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

In recent years, a differentiation has been made between two syndromes that are characterized by brief abnormal paroxysmal movements occurring principally at night: 1, hypnogenic paroxysmal dystonia (HPD), sometimes considered a particular form of dystonia similar to paroxysmal kinesigenic choreoathetosis, and 2, mesiofrontal epilepsy. Whether HPD is a distinct syndrome is not clear. Twenty-three patients, 11 men and 12 women, were hospitalized between 1985 and 1989 for examination of this type of abnormal paroxysmal movements (APM) occurring at night. In order to clarify the physiopathology of these abnormal nocturnal movement as focal epilepsy or a particular form of dystonia, we analyzed the personal and familial antecedents of all 23 patients, the polygraphic records during waking and sleep periods, and the results of neuroradiological examinations. Four patients were examined by positron emission tomography (PET) using i8F deoxyglucose. Symptoms first appeared between 3 and 28 years of age (M, 10.1) and developed over 1 to 20 years (M, 10.1). APM clearly occurred more commonly (greater than 90%) during sleep, usually during phases of slow-wave sleep. The sleeping patient opened his eyes and the motor signs then variously associated affective facial expression; axial postural modifications; tonic, dystonic or choreic postural movements of the limbs; pedalling; automatisms; disordered agitation and vocalization. The seizure was abruptly interrupted after 10 to 60 seconds. There was usually no postictal confusion. Thirteen patients clearly had clear epileptic antecedents: in 9, generalized tonic-clonic seizures; in 4, focal epileptic status. During nocturnal polygraphic recording, 6 patients presented a generalized seizure following a period of APM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Postures and abnormal paroxysmal movements during sleep: hypnogenic paroxysmal dystonia or partial epilepsy?]. 190 68

In the central nervous system, adenosine has been shown to be a major regulator of neuronal activity in convulsive disorders, mainly via the A1 receptor subtype. In a previous work, we have shown that seizures lead to an age-dependent upregulation of cerebral adenosine A1 sites measured in isolated rat cerebral membranes. However, information concerning regional changes in the receptor density was so far lacking. In the present study, the effects of bicuculline-induced seizures were investigated by quantitative autoradiography of central adenosine A1 receptors in developing rats and in adults. Animals were sacrificed 30 min after an intraperitoneal injection of either saline or a convulsive dose of bicuculline. Adenosine A1 receptors in brain sections were labeled by [3H]N6-cyclohexyladenosine (CHA), a potent receptor agonist. Generalized seizures induced a widespread increase in CHA-specific binding, with a marked enhancement in structures that mediate seizure activity, such as substantia nigra, amygdala, septum and hippocampus. Moreover, the addition of guanylyl-5'-imidodiphosphate, a GTP analogue, to the incubation medium reduced CHA binding by the same order of magnitude whether rats were given saline or bicuculline, suggesting that additional adenosine A1 receptors are also functionally linked to G proteins. The age-related postictal increase in adenosine receptors might contribute to facilitate adenosine anticonvulsant effect, especially in newborns.
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PMID:Autoradiographic changes in brain adenosine A1 receptors and their coupling to G proteins following seizures in the developing rat. 191 42

There is little evidence for significant intellectual deterioration in well-controlled seizure disorders. With recurrent convulsive seizures, the picture is less clear and depends on severity, type, age of onset, and frequency of toxic levels of antiepileptic drugs (see Table 1). In the interictal state, deficits in verbal language and memory have been observed, especially in patients with complex partial seizure foci in the left (dominant) hemisphere. The memory deficits appear to affect new learning and retention of material; the verbal deficits are more subtle, affecting word-finding, verbal fluency, and comprehension abilities. Both of these changes may either go unnoticed by the patient in day to day activities or be attributed to the effects of antiepileptic medication. Antiepileptic drugs can also affect interictal cognitive functioning. The worst of these appears to be phenobarbital; phenytoin has an intermediate effect; valproic acid and carbamazepine as single agents seem to produce fewer adverse effects. However, individual patients may be particularly sensitive to cognitive side effects of certain drugs. Finally, attention deficits and slowing of cognitive processes, either chronically or intermittently, appear to affect all seizure patients to some extent. The syndrome is more prominent in frontal or generalized seizure patterns. The intermittent nature of these disturbances has been emphasized in recent research on subclinical interictal spike-wave electrical phenomena.
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PMID:Interictal cognitive changes in epilepsy. 192 32

Women with epilepsy account for approximately 0.5% of all pregnancies. Their pregnancies are high risk because of an increased frequency of maternal seizures, complications of pregnancy, and adverse pregnancy outcomes. The increase in seizure frequency is associated with a progressive decline in antiepileptic drug (AED) levels during pregnancy even with constant dosing. Fetal deaths after a generalized seizure, although rare, have been reported, and a marked decline in fetal heart rate has been demonstrated after such seizures during delivery. AEDs have been implicated in causing a twofold increase in the rate of congenital malformations, a variety of minor physical anomalies, mostly involving the midface, and a neonatal hemorrhagic disorder. The clinician caring for a pregnant woman with epilepsy is therefore faced with a dilemma and must carefully chart a middle ground providing effective seizure control while minimizing fetal exposure to AEDs.
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PMID:Pregnancy and epilepsy. 195 12

Intrahippocampal implants of noradrenaline-rich neural tissue from the fetal locus coeruleus region suppress development of seizures induced by hippocampal kindling stimulation in hyperexcitable, noradrenaline-depleted rats. In the present study the intracerebral microdialysis technique has been used to monitor seizure-induced release of noradrenaline from such grafts. The steady-state output of noradrenaline in the hippocampus of grafted animals (previously treated with intraventricular 6-hydroxydopamine) was similar to the baseline level in normal rats. A generalized seizure gave rise to a threefold increase of hippocampal noradrenaline levels as compared to baseline (15-min samples) in both normal and grafted animals. The maximal increase of extracellular noradrenaline levels occurred within 2-4 min after the onset of seizure activity and the levels then tapered off, reaching baseline after another 6-8 min. In 6-hydroxydopamine-treated animals without grafts baseline noradrenaline levels were markedly reduced compared to those of normal rats and only minor changes were observed in response to seizures. This supports the theory that the high extracellular noradrenaline concentrations measured in conjunction with seizures originate from the grafts. A knife cut transecting the ascending bundle from the locus coeruleus led to a marked attenuation of the seizure-induced increase of noradrenaline release in normal animals. In the intact brain, and probably also in the grafts, this response thus seems to be dependent on impulse flow in locus coeruleus neurons and only to a minor extent on local regulatory mechanisms in the hippocampus. In conclusion, the present study demonstrates that grafted locus coeruleus neurons are able to restore both basal and seizure-induced extracellular noradrenaline levels in the hippocampus.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Host regulation of noradrenaline release from grafts of seizure-suppressant locus coeruleus neurons. 198 32

These behavioral studies provide abundant evidence of the close interrelation between seizure activity and behavior. They reaffirm the point already made several times in this chapter: Seizures do not occur in a behavioral vacuum. They also strengthen the theoretical framework which provides for behavioral treatment of patients with epilepsy. With the detailed knowledge that we now have of the epilepsy focus and the way that it is connected to the surrounding cerebral mechanisms, it really is not surprising that seizure control is significantly influenced by altering the outlook and behavior of the patient with epilepsy. Seizures should not be thought of as arising randomly. They occur, in the case of focal seizures, when the pools of group 2 neurons are sufficiently excited for seizure activity to spread. Generalized seizures occur when the level of cortical excitability or of corticoreticular excitation has reached a point at which thalamic recruiting volleys generalize and start to spread. In the case of the focal epilepsies, a detailed clinical history should be taken as to the nature and characteristics of the aura; the history should also include details regarding the form that the seizure generalization or spread may take. This information allows the accurate location of the seizure focus, as well as of the cerebral structures through which the seizure discharge passes. The position of the focus will determine the relationship between the individual and his epilepsy. It will define those aspects of the psychic life or behavior of a patient which will both trigger and inhibit seizure activity. Detailed discussion of this information with the patient will help him to understand that his seizures are not part of a random process but are, instead, intimately related to how he feels, what he is doing, and what he is thinking. A complete treatment of epilepsy is not just the administration of drugs; rather, it also includes (a) teaching the patient about his brain and its functioning and (b) how the patient's feelings, thinking, and behavior can all be used in the control of his epilepsy.
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PMID:Evocation and inhibition of seizures. Behavioral treatment. 200 5

A patient presented without symptoms 30 minutes after ingesting acetonitrile, also known as methylacyanide. He had prompt gastric lavage and activated charcoal administration. Hours later, the onset of clinical toxicity was heralded by mental status abnormalities and vomiting prior to a generalized seizure. Following administration of sodium thiosulfate, the patient made an uneventful recovery. A blood cyanide level drawn shortly after presentation, but reported after the patient had been discharged, documented significant exposure. During hospitalization, cyanide toxicity was inferred from the history of ingestion of acetonitrile, plus a significant absence of venous blood hemoglobin desaturation. Because even small amounts can be harmful and toxicity is delayed, all acetonitrile ingestions should be presumed dangerous. Patients should be observed and repeatedly evaluated for at least 24 hours. In the absence of cyanide level determinations, lethargy, vomiting, seizures, and the lack of normal venous blood hemoglobin desaturation are clues to cyanide toxicity.
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PMID:Cyanide toxicity from acetonitrile-containing false nail remover. 201 1

Kindling was induced in rats by electrical stimulation of the lateral portion of the substantia innominata (SI). The pattern of seizure development was similar to that of amygdala (AM) kindling. However, lateral SI kindling was associated with ipsilateral head turning as an initial manifestation. In addition, lateral SI kindling had a higher afterdischarge threshold than AM kindling, and the generalized seizure triggering threshold was more unstable in SI kindling than in AM kindling. These findings suggest that lateral SI participates in, but is not essential for, AM seizure development in rats.
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PMID:Comparison between substantia innominata and amygdala kindling in rats. 207 96

The transferability between amygdaloid bicuculline kindling and electrical kindling was studied in rats. Electrically kindled animals exhibited stage 5 generalized seizures on the first injection of bicuculline, in contrast to the 3-7 injections required in controls. Similarly, bicuculline-kindled animals reached stage 5 after significantly fewer electrical stimulations than controls; two-thirds of the bicuculline-kindled animals began in stage 1 but skipped stages 3 and 4 on their way to stage 5. These data indicate that a common generalization mechanism exists in both types of kindling, but the process of progression from local seizure to generalized seizure may be immature in bicuculline kindling.
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PMID:Common epileptic pathway in amygdaloid bicuculline and electrical kindling demonstrated by transferability. 208 82

Sleep and sleep deprivation are often used for EEG activation in epilepsy. We compared postprandial naps and day-long sleep deprived EEGs in 36 patients with generalized seizures, 57 complex partial seizure patients, and 7 individuals with mixed seizure disorders. Ten of 36 generalized seizure patients had normal sleep and sleep deprived EEGs, while both were normal in 16 of 57 partial seizure patients. Both were abnormal in 18 of 36 generalized and 22 of 57 partial epileptics. Seven generalized seizure patients had epileptiform discharges or seizures during afternoon naps but normal sleep deprived EEGs. No partial seizure patients had normal sleep deprived EEGs and abnormal nap, but 29 of 57 had abnormalities or seizures only with sleep deprivation. All 7 mixed seizure patients had abnormal sleep and sleep deprived studies, and 6 had seizures, 4 on both studies. Natural sleep may facilitate the appearance of generalized seizures or epilepti-form discharges, while sleep deprivation may accentuate the yield of EEG abnormality in partial epilepsy. Either is likely to be abnormal in patients with mixed seizures and encephalopathy. Natural sleep and sleep deprived EEGs are an appropriate combination in the evaluation of refractory seizures.
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PMID:Sleep and sleep deprived EEG in partial and generalized epilepsy. 211 Oct 70


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