma-aminobutyric acid (GABA)ergic inhibition and their reduction of repetitive firing occur at concentrations of unbound drug comparable to those that block absence seizures or stop clinical SE in patients. Thus, it is likely that these actions contribute to antiepileptic and anti-SE efficacy of the benzodiazepines. A predictable sequence of progressive electroencephalographic (EEG) changes during the course of generalized convulsive SE, both in humans and in experimental models, has been recently described. The homology of the sequence of EEG patterns in patients and in experimental models supports the concept that animal models should be useful in evaluating the treatment of clinical SE, and benzodiazepines are effective in stopping SE in a number of animal models. Late SE in animals, however, as in humans, is less responsive to treatment than is early SE. Forty-seven clinical studies in which clonazepam, diazepam, or lorazepam was used in the treatment of SE have been reported. Overall, lasting control of SE was achieved in 79% of the 1,346 patients in these noncontrolled studies. However, no data yet exist to differentiate the efficacy of 1 of the benzodiazepines from that of the others. Therefore, the choice of benzodiazepine is best determined by availability and by pharmacokinetic differences. Because of a much smaller volume of distribution of unbound drug, lorazepam appears to have a significantly longer effective duration of action against SE than does diazepam, which is rapidly redistributed to lipid stores in the body after intravenous administration. For this reason, we now use lorazepam in the initial treatment of patients with generalized convulsive SE.

Myoclonic status epilepticus A clinical and electroencephalographic study

Abstract: We reviewed the clinical features and ictal EEGs in 23 adults with myoclonic status epilepticus (MSE). Anoxic encephalopathy was the most common cause of MSE, occurring in 15 patients; 8 developed MSE within 14 hours following the anoxic insult. Metabolic encephalopathies were present in 4 patients, while 2 had degenerative CNS disorders. In 2 patients with generalized epilepsy, MSE developed during a medication change. Five types of EEG patterns were associated with MSE. Generalized periodic complexes (usually spikes, polyspikes, or sharp waves), often with attenuation of background activity between complexes (11 patients) or a burst-suppression pattern (4 patients), were the most common types. Outcome was poor: 20 patients died without regaining consciousness, while 1 remains in a vegetative state. The 2 patients with generalized epilepsy, both of whom were conscious during MSE, survived without sequelae.

Epileptic seizures in thrombotic stroke.

Abstract: Epileptic seizures due to thrombotic cerebral infarction were studied in 118 patients. The occurrence of seizures had a bimodal distribution with one peak period within 2 weeks and another peak period from 6 to 12 months after stroke. Four patients had seizures preceding stroke, while 23 patients without a history of previous stroke had “silent infarct” on the CT scan. Fifteen patients (13%) had status epilepticus. Simple partial seizures occurred in 56% of patients, complex partial seizures in 24% and generalized tonic-clonic seizures in 4%. Epilepsy developed in 35% of patients with early seizures and in 90% of patients with late seizures.

Status epilepticus: the next decade.

Abstract: Advances in the treatment of status epilepticus (SE) in the past decade have significantly improved the prognosis for this condition. Although currently available intervention techniques can eliminate mortality attributable to seizures, death associated with SE is usually caused by the disorder that precipitated the SE. Therefore, since currently available drugs for the treatment of SE possess significant shortcomings, new treatment modalities must be developed.

Prolonged postictal encephalopathy

Abstract: Eleven patients (6 males, 5 females; ages 7.5 to 40 years, mean 27.8) had prolonged postictal confusion lasting from 4 to 10 days. During that time, the EEG showed a typical encephalopathic pattern. Comprehensive evaluation ruled out the possibility of metabolic, toxic, drug-related, or ongoing nonconvulsive status epilepticus. We have designated this syndrome as prolonged postictal encephalopathy (PPIE). Nine of 11 patients were mildly to borderline mentally retarded. Ten had previous episodes of status epilepticus. Nine of 11 had minimal structural abnormalities (mainly diffuse cortical atrophy). Nine patients had multiple recurrent episodes of PPIE. All episodes occurred following a cluster of seizures: in 8 patients after a cluster of generalized tonic-clonic seizures, in 2 after complex partial seizures, and in 1 patient after a cluster of atypical absence seizures. This series suggests that vulnerability to develop PPIE exists in patients with diffuse structural abnormalities, mild to borderline mental retardation, a history of status epilepticus, and a tendency of seizures to cluster.

Therapeutic drug monitoring of anticonvulsants. State of the art.

