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Query: UMLS:C0036572 (seizures)
80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This paper reviews a series of previous reports which summarize the physiology of chronic experimental epileptic foci in monkeys. It is shown that such monkeys can be trained to bidirectionally control the firing rates of normal and epileptic neurons which comprise the epileptic focus. As a result of this acquired operant performance, the monkeys show both a decrease in clinical seizures as well as a decrease in single unit epileptic activity. The EEG correlate of this change in single unit epileptic activity is generalized EEG desynchronization. The conclusion from these data would indicate epileptic neurons can be operantly controlled from and this control is not correlated with any specific EEG pattern. This brings to question the specificity of the SMR in EEG biofeedback paradigms which treat human epilepsy. This author feels that the result from such biofeedback studies are the result of the patient learning to manipulate electrical events within the CNS pathways through which the seizures propagates and is not contingent upon specific EEG frequencies.
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PMID:Operant conditioning of epileptic neurons in monkeys and its theoretical application to EEG operant conditioning in humans. 41 Oct 99

After 1 year of SMR biofeedback training of a severe epileptic teenage male, incidence of atonic seizures decreased from 8/hr to less than 1/3 hr. SMR increased from 10% to 70%. Epileptiform discharges decreased from 45% to 15%. Unknown to the patient, his family, or certain members of our research staff, noncontingent feedback was introduced on 7/22/74, ending 9/11/74. A significant decrease occurred for SMR (down 8%), and a significant increase for epileptiform discharges (up 4%). Rate of seizures increased, but was not statistically significant over preceding months of contingent feedback. Incidence of seizures associated with urine loss increased from approximately 6/month to 23/month during noncontingent feedback, a significant increase. Urine-loss results suggest that although seizures did not become more frequent, those the patient did experience were "harder," i.e., more severe. Contingent feedback was reinstituted following the 7-wk sham, and recovery of all variables to their former levels (prior to sham) occurred.
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PMID:Effects of sham feedback following successful SMR training in an epileptic: follow-up study. 99 Mar 51

These studies concern the EEG rhythms of the sensory motor cortex in cats. The cat generates a 12H to 16Hz rhythm related to the MU (Rolandic) rhythm in man. The behavioral state required to generate the rhythm in man and the cat requires complete immobility and alertness. The MU rhythm in man centers around 9Hz and in the cat at 12Hz to 16Hz. This rhythm is used in the biofeedback training for the treatment of intractable seizures in man. It has also been used (12 Hz to 16 Hz) experimentally in animals. It is necessary to enhance the MU rhythm and simultaneously depress the seizure activity. Our interest has been to detect and enhance the SMR rhythm (12 H to 16 Hz) in the cat. We found that when it is enhanced it also enhances the amplitude of auditory evoked potentials in other brain regions.
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PMID:Autoregressive spectral filter studies on the sensorimotor rhythm EEG state variable. 233 63

The author reviews the use of operant conditioning to alter electroencephalogram (EEG) patterns. A discrete rhythmic EEG pattern directly related to modulation of motor patterns (sensorimotor rhythm, SMR) was brought under voluntary control in the cat. This technique was modified for use in epileptic human volunteers in order to reduce motor seizures. The use of a newer experimental design and its successful application in one subject is described.
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PMID:EEG biofeedback: physiological behavior modification. 730 Dec 28

The present review aims at highlighting selective aspects of the medical risks in epilepsy and their prevention. Emphasis is put on accidents and physical injuries, including risk factors and effectiveness of prevention; mortality, its causes, risk factors and prevention of seizure-related deaths, as well as traffic accidents, their risk factors and the effectiveness of prevention. Accidents and injuries are slightly more frequent among people with epilepsy than in the general population. This increased risk is probably most prevalent in patients with symptomatic epilepsy and frequent seizures, most often in combination with associated handicaps. The majority of accidents are trivial and occur at home. The most frequent injuries among patients with epilepsy are contusions, wounds, fractures, abrasions and brain concussions. The standardised mortality ratio (SMR; the ratio of observed number of deaths in a population with epilepsy to that expected, based on age and sex-specific mortality rates in a reference population) in population-based studies of epilepsy is 2-3 compared to the general population. This increased mortality is largely related to the etiology of the epilepsy and is probably not influenced by the treatment of the epilepsy. On the other hand, most fatalities in patients with chronic, therapy resistant epilepsy seem to be seizure-related and often sudden unexpected deaths (SUDEP). The frequency of such seizure-related deaths is most likely to be reduced by intensified treatment aiming at early seizure control, although appropriate studies for definitive evidence are still lacking. Apparently, there is an increased rate of traffic accidents in drivers with epilepsy, even if population-based prospective data are lacking. Many of these accidents are seizure-related. Probably, the extent to which physicians report their patients with uncontrolled epilepsy to the authorities is too low, but this has not yet been explored. Moreover, the preventive measures in legislation may be ignored by many people with epilepsy.
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PMID:Medical risks in epilepsy: a review with focus on physical injuries, mortality, traffic accidents and their prevention. 1527 65

