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

The authors describe a child with a ventriculo-peritoneal shunt in place for 5 years who presented with 'postural' seizures (seizures on sitting upright, which resolved on recumbency). On shunt tap, the cerebrospinal fluid was obtained freely, but required gentle aspiration with a syringe in the recumbent position, suggesting very low intracranial pressure. Contrast magnetic resonance imaging showed pachymeningeal enhancement and enlargement of the pituitary gland diagnostic of intracranial hypotension along with well-decompressed ventricles. At the time of revision of the shunt, no evidence of malfunction was found and the valve was changed to one with a higher opening pressure. Following this, she became asymptomatic and seizure free. This case illustrates the fact that following shunting, intracranial hypotension may also predispose to seizures, and should be kept in mind while managing these patients.
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PMID:Seizure as a manifestation of intracranial hypotension in a shunted patient. 1663 18

Multiple simultaneous intracerebral hemorrhages (ICH) are uncommon. We report the case of an 80-year-old woman with previous diagnosis of normal pressure hydrocephalus and who was brought to our hospital with altered mental status and urinary incontinence. Medical history of hypertension, hematological disorders or severe head trauma was absent. Platelet count and coagulation profile were unremarkable. An initial head computed tomography (CT) showed sulcal enlargement and ventricular dilatation, but no evidence of ICH. A tap test indicated as a guide to case selection for shunt surgery accidentally resulted in cerebrospinal fluid (CSF) overdrainage. The patient presented sudden neurological deterioration, with sluggishly responsive pupils and generalized tonic-clonic seizures. A new head CT demonstrated multiple supra and infratentorial ICH. The patient became comatose and had a fatal course. Hence, CSF overdrainage may either cause or precipitate multiple simultaneous ICHs, affecting both the infratentorial and supratentorial regions.
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PMID:Multiple simultaneous intracerebral hemorrhages following accidental massive lumbar cerebrospinal fluid drainage: case report and literature review. 1711 57

Kindling is a model in which an initially subconvulsive electrical stimulation of certain brain areas eventually develops a generalized seizure that produces behavioral and long term neuronal changes. In the present study we evaluated if kindling can modify conditioning taste aversion (CTA). In this paradigm animals acquire aversion to saccharin when it is presented as the conditioned stimulus (CS) followed by an injection of lithium chloride (LiCl) that induces a gastric irritation as the unconditioned stimulus (US). Male Wistar rats were implanted with bipolar electrodes aimed at the right amygdala (AMG) or at the right insular cortex (IC). The animals were stimulated daily until they reached stages 2-4 (intermediate) or until kindling was fully established (three consecutive stage 5 seizures). At least two weeks after kindling stimulation had ceased the animals were deprived of water for 24 h and given 10-min drinking sessions twice a day for 4 days. On day 5 (morning session) tap water was replaced by saccharin solution (0.1%), 20 min later the animals were injected with LiCl (7.5 ml/kg i.p., 0.2 M) to induce gastric malaise or taste aversion. After three more days of baseline consumption, water was substituted by a fresh 0.1% saccharin solution to test the aversion. AMG-kindling delayed the extinction of CTA. Animals with kindling in the IC had a higher retention than the sham kindling group; that is, they drank significantly less saccharin solution than the other groups. The results of the present experiment show that local modification of brain function induced by kindling stimulation can prolong the aversive effects of CTA.
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PMID:Kindling increases aversion to saccharin in taste aversion learning. 1714 Jul 39

A review of U.S. poison center data for 2004 showed over 40,000 exposures to salicylate-containing products. A guideline that determines the conditions for emergency department referral and pre-hospital care could potentially optimize patient outcome, avoid unnecessary emergency department visits, reduce health care costs, and reduce life disruption for patients and caregivers. An evidence-based expert consensus process was used to create the guideline. Relevant articles were abstracted by a trained physician researcher. The first draft of the guideline was created by the lead author. The entire panel discussed and refined the guideline before distribution to secondary reviewers for comment. The panel then made changes based on the secondary review comments. The objective of this guideline is to assist poison center personnel in the appropriate out-of-hospital triage and initial out-of-hospital management of patients with a suspected exposure to salicylates by 1) describing the process by which a specialist in poison information should evaluate an exposure to salicylates, 2) identifying the key decision elements in managing cases of salicylate exposure, 3) providing clear and practical recommendations that reflect the current state of knowledge, and 4) identifying needs for research. This guideline is based on an assessment of current scientific and clinical information. The expert consensus panel recognizes that specific patient care decisions may be at variance with this guideline and are the prerogative of the patient and the health professionals providing care, considering all of the circumstances involved. This guideline does not substitute for clinical judgment. Recommendations are in chronological order of likely clinical use. The grade of recommendation is in parentheses: 1) Patients with stated or suspected self-harm or who are the victims of a potentially malicious administration of a salicylate, should be referred to an emergency department immediately. This referral should be guided by local poison center procedures. In general, this should occur regardless of the dose reported (Grade D). 2) The presence of typical symptoms of salicylate toxicity such as hematemesis, tachypnea, hyperpnea, dyspnea, tinnitus, deafness, lethargy, seizures, unexplained lethargy, or confusion warrants referral to an emergency department for evaluation (Grade C). 3) Patients who exhibit typical symptoms of salicylate toxicity or nonspecific symptoms such as unexplained lethargy, confusion, or dyspnea, which could indicate the development of chronic salicylate toxicity, should be referred to an emergency department (Grade C). 4) Patients without evidence of self-harm should have further evaluation, including determination of the dose, time of ingestion, presence of symptoms, history of other medical conditions, and the presence of co-ingestants. The acute ingestion of more than 150 mg/kg or 6.5 g of aspirin equivalent, whichever is less, warrants referral to an emergency department. Ingestion of greater than a lick or taste of oil of wintergreen (98% methyl salicylate) by children under 6 years of age and more than 4 mL of oil of wintergreen by patients 6 years of age and older could cause systemic salicylate toxicity and warrants referral to an emergency department (Grade C). 5) Do not induce emesis for ingestions of salicylates (Grade D). 6) Consider the out-of-hospital administration of activated charcoal for acute ingestions of a toxic dose if it is immediately available, no contraindications are present, the patient is not vomiting, and local guidelines for its out-of-hospital use are observed. However, do not delay transportation in order to administer activated charcoal (Grade D). 7) Women in the last trimester of pregnancy who ingest below the dose for emergency department referral and do not have other referral conditions should be directed to their primary care physician, obstetrician, or a non-emergent health care facility for evaluation of maternal and fetal risk. Routine referral to an emergency department for immediate care is not required (Grade C). 8) For asymptomatic patients with dermal exposures to methyl salicylate or salicylic acid, the skin should be thoroughly washed with soap and water and the patient can be observed at home for development of symptoms (Grade C). 9) For patients with an ocular exposure of methyl salicylate or salicylic acid, the eye(s) should be irrigated with room-temperature tap water for 15 minutes. If after irrigation the patient is having pain, decreased visual acuity, or persistent irritation, referral for an ophthalmological examination is indicated (Grade D). 10) Poison centers should monitor the onset of symptoms whenever possible by conducting follow-up calls at periodic intervals for approximately 12 hours after ingestion of non-enteric-coated salicylate products, and for approximately 24 hours after the ingestion of enteric-coated aspirin (Grade C).
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PMID:Salicylate poisoning: an evidence-based consensus guideline for out-of-hospital management. 1736 28

Bacterial meningitis due to Streptococcus pneumoniae is associated with a significant mortality rate and persisting neurologic sequelae including sensory-motor deficits, seizures, and impairments of learning and memory. Creatine kinase (CK) is an effective buffering system of cellular ATP levels in high-energy consuming tissues; a decrease in CK activity is associated with a neurodegenerative pathway that results in neuronal loss. Thus, the aim of this study was to evaluate brain CK activity after pneumococcal meningitis. The animals underwent a magna cistern tap receiving either sterile saline as a placebo or an equivalent volume of a S. pneumoniae suspension; they were killed 6, 12, 24 and 48h after that, the brain was removed and hippocampus, striatum, cerebellum, cerebral cortex and prefrontal cortex were dissected and used for the determination of CK activity. We verified that CK activity was not altered 6 and 12h after meningitis. Interestingly, 24h after the induction of the meningitis we observed a decrease in CK activity. Finally, CK activity was not altered 48h after meningitis. Although it is difficult to extrapolate our findings to the human condition, the inhibition of brain CK activity may be involved in the pathogenesis of pneumococcal meningitis.
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PMID:Brain creatine kinase activity after meningitis induced by Streptococcus pneumoniae. 1940 53

Bacterial meningitis due to Streptococcus pneumoniae is associated with a significant mortality rate and persisting neurologic sequelae including sensory-motor deficits, seizures, and impairments of learning and memory. The presence of proliferating bacteria within the subarachnoid and ventricular space compartments triggers an intense inflammatory host response at killing the invading microorganism. Proinflammatory mediators released in the process include tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1beta, IL-6. TNF-alpha have several effects, including cytotoxicity, antiviral activity, transcription factor activation, and immune response regulation. Thus, the aim of this study was to verify the levels of the TNF-alpha after pneumococcal meningitis in male Wistar rats. The animals underwent a magna cistern tap receiving either 10 microL sterile saline as a placebo or an equivalent volume of a S. pneumoniae suspension at the concentration 5 x 10(9)cfu/mL. The animals were killed at 0, 6, 12, 24, 48 and 96 h after induction. The brain was removed and hippocampus, cortex, prefrontal and cerebrospinal fluid (CSF) were isolated and used for the determination of TNF-alpha levels. We found an increase in TNF-alpha levels at 6h after induction of the meningitis in the hippocampus (p<0.01), frontal cortex (p<0.05), and cerebrospinal fluid (p<0.001).There was no alteration in the cortex. Our data suggest that TNF-alpha is involved in the pathophysiology of the pneumococcal meningitis and could be investigated as a putative biomarker for brain damage in the first hours.
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PMID:Tumor necrosis factor alpha (TNF-alpha) levels in the brain and cerebrospinal fluid after meningitis induced by Streptococcus pneumoniae. 1983 31

Bacterial meningitis caused by Streptococcus pneumoniae is associated with a significant mortality rate and persisting neurologic sequelae, including sensory-motor deficits, seizures, and impairment of learning and memory. The presence of proliferating bacteria within the subarachnoid and ventricular space compartments triggers an intense inflammatory host response at killing the invading microorganism. Proinflammatory mediators released in the process, including tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1beta, and IL-6, were shown to contribute to the development of brain injury in bacterial meningitis. Thus, the aim of this study was to verify the levels of the TNF-alpha, IL-1beta, IL-6, and CINC-1 in the rat brain after pneumococcal meningitis. The animals underwent a magna cistern tap receiving either 10 microL of sterile saline as a placebo or an equivalent volume of a S. pneumoniae suspension at the concentration of 5x10(9) cfu/mL. The placebo group was killed immediately after the induction and the meningitis group at 0, 6, 12, 24, 48, and 96h after induction. The brains were removed followed by the isolation of the hippocampus and prefrontal cortex for determining TNF-alpha, IL-1beta, IL-6, and CINC-1 levels. In the hippocampus we found increased levels of the TNF-alpha only at 6h (p<0.01; F=3.777); CINC-1 levels increased at 6 and 24h (p<0.001; p<0.05; F=15.05); and IL-6 and IL-1beta levels were not altered. In the prefrontal cortex, the TNF-alpha levels were found to be increased only at 6h (p<0.05; F=4.921); IL-6 (p<0.05; F=11.69) and IL-1beta (p<0.001; F=132.0) levels were found to be increased only at 24h after meningitis induction; and CINC-1 levels were found to be increased at 6, 12, and 24h (p<0.01; p<0.01; p<0.01; F=16.86) after meningitis induction. Our data suggest that cytokine/chemokine levels can be putative biomarkers of brain damage in the first hours of the pneumococcal meningitis.
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PMID:TNF-alpha, IL-1beta, IL-6, and cinc-1 levels in rat brain after meningitis induced by Streptococcus pneumoniae. 2020 93

Bacterial meningitis due to Streptococcus pneumoniae is associated with a significant mortality rate and persisting neurologic sequelae including sensorymotor deficits, seizures, and impairments of learning and memory. The presence of proliferating bacteria within the subarachnoid and ventricular space compartments triggers an intense inflammatory host response. Proinflammatory mediators released in the process include tumor necrosis factor alpha (TNF-alpha), interleukin (IL)-1beta, IL-6, and all of which have been shown to contribute to the development of brain injury in bacterial meningitis. The animals underwent a magna cistern tap receiving either 10muL sterile saline as a placebo or an equivalent volume of a S. pneumoniae suspension at the concentration 5x10(9)cfu/mL. Ten days after induction we evaluated depressive-like behavior by using the forced swimming test and verified the levels of the TNF-alpha, IL-1beta, IL-6 and CINC-1 in the brain of rats induced to pneumococcal meningitis. In the forced swimming test we observed a significant increase in the immobility time in the meningitis group compared to the sham group (p<0.05). The TNFlevels were found increased in the prefrontal cortex (p<0.05, F=4.921), but not hippocampus. The IL-6, CINC-1 and IL-1beta levels presented no alteration in both prefrontal cortex and hippocampus 10 days after meningitis induction by S. pneumoniae. These findings suggest that the meningitis model could be a good research tool for the study of the biological mechanisms involved in the behavioral alterations secondary to pneumococcal meningitis.
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PMID:Depressive-like-behavior and proinflamatory interleukine levels in the brain of rats submitted to pneumococcal meningitis. 2045 Sep 61

The present study is concerned with the human factors that contribute to violations in aviation maintenance. Much of our previous research in this area has been based on safety climate surveys and the analysis of relations among core dimensions of climate. In this study, we tap into mainstream psychological theory to help clarify the mechanisms underlying the links between climate and behavior. Specifically, we demonstrate the usefulness of Ajzen's (1991, 2001) Theory of Planned Behavior (TPB) to understanding violation behaviors in aircraft maintenance. A questionnaire was administered to 307 aircraft maintenance workers. Constructs measured by the survey included perceptions of management attitudes to safety, own attitudes to violations, intention to violate, group norms, workplace pressures, and violations. A model based on the TPB illustrated hypothetical connections among these variables. Path analyses using AMOS suggested some theoretically justifiable modifications to the model. Fit statistics of the revised model were excellent with intentions, group norms, and personal attitudes combining to explain 50% of the variance in self-reported violations. The model highlighted the importance of management attitudes and group norms as direct and indirect predictors of violation behavior. We conclude that the TPB is a useful tool for understanding the psychological background to the procedural violations so often associated with incidents and accidents.
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PMID:Safety climate and the theory of planned behavior: towards the prediction of unsafe behavior. 2053 1

This study was designed to determine the effect of different concentrations of lead acetate on seizure threshold. Balb\c male mice were randomly divided into one control group provided with tap water and four experimental groups received lead acetate in drinking water for 30 days at concentrations of 50, 100, 200 and 400 ppm. Intravenous infusion of pentylenetetrazole (PTZ) was used to induce seizure signs and elapsed time was recorded to calculate the threshold dose. At the end of the experiments blood samples were taken to measure the blood lead level. Threshold doses of PTZ were significantly lower in 100, 200 and 400 ppm lead exposed groups for the induction of all seizure stages. Blood lead level increased in all experimental groups compared to control dose-dependently. Considering the lack of any response induced by 50 ppm concentration of lead, it may be concluded that 100 ppm of lead was the minimal effective dose. Therefore, lead acetate at a concentration of 100 ppm that produces similar blood level in human populations approves the enhancement of convulsive attack risk. Considering the effect of low levels of lead in the reduction of seizure threshold, more investigations should be carried out to clarify the exact mechanisms.
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PMID:Effect of short-term lead exposure on PTZ-induced seizure threshold in mice. 2067 92


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