Abstract: There is considerable interindividual variation in the relationship between control of seizures and the serum anticonvulsant concentration. The minimum effective serum concentration is dependent on the type and severity of the epilepsy, and varies from patient to patient. The therapeutic range should be used as a guide to adjust the dose in order to further improve seizure control or reduce toxicity; the latter is more likely with higher serum concentrations, but can also be present when concentrations are low. A request for the serum concentration of an anticonvulsant should be made only for good clinical reasons, and an interpretation of that concentration can only be made if all the relevant clinical details are available. Indications for the measurement of serum anticonvulsant concentrations include poor seizure control, toxicity, suspected gross noncompliance, status epilepticus and the elapse of 2 to 4 weeks after the initiation of therapy. Additional drug therapy, pregnancy or illness may alter drug disposition in a well controlled patient and therapeutic drug monitoring may, therefore, help to prevent seizures secondary to these changes. The measurement of anticonvulsants in saliva as opposed to serum may be of benefit in some patients.

Status Epilepticus after Ligation of Portosystemic Shunts

Abstract: Status epilepticus developed in four dogs, 2 to 3 days after ligation of an extrahepatic portosystemic shunt. Pentobarbital or phenobarbital intravenously was required to control seizure activity. Two dogs treated with phenobarbital recovered. Exacerbation of hepatic encephalopathy secondary to metabolic changes after surgery may be a cause of this syndrome. A treatment protocol for status epilepticus after ligation of a portosystemic shunt is proposed.

Comparison of Midazolam and Diazepam by the Intramuscular Route for the Control of Seizures in a Mouse Model of Status Epilepticus

Abstract: A model system is described in which sustained clonic seizures are produced by a combination of phenytoin (PHT) and pentylenetetrazol (PTZ) in the mouse, the former agent preventing the terminal tonic spasms produced by the latter. In this system, midazolam (MDL), a water-soluble benzodiazepine, was compared with diazepam (DZP), a sparingly soluble agent which is widely used to treat status epilepticus (SE) in humans. Both agents were administered intramuscularly (i.m.) in approximately equieffective doses in animals exhibiting clonic seizure activity. MDL proved to be about twice as potent as DZP. Whereas control animals convulsed for a period of approximately 90 min, those treated with DZP 0.2 and 0.4 mg/kg convulsed for 7.8 and 3.9 min, respectively; mice receiving MDL 0.1 and 0.2 mg/kg convulsed for 1.9 and 1.4 min, respectively. MDL arrested seizures substantially more rapidly than diazepam (p less than 0.05). These data suggest that MDL has sufficiently rapid anticonvulsant action to merit evaluation for control of SE in humans when a rapidly absorbed antiepileptic drug (AED) is needed and intravenous (i.v.) administration is not feasible.

Benign neonatal seizures.

Abstract: Benign neonatal seizures is a rare but increasingly recognized syndrome characterized by seizures in the neonatal or infantile period. Two forms are recognized: familial and nonfamilial. In both instances, the seizures may be quite severe, and status epilepticus is common. The nonfamilial form is characterized by idiopathic, self-limited seizures occurring in previously normal neonates. The seizures most commonly occur at day 5 and have been called "fifth-day fits" by some authors. Familial seizures most frequently have their onset during the first week of life, but onset may occur as late as early infancy. These seizures may recur for several months before resolving. No cause is found for the seizures, and the patient appears healthy during the interictal period. The family history reveals benign neonatal seizures in other family members. Although the prognosis is favorable in both syndromes, seizures may occasionally occur later in life in the familial form. The familial form of benign neonatal seizures is autosomal dominant, and the gene has been localized to chromosome 20.

Lorazepam treatment of experimental status epilepticus in the rat: Relevance to clinical practice

Abstract: We studied the efficacy, pharmacokinetics, and brain entry of lorazepam in the treatment of status epilepticus (SE) using a rat model of secondarily generalized convulsive SE. Lorazepam entered the bloodstream rapidly following intraperitoneal injection. Brain concentrations peaked 10 minutes after peak serum levels were achieved. Lorazepam remained in brain longer than in serum, leading to increasing brain: serum ratios over time once peak serum levels had been reached. Free lorazepam was 9.1% of the total concentration in serum, a fraction similar to that which has been reported for humans. The median effective dose for control of generalized tonic-clonic seizures in this model was 0.94 mg/kg, which would produce a serum concentration of 196 ng/ml. Rats in SE had higher serum lorazepam concentrations than controls given the same doses, but lower brain: serum ratios, perhaps due to lactic acidosis during SE. Our data confirmed clinical reports of lorazepam9s effectiveness as a treatment for SE and suggest that a target serum concentration of 200 ng/ml should be effective in most cases and provide seizure protection for 24 hours following treatment.