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

1. The temporal lobe status appears at a rate of once every 3-5 minutes. 2. The duration of a single temporal lobe seizure is varied, ranging from 10 seconds to 140 seconds. 3. The EEG during seizures is characterized by a generalization of 15-32 Hz recruiting epileptic rhythm which may become 3-7 Hz slow waves later in some cases, 3-7 Hz paroxysmal rhythmic waves. 4. The clinical symptoms are colorful, including apnic seizures, verbal automatism, facial muscle twitching, versive seizure and tonic seizure. The clinical symptoms depend on the size and depth of focus and the scope of propagation of discharge. 5. Generalization cannot be attained merely by the firing of focus that has been formed secondarily. The firing of primary focus is indispensable as the condition for generalization. 6. The focus depends more on the time of the disappearance of discharges than on the site of the primary onset of paroxysm. Particularly important is the length of duration of ictal discharges. 7. The cortico-cortical synapse and the cortico-subcortical pathways were considered the sources of epileptic propagation.
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PMID:Clinical and electroencephalographic study of temporal lobe status. 721 66

Rats repeatedly injected with initially subconvulsive doses of pentylenetetrazol (PTZ) eventually became sensitized to the drug (displayed twitching and myoclonic jerks). Other rats injected with increased doses of PTZ displayed both sensitization and generalized convulsions. Both groups subsequently developed generalized amygdaloid kindled seizures significantly faster than control rats, but did not differ significantly from each other in their rate of kindling. These results indicate that substantial transfer facilitation of electrical kindling occurs whether sensitization alone, or sensitization together with convulsions are induced by injection of PTZ.
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PMID:Transfer of pentylenetetrazol sensitization to amygdaloid kindling. 729 Dec 55

Kindling of the cingulate cortex in the Senegalese baboon Papio papio led to a protracted nonconvulsive seizure state characterized by immobile staring with (anterior cingulate, AC) or without (posterior cingulate, PC) widening of eyelids and neck flexion, followed by postictal visual searching behavior. Despite early bilateral spread of EEG discharges, ictal and interictal patterns remained persistently asymmetric. Secondary generalization was rapid and predictable once contralateral lower facial twitching associated with sustained adversion developed. After the primary site had been kindled, stimulation of the contralateral homotopic posterior cingulate cortex readily produced afterdischarge. However, it remained localized and kindling growth did not occur. The findings suggest that (a) the cingulate cortex can support nonconvulsive seizures; (b) cingulate seizures are accompanied by asymmetric convexity EEG discharges indicating its lateralized onset; (c) further evolution to convulsive seizures after kindling of cingulate cortex requires access to the ipsilateral frontocentral cortex responsible for facial twitching; and (d) the development of focal epileptogenesis at one cingulate site interferes with clinical seizure development at the homotopic contralateral site.
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PMID:Cingulate kindling in Senegalese baboons, Papio papio. 758 60

In Genetic Absence Epilepsy Rats from Strasbourg (GAERS), 100% of the animals present recurrent generalized non-convulsive seizures characterized by bilateral and synchronous spike-and-wave discharges (SWD) accompanied with behavioural arrest, staring and sometimes twitching of the vibrissae. Spontaneous SWD (7-11 cps) start and end abruptly on a normal background EEG at a mean frequency of 1.5 per min. Drugs effective against absence seizures in humans suppress the SWD dose-dependently, whereas drugs specific for convulsive or focal seizures are ineffective. Depth EEG recordings and lesion experiments show that SWD in GAERS depend on cortical and thalamic structures with a possible rhythmic triggering by the lateral thalamus; GABAA and GABAB receptors seem to play a critical role. SWD are genetically determined with an autosomal dominant inheritance. The variable expression of SWD in offspring from GAERS and control reciprocal crosses may be due to the existence of multiple genes.
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PMID:Genetic Absence Epilepsy in Rats from Strasbourg (GAERS). 764 44

