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)

A middle-aged aboriginal man with a history of alcoholism and gastrectomy was diagnosed as having bacterial meningoencephalitis based on the typical clinical manifestations, laboratory findings, and treatment responses. During the recovery stage, he developed consciousness disturbance, seizures, severe diarrhea, and respiratory failure that led us to search for other possibility of the diagnosis. The eosinophilia and repeated stool examinations helped us to make the diagnosis of disseminated strongyloidiasis. In this patient the initial bacterial meningitis was followed by S. stercoralis hyperinfection. Despite treatment with strong antimicrobial agents, the patient died. This case could serve as a reminder to physicians to be alert for strongyloidiasis superimposed on bacterial meningitis.
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PMID:Fatal meningoencephalitis caused by disseminated strongyloidiasis. 1583 86

Nerve agents are organophosphate compounds similar to those used as pesticides but with much higher toxicity. They all block the activity of the enzyme acetylcholine esterase. Victims are intoxicated by absorption of the toxin via exposed skin or, more commonly, via inhalation of the poisonous gas. The resultant clinical picture is of hyperstimulation of both the nicotinic and muscarinic cholinergic system, which, if not promptly treated, leads to severe muscle paralysis, cardiac brady-asystole, hypersecretion from secretory glands, respiratory failure, seizures, coma and death. If antidotal drugs are promptly administered, the clinical severity of the poisoning is attenuated or complete abortion of symptoms is obtained. The main therapeutic strategies include atropine and oximes that counteract the nerve-agent-induced muscarinic and nicotinic cholinergic symptoms, respectively. Anticonvulsants and sedatives are used to treat central nervous system acetylcholine esterase disarray. This review summarizes the biochemistry and pathophysiology of anticholinesterase poisoning, the relevant clinical manifestations and the currently available therapeutic strategies.
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PMID:Pathophysiological and clinical aspects of combat anticholinesterase poisoning. 1584 47

Patients with Leigh syndrome classically present in early childhood with developmental regression, ataxia, and hypotonia with subsequent respiratory and brainstem dysfunction. However, the clinical presentation can be highly variable. This report presents five cases of Leigh syndrome with atypical presentations. The first patient is a 17-month-old female who presented with progressive limb weakness diagnosed as Guillain-Barre syndrome. Postmortem examination demonstrated Leigh syndrome confined to the spinal cord. The case series then describes two sisters one of whom presented at 11 years of age with central respiratory failure and encephalopathy. Her 15-year-old sister presented with a progressive diplegia. The fourth patient presented with bronchiolitis and apnea at 3 months of age due to bilateral brainstem lesions. Her second cousin presented at 6 months of age with hypotonia, blindness, and tonic seizures. All patients had laboratory and radiologic findings consistent with Leigh syndrome. Evidence of spinal cord involvement was observed on magnetic resonance imaging in four of the five patients. Leigh syndrome can involve any level of the neuroaxis, resulting in a wide variety of presentations. Many atypical variants are observed, of which clinicians should be aware. Evidence of brainstem or spinal cord involvement should also be sought in patients with Leigh syndrome.
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PMID:Atypical presentations of leigh syndrome: a case series and review. 1586 34

Ergot toxicity in the newborn usually manifests itself as respiratory depression, cyanosis, oliguria, and seizures. Death is usually caused by respiratory failure. A limited number of neonatal cases have been reported worldwide, and almost all cases involved confusion of maternal methylergonovine with neonatal vitamin K. Previous case reports provided little information regarding the effectiveness and dosing of antidotal therapy, especially sodium nitroprusside. A full-term male infant was inadvertently given methylergonovine instead of naloxone at birth. Several hours later, he required intubation for respiratory failure. Peripheral perfusion, ventilation, and renal function improved rapidly with nitroprusside infusion, and he was extubated on the third hospital day. Even asymptomatic newborns should be transferred to a neonatal intensive care unit for close observation after methylergonovine administration because toxicity can be life threatening. Rapid recognition of the therapeutic error, ventilatory support, and prompt administration of sodium nitroprusside should lead to a good outcome.
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PMID:Neonatal ergot poisoning: a persistent iatrogenic illness. 1604 32

Serious complications after carbamazepine poisoning, such as coma, seizures, respiratory failure, cardiac conduction abnormalities, and death are more likely with serum levels greater than 170 micromol L(-1). We report a case of a single massive carbamazepine overdose in a 19-year-old male, following attempted suicide, without prior history of seizure disorder. On admission, three hours after ingestion, serum carbamazepine concentration was 179 micromol L(-1) and Glasgow Coma Scale scored 6. The patient was intubated and treated with multiple doses of activated charcoal for 48 hours. Twelve hours after ingestion, two repeated generalised myoclonic seizures were noted when serum carbamazepine levels peaked at 181 micromol L(-1), and were successfully treated with diazepam. Carbamazepine serum level fell within the therapeutic range 63 hours after ingestion and the patient was discharged without any long-term sequelae. As there is no antidote for carbamazepine poisoning, supportive treatment remains the only, but usually potent option.
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PMID:Multidose activated charcoal in the treatment of carbamazepine overdose with seizures: a case report. 1637 May 16

Protozoan infections in organ transplant recipients are rare. We report a fatal case of disseminated acanthamoebiasis in a bilateral lung transplant recipient that presented with cutaneous lesions, respiratory failure, and seizures. Acanthamoeba infection may be identified in transplant recipients with exposure to water who develop non-healing cutaneous ulcers with granulomatous inflammation. Cutaneous lesions are the initial manifestation of infection and a harbinger of dissemination. Early institution of combination anti-microbial therapy is therefore necessary for effective treatment and prevention of lethal spread to the central nervous system.
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PMID:Disseminated acanthamoebiasis after lung transplantation. 1644 27

Vigabatrin, a structural analogue of gamma-aminobutyric acid (GABA), is used for the treatment of generalized and partial seizures in infants. The drug inhibits the GABA transaminase and elevates the GABA concentration in the brain. Here we present the vigabatrin experience in two patients with early myoclonic encephalopathy owing to nonketotic hyperglycinemia (glycine encephalopathy). Both patients had early infantile seizures characterized by fragmentary myoclonic jerks associated with burst-suppression pattern on electroencephalography. Nonketotic hyperglycinemia was diagnosed with elevated cerebrospinal fluid and plasma glycine levels. The seizures were initially thought to be infantile spasms, and vigabatrin (50 mg /kg/day) was started for the treatment of seizures. Rapidly progressive deterioration was noticed after a few days. Acute encephalopathy associated with sleepiness and respiratory failure developed. Vigabatrin produced acute encephalopathy, which regressed in a few days after vigabatrin was stopped in the first patient. However, in the second case, despite the discontinuation of vigabatrin, there was no recovery of general conditions. Our observations in two cases indicate the risk of using vigabatrin in patients with nonketotic hyperglycinemia. The elevated GABA concentration in the brain can enhance the encephalopathy, together with the elevated levels of glycine. (J Child Neurol 2006;21:82-84).
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PMID:Vigabatrin caused rapidly progressive deterioration in two cases with early myoclonic encephalopathy associated with nonketotic hyperglycinemia. 1655 61

Episodes of psychogenic nonepileptic status epilepticus (PNESE) characterized by pronounced generalized motor features were compared with those of refractory generalized convulsive status epilepticus. Patients with PNESE were younger, had port systems implanted more frequently, received higher doses of benzodiazepines until seizure termination or respiratory failure, and had lower serum creatine kinase levels.
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PMID:Diagnosis of psychogenic nonepileptic status epilepticus in the emergency setting. 1676 30

Seven Chinese patients (5 males and 2 females) with vaccination-induced acute metabolic crisis were reported. Only one male with 21-hydroxylase deficiency had been diagnosed before vaccination. In the remaining six patients, the preexisting diagnoses were not confirmed before the vaccination. Acute metabolic crisis occurred in seven patients between 3 and 12 hours after the administration of Japanese encephalitis, diphtheria, and tetanus toxoids and acellular pertussis, hepatitis B, or measles vaccines. Patients 1 and 2 displayed acute adrenal insufficiencies at the ages of 5 years and 3 months, respectively. Patient 3 had presented with mild motor retardation previously. Patients 4 to 7 were previously healthy, but suffered from fever, seizures, coma, acidosis, and hypoglycemia after being vaccinated. Glutaric aciduria type 1 was evident in case 4. Leigh syndromes were present in Patients 5, 6, and 7. They all died from respiratory failure before 2 years of age. Symmetric foci, cystic cavitations with neuronal loss, and vascular proliferation were observed by postmortem examination. Among the seven patients, although the vaccines were not the primary cause of the acute metabolic crisis, the severe acute episodes occurred coincidentally.
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PMID:Acute metabolic crisis induced by vaccination in seven Chinese patients. 1687 7

Nerve agents (NA) are simple and cheap to produce but can produce casualties on a massive scale. They have already been employed by terrorist organizations and rogue states on civilians and armed forces alike. By inhibiting the enzyme acetylcholine esterase, NAs prevent the breakdown of the neurotransmitter acetylcholine. This results in over-stimulation of muscarinic and nicotinic receptors in the autonomic and central nervous systems and at the neuromuscular junction. Increased parasympathetic stimulation produces miosis, sialorrhea, bronchospasm and bronchorrhea. Effects at the neuromuscular junction cause weakness, fasciculations, and eventually paralysis. Central effects include altered behavior and mental status, loss of consciousness, seizures, or apnea. Most deaths are due to respiratory failure. Treatment with atropine competitively blocks the parasympathetic effects. Oximes like pralidoxime salvage acetylcholine esterase by "prying off" NA, provided the attachment has not "aged" to an irreversible bond. This reverses weakness. Benzodiazepines like diazepam are effective against NA induced seizures. Mortality has been surprisingly low. If victims can survive the first 15 to 20 min of a vapor attack, they will likely live. The low mortality rate to date underscores that attacks are survivable and research reveals even simple barriers such as clothing offer substantial protection. This article reviews the properties of NAs and how to recognize the clinical features of NA intoxication, employ the needed drugs properly, and screen out anxious patients who mistakenly believe they have been exposed.
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PMID:The acute treatment of nerve agent exposure. 1694 86


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