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)

We measured total creatine kinase (CK), CK-MB isoenzyme, and the MB isoforms in 202 serum and plasma samples from nine groups of patients and normal individuals: 39 with acute myocardial infarction (MI), divided according to time between the onset of chest pain and blood collection (1-6 h, 7-12 h, and 13-48 h); 26 with chest pain for whom an MI was ruled out, sampled at admission; 17 undergoing bypass surgery or cardiac catheterization, sampled within 6 h after either procedure; 17 with acute skeletal muscle injury, sampled within 8 h after injury; 30 marathon runners immediately after a race; 17 runners and other athletes > 12 h after training or a race; 12 with cerebral injury or seizures, sampled at admission; 8 with closed head injury, sampled at admission; and 38 normal subjects. CK-MB (relative index) and MB isoforms (MB2/MB1) were respectively increased in 15% and 75% of MI patients 1-6 h after onset, 94% and 94% after 7-12 h, and 88% and 8% after 12 h, and in 87% and 82% of cardiac surgery patients. MB isoforms were increased in most patients with acute skeletal muscle trauma and in subjects examined after exercise, but were within normal limits in patients for whom MI was ruled out, patients with cerebral trauma, and normal individuals. The relative index of MB/total CK was normal in essentially all individuals in the last groups, including those with acute skeletal muscle trauma. We concluded that the CK-MB isoform ratio is increased in both acute skeletal muscle injury and MI. The isoform ratio is most useful for distinguishing recent from old (> 12 h) injury.
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PMID:Creatine kinase MB isoforms in patients with skeletal muscle injury: ramifications for early detection of acute myocardial infarction. 145 74

We examined 348 patients who underwent thrombolytic treatment for acute myocardial infarction. Nine patients (2.58%) developed neurological complications related directly or indirectly to this procedure. Cerebral hemorrhage occurred in 3 patients; 2 patients had transient ischemic attacks, 1 had syncope, another had psychomotor agitation and 2 patients presented seizures during the infusion of the thrombolytic agent, without hemodynamic abnormalities. This latter feature had never been described before.
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PMID:Neurological complications after thrombolytic treatment for acute myocardial infarction: emphasis on unprecedented manifestations. 162 95

The toxicities of cocaine are far-ranging. They include sudden death, acute medical and psychiatric illness, infectious complications, reproductive disturbances, trauma, criminal activities and societal disruption, including child neglect and abuse and lost job productivity. This chapter focuses on the medical complications. Medical complications in general reflect the intense sympathomimetic activities of cocaine ('sympathetic neural storm'). Psychiatric complications include acute anxiety or panic and paranoid psychosis. Cardiovascular complications include arrhythmias and sudden death, acute myocardial infarction, myocarditis, dissecting aneurysm and bowel infarction. Neurological complications include seizure, intracerebral haemorrhage and brain injury due to hyperthermia and/or seizures, and headache. The incidence of medical complications has been estimated using two databases collected prospectively in the United States. In 1989 and 1990 cocaine ranked first in total encounters, major medical complications and drug-related deaths. An attempt was made to assess the intrinsic toxicity of cocaine by computing the incidence of adverse health outcomes per population of drug abusers. Rates of emergency department visits and deaths were 15.1 and 0.5 respectively, per 1000 persons using drugs in the past year. The magnitude of the cocaine problem, while considerable, is relatively small compared with that of cigarette smoking or alcohol abuse.
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PMID:How toxic is cocaine? 163 9

21 patients with acute myocardial infarction and ventricular arrhythmia of Lown class II-IIIB of acute onset received a short infusion of (50 mg/5 min) ajmaline (Gilurytmal). 6 of the patients had normal kidney and liver function (Group 1), 4 patients had acute renal failure and hemodialysis treatment (Group 2), 4 patients had impaired hepatic function (Group 3), 3 patients had cardiogenic shock (Group 4), and 4 patients had been pretreated with phenobarbital for seizures for at least 5 days (Group 5). A distribution half-life of 6 +/- 1 min and an elimination half-life of 95 +/- 6 min was determined in Group 1. The total plasma clearance was significantly lower in patients with impaired liver or cardiac function and significantly higher in Group 5, whereas impaired renal function did not affect total plasma clearance. After short infusion, ventricular arrhythmia of Lown II-IIIB completely disappeared for at least 16 to 36 min (mean: 19 min), which was associated with an ajmaline plasma level of 0.1-0.45 micrograms/ml. Additionally, steady-state plasma levels of ajmaline were determined after continuous infusion of 10-50 mg/h to 16 patients (Group 6) with ventricular arrhythmia of acute onset (Lown class IVA-V). Ventricular arrhythmia completely disappeared or at least changed to lower Lown classes at ajmaline plasma levels of 0.4-2.0 micrograms/ml. The ajmaline plasma protein binding was 76 +/- 9%. Ajmaline had a special affinity to alpha 1-acid glycoprotein.
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PMID:Pharmacokinetics and antiarrhythmic efficacy of intravenous ajmaline in ventricular arrhythmia of acute onset. 259 21