Pilocarpine administration to lithium chloride-pretreated rats results initially in discrete convulsive seizures, each behaviorally and electroencephalographically terminated, which then progress to convulsive activity with waxing-and-waning behavioral and electrographic severity; finally, a continuous convulsive state ensues, associated electrographically with continuous fast spiking. This stage does not last indefinitely but is followed by a dramatic electrographic change to periodic epileptiform discharges. The purpose of the present study was to determine with the 14C-2-deoxyglucose functional mapping technique what changes occur in the seizure anatomic substrate during and after this transition, in order to enable inferences about underlying mechanisms. Behavior associated with early and late continuous fast spiking consisted of head twitching; corresponding deoxyglucose autoradiographs displayed seizure-induced intense glucose utilization in most forebrain areas; extranigral brainstem was normal. At 2-3 h of status, fast spiking became interrupted by flat periods; periodic complexes soon dominated the electroencephalogram. Behaviorally, convulsive severity increased. Despite this dramatic electrographic evolution, little change in generalized forebrain metabolic hyperactivation occurred, except that the zona incerta/pretectal/superior colliculus complex displayed markedly increased activity. Deoxyglucose studies in late stages of periodic epileptiform discharges established a sequence of further changes. In late periodic discharges with clonic jerks, at 4 h after status entry, generalized forebrain hyperactivation still prevailed, but to a lesser degree than in early periodic discharges with clonic jerks. At a still later stage, late periodic discharges, subtle convulsive, autoradiographs revealed constriction of the seizure-activated anatomic substrate: hyperactivation was lost in most of neocortex and thalamus, and in caudal olfactory structures, cortical amygdala, and entorhinal areas, but retained in deep occipital cortex and many limbic areas. In the last stage, late periodic discharges, electrical, not associated with convulsive behavior, autoradiographs revealed residual activation in only Ammon's horn; in contrast, much of the forebrain displayed below-normal glucose utilization. These results demonstrate that in the later stages of status epilepticus, the transition from fast spiking to periodic complexes is not associated with a reduction in the seizure anatomic substrate. The electrographic entity of periodic epileptiform discharges is not anatomically or behaviorally homogeneous, but proceeds through successive stages characterized initially by a reduction of glucose utilization within generalized seizure-activated forebrain, then a contraction of the seizure anatomic substrate. Possible mechanisms underlying the transition to periodic complexes are discussed.
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PMID:Functional mapping of the late stages of status epilepticus in the lithium-pilocarpine model in rat: a 14C-2-deoxyglucose study. 775 76

Ifosfamide, a nitrogen mustard derived alkylating agent commonly used in the treatment of solid tumors, has been associated with neurotoxicity in 5-33% of treated patients. Encephalopathy most often occurs during or shortly following drug administration, with increased drowsiness or irritability, confusion, hallucinations, visual blurring, extrapyramidal dysfunction, cranial nerve abnormalities, incontinence, generalized muscle twitching, seizures, and coma reported in infants, children, and older adults. While most reported neurologic abnormalities associated with ifosfamide have been reversible, encephalopathy resulting in death has occurred. We now report an infant who developed ifosfamide-induced encephalopathy, loss of developmental milestones, progressive brain atrophy, and cessation of cranial growth. This is the first case of cerebral atrophy and loss of developmental milestones that has been reported in a pediatric patient treated with ifosfamide. Given the efficacy of this anti-neoplastic agent and its increasing use in pediatrics, further investigation is indicated, especially in infants where brain growth is ongoing.
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PMID:Cerebral atrophy in an infant following treatment with ifosfamide. 805 12

A 73-year-old woman (patient 1) developed progressive mental deterioration at age 63, and seizures at age 70. On examination, she showed severe dementia, tonic clonic convulsion, hypotonia and muscular wasting. There was neither myoclonus nor cerebellar ataxia. Brain CT revealed a low density area in the right occipital lobe. A 44-year-old man (son of the patient 1) developed unsteady gait at age 15, muscle twitching at age 18 and then noticed speech disturbance at age 35. He had no history of convulsive seizure. Neurological examination showed cerebellar ataxia, myoclonus in the extremities and mild muscular weakness. His intelligence was normal. Brain CT showed moderate atrophy of the pons and the cerebellum. Both cases showed the same mitochondrial DNA mutation as reported previously in patients with MERRF. However, the clinical features, the age of onset and the brain CT findings were totally different between these 2 cases. In the progress of mitochondrial genetic analysis, atypical forms in MERRF like the patient 1 would increase in number, and the wide variation of clinical symptoms should be considered.
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PMID:[Two cases of MERRF (myoclonus epilepsy associated with ragged red fibers) showing different clinical features in the same family]. 812 82

