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

With the use of a time-synchronized video and polygraphic recording system, 5,042 infantile spasms were monitored and analyzed in 24 infants aged 1 to 43 months. Of these, 33.9% were flexor, 22.5% extensor, and 42.0% mixed flexor-extensor. Sometimes the spasms were followed by a period of akinesia and diminished responsiveness lasting up to 90 seconds, and rarely (1.0%) this "arrest" effect constituted the entire seizures. More than one type of seizure occurred in 21 of the 24 infants. In the same number, 78.3% of the seizures occurred in clusters, and the intensity and frequency of the spasms in each cluster often increased to a peak, then progressively decreased until they stopped. Predominantly, the clusters occurred soon after arousal from sleep. The number of seizures occurring at night (55.2%) was similar to the diurnal number (44.8%). The electroencephalographic seizure pattern was variable, but a marked generalized attenuation of electrical activity was a feature of 71.7% of the attacks. Attenuation episodes of similar degree and duration occurred with no evidence of a seizure.
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PMID:Precise characterization and quantification of infantile spasms. 53 18

Intracerebroventricularly applied pilocarpine (2.4 mg/2 microliters) immediately produced symptoms of epilepsy, ranging from akinesia to motor seizures, in rats. Whereas ACTH-(1-39), ACTH-(1-24), ACTH-(1-18), ACTH-(1-16) and ACTH-(18-39) were not active, subcutaneous pretreatment with smaller ACTH-like fragments, such as ACTH-(4-9), ACTH-(4-10), ACTH-(4-10)(7D-Phe), ACTH-(7-16), and Org2766, reduced the severity of the epilepsy. Moreover, fewer rats developed motor seizures. Thus, ACTH fragments devoid of peripheral endocrine activity reduce pilocarpine-induced epileptiform activity in rats. A narrow bell-shaped dose-response relationship was found. Except for ACTH-(7-16), which was active in a dose of 1 and 10 micrograms/rat s.c., the other fragments were only active at one dose (10 micrograms/rat). The anti-epileptic properties appeared to reside in the sequence 1-16, and more specifically in the sequences 4-7 and 7-16, of the ACTH molecule.
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PMID:ACTH: a structure-activity study on pilocarpine-induced epilepsy. 133 45

Behavioral, electroencephalographic and morphological changes induced by systemic administration of pilocarpine hydrochloride were studied in 3-90-day-old rats. Pilocarpine, 100, 200 and 380 mg/kg, presented a characteristic array of behavioral patterns in developing rats. Hyper- or hypoactivity, tremor, loss of postural control, scratching, head bobbing and myoclonic movements of the limbs dominated the behavior in 3-9-day-old rats. No overt motor seizures were observed in this age group. More intense behavioral signs evolving in some animals to limbic seizures and status epilepticus occurred when pilocarpine was administered in 12-day-old-rats. The electrographic activity in these animals progressed from low voltage spiking registered concurrently in the hippocampus and cortex during the first week of life into localized epileptic activity in the hippocampus, which spread to cortical recordings during the second week of life. No morphological alterations were detected in the brains of 3-12-day-old rats subjected to the action of pilocarpine, 100-380 mg/kg. The adult pattern of behavioral and electroencephalographic sequelae after pilocarpine was encountered in 15-21-day-old rats. Akinesia, tremor and head bobbing progressed in 15-21-day-old rats given pilocarpine, 100-380 mg/kg, to motor limbic seizures and status epilepticus. The lethal toxicity of pilocarpine reached 50% during the third week of life. This increased susceptibility to the convulsant action of pilocarpine was characterized by a shortened latency for behavioral and electrographic signs, and an increased severity of seizures relative to older and younger rats. In 15-21-day-old rats subjected to pilocarpine-induced convulsions high voltage fast activity superposed over hippocampal theta-rhythm, progressed into high voltage spiking and spread to cortical records. The electrographic activity became well synchronized and then developed into seizures and status epilepticus. Morphological analysis of frontal forebrain sections in 15-21-day-old rats which underwent status epilepticus after pilocarpine revealed no damage or an attenuated pattern of damage. In 15-21-day-old rats which presented epilepsy-related brain damage, morphological breakdown was seen in the hippocampus, amygdala, olfactory cortex, neocortex and certain thalamic nuclei. No damage was detected in the substantia nigra and lateral thalamic nucleus. An adult pattern of the damage to the brain, in terms of extent and topography, was present in 4-5-week-old rats.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:The susceptibility of rats to pilocarpine-induced seizures is age-dependent. 344 Feb 12

Forty-three patients affected with Alzheimer's disease were identified in a kindred of Italian origin, emigrated in part to the U.S.A. and France. Thirteen were known by history, 21 by medical record, and 9 by personal examination, of whom 5 were confirmed histopathologically. The clinical picture was fairly uniform: the first symptom was memory loss beginning around age 40. Psychotic-like symptoms often followed, with rapid evolution into profound dementia, and death around age 50. Akinesia was prominent at a late stage, often with myoclonus. Grand mal seizures sometimes occurred, with occasional interictal spike and wave discharge; repetitive paroxystic periodic discharges were never recorded. A genealogical study, as far as possible free from line bias, has been conducted mainly by analysis of municipal records. 1 435 subjects in 10 generations, linked to affected subjects through ascent/descent or marriage, were listed in a computer file; the corresponding genealogical tree or selected part thereof are generated by computer. Application of Bayesian techniques to demographic data makes possible an estimation of disease probability in subjects for which no clinical data were available: such an estimate was confirmed by the later discovery of a living patient in descent of a subject with 0.7 estimated disease probability. No patient was found in descent from an inbred union known as such. Patients are the only transmitters. The sex ratio is not significantly different from 1. There is no detectable maternal effect. The segregation ratio, as calculated from extensively known sibships, lies in the range 0.65 to 0.89; the lower value itself is significatively higher than the 0.5 value expected in an autosomal dominant monogenic Mendelian transmission. An environment factor is ruled out by the diversity of locations and circumstances in kindred members. Such a kindred may represent an useful model for fundamental studies in Alzheimer's disease and senile dementia of the Alzheimer type.
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PMID:[Alzheimer's presenile dementia transmitted in an extended kindred]. 400 7

Paroxysmal symptoms are described in 14 patients with undoubted or suspected multiple sclerosis (MS). In seven of the patients the paroxysms were the first symptom of the disease, although only one has developed definite MS so far. The clinical features have been compared with 153 patients previously reported in the literature which has been reviewed, with special reference to 36 in whom paroxysmal symptoms were the initial manifestations of MS. Attention has been focused on paroxysmal symptoms of brain stem and spinal cord origin of the following types: paroxysmal dysarthria and ataxia, diplopia, tonic seizures, paroxysmal akinesia, paroxysmal sensory disturbances and pains. Examples of each type have been reported as the first symptoms of MS with remissions ranging from less than one to 21 years before other manifestations of MS have developed.
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PMID:Paroxysmal symptoms as the first manifestations of multiple sclerosis. 737 30

Several symptom complexes in multiple sclerosis (MS) are found in unusual circumstances but are characteristic of the disease. Most of these are amenable to treatment and will be confronted by the physiatrist treating patients who have MS. This article begins by addressing paroxysmal symptoms such as trigeminal neuralgia, paroxysmal dysarthria and ataxia, parathesia and pain, paroxysmal itching, and akinesia. Seizures, adventitious movements, fatigue, and complications related to pregnancy also are addressed.
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PMID:Multiple sclerosis potpourri. Paroxysmal symptoms, seizures, fatigue, pregnancy, and more. 989 8

1. Excessive excitation of brain neurons by the excitatory neurotransmitter, glutamate, induces a cascade of events leading to increased intracellular Ca++, neuronal degeneration and death. 2. Recent in vitro research has demonstrated that a natural cationic amphiphile in the brain, lysosphingomyelin, may be able to prevent neuronal degeneration by repressing phosphosinositidase-C overactivation induced by excessive excitation of the metabotropic glutamate receptor. 3. This research tested the latter finding in vivo in a rat model of glutamate excitotoxicity. Intracerebroventricular (i.c.v.) administration of the Group 1 metabotropic glutamate receptor (mGluR) agonist, quisqualate, produced seizures, akinesia, destruction of hippocampal pyramidal cell dendritic microtubule-associated protein-2, and major loss of hippocampal CA sector neurons. 4. Prophylactic i.c.v. infusion of lysosphingomyelin powerfully attenuates these quisqualate-induced behaviors and prevents neuronal degeneration. 5. Lysosphingomyelin may be of clinical use in allaying progressive Group 1 mGluR-induced hippocampal cognitive and motor disorders including Alzheimer's disease, brain seizure, and stroke.
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PMID:Lysosphingomyelin prevents behavioral aberrations and hippocampal neuron loss induced by the metabotropic glutamate receptor agonist quisqualate. 1050 81

In this study, the behavioral and electroencephalographic (EEG) analysis of seizures induced by the intrahippocampal injection in rats of granulitoxin, a neurotoxic peptide from the sea anemone Bunodosoma granulifera, was determined. The first alterations occurred during microinjection of granulitoxin (8 microg) into the dorsal hippocampus and consisted of seizure activity that began in the hippocampus and spread rapidly to the occipital cortex. This activity lasted 20-30 s, and during this period the rats presented immobility. During the first 40-50 min after its administration, three to four other similar short EEG seizure periods occurred and the rats presented the following behavioral alterations: akinesia, facial automatisms, head tremor, salivation, rearing, jumping, barrel-rolling, wet dog shakes and forelimb clonic movements. Within 40-50 min, the status epilepticus was established and lasted 8-12 h. These results are similar to those observed in the acute phase of the pilocarpine model of temporal lobe epilepsy and suggest that granulitoxin may be a useful tool not only to study the sodium channels, but also to develop a new experimental model of status epilepticus.
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PMID:Behavioral and electroencephalographic analysis of seizures induced by intrahippocampal injection of granulitoxin, a neurotoxic peptide from the sea anemone Bunodosoma granulifera. 1137 71

The effects of four organophosphorous compounds, three oximes and atropine sulphate, injected through an indwelling cannula into the third ventricle of unanaesthetized dogs were examined. The effects of 200 mug of dyflos were involuntary micturition, defaecation, akinesia of hind limbs and pronounced disturbances of awareness; those of 100 mug of ethyl pyrophosphate were tremor, restlessness and signs of fear; 500 mug to 5 mg of dyflos and 250 mug to 500 mug of ethyl pyrophosphate caused vomiting, salivation, twitches of facial muscles and recurrent epileptiform seizures. The injection of 40 to 80 mg of dimefox and of 50 mg of schradan elicited involuntary micturition, vomiting, salivation and defaecation. These effects occur probably after these substances have passed into the blood stream and have been converted in the liver to potent anticholinesterases. This view is supported by the finding of reduced blood cholinesterase activity. At a dose level of 12.5 mg, 1,1'-trimethylenebis(4-hydroxyiminomethylpyridinium bromide) produced strong convulsions. At this dose level pralidoxime iodide and diacetyl monoxime produced no observable effects. Atropine sulphate in a dose of 1 mg caused disturbances in consciousness and behaviour followed by convulsions. Intraventricular atropine and to a minor extent intraventricular oximes were able to antagonize the effects of intraventricular ethyl pyrophosphate. Pralidoxime iodide exerted a strong antagonistic effect also on intravenous injection.
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PMID:Effects of organophosphorous compounds, oximes and atropine injected into the third ventricle of unanaesthetized dogs. 1388 82

Rolandic mu rhythm is usually limited to brief stretches of 0.5 to 2 sec duration. Two observations of status-like enhancement of mu rhythm have prompted this report. In both cases, 4-hour EEG-Video-Monitoring was used. Clinically, the reported cases differed considerably. Case 1 showed nearly continuous mu activity associated with general motionlessness: akinesia/amimia but without rigidity, caused by frontal lobe impairment due to multiple sclerosis. In Case 2, an impressive mu-status started in drowsiness and was presumably attributable to levitiracetam (which had rendered seizure-free the patient's formerly severe case of temporal lobe epilepsy). Mu rhythm status, thus far, is an unknown EEG entity. It can be caused by impaired fronto-motor input and may also constitute a medication-effect (levitiracetam).
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PMID:"Mu rhythm status" and clinical correlates. 1516 15


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