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Query: UMLS:C0040822 (tremor)
 18,428 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Electroencephalographic activity of the frontal cortex, cerebellar vermis, and superior vestibular nucleus was recorded in awake rats during the high pressure nervous syndrome (HPNS) by means of permanently implanted electrodes. Power-spectrum analysis revealed a decline in the faster frequencies and an increase in the slow frequences as the seizure end-point was approached. Effects of compression to 4500 fsw varied from severe tremor and myoclonic jerks to status epilepticus, with seizures occurring at an average depth of 3560 fsw. In all animals, multifocal-spiking activity progressed in severity with increasing depth. The predominant seizure pattern observed was a spike and slow-wave pattern reminiscent of absence seizures. Initial evidence of generalized seizure activity was equally divided between the cerebellum and cortex. It is concluded that the cerebellum participates in HPNS seizures. Possible evolution of the syndrome by loss of Purkinje cell inhibitory influence on subcortical sites that modulate cortical excitability is discussed.
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PMID:Cerebellar and cerebral electroencephalogram during the high pressure nervous syndrome (HPNS) in rats. 60 10

Lithium is known to potentiate the ability of pilocarpine to induce status epilepticus in rats. The goal of this study was to determine whether lithium could potentiate pilocarpine-induced seizures in developing animals. Behavioral, electroencephalographic (EEG), and histopathological changes induced by systemic administration of lithium (3 meq/kg) followed 20 h later by pilocarpine (3, 10, 30, 60 mg/kg) were studied in 3-30-day-old rats. Lithium followed by pilocarpine (30 and 60 mg/kg) induced hyperactivity, tremor, loss of postural control and scratching but no electrographic seizures in 3-8-day-old rats. In the 7-10-day-old animals pretreatment with lithium and pilocarpine 60 mg/kg induced status epilepticus with sustained myoclonus and continuous bilateral synchronous spike and sharp wave, but doses of pilocarpine lower than 60 mg/kg had no effect. The susceptibility to lithium-pilocarpine-induced status epilepticus increased markedly during the third postnatal week of life. During this time period, rats treated with lithium (3 meq/kg) plus pilocarpine 10 mg/kg exhibited behavioral and EEG manifestations of status epilepticus. The same combination of lithium and pilocarpine failed to induce status epilepticus either before or after the third week of life. Histopathological analysis of the brains of the animals used in these studies failed to demonstrate the widespread damage reported in adult rats that have undergone lithium-pilocarpine-induced status epilepticus.
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PMID:Ontogenic study of lithium-pilocarpine-induced status epilepticus in rats. 132 90

A five-year-old male was admitted to the hospital with generalized seizures. Enlarged lymph nodes raised the suspicion of cat-scratch disease. The diagnosis was confirmed by a positive history of a cat bite, typical histopathologic findings in the biopsy of the lymph nodes, and a positive skin test. Brain CT scan and LP were repeatedly normal. The clinical course was remarkable for recurrent episodes of status epilepticus refractory to usual anticonvulsant therapy and prolonged encephalopathy consisting of mental confusion, hemiparesis, tremor, chorea, and vomiting. All neurologic symptoms gradually resolved within nine months, without sequelae. Cat-scratch encephalopathy should be suspected in a child presenting with status epilepticus and enlarged lymph nodes. Aggressive and prolonged anticonvulsant therapy is strongly recommended.
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PMID:Cat-scratch encephalopathy presenting as status epilepticus and lymphadenitis. 232 Apr 87

