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

High-voltage electrical injuries may be devastating, with extensive burns, cardiac arrest, amputations, and long, complicated hospitalizations. Low-voltage injuries, after other pathologic and high-voltage sources are ruled out, tend to be rather benign acutely although they may have significant long-term morbidity, including chronic pain syndromes. Lightning injuries affect 800 to 1000 persons per year. In lightning injury, cardiac arrest is the main cause of death, burns tend to be superficial, ad injuries often are what one would expect of short-circuiting or overloading the body's electrical systems (tinnitus, blindness, confusion, amnesia, cardiac arrhythmias, and vascular instability). Although high-voltage injuries may require the services of trauma surgeons, in general, therapy for low-voltage and lightning injury is supportive and involves cardiac resuscitation for the more seriously injured and supportive care for the less severely injured. Long-term problems from sleep disturbances, anxiety attacks, pain syndromes, peripheral nerve damage, fear of storms (for lightning patients), and diffuse neurologic and neuropsychologic damage may occur in both electrical and lightning patients. Other sequelae--such as seizures or severe brain damage from hypoxia during cardiac arrest and spinal artery syndrome from vascular spasm--are indirect results of electrical and lightning injury.
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PMID:Emergent care of lightning and electrical injuries. 857 Sep 29

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

There is an intricate reciprocal relationship between epilepsy and sleep. The seizure threshold is often affected by changes in the level of arousal; certain seizure types occur predominantly or almost exclusively during sleep or upon awakening; many epileptiform electroencephalogram abnormalities are activated by sleep or sleep deprivation. Inversely, certain epilepsies are often associated with sleep disturbances, and epilepsy can affect sleep patterns and sleep architecture. Also, it may be difficult to differentiate certain nocturnal nonepileptic events from epileptic seizures occurring during sleep. Finally, antiepileptic drugs used in the treatment of sleep-related epilepsies can have an effect on sleep. The following is an analysis and review of these complex interactions between epilepsy and sleep.
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PMID:The relationship between sleep and epilepsy in children. 879 39

Mirtazapine is a unique antidepressant that refines the specificity of effects on noradrenergic and serotonergic systems. It is an antagonist of presynaptic alpha 2-adrenergic autoreceptors and heteroreceptors on both norepinephrine and serotonin (5-HT) presynaptic axons, plus is a potent antagonist of postsynaptic 5-HT2 and 5-HT3 receptors. The net outcome of these effects is increased noradrenergic activity together with specific increased serotonergic activity, especially at 5-HT1A receptors. This mechanism of action maintains equivalent antidepressant efficacy but minimizes many of the adverse effects common to both tricyclic antidepressants and selective serotonin reuptake inhibitors. Mirtazapine has an onset of clinical effect in 2-4 weeks similar to other antidepressants, although sleep disturbances and anxiety symptoms may improve in the first week of treatment. It has minimal cardiovascular and anticholinergic effects, and essentially lacks serotonergic effects such as gastrointestinal symptoms, insomnia, and sexual dysfunction. Sedation, increased appetite, and weight gain are more common with mirtazapine than with placebo. An elimination half-life of 20-40 hours enables once-daily bedtime dosing. The recommended initial dosage is 15 mg once/day at bedtime, with an effective daily dosage range of 15-45 mg. Cases of overdose of up to 975 mg caused significant sedation but no cardiovascular or respiratory effects or seizures.
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PMID:Mirtazapine: an antidepressant with noradrenergic and specific serotonergic effects. 901 62

Vigabatrin (VGB) has been shown through several studies to be safe and effective as add-on therapy, particularly for the treatment of partial seizures in patients with severe epilepsies followed for years in hospital-based clinics. We now report additional clinical experience with VGB arising from an open trial of add-on VGB therapy in patients with relatively few seizures followed by qualified neurologists in private practice (the French Neurologists Sabril Study Group). VGB was administered to 397 patients aged 12-74 years (mean age = 37.5 +/- 13.8 years) who presented with no more than seven partial seizures of any type per month during a 3-month baseline period (mean number of seizures = 3.7 +/- 1.9/month). Simple partial seizures were reported in 121 (30.5%) patients, complex partial seizures in 282 (71.0%) and seizures with secondary generalization were reported in 111 (28.0%). The mean number of associated antiepileptic drugs (AEDs) was 1.9 +/- 0.9 and the mean dose of VGB was 2.21 +/- 0.64 g/day. Following introduction of VGB, 53 (13.4%) became seizure-free and remained so during the whole trial. During the fourth month of treatment, 158 patients (39.8%) had no seizures at all and a further 69 (17.4%) had their seizure frequency reduced by more than 50%. Secondary generalization was controlled during the whole period of treatment in 55 out of 97 patients (56.7%), 17 of which remained free of all types of partial seizures. VGB showed a good tolerability profile; adverse experiences more frequently reported were drowsiness and sleep disturbances. No action was necessary in the great majority of cases; the dose was reduced in 26 (6.5%) and VGB was discontinued in 32 (8%) patients. These data provide additional evidence that VGB can be used safely early on to treat patients with mild to moderate partial epilepsies. Secondary generalization was controlled in the majority of patients. Factors associated with the everyday clinical use of VGB, that resulted from a series of organized meetings with the investigators, are discussed.
Seizure 1997 Jun
PMID:Multicentre clinical evaluation of vigabatrin (Sabril) in mild to moderate partial epilepsies. French Neurologists Sabril Study Group. 920 52

