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

Paradoxical or "forced" normalization of the EEG of patients with epilepsy was first described by Landolt in 1953. It refers to conditions where disappearance of epileptiform discharge from the routine scalp EEG is accompanied by some kind of behavioral disorder. The best known of these is a paranoid psychotic state in clear consciousness, which is also known as "alternative" psychosis. Thus, the issue is related to much older observations which indicated a "biological antagonism" between productive psychotic symptomatology and epileptic seizures, which led to the therapy of psychoses with artificially induced convulsions. Apart from psychotic episodes, the clinical manifestations of PN comprise dysphoric states, hysterical and hypochondriacal syndromes, affective disorders, and miscellanea. PN can be observed in both generalized and localization-related epilepsies as a rare complication. A subset where it is more frequently seen are in adults with persistent absence seizures when the latter become finally controlled by succinimide therapy. These seem to be the drugs with the highest hazard of precipitation of PN, but all other AEDs have also been suspected. Sleep disturbance by succinimide treatment may play a crucial role, but a variety of other factors are also involved, including psychosocial factors. The pathogenesis of this condition has given rise to some debate but remains still unresolved. Eleven of the most important hypotheses have been discussed and seem to converge into a more comprehensive hypothesis which basically assumes that, during PN, the epilepsy is still active subcortically, perhaps with spread of discharge along unusual pathways. This activity is supposed to provide energy and, possibly, some of the symptoms included in the psychotic syndrome. A critical clinical condition results, usually with a dysphoric symptomatology, where a development towards psychosis is impending but still depends on the presence or absence of a variety of risk factors. Along with neurophysiological factors such as powerful inhibition of the spread of epileptic discharge, these may also include biographic factors such as the repeated experience of ictal sudden, unexpected loss of consciousness. Because during PN there presumably is ongoing epileptic activity, the differences with respect to other psychotic conditions in epilepsy are probably subtle rather than fundamental. Thus, it could be that ictal psychosis is characterized by a direct expression of epileptic activity, whereas in postictal psychosis a momentum of exhaustion may be added; moreover, in PN the prevailing pathogenic factor could be an abnormally high level of balance between excitatory and inhibitory processes.
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PMID:Acute behavioral symptomatology at disappearance of epileptiform EEG abnormality. Paradoxical or "forced" normalization. 200 2

Three hundred cases of tuberous sclerosis were surveyed by postal questionnaire, including 240 cases with learning difficulties. People who have tuberous sclerosis and severe learning disabilities also have a higher frequency of epileptic seizures than people with learning difficulties from all causes. Pervasive developmental disorder and hyperactive behaviour are behavioural features of the disorder. Sleep problems and the level of vigilant care required because of seizures or behaviour have implications on the level of service needed to support people with tuberous sclerosis in the community.
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PMID:Development, behaviour and seizures in 300 cases of tuberous sclerosis. 768 10

Whereas early formulations of addictive behaviour placed great emphasis upon withdrawal as a defining feature, current views focus more upon compulsive use as its central characteristic. However, the withdrawal syndrome continues to occupy an important place in the study of the addictions. It is interesting both in its own right and in relation to the development and maintenance of the compulsive use of drugs. Despite the attention devoted to withdrawal phenomena over many years, precise demarcation of the withdrawal symptoms associated with drugs of dependence has proved difficult to achieve. Withdrawal from all drugs of dependence appears to lead to mood disturbances although the extent to which these are due to the pharmacological actions of the drugs or to other physiological or psychological processes is unclear. Sleep disturbance is also common, although again direct links with the pharmacological actions of the withdrawn drug are yet to be established. Withdrawal from alcohol, benzodiazepines and opiates is often associated with somatic symptoms. In the former two cases, these can involve sweating, tremor and occasionally seizures. Perceptual disturbances have also been reported. In the case of opiates, flu-like symptoms are often reported, including muscle aches and gastric disturbances. In the case of nicotine, heightened irritability has been established as a direct pharmacological withdrawal effect. Characterization of stimulant withdrawal is still uncertain. There is little evidence of somatic symptoms but depression may occur as a result of a physiological rebound. There is also uncertainty over what role pharmacological withdrawal symptoms play in maintaining compulsive use.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Overview: a comparison of withdrawal symptoms from different drug classes. 784 60

