Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0036572 (seizures)
 80,221 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Recent studies have demonstrated that intramuscular administration of thyrotropin-releasing hormone (TRH) or its analogue improves various clinical aspects of intractable epilepsy such as Lennox-Gastaut syndrome, West syndrome, and myoclonus epilepsy. Other clinical studies reported efficient property of intravenous TRH against status epilepticus. However, it is also true that intravenous TRH produces epileptic seizures in patients with epilepsy or organic brain damage. Thus, the utility of intravenous TRH for the treatment of status epilepticus seems to be equivocal. To further explore the problem in this regard, we examined the effect of TRH on limbic status epilepticus in rats. Thirty-eight male Wistar rats weighing 180-220g were used. Status epilepticus was induced by intracerebral injection of a combination of 200 micrograms of dibutyryl-cAMP (db-cAMP) and 67.2ng of ethylenediaminetetraacetic acid (EDTA) into the amygdala (AM) through an implanted cannula. 30 min later, TRH or vehicle (distilled water) was administered intravenously (i.v.) or intracerebroventricularly (i.c.v.). Although 3 mg/kg of TRH (n = 9), when injected i.v., did not alter the pattern of electroclinical ictal responses induced by db-cAMP/EDTA, 25 mg/kg (n = 5) and 50 mg/kg (n = 5) of TRH significantly exaggerated EEG and/or behavioral ictal seizures, beginning immediately after the injection and lasting for more than 30 min. With 50 mg/kg of TRH, the exaggerated seizure patterns were followed by marked suppression of electroclinical seizures. 50 micrograms of i.c.v. TRH (n = 5), like higher doses of i.v. TRH, caused a slight, but not a significant, build up of electroclinical ictal seizures, beginning immediately after the injection and lasting for about 30 min.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:[Effects of thyrotropin-releasing hormone (TRH) on status epilepticus in rats]. 190 68

Brain edema and intracranial hypertension are a major cause of death in fulminant hepatic failure. We have shown that brain water measured in rats after hepatic devascularization (portacaval anastomosis followed in 24 to 48 hr by ligation of the hepatic artery) increases with the progression of encephalopathy. In this study, we examined whether intracranial hypertension develops in this model of fulminant hepatic failure. Using a fiberoptic pressure transducer, intracranial pressure rose from 3.3 +/- 1.1 mm Hg to 23.7 +/- 2.7 mm Hg (mean +/- S.E.M.) by the time the corneal reflex was lost; intracranial pressure was unchanged in control rats. Immediately after ligation of the hepatic artery, intracranial pressure was normal and remained stable until the last hours of the experiment, when it progressively rose, suggesting a loss of intracranial compliance. In addition, sudden and short episodes of marked increases in intracranial pressure (greater than 50 mm Hg) not related to seizure activity markedly decreased cerebral perfusion pressure. Internal carotid artery blood flow, an indirect measure of cerebral perfusion, decreased 29% +/- 12% by the end of the experiment. The time elapsed from ligation of the hepatic artery until loss of the corneal reflex (range 340 to 940 min) was related to the change in cerebral perfusion pressure, suggesting that an increase in systemic arterial pressure at the time of the initial rise in intracranial pressure may result in an increased length of survival. In this animal model, widely used to study the pathogenesis of hepatic encephalopathy, intracranial hypertension invariably appears in the terminal phase of the course. The development of intracranial pressure waves may be an indication that brain herniation is imminent.
 ...
PMID:Intracranial pressure waves and intracranial hypertension in rats with ischemic fulminant hepatic failure. 191 75

Three patients with hyponatremia were found at an residential home of mental developmental delay. Because pimozide had been administered to all of them, it was suggested that pimozide might have induced compulsive water drinking resulting in hyponatremia. To my knowledge, there has been no previous report that pimozide may induce hyponatremia. As children with mental developmental delay and/or autism frequently develop epilepsy, hyponatremia should be included in the differential diagnosis of convulsive seizures. Particularly when antipsychotic drugs such as pimozide have been given, we should pay attention to polydipsia, polyuria and/or general malaise and prevent hyponatremia.
 ...
PMID:[Three cases of hyponatremia during administration of pimozide]. 193 Nov 69