Mortality in people with epilepsy has been studied in many different populations. In population-based incidence cohorts of epilepsy with 7-29 years follow-up, there was up to a threefold increase in mortality, compared to the general population (standardized mortality ratios [SMR] ranged from 1.6 to 3.0). When studies include selected epilepsy populations where patients with frequent and severe seizures are more common, the mortality is even greater. Relative survivorship (RS) following the diagnosis of epilepsy was 91%, 85%, and 83% after 5, 10, and 15 years, respectively. In a population with childhood-onset epilepsy, RS was 94% and 88% after 10 and 20 years. The level of increased mortality is affected by several factors. In idiopathic epilepsy where the causes of seizures are unknown, the results are conflicting. There was no significant increase in mortality in studies from Iceland, France, and Sweden, a barely increased risk in a study from the United Kingdom, and a significantly increased risk in a study from the United States. In contrast, all studies report a significant increased mortality in remote symptomatic epilepsy (standardized mortality ratios [SMRs] ranging from 2.2 to 6.5). The highest mortality is found in patients with epilepsy and neurodeficits present since birth, including mental retardation or cerebral palsy (SMRs ranging from 7 to 50). Mortality is also affected by age, with the highest SMRs in children, the combined effect of low mortality in the reference population, and high mortality in children with neurodeficits and epilepsy. The highest excess mortality is found in the elderly, > or =75 years. A pronounced increase in mortality is found during the first year following the onset of seizures due to underlying severe diseases. The increased mortality remains in different studies 2-14 years following diagnosis. Most of the factors responsible for the increased mortality are related to the underlying disorder causing epilepsy with pneumonia, cerebrovascular disease, and neoplastic disorders (risk remains elevated when primary brain tumors are excluded), as the most frequently recorded causes. The most common direct seizure-related cause of death in adolescents and young adults is sudden unexpected death, which is 24 times more common than in the general population.
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PMID:Mortality of epilepsy in developed countries: a review. 1639 74

This review traces the application of electroencephalographic (EEG) operant conditioning, or biofeedback, from animal research to its emergence as an alternative treatment for the major types of seizure disorder. Initial animal studies focusing on brain mechanisms that mediate learned behavioral inhibition revealed a uniquely correlated 12- to 15-Hz EEG rhythm localized to sensorimotor cortex. We labeled this the sensorimotor rhythm, or SMR. The similarity of the SMR to the known EEG spindle pattern during quiet sleep led to the novel idea of attempting to increase the SMR using EEG operant conditioning. The hypothesis was that this might produce a corresponding increase in sleep spindle activity, thus establishing a common EEG marker for the state of motor inhibition. Results supported this hypothesis but led also to the accidental discovery of an anticonvulsant effect on drug-induced seizures in cats and monkeys. Continuing animal studies identified a pattern of neurophysiologic responses correlated with the SMR in primary motor pathways. These and other findings were indicative of reduced motor excitability. Simultaneously, we undertook studies in human epileptic subjects that documented a significant reduction in seizure incidence and severity, together with EEG pattern normalization. This work expanded internationally, resulting in numerous well-controlled group and single-case studies summarized in recent meta-analyses. Exciting new findings in functional neuroimaging/EEG correlation studies provide a rational model for the basis of these clinical effects. In recognition of the diversity of clinical applications of EEG biofeedback and the complexity of seizure disorders, this review also details specific methods used in our EEG biofeedback program.
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PMID:Biofeedback in the treatment of epilepsy. 2062 79

We examined mortality in early onset (age<12 months) epilepsy in a population-based group of children. Children with early onset epilepsy were significantly more likely to die (case fatality, CF 8/60 versus 8/407, p<0.001; mortality rate, MR 14.5/1000 versus 2/1000 person years; standardized mortality ratio, SMR 22.25 versus 5.67). Mortality was greater in children with malignant neonatal (age<1 month) epilepsy (CF 4/12 versus 12/450, p<0.001; MR 54/1000 person years versus 2.7/1000 person year; SMR 46.55 versus 7.22). Given that only 1/8 early onset epilepsy deaths was seizure-related, mortality appears to be more affected by underlying etiology.
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PMID:Early onset epilepsy is associated with increased mortality: a population-based study. 2358 6