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

"I think it's time," said Bruce, between sobs. I knew my husband meant it was time to help our son Roger die. Roger entered our family 18 years ago. He was a tiny (1 lb., 12 oz.) premature baby I met in the NICU. Because normal gestational age at birth is 38 to 41 weeks, Roger's gestational age of 28 weeks made him extremely vulnerable to many medical complications, such as chronic respiratory problems, intracranial hemorrhage, mental retardation, and seizures. He experienced all of these complications during his life.
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PMID:A time for dying. Working through end-of-life decisions. 1082 87

Brucellosis is an infectious disease with multisystemic involvement caused by the genus Brucella. Neurological complications, including meningitis, meningoencephalitis, myelitis-radiculoneuritis, brain abscess, epidural abscess and meningovascular syndromes, are rarely encountered. We present a patient with epileptic seizures and aggressive mood due to chronic neurobrucellosis of 2.5 y duration, which was misdiagnosed as bacterial meningitis and epilepsy. This form of presentation has not previously been reported in the English language literature. We conclude that the diagnosis of neurobrucellosis should be considered in patients presenting with recurrent or chronic meningitis syndromes with or without seizure from endemic areas for brucellosis.
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PMID:Epileptic seizure: an atypical presentation in an adolescent boy with neurobrucellosis. 1223 82

Epilepsy is a common neurological disorder; however, in Nigeria and other tropical regions, the causes of epileptic seizures differ greatly in etiology. This paper is an attempt to highlight some possible microbiological aspects of epileptic seizures. A literature review was carried out to identify the extent to which microbial infections were involved in the elicitation of epileptic seizures. Data were collected from several clinics in the community and hospitals in Nigeria and correlated with the evidence from the literature review. It was found that different microbial agents including viral, bacterial, protozoa, and fungal agents were involved in several aspects of epileptic seizures. Malaria was found to cause more than 88% of childhood epileptic seizures and 12% of adult seizures. Generalized tonic-clonic seizures occurred in more than 40% of adult patients. Partial seizures were uncommon. Cases of epileptic seizures associated with bacteria (e.g., brucellosis), viral, fungal, and protozoa infections were frequently reported. Malaria, tapeworm, and cysticercosis were some of the common infectious causes of epilepsy; however, in some cases, the cause remained unknown. From these findings, it was evident that microbiological aspects of epilepsies are possible research areas that might be developed. It is believed that the unraveling of the various microbiological factors in epileptic seizures would have important implications for understanding the underlying neurobiology, evaluating treatment strategies, and perhaps planning health-care resources for the affected. It will also help to improve the prognostic factors in initial seizure symptomatic etiology and presence of any structural cerebral abnormalities.
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PMID:Clinical microbiological aspects of epileptic seizures in the tropical countries with specific focus on Nigeria. 1591 94

Prolonged or excess stimulation of excitatory amino acid receptors leads to seizures and the induction of excitotoxic nerve cell injury. Kainic acid acting on glutamate receptors produces degeneration of vulnerable neurons in parts of the hippocampus and amygdala, but the exact mechanisms are not fully understood. We have here investigated whether the anti-apoptotic protein Bruce is involved in kainic acid-induced neurodegeneration. In the rat hippocampus and cortex, Bruce was exclusively expressed by neurons. The levels of Bruce were rapidly downregulated by kainic acid in hippocampal neurons as shown both in vivo and in cell culture. Caspase-3 was activated in neurons exhibiting low levels of Bruce causing cell death. Likewise, downregulation of Bruce using antisense oligonucleotides decreased viability and enhanced the effect of kainic acid in the hippocampal neurons. The results show that Bruce is involved in neurodegeneration caused by kainic acid and the downregulation of the protein promotes neuronal death.
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PMID:Bruce/apollon promotes hippocampal neuron survival and is downregulated by kainic acid. 1623 53

Citalopram, a selective serotonin reuptake inhibitor, is generally considered to be of low toxicity. However, serotonin syndrome, seizures, electrocardiographic abnormalities as well as respiratory failure and death have been described in patients with citalopram overdose. The mechanisms of severe toxicity remain unclear. Our objective was to study the mechanisms of death following high-dose citalopram administration in Sprague Dawley rats. The median lethal dose (MLD) of intraperitoneal (i.p.) citalopram was measured using Dixon & Bruce's up-and-down method at 102 mg/kg. Dose-effect relationships of citalopram-induced clinical features, alterations in arterial blood gas and plethysmography, and disturbances in blood lactate, plasma and platelet serotonin concentrations were studied. Seizures were significantly increased in rats receiving 80% and 120% of citalopram MLD versus controls (p<0.05 and p<0.01, respectively). A significant decrease in body temperature was observed after 90 min in rats treated with doses >60% MLD in comparison to controls (p<0.05). The occurrence of serotonin behavioural syndrome was comparable in all groups. Citalopram administration did not result in significant hypoxemia, hypercapnia and lactate elevation. However, a significant moderate increase in the inspiratory time (p<0.05) accompanied with an expiratory braking was observed. A significant dose-related linear decrease in platelet serotonin and increase in plasma serotonin concentrations were measured (p<0.05). Pre-treatments of rats receiving 120% of citalopram MLD with diazepam (1.77 mg/kg) and cyproheptadine (17.1mg/kg) prevented seizures and death, but propranolol pre-treatment was ineffective. Neuroprotection with diazepam and cyproheptadine was not associated with decreased serotonin plasma concentrations. In conclusion, citalopram-induced deaths resulted from seizures in relation to serotonin release, whilst respiratory and metabolic toxicity was mild. Our observations support the role of serotonin-induced neurotoxicity in citalopram overdose and suggest that cyproheptadine and benzodiazepines, but not beta-blockers, may have a role in the management of citalopram toxicity.
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PMID:Mechanisms of high-dose citalopram-induced death in a rat model. 2295 78

A 3-year-old male child presented with moderate-to-high grade fever and non-projectile vomiting, generalised seizures and altered sensorium for 1&emsp14;month. CT scan revealed a communicating hydrocephalus with no basal exudates. The microbiological tests were negative for Streptococcus pneumoniae, Haemophilus influenzae, Neisseria meningitides, brucellosis, cryptococcosis, HIV and Mycobacterium tuberculosis. Intracranial pressure was relieved by ventriculo-peritoneal shunt, and the child was empirically started on ceftriaxone, and antitubercular therapy with isoniazid, rifampicin, ethambutol and streptomycin, along with steroids and supportive treatment for seizures. The symptoms persisted. On further investigation the cerebrospinal fluid showed growth of Acanthamoeba spp., following which the initial treatment was stopped and a combination antiamoebic regimen of cotrimoxazole, rifampicin and ketoconazole was started, after which he showed clinical improvement. The treatment was continued for 6&emsp14;months and on follow-up at 1, 3 and 6 months, there was a remarkable clinical improvement with no residual symptoms.
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PMID:Central nervous system infection with Acanthamoeba in a malnourished child. 2309 78

Parainfectious disorders of the nervous system encompass those meningo-encephalo-radiculomyelitic conditions that are temporally associated with a systemic infection, antigenic stimuli, or toxin exposure, in the absence of evidence of direct neuronal infection or invasion of the central nervous system (CNS) or peripheral nervous system (PNS). Pathogenetic mechanisms can be due to immune-mediated processes (such as bystander activation, molecular mimicy) or the inciting insult can be due to toxic factors, as in the case of botulism. A myriad of clinical manifestations can occur including headache, seizures, and mental status changes, ranging from mood and behavioral disturbances to varying levels of alteration in consciousness. Focal neurological deficits can include aphasia, hemiparesis, or paraparesis. The PNS can also be affected leading to cranial nerve involvement, focal or multifocal neuropathies, and dysfunction of the autonomic nervous system. Diagnosis is based not only on the history, examination, laboratory, and neuroimaging data but also on epidemiological factors. The parainfectious disorders covered in this review are cat scratch disease, Lyme borreliosis, legionellosis, brucellosis, botulism, pertussis, and mycoplasma. Each is associated with a distinct organism, has both systemic and neurological manifestations, and has a different epidemiological profile.
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PMID:Parainfectious meningo-encephalo-radiculo-myelitis (cat scratch disease, Lyme borreliosis, brucellosis, botulism, legionellosis, pertussis, mycoplasma). 2362 29

Cerebral venous sinus thrombosis is a rare form of stroke caused by thrombosis in venous sinuses of the brain. In this study, we reported on a patient with venous sinus thrombosis and brucellosis who presented with uncontrolled seizure despite being treated with anti-epileptic drugs at high doses. The case was a 33-year-old woman with a history of controlled complex partial seizure who presented with headache, asthenia, and uncontrolled seizure for one month. She was febrile and a brain CT scan indicated hemorrhagic focus in the left posterior parietal and the temporal lobe. Magnetic resonance imaging and magnetic resonance venography also proved venous sinus thrombosis in the left transverse sinus. Besides [In addition], a laboratory assessment confirmed brucellosis. Following the treatment with anti-coagulant, anti-brucellosis, and anti-epileptic agents, the patient was discharged in good condition with medical orders. Clinical suspicion and accurate evaluation of a patient's history is the most important clue in diagnosis and treatment of brucellosis and cerebral venous sinus thrombosis, especially in uncontrolled seizure in patients who had previously been under control.
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PMID:Uncontrolled seizures resulting from cerebral venous sinus thrombosis complicating neurobrucellosis. 2425 Jan 68

We report a rare case of brucellosis with Parkinsonian-like tremor and simple partial motor seizure. This patient worked as a sheep butcher and the sheep were imported from brucellosis-endemic areas. He presented with classical manifestations of brucellosis; infection was confirmed using the Rose Bengal Plate and Standard Tube Agglutination tests. The patient also suffered from headache, partial seizures, changes of personality and static tremor of both upper limbs. After anti-infection therapy, but without the use of anti-Parkinson drugs, the patient fully recovered and remained free of Parkinsonian-like tremor. Brucellosis can present with atypical symptoms, clinicians should widen their diagnostic view of brucella infection.
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PMID:A case of brucellosis displaying Parkinsonian-like tremor. 2433 51

Poisoning with opioid analgesics including tramadol represents a challenge. Tramadol may induce respiratory depression, seizures and serotonin syndrome, possibly worsened when in combination to benzodiazepines. Our objectives were to investigate tramadol-related neurotoxicity, consequences of diazepam/tramadol combination, and mechanisms of drug-drug interactions in rats. Median lethal-doses were determined using Dixon-Bruce's up-and-down method. Sedation, seizures, electroencephalography and plethysmography parameters were studied. Concentrations of tramadol and its metabolites were measured using liquid-chromatography-high-resolution-mass-spectrometry. Plasma, platelet and brain monoamines were measured using liquid-chromatography coupled to fluorimetry. Median lethal-doses of tramadol and diazepam/tramadol combination did not significantly differ, although time-to-death was longer with combination (P=0.04). Tramadol induced dose-dependent sedation (P<0.05), early-onset seizures (P<0.001) and increase in inspiratory (P<0.01) and expiratory times (P<0.05). The diazepam/tramadol combination abolished seizures but significantly enhanced sedation (P<0.01) and respiratory depression (P<0.05) by reducing tidal volume (P<0.05) in addition to tramadol-related increase in respiratory times, suggesting a pharmacodynamic mechanism of interaction. Plasma M1 and M5 metabolites were mildly increased, contributing additionally to tramadol-related respiratory depression. Tramadol-induced early-onset increase in brain concentrations of serotonin and norepinephrine was not significantly altered by the diazepam/tramadol combination. Interestingly neither pretreatment with cyproheptadine (a serotonin-receptor antagonist) nor a benserazide/5-hydroxytryptophane combination (enhancing brain serotonin) reduced tramadol-induced seizures. Our study shows that diazepam/tramadol combination does not worsen tramadol-induced fatality risk but alters its toxicity pattern with enhanced respiratory depression but abolished seizures. Drug-drug interaction is mainly pharmacodynamic but increased plasma M1 and M5 metabolites may also contribute to enhancing respiratory depression. Tramadol-induced seizures are independent of brain serotonin.
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PMID:Mechanisms of tramadol-related neurotoxicity in the rat: Does diazepam/tramadol combination play a worsening role in overdose? 2764 27


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