A 43-year-old male was referred by a veterinarian who evaluated his dog for a seizure and suspected a toxic lead exposure for both. He refurbished houses, removing old paint, and complained of decreased cognition, fatigue, and muscle cramps. He had a depressed affect, postural tremor, right arm weakness with partial denervation on EMG, and borderline-low sensory nerve action potential (SNAP) amplitudes. A mild anemia and elevated serum and urine lead levels supported a diagnosis of lead neuropathy. Chelation therapy increased urine lead excretion without symptomatic improvement. His brother worked part-time with him and developed similar findings, but also had difficulty chewing, dysphagia, perioral twitching, gynecomastia, and multifocal denervation of extremity and facial muscles. His lead levels were not elevated, but an androgen receptor mutation identified on the X chromosome for both brothers confirmed the diagnosis of X-linked bulbospinomuscular atrophy (Kennedy's disease).
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PMID:X-linked bulbospinomuscular atrophy (Kennedy's disease) masquerading as lead neuropathy. 817 Apr 88

Generalised or partial seizures are a common problem with many supratentorial gliomas. Their underlying pathophysiological mechanisms are poorly understood. To investigate this problem clinical and EEG seizure thresholds were investigated in experimental rodent gliomas using the epileptogenic drug pentylenetetrazole (PTZ). Mixed C6/A15A5 malignant gliomas were grown in adult Wistar rats after unilateral stereotactic implantation of a 50:50 cell mix into the caudoputaminal region. Eleven to 14 days later EEG (raw and spectrally analysed) was recorded bilaterally from the frontal and parietal regions under mixed alpha-chloralose and urethane anaesthesia. Baseline EEG (15 minutes), EEG during and after (30 minutes) PTZ infusion (100 microliters/min) and the time to appearance of seizure manifestations after starting PTZ were recorded. Fourteen animals were studied (5 normal, 5 with tumours, 4 sham implants) and mean BP, PaCO2, PaO2 and temperature were similar in the three groups. Baseline raw EEG showed predominate slow wave activity with lower amplitude and less spontaneous activity overlying tumours. Following PTZ infusion a sequence of vibrissal twitching (following a mean of 14.5 mg/kg PTZ in control and sham animals); jaw/nasal twitches (17.5 mg/kg); fore and hind limb jerking (46 mg/kg); myoclonic jerking (47 mg/kg); and status (77.5 mg/kg) was observed. The seizure thresholds for all PTZ induced seizure phenomena were, except for status epilepticus, highest in the tumour bearing animals. The time to 70% seizure activity on the EEG was also significantly longer in the tumour bearing animals. Spectral analysis of the EEG, although showing increased alpha and theta activity after PTZ infusion, did not discriminate between the three experimental groups either before or after PTZ activation. These studies have confirmed that experimental gliomas alter baseline EEG and both the EEG and behavioural response to PTZ. The reasons for the raised seizure threshold in the glioma bearing animals and the relevance of this experimental paradigm to human tumour associated epilepsy are discussed.
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PMID:The effects of malignant glioma on the EEG and seizure thresholds: an experimental study. 873 86

The diagnosis and treatment of epilepsy relies heavily on descriptions of behavioral changes noted during seizure episodes. A pilot study was completed to determine the frequency of occurrence of behaviors commonly associated with seizures in a pediatric population (n = 153). Caretakers of the children (ages = 4 months to 19 years) were asked to respond to a checklist containing 40 behavioral descriptors. Thirteen descriptors were found to differentiate between seizure and nonseizure events. Twelve of these behaviors were endorsed significantly more frequently by caretakers of children with seizures including the following: does not remember what happened, moves mouth funny, drools, jerking/twitching, becomes stiff, changes in breathing, stares off, bites or chews tongue, eyes look glassy, will not respond, mumbles or slurs words, and eyes or head turn to one side. One behavior, fidgets in seat, was significantly more associated with nonseizure episodes. The behavioral descriptors may be presented in a checklist format or incorporated within a clinical interview in primary care settings for initial screening of children with possible seizure disorders.
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PMID:Behavioral descriptors that differentiate between seizure and nonseizure events in a pediatric population. 880 42


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