The main interest in the association between sleep and temporal lobe dysfunction is based on the activation of ictal and interictal epileptic phenomena. The clinical semiology of NREM and REM parasomnias may resemble complex partial seizures. The differentiation between epilepsy and dissociated states of wakefulness and sleep is of high diagnostic and therapeutic importance. Systems within temporal lobe structures are also responsible for disturbed sleep or dyssomnia. The limbic brain is connected with different nodal points in the network underlying sleep organisation and participates in both sleepinducing and arousal mechanisms. Experimental amygdala kindling, an animal epilepsy model involving temporal structures, induces disturbed sleep patterns favouring waking and light sleep. In epilepsy unstable disrupted and superficial sleep patterns prevail without overt seizures. Sleep-fragmentation and deprivation may impair daytime functioning and cognitive performance by lowering the seizure-threshold. The recognition of dyssomnia and of excessive sleepfragmentation and sleepiness has obvious implications for behavioural and drug treatment.
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PMID:Sleep and the temporal lobe. 866 24

By means of parental questionnaires, sleep disturbances were assessed in 79 schoolchildren with epilepsy (mean age 10.12, range 5-16 years) for comparisons with 73 healthy control children matched for gender and to within a maximum of 6 months of age. The daytime behaviour of the children with epilepsy was also assessed by questionnaire. The children with epilepsy were considered representative of such children under general paediatric care. Sleep disturbance was classified into five basic types (poor quality sleep, anxieties about sleep, disturbances during sleep, symptoms of disordered breathing during sleep and short duration sleep) and the behaviour questionnaire provided scores on five factors (conduct problems, hyperactivity, attention problems, anxiety and physical complaints). Compared with normal controls children with epilepsy showed much higher rates of sleep disorders, particularly poor quality sleep and anxieties about sleep. In children aged 5-11 years associations were found between disturbed daytime behaviour and sleep problems, particularly poor quality sleep. There was also a significant association between seizure frequency and anxieties about sleeping. This study highlights the potentially serious psychological and other developmental implications of persistent sleep disturbance to children with epilepsy, and the need for further research on specific types of epilepsy with careful identification of the nature of both sleep disturbance and related psychological dysfunction.
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PMID:Sleep disorders and their relationship to psychological disturbance in children with epilepsy. 946 76

The purpose of this study is to review clinical features of children with moderate to severe Periodic Limb Movement Disorder (PLMD). Because of our interest in both Restless Legs Syndrome (RLS) and Attention-Deficit Hyperactivity Disorder (ADHD), many of our patients had one or both of these conditions. We did a retrospective review of 129 children and adolescents who were found to have Periodic Limb Movements in Sleep (PLMS) > 5/hour of sleep. Sixty five had PLMS of 5-10/hour of sleep, 48 had PLMS of 10-25/hour of sleep and 16 had PLMS > 25/hour of sleep. One hundred and seventeen of the original 129 had ADHD. Stimulant medication did not seem to play a role in the production of PLMS. In only 25 of the 129 cases did parents note the presence of PLMS before being specifically asked to look, and even after specific instructions to look, PLMS were not noted by the parents in 39 patients. The sub-group of 16 children and adolescents--6 female, 10 male (average age 11.1 years--range 6-17 years) with moderate to severe PLMS > 25/hour of sleep are described in more detail. Fifteen of the 16 patients had ADHD. Four of the 16 had RLS and 10 of 13 patients for whom a family history was available had a parent with RLS. Two of the 16 patients had their PLMS initially misdiagnosed as seizures. Sleep disturbance was present in all 16 patients and 7 of the 16 had daytime somnolence which resolved with dopaminergic medications. To our knowledge this is the first clinical series of moderate to severe PLMS in children and adolescents to be fully described in the literature.
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PMID:Moderate to severe periodic limb movement disorder in childhood and adolescence. 1034 79

Sleep disturbance in patients with epilepsy is frequently overlooked, but may contribute to decreased daytime functioning and increased seizure activity. Although complicated, the relationship between sleep and epilepsy is becoming clearer. Sleep, and particularly deep non-rapid-eye-movement sleep, increase interictal epileptiform activity. Sleep increases certain seizure types and the rate of generalization of partial seizures, however rapid-eye-movement sleep seems to suppress seizures. Sleep disorders, particularly sleep apnea, exacerbate seizures. Seizures, in turn, can disrupt sleep structure, particularly rapid-eye-movement sleep. An understanding of these relationships is important in seizure control and in maximizing the quality of life for patients with epilepsy.
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PMID:Sleep and epilepsy. 1098 75

Quality sleep is essential for patients with epilepsy, but this aspect of their treatment is frequently overlooked. Sleep disturbance can result in daytime drowsiness, worsening memory, and deteriorating seizure control. In a few patients, recognition and treatment of a coexisting sleep disorder can make the difference between complete seizure control and refractory epilepsy. Sleep has effects on interictal epileptiform discharges, with particular implications for diagnostic studies. Sleep disorders can coexist with epilepsy, leading to errors in diagnosis and worsening of seizures. Some specific syndromes demonstrate unique properties related to sleep. Seizures themselves disrupt sleep, even when occurring during the day, with the potential for persistent drowsiness and, perhaps, further memory dysfunction. Finally, most patients with epilepsy are treated with anticonvulsant drugs, some of which can have adverse (or beneficial) effects on sleep.
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PMID:Sleep and epilepsy. 1252 57

Sleep disturbance is common in epilepsy, the nature of sleep disturbances in epilepsy is diverse, and the etiologies are complex. Evidence suggests that having epilepsy and the occurrence of seizures, as well as some AEDs, are associated with significant sleep disruption. The occurrence of seizures can have profound effects on sleep architecture lasting much longer than the postictal period. Persistent daytime drowsiness in patients with epilepsy is not always due to the side effects of some AEDs and may be independently linked with sleep fragmentation. Significant sleep disruption in epilepsy has been associated with impaired quality of life and impaired seizure control. All aspects of sleep medicine are important in the management of epilepsy and are confounded by the occurrence of seizures, the location of seizures, and the beneficial and detrimental effects of AEDs. Sleep should be proactively evaluated, and sleep disturbances should be treated as part of the total care of patients with epilepsy.
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PMID:Epilepsy and sleep disturbance. 1452 82

Photic hypersensitivity may induce various signs of nervous hypersensitivity, including diurnal cephalalgias, anxiety, dyssomnia, seizures, fatigue and/or myalgias. The patients usually present both dishabituation and generalization in response to repetitive light stimuli instead of habituation as in normal subjects. These clinical manifestations appear when light intensity is maximum (daytime; spring and summer) in magnesium-depleted patients with hypofunction of the biological clock. The best photic hypersensitivity management involves darkness therapy, either darkness per se or darkness-mimicking agents. To detect efficiently the best drugs that may be used in the treatment of disorders due to photosensitive magnesium depletion, we are proposing a simple and reproducible actimetry-based test in a murine photosensitive magnesium depletion model. Photostimulation using a stroboscope (100 J, 50 Hz) was performed on magnesium-deficient and control mice. It led to habituation with a decreased activity in response to intermittent light stimulation in control mice, whereas it induced in magnesium-deficient mice both sensitization (or potentiation), with nervous hyperexcitability, and generalization, involving sound hypersensitivity, after visual stimulation. In preclinical evaluation, this test provides a valuable animal model to study the neuroprotective effect of drugs in photosensitive syndromes, which often associate sensitization and generalization to various stimuli.
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PMID:A new actimetry-based test of photic sensitization in a murine photosensitive magnesium depletion model. 1639 16


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