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 ontogenetic framework onto which a child's sleep is constructed undergoes significant developmental alterations during early life. Sleep state behaviors, in large part, reflect continuities from fetal through neonatal time periods. Major changes in sleep organization subsequently occur throughout infancy. Maturational expressions of sleep behaviors must be understood by the pediatric neurologist before specific physiologic phenomena can be assessed as transient sleep disturbances or clinically relevant sleep disorders. The first part of this two-part review article focuses on the major aspects of developmental sleep physiology in the first few months of life. Recognition of age-specific electroencephalographic/polysomnographic patterns will facilitate the child neurologist's evaluation of the newborn with suspected seizures and interictal encephalopathies, as well as the prediction of neurologic sequelae.
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PMID:Understanding sleep ontogeny to assess brain dysfunction in neonates and infants. 979 51

Adverse effects associated with antidepressant drug therapy rarely cause significant morbidity or mortality. Nevertheless, the successful management of patients with depression requires recognition of potential adverse effects that have serious consequences, which include the discontinuation of otherwise effective therapy. The aim of this overview is to highlight the more common and potentially deleterious adverse effects of both older and newer classes of antidepressant drugs. Major adverse effects attributed to the tricyclic antidepressant drugs (TCAs) include conduction defects and lethal overdose. Most worrisome with the selective serotonin reuptake inhibitor drugs (SSRIs) is the serotonin syndrome. Although rare, this syndrome can be insidious and lethal. Recent trends toward the use of medication combinations and augmentation therapies significantly enhance the risk of serotonin syndrome. Cognitive impairment also may occur, especially with the TCAs. Apathy is occasionally a problem with SSRI therapy. The syndrome of inappropriate antidiuretic hormone (SIADH) has been reported with most antidepressant drugs but appears to be more common with serotonergic agents and in elderly patients. Although seizures are uncommon in patients receiving antidepressant therapy, the risk must be understood by both the patient and the clinician. Adverse effects related to sexual function are common, especially with TCAs, SSRIs, and venlafaxine. Sexual dysfunction often leads to noncompliance and self-discontinuation of therapy. Sleep disturbances are common in patients with depression, and recent data illustrate how crucial sleep regulation is to mood. Antidepressant drugs vary in their sleep effects. Although antidepressant drugs can cause a variety of adverse effects, these drugs save lives and their benefits far exceed their risks.
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PMID:Antidepressant drugs: disturbing and potentially dangerous adverse effects. 979 63

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

Angelman syndrome is an inherited disorder that includes severe mental retardation and epilepsy. Patients have no speech, puppet-like gait with jerky movements, hyperactivity, disturbed sleep, bouts of inappropriate laughter, a pronounced jaw, and widely spaced teeth. The syndrome results from deletion or mutation within maternal chromosome 15q11-q13. Considerable evidence suggests that the gene or genes responsible for Angelman syndrome are expressed only from the maternal chromosome 15, a situation known as parental imprinting. This epigenetic marking of certain regions of the parental genomes is characterized by parent-of-origin-specific allelic DNA methylation, allele-specific DNA replication timing, and physical pairing of the two chromosome 15 homologues. Imprinting is important for normal development, and its disregulation causes several human disorders. The epilepsy of Angelman syndrome has been studied and indicates a rather typical electroencephalographic abnormality with slowing and notched wave and spikes. Various types of seizures occur, usually including myoclonus and atypical absence. Variable severity among patients suggests potential molecular diversity in the genetic mechanism, possibly the involvement of more than one gene. Angelman syndrome can arise from the following molecular genetic defects: a deletion in 15q11-q13 that covers the Angelman gene or genes, mutations that alter imprinting, and paternal uni-parental disomy for the region. Another 20% or so of patients with clinical symptoms of Angelman syndrome have none of these three defects but are believed to have mutations in one or more genes in the region, and this may be familial. The UBE3A gene, which codes for the enzyme ubiquitin protein ligase involved in protein degradation and processing, has been found to be mutated in many but not all of patients with Angelman syndrome and can be considered a major Angelman candidate gene. Other potential candidate genes in the region include a cluster of three GABAA receptor subunits, which are involved in inhibitory synaptic transmission in the brain. The GABRB3 gene, which codes for the beta 3 subunit, is deleted in most persons with Angelman syndrome. The absence of this gene in mice causes craniofacial abnormalities and neurologic impairment with seizures. The exact role of UBE3A and GABRB3 in the syndrome and their imprinting status are under investigation.
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PMID:Parental imprinting and Angelman syndrome. 1051 31


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