High-dose treatment with pilocarpine hydrochloride, a cholinergic muscarinic agonist, induces seizures in rodents following systemic or intracerebral administration. Pilocarpine seizures are characterized by a sequential development of behavioral patterns and electrographic activity. Hypoactivity, tremor, scratching, head bobbing, and myoclonic movements of the limbs progress to recurrent myoclonic convulsions with rearing, salivation, and falling, and status epilepticus. The sustained convulsions induced by pilocarpine are followed by widespread damage to the forebrain. The amygdala, thalamus, olfactory cortex, hippocampus, neocortex, and substantia nigra are the most sensitive regions to epilepsy-related damage following convulsions produced by pilocarpine. Spontaneous seizures are observed in the long-term period following the administration of convulsant doses of pilocarpine. Developmental studies show age-dependent differences in the response of rats to pilocarpine. Seizures are first noted in 7-12 day-old rats, and the adult pattern of behavioral and electroencephalographic sequelae of pilocarpine is seen in 15-21-day-old rats. During the third week of life the rats show an increased susceptibility to the convulsant action of pilocarpine relative to older and younger animals. The developmental progress of the convulsive response to pilocarpine does not correlate with evolution of the brain damage. The adult pattern of the damage is seen after a delay of 1-2 weeks in comparison with the evolution of seizures and status epilepticus. The susceptibility to seizures induced by pilocarpine increases in rats aged over 4 months. The basal ganglia curtail the generation and spread of seizures induced by pilocarpine. The caudate putamen, the substantia nigra, and the entopeduncular nucleus govern the propagation of pilocarpine-induced seizures. The antiepileptic drugs diazepam, clonazepam, phenobarbital, valproate, and trimethadione protect against pilocarpine-induced convulsions, while diphenylhydantoin and carbamazepine are ineffective. Ethosuximide and acetazolamide increase the susceptibility to convulsant action of pilocarpine. Lithium, morphine, and aminophylline also increase the susceptibility of rats to pilocarpine seizures. The pilocarpine seizure model may be of value in designing new therapeutic approaches to epilepsy.
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PMID:Review: cholinergic mechanisms and epileptogenesis. The seizures induced by pilocarpine: a novel experimental model of intractable epilepsy. 264 33

We report an infant with Shaken Baby syndrome (SBS) who presented with status epilepticus. The initial evaluation with computerized axial tomography (CAT scan) of the head was normal, and there was no history or physical finding consistent with physical abuse or shaking. This prompted an extensive evaluation to determine the etiology of the seizures. An ophthalmology consultation revealed the presence of severe bilateral retinal hemorrhages, which raised the possibility of SBS. Magnetic resonance imaging (MRI) showed cerebral hemorrhages, hemorrhagic contusions, and bilateral subtemporal subdural hematomas. This is the first reported case of SBS diagnosed by magnetic resonance imaging following a normal initial CAT scan. MRI may be a valuable tool in the diagnosis of brain injury in SBS and may be particularly valuable when the CAT scan of the head is normal, the etiology of neurologic injury is unclear, and the presence of retinal hemorrhages raises the suspicion of SBS.
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PMID:Shaken baby syndrome diagnosed by magnetic resonance imaging. 269 92

Venom was microinjected into the dorsal hippocampus of rats and electroencephalographic recordings were obtained from the hippocampus and occipital cortex. Behavioural alterations consisted of circling, wet shaking and scratching that evolved to head and body jerks and isolated clonic episodes and then to wild running followed by tonic-clonic generalized seizures and status epilepticus. Electroencephalographic alterations consisted of high frequency and high voltage spikes together with epileptiform seizures beginning in the hippocampus and evolving to the cortex. However there was only a poor electrographic-behavioural correlation between the generalized tonic-clonic seizures preceded by wild running and the electrical recordings from hippocampus and occipital cortex. Histology revealed lesions at the site of injection as well as at distant sites. Severity of neuronal damage was associated with seizure intensity. Damaged areas were almost the same as found within other models of epilepsy. Nevertheless a remarkable difference was the highly lesioned hypothalamus seen in this experiment. We discuss our results in relation to results obtained with other methods of inducing epilepsy. This venom may be a useful tool for studying the nervous system.
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PMID:Behavioural, electroencephalographic and neuropathological effects of the intrahippocampal injection of the venom of the South American rattlesnake (Crotalus durissus terrificus). 271 90

A case of status epilepticus with transient motor deficit is reported in a 66 year old male treated with fluvoxamine. Fluvoxamine is supposed to induce few epileptic seizures. The patient had no previous history of epilepsy. Two factors seem to have favoured the occurrence of epilepsy: presence of an incipient arteriopathic impairment, cortical and subcortical brain atrophy and perhaps drug overdosage causing a tremor in the days before the epileptic fit.
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PMID:[Epileptogenic action of fluvoxamine. Apropos of a case]. 311 16