To elucidate the mechanism of anticonvulsant action of peony root and to determine the relative contributions of pure component substances, the water, water/acetone and methanol extracts of peony roots, paeoniflorin, albiflorin and pentagalloylglucose were studied in rats using the EEG power spectrum changes induced by pentylenetetrazol administration and the extracellular calcium and potassium concentration changes related to seizure activity. The water extract of peony roots, albiflorin and pentagalloylglucose given orally completely inhibited the EEG power spectrum changes as well as the extracellular calcium and potassium concentration changes related to seizure activity. The water/acetone and methanol extracts and paeoniflorin were relatively less potent. These findings suggested that the anticonvulsant action of peony roots is due primarily to albiflorin and the gallotannin fraction. Albiflorin and pentagalloylglucose appear to manifest their anticonvulsant action due to inhibition of the seizure-related decrease of extracellular calcium and consequent intracellular calcium increase.
 ...
PMID:Inhibitory effect of peony root extract on pentylenetetrazol-induced EEG power spectrum changes and extracellular calcium concentration changes in rat cerebral cortex. 194 64

This study reports the results of an epidemiologic survey for the detection of Taenia solium in a rural village of 559 inhabitants in Sinaloa, Mexico, as well as a large scale treatment of the population with praziquantel. The study was carried out in two stages. In stage 1, serial stool analysis of 392 persons detected a cluster of three T. solium tapeworms. A fourth T. solium tapeworm was detected through a household census, giving a 1.32% prevalence rate for this helminth. Over 70% of the population over five years of age was treated with a 10 mg/kg dose of praziquantel, and no additional tapeworms were found. Environmental studies for the detection of Taenia sp. eggs in soil, water, and and objects from the houses of tapeworm-infected individuals showed only one soil sample containing eggs compatible with Taenia sp. A total of 72 domestic pigs were examined for the presence of cysticerci under the tongue. One animal had cysts, and belonged to a household that had two T. solium tapeworm infections. Stage 2 of the study was carried out one year after large scale antihelminthic treatment (LSAT), and no infections with Taenia sp. eggs were found. No cysticercus-infected pigs were detected. Intestinal parasitosis decreased from 69.2% to 37.5%. It is concluded that LSAT with praziquantel is efficient in decreasing endemic foci of T. solium. Seropositivity to T. solium bladder fluid antigens was tested by enzyme-linked immunosorbent assay and found to be 11% before LSAT and 7% one year later. In family members living with T. solium tapeworm carriers, the number of seropositive individuals was 28%. The relative risk ratio of seropositivity for persons living in the same household with a T. solium tapeworm carrier was 2.95. Positive response was significantly higher in the 30-39-year-old age group, in which 30% were seropositive in stage 1, compared with 7% one year after LSAT. High seropositivity rates were significantly associated with tapeworm clusters as well as with individuals with a clinical history of seizures.
 ...
PMID:Epidemiologic study and control of Taenia solium infections with praziquantel in a rural village of Mexico. 195 62

While the cause of Parkinson's disease (PD) remains unknown, recent evidence suggests that certain external factors, ie, environmental agents, may act as neurotoxins, initiating the chain of oxidative reactions that ultimately destroy neurons in the substantia nigra. Young-onset PD might result from greater exposure to a putative neurotoxin. This hypothesis has rekindled interest in the epidemiology of PD. We therefore conducted a detailed analysis of various environmental exposures and early life experiences in 80 patients with old-onset PD (at an age older than 60 years), 69 young-onset patients (younger than 40 years), and 149 age- and sex-matched control subjects. Contrary to previous reports, we were unable to implicate well water or exposure to herbicides, pesticides, or industrial toxins as significant PD risk factors. A residential history of rural living was reported by more patient cases than control subjects and was marginally significant. On the other hand, at least one episode of head trauma "severe enough to cause vertigo, dizziness, blurred or double vision, seizures or convulsions, transient memory loss, personality changes, or paralysis" occurred significantly more often prior to disease onset in patients with both young-onset and old-onset PD than in control subjects (odds ratio = 2.7). When adjusted for head trauma and rural living, smoking was inversely associated with PD, as has been previously reported (odds ratio = 0.5). There were no significant differences in early life experiences or environmental exposures between young-onset and old-onset patients. We suggest that the risk of developing PD is influenced by a variety of factors.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:The epidemiology of Parkinson's disease. A case-control study of young-onset and old-onset patients. 195 12

A case of psychogenic polydipsia is presented. A 40 year old female was brought to the emergency room after a sudden seizure at home. The patient had spontaneous eye opening, was making incomprehensible sounds and had abnormal and agitated flexion of the limbs. Severe cerebral edema was seen on the computed tomogram. The patient was found to have hypotonic polyuria and hyponatremia. Two months previously, the patient had stopped taking bromazepam (a benzodiazepine) and on the advice of a neighbour had taken plenty of water to avoid withdrawal symptoms. The diagnosis and therapy are discussed.
 ...
PMID:[Psychogenic polydipsia: pronounced cerebral edema after exaggerated consumption of boiled water]. 200 20

Two groups of rats with electrolytic lesions of the medial and upper septal area (MUL) or, alternatively, of the anteroventral portion of the third ventricle (AV3V) and a third group of sham-operated rats were water loaded and received three carbachol injections into the locus coeruleus according to the following schedule: 1) prelesion, 2) on the second postlesion day and 3) on the seventh postlesion day. Both MUL and AV3V lesions inhibited the carbachol-induced natriuresis on the second postlesion day. Recovery was almost complete after MUL but not after AV3V lesion on the seventh day. Water deprivation also reduced the carbachol-induced natriuresis but passive hydration of AV3V animals did not avoid the impairment induced by the lesion. Transient seizure phenomena such as clonic convulsions, salivation and analgesia subsequent to carbachol injection were not altered by the lesions.
 ...
PMID:Natriuresis, not seizures, induced by cholinergic stimulation of the locus coeruleus is affected by forebrain lesions and water deprivation. 201 79

There are a number of clinical situations where overhydration may occur. If the reduction in plasma osmolality is acute, passive water influx swells brain cells, shrinking the extracellular space around them. It is during this time that susceptibility to generalized tonic-clonic seizure dramatically increases. Common clinical examples include hastened rehydration therapy, the dialysis disequilibrium syndrome, compulsive polydipsia, the syndrome of inappropriate ADH secretion (SIADH) and post-TURP syndrome. Treatments that tend to restore normal cellular volume (dehydration, mannitol infusion) help protect against this form of seizure. Support for a correlation between plasma osmolality and seizure susceptibility is scattered amongst the literature of several medical disciplines and spans almost 70 years. However a cellular basis to explain how overhydration might promote epileptiform activity has been examined only recently. The neocortical and hippocampal brain slice preparations permit an examination of how acute osmotic change alters cortical excitability independent of vascular damage, brain compression or other factors secondary to brain swelling. Electrophysiological evidence indicates that hyposmolality promotes epileptiform activity by strengthening both excitatory synaptic communication in neocortex and field effects among the entire cortical population. Moreover there is little evidence that associated hyponatremia in itself leads to increased CNS excitability. Such findings help in understanding how rapid lowering of plasma osmolality in clinical situations can promote the hyperexcitability associated with generalized tonic-clonic seizure.
 ...
PMID:Seizure and acute osmotic change: clinical and neurophysiological aspects. 202 29

The cerebral protective effect of eptazocine, an opioid mu-antagonist-kappa-agonist, was investigated using mice and rats subjected to ischemia. 1) Decapitation or concussive head injury (20 g, 30 cm)-induced ischemia in mice: Eptazocine (3,10 mg/kg) prolonged the gasping duration or the survival time in a dose-dependent manner. 2) Ischemic brain edema induced by bilateral carotid arterial occlusion (BLCO) in rats: Administration of eptazocine just after BLCO treatment significantly prevented the incidence of ischemic seizures, lethality and an increase in cerebral water content. 3) Acute ischemic changes in cerebral energy metabolism in mice: 2-min BLCO treatment decreased the cerebral contents of phosphocreatine and ATP, and it increased the contents of AMP and lactate, resulting in a 34% decrease in energy charge potential and an increase in lactate/pyruvate ratio. Such changes were improved by eptazocine (3, 10 mg/kg) and ethylketocyclazocine (3 mg/kg), a kappa-agonist. 4) Respiratory function in mouse brain mitochondria preparations: Eptazocine increased the State 3 respiration and respiratory control index (RCI:State 3/State 4), and it prevented a decrease in RCI induced by 3-min ischemia. These results suggest that eptazocine may improve cerebral ischemic disorders through an activation and/or protection of mitochondrial energy-producing systems.
 ...
PMID:[Protective effect of eptazocine, a novel analgesic, against cerebral ischemia in mice and rats]. 205 80


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>