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 22 year-old woman with a seven year history of (SLE) was readmitted because of oliguria, edema, dyspnea and arterial hypertension. She had a previous biopsy diagnosis of focal glomerulonephritis, (WHO III b), and had been treated with immunosuppressors and steroids. Laboratory data showed lupus activity, AHM with thrombocytopenia, nephrotic-range proteinuria and renal failure. A second renal biopsy was performed showing diffuse proliferative nephritis, (WHO IV), in association with noninflammatory necrotizing vasculopathy with luminal obliteration. She started with hemodialysis and was subsequently treated with methylprednisolone pulses, plasmapheresis, cyclophosphamide and oral steroids. During the inpatient period, she had generalized seizures, acute lung injury and pulmonary hemorrhage. These complications, the AHM and the thrombocytopenia receded totally. Renal function was never resumed. We emphasize that this association of diffuse proliferative nephritis with noninflammatory necrotizing vasculopathy is not infrequent and has a poor renal prognosis. The AHM with thrombocytopenia was interpreted as secondary to endothelial cell damage due to vasculopathy.
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PMID:[Renal vascular lesion and microangiopathic hemolytic anemia in systemic lupus erythematosus]. 953 30

A 61-year-old woman presented to the emergency department after experiencing palpitations, shortness of breath, and syncope while taking a shower. Her husband revived her with mouth-to-mouth resuscitation. She had had a similar episode three days earlier while making her bed and had lost consciousness for about 10 sec. She did not appear to have had a seizure. Five months earlier, while taking a walk, she had experienced dizziness, dyspnea, and chest pressure lasting about an hour. A workup at that time included cardiac catheterization, lung scanning, and esophagogastroduodenoscopy, but no abnormality was found. Lower extremity edema was noted.
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PMID:Syncope two years after hysterectomy. 1004 58

The authors administered the Medical Outcomes Study (MOS 20) Short Form Health Survey to 369 persons with HIV disease. The MOS survey measures six domains of health: physical function, role function, social function, mental health, health perception, and pain. Additional data included sociodemographics, HIV risk group, time since HIV diagnosis, symptoms (dyspnea, diarrhea, fever, chills, sweats, weight loss, weakness, numbness, memory trouble, seizures), and CD4 lymphocyte count within 3 months of the MOS survey. Bivariate analyses revealed worse MOS scores associated with older age in five health domains: physical function (p less than .01), health perception (p <.10), role function (n.s.), social function (n.s.), and mental health (n.s.). Older subjects reported less pain. When controlling for CD4 count and for sociodemographic and clinical variables, older age was significantly (p less than .05) associated with worse MOS scores in physical function, social function, and health perception, nonsignificantly associated with worse MOS scores in role function and mental health, and nonsignificantly associated with less reporting of pain.
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PMID:The impact of age on the quality of life in persons with HIV infection. 1016 53

Vagus nerve stimulation is an empirically based method for treatment of epilepsy by repeated stimulation of the left vagus nerve through implanted electrodes. Despite studies in animals and man, which show changes in brain electrophysiology, metabolism and neurochemistry, the mode of action remains unknown. Clinical testing has presented methodological challenges, as it is difficult to assess under double blind conditions a treatment which requires surgery and produces a sensation every time the stimulator comes on. This has nevertheless been successfully addressed in parallel design, controlled trials comparing high and low stimulation schedules. These have been performed in adults with medically intractable partial seizures, and demonstrated efficacy, safety and good tolerability. Efficacy, both in the controlled trials and in numerous reports arising from the considerable post-marketing experience is modest. Some 30% of patients achieve a 50% seizure reduction after 3 months of treatment, but this proportion progressively increases to about 50% after 18 months. Side-effects comprise: discomfort in the face or neck when the stimulator is activated, coughing, breathlessness on exertion and hoarseness of voice. All are related to intensity of stimulation and rapidly habituate in most subjects. In those patients who respond, a stimulus level can therefore generally be found which is acceptable to the subject. No indication other than refractory partial seizures in adults has been the subject of controlled trials, but post-marketing experience and uncontrolled reports indicate comparable efficacy and safety in a wide range of epilepsies, partial and generalized, idiopathic, cryptogenic, or symptomatic, in patients of all ages.
Seizure 2000 Apr
PMID:Vagus nerve stimulation for epilepsy: a review. 1077 11

Acute viral myocarditis is an uncommon but potentially fatal illness in children. Patients with myocarditis may present with nonspecific symptoms or atypical findings that make diagnosis in the emergency department difficult. We describe a previously healthy 14-month-old child with difficulty breathing and a tonic-clonic seizure who was subsequently found to have ECG changes and cardiac marker elevation consistent with acute myocardial infarction. The patient was immediately transferred from our community hospital ED to our tertiary care children's hospital. Shortly after admission, the patient developed intractable nonperfusing ventricular arrhythmias necessitating extracorporeal membrane oxygenation. Cardiac function did not recover, and the patient required heart transplantation before cessation of bypass. Serology and anatomic pathology confirmed coxsackievirus B myocarditis. This case illustrates (1) the nonspecific presentation of myocarditis as dyspnea and seizure, (2) the manner in which myocarditis can mimic myocardial infarction, and (3) the importance of early diagnosis in the ED and transfer to a tertiary care facility.
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PMID:Viral myocarditis presenting with seizure and electrocardiographic findings of acute myocardial infarction in a 14-month-old child. 1082 77

During the period from 1984 to 1997, 85 bacterial meningitis neonates with positive cerebrospinal fluid cultures were treated. The ages of these patients ranged from 1 to 28 days. The male to female ratio was 1.7 to 1. The most common causative agent was group B beta-hemolytic streptococci (GBS, 31.8%), followed by Escherichia coli (20%), Proteus mirabilis (7.1%), Enterobacter cloacae (5.9%), other streptococci excluding Streptococcus pneumoniae (5.9%), Chryseobacterium meningosepticum (5.9%), enterococci (4.7%), and Klebsiella pneumoniae (3.5%). Among the 85 patients treated, 51 (60%) were younger than 7 days old. Among them, dyspnea was the most common clinical manifestation. In contrast, fever and diarrhea were seen more frequently in neonates with late onset of disease (after seven days of age). Ampicillin and cefotaxime were the most commonly used antibiotics. The most frequently encountered complications were hydrocephalus and seizures. Since 1991, GBS has overtaken E. coli as the leading cause of neonatal bacterial meningitis. This was accompanied by a fall in the mortality rate, but a sustained high incidence of complications and sequelae. The results of this study highlight the importance of developing strategies to prevent group B streptococcal infection.
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PMID:Characteristics of neonatal bacterial meningitis in a teaching hospital in Taiwan from 1984-1997. 1091 79

Hypocalcemia is a relatively uncommon reversible cause of congestive heart failure. There are a few reports of hypocalcemic children who developed congestive heart failure associated with hypoparathyroidism. In all these patients, however, cardiac failure did not occur before the age of nine years. In addition, other striking noncardial manifestations of hypoparathyroidism, e.g., convulsive seizures, had been present prior to cardiac symptoms. We report on a 3.7 year old girl with mitral insufficiency and severe cardiac failure due to hypocalcemia secondary to familial hypoparathyroidism. The infant's mother was suffering from idiopathic hypoparathyroidism, but her own history lacked any evidence for parathyroid hormone deficiency. On admission, she presented with fatigue, dyspnea, and pedal edema. Liver edge was palpable 4 cm below the right costal margin, and a 3/6 systolic murmur was heard. A chest x-ray showed cardiac enlargement; electrocardiogram demonstrated a prolonged QTc interval of 0.46 s. The echocardiography revealed a cleft in the mitral valve with mitral insufficiency and markedly reduced contractility of the left ventricle. Laboratory studies demonstrated a low total serum calcium level of 1.3 mmol/l; serum magnesium level was slightly decreased (0.5 mmol/l), and parathyroid hormone level was not detectable. Partial monosomy of chromosome 22 was excluded. Ophthalmological examination, audiometry, and renal ultrasonogram were normal. Oral calcium supplementation and anticongestive therapy with metildigoxin, furosemid, and captopril was initiated but no improvement of the heart failure occurred. However, normalization of serum calcium level by calcium infusions caused prompt clearing of the clinical symptoms, complete normalization of liver size, reduction of cardiac enlargement (thoracic ratio decreased from 0.68 to 0.57), and marked improvement in contractility (left ventricular shortening fraction increased from 21% to 34%). The QTc interval decreased to 0.39 s. The successful treatment following normalization of serum calcium level proved the superiority of hypocalcemia over mitral valve insufficiency in the etiology of the cardiac failure. To our knowledge, this is the first report of congestive heart failure due to hypocalcemia as the first manifestation of hypoparathyroidism in childhood. Hypocalcemia should be kept in mind in any congestive heart failure in children with or without underlying cardiac malformation.
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PMID:[Hypocalcemia-induced heart failure as the initial symptom of hypoparathyroidism]. 1102 Dec 71

Ramaria flavo-brunnescens collected in autumn from 1990 to 1994 was orally administered to 11 sheep. These animals were dosed with 100-430 g/kg bw administered over 3-13 d. Six sheep showed clinical signs and 4 of them died. The mininum toxic dose was of 150 g/kg bw. Clinical signs were anorexia, hyperthermia, dyspnea, polyuria, ataxy, muscle tremors and seizures. The eyes had hyperemia of the sclera and, in some cases, hemorrhages of the anterior chamber or corneal opacity. Sheep dosed with higher doses had ulcerations of the tongue and necrotic lesions in the hooves. The main histologic lesions of the feet and tongue were miopachynsis and endotelial degeneration followed by degeneration, necrosis and ulceration of the epithelium. Hemorrhages of the anterior chamber, and severe congestion and hemorrhages of the iris, ciliary body and process were observed in the eyes. Congestion and perivascular hemorrhages occurred in the central nervous system. The similarity of clinical signs and pathologic lesions induced by R flavo-brunnescens and those caused by ergotism in cattle and sheep suggests the presence ofa vasoactive constrictive substance in the mushroom. Fresh R flavo-brunnescens dosed in autumn 1993 was not toxic at doses of 200-400 g/kg demonstrating variations in the toxicity of the mushroom from year to year.
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PMID:Experimental intoxication by the mushroom Ramaria flavo-brunnescens in sheep. 1111 35

Pulmonary oedema with severe, dramatic course following CNS injury was termed neurogenic pulmonary oedema (NPO). NPO was mainly described as a consequence of grand mal seizures, subarachnoid bleeding, intracranial bleeding or head injury. However, the pathogenesis of NPO is not entirely clear yet. In the majority of cases, early or classic symptoms of pulmonary oedema are evident from several minutes up to several hours after CNS damage. Dyspnoea, chest pain, bloody expectoration are observed shortly after consciousness disorders, although NPO may occasionally be diagnosed on the basis of chest x-ray in patients with no clinical symptoms. Tachypnoea, tachycardia, rales without any changes in cardiac system are usually observed during physical examination. The ailments withdraw quickly in the majority of patients, who may require oxygen therapy at most. NPO has been well-known in adults, but our knowledge of its occurrence in children is still rather sparse. The current work presents a case of a 13-year-old boy with pulmonary oedema as a post-seizure complication.
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PMID:Neurogenic pulmonary oedema in a 13-year-old boy in the course of symptomatic epilepsy--case report. 1120 46

Specific recommendations on how to deal with drug overdoses and how to identify an individual who has overdosed are provided. Some signs of overdose are pallor, limpness, difficulty breathing, foaming at the mouth, vomiting and seizures. An overdose may be fatal. If a person is overdosing, check the person's pulse and respiration and try to revive him by using cold water on the face. If possible, get them up and walking and try to keep them talking. It may be necessary to call an ambulance. Steps not to take are listed. Finally, information about needle exchange programs is provided.
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PMID:[Drug overdoses: how to identify them and what to do about them]. 1136 31


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