Lipid chemical analysis of a case of membranous lipodystrophy (Nasu-Hakola disease) was reported. The case is a 43 yr-old man (at death). Onset of the disease was at his age of 10 when he had complained of leg pain. Since his age of 14, he had bone fractures of the lower extremities many times. At the age of 35, he was admitted to a hospital for the neurological examination. At that time, he showed exaggerated tendon reflexes and intension tremor of the upper extremities. He was euphoric and demented. His IQ was 31. Histological examination of biopsy specimen from the bone marrow revealed the typical membrano-cystic lesion. He had status epilepticus which was followed by comatous state for a week. The disease progressed gradually and he fell into decorticated state. He died at the age of 43. The total clinical course was 33 years. The brain weighed 680 g. Remarkable atrophy was observed in the whole brain. Loss of nerve cells in the upper layers of the cortex was marked. There were loss of myelin sheath and severe gliosis in the white matter. A part of the brain, liver and subcutaneous fat was frozen at the time of autopsy for the chemical examination. Quantitative determination of cholesterol, glycolipid, phospholipid, free fatty acid in the brain and liver, cholesterol, free fatty acid, triglyceride in the subcutaneous fat were carried out. Cholesterol was decreased about 33% in the cortex and 42% in the white matter in comparing with those of controls and the content of cerbroside in the white matter was about 1/3 of that of controls.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Lipid chemical study of an autopsy case of Nasu-Hakola disease]. 337 Jan 66

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

Bicuculline methiodide (0.5-3 nmol) and picrotoxin (0.5-4 nmol) were injected uni- or bilaterally into the rat amygdala and the resulting behavioural, electroencephalographic and morphological alterations were studied. In rats treated unilaterally with lowest doses of either bicuculline or picrotoxin (0.5 and 1 nmol) increase in the locomotor activity, occasional myoclonus of the hindlimbs and wet dog shakes were observed. At doses of 2-3 nmol, both gamma-aminobutyrate antagonists produced a sequence of repetitively occurring behavioural alterations including limbic gustatory automatisms, tremor and myoclonus of the forelimbs, head nodding and rearing, that developed over 15-30 min and built up progressively into the recurrent motor limbic seizures lasting for 1-6 h. In animals injected bilaterally with either bicuculline (0.5-3 nmol) or picrotoxin (0.5-3 nmol) motor limbic seizures rapidly developed into the status epilepticus lasting for several hours. Bicuculline and picrotoxin produced both ictal and interictal epileptiform activity in the electroencephalogram. A spectrum of electroencephalographic changes consisted of high voltage fast activity, slow and fast voltage spiking, paraoxysmal bursts and periods of postictal depression. The earliest electrographic alterations appeared in the amygdala and then rapidly spread to cortical areas. Electrographic seizures started 1-10 min after unilateral injections of large doses of bicuculline and pictrotoxin (2-4 nmol). Ictal periods lasted for 1-2 min, recurred every 5-10 min and were followed by periods of depression of the electrographic activity. Bilateral injections of large doses of both gamma-aminobutyrate antagonists (2-3 nmol) resulted in the status epilepticus. Morphological examination of frontal forebrain sections with light microscopy revealed a widespread damage to the amygdala, olfactory cortex, substantia nigra, thalamus, hippocampus and neocortex. Pretreatment of animals with diazepam prevented the build-up of convulsive activity and brain damage produced by bicuculline or picrotoxin. Muscimol retarded the appearance and shortened the duration of convulsive activity, but did not alter the sequence and intensity of seizures. The results indicate that gamma-aminobutyrate antagonists, bicuculline and picrotoxin when directly applied to the amygdala can elicit in rats motor limbic seizures, epileptic changes in the electroencephalogram indicative of repetitive limbic seizures, and status epilepticus accompanied by seizure-related brain damage.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Injections of picrotoxin and bicuculline into the amygdaloid complex of the rat: an electroencephalographic, behavioural and morphological analysis. 397 84


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