The increasingly widespread use of cocaine in the United States has been accompanied and perhaps exacerbated by the misconception that the drug is not associated with serious medical complications. In particular, the potential for cocaine to precipitate life-threatening cardiac events needs to be reemphasized. We report the clinical and pathological findings in seven people in whom nonintravenous "recreational" use of cocaine was temporally related to acute myocardial infarction, ventricular tachycardia and fibrillation, myocarditis, sudden death, or a combination of these events. We also review data on 19 previously reported cases of cocaine-related cardiovascular disorders. Analysis of all 26 patients indicated the following findings: the cardiac consequences of cocaine abuse are not unique to parenteral use of the drug, since nearly all the patients took the drug intranasally; underlying heart disease is not a prerequisite for cocaine-related cardiac disorders; seizure activity, a well-documented noncardiac complication of cocaine abuse, is neither a prerequisite for, nor an accompanying feature of, cardiac toxicity of cocaine; and the cardiac consequences of cocaine are not limited to massive doses of the drug. Although the pathogenesis of cardiac toxicity of cocaine remains incompletely defined, available circumstantial evidence suggests that cocaine has medical consequences that are equal in importance to its well-documented psychosocial consequences.
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PMID:Acute cardiac events temporally related to cocaine abuse. 378 95

Recovery from prolonged cold water submersion is well documented in children but rare in adults. In the few adult cases reported, significant body cooling occurred (rectal temperature ranging from 22 degrees to 32 degrees C) and the victims were relatively young (< 40 years). We report a case of a 62-year-old man who was submersed in 2 degrees to 3 degrees C water for 15 minutes (time from initial submersion to intubation = 22 minutes). At the time of rescue, he had no vital signs, received prehospital Advanced Life Support, and was transported to hospital. On arrival at hospital, the patient remained in full cardiopulmonary arrest with an agonal ECG rhythm and had an initial pH of 6.77. Initial rectal temperature was near normal (36 degrees C) but subsequently dropped to 33 degrees C. The patient was resuscitated, rewarmed by forced-air warming, and treated for acute myocardial infarction, pulmonary edema, and generalized seizures. He was discharged after 27 days with minor neurologic abnormalities. Given the near-normal initial rectal temperature, preferential brain cooling may have been at least partially responsible for the positive neurologic outcome.
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PMID:Recovery of a 62-year-old man from prolonged cold water submersion. 943 57

Focal deficits, seizures and epilepsy, altered consciousness, and disturbed behaviours can complicate heart diseases and their medical treatment as well as cardiological procedures and cardiac surgery. Neurological complications of common cardiac conditions are discussed. These cardiac conditions are acute myocardial infarction and ischaemic heart disease, atrial fibrillation and cardiac arrhythmias, congestive heart failure, valvular heart diseases, infective endocarditis, congenital heart disease, invasive cardiological procedures and cardiac surgery. As transient ischaemic attack, stroke, seizures and epilepsy are the most common neurological complications, their management is also reviewed. Precautions should be taken to prevent neurological complications of heart disease. Regular surveillance for these complications would allow early diagnosis and initiation of appropriate management.
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PMID:Neurological complications of heart disease. 948 97

To explore the natural history of critically ill patients with acute renal failure due to acute tubular necrosis, we evaluated 256 patients enrolled in the placebo arm of a randomized clinical trial. Death and the composite outcome, death or the provision of dialysis, were determined with follow-up to 60 d. The relative risks (RR) and 95% confidence intervals (95% CI) associated with routinely available demographic, clinical, and laboratory variables were estimated using proportional hazards regression. Ninety-three (36%) deaths were documented; an additional 52 (20%) patients who survived received dialysis. Predictors of mortality included male gender (RR, 2.01; 95% CI, 1.21 to 3.36), oliguria (RR, 2.25; 95% CI, 1.43 to 3.55), mechanical ventilation (RR, 1.86; 95% CI, 1.18 to 2.93), acute myocardial infarction (RR, 3.14; 95% CI, 1.85 to 5.31), acute stroke or seizure (RR, 3.08; 95% CI, 1.56 to 6.06), chronic immunosuppression (RR, 2.37; 95% CI, 1.16 to 4.88), hyperbilirubinemia (RR, 1.06; 95% CI, 1.03 to 1.08 per 1 mg/dl increase in total bilirubin) and metabolic acidosis (RR, 0.95; 95% CI, 0.90 to 0.99 per 1 mEq/L increase in serum bicarbonate concentration). Predictors of death or the provision of dialysis were oliguria (RR, 5.95; 95% CI, 3.96 to 8.95), mechanical ventilation (RR, 1.53; 95% CI, 1.07 to 2.21), acute myocardial infarction (RR, 1.95; 95% CI, 1.24 to 3.07), arrhythmia (RR, 1.51; 95% CI, 1.04 to 2.19), and hypoalbuminemia (RR, 0.56; 95% CI, 0.42 to 0.74 per 1 g/dl increase in serum albumin concentration). Neither mortality nor the provision of dialysis was related to patient age. These observations can be used to estimate risk early in the course of acute tubular necrosis. Furthermore, these and related models may be used to adjust for case-mix variation in quality improvement efforts, and to objectively stratify patients in future intervention trials aimed at favorably altering the course of hospital-acquired acute renal failure.
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PMID:Predictors of mortality and the provision of dialysis in patients with acute tubular necrosis. The Auriculin Anaritide Acute Renal Failure Study Group. 955 72

We report a 45-year-old man with monocytosis and right hemiparesis. The patient suffered from an acute myocardial infarction from which he recovered completely when he was 42 years old. One year prior to his death, he was found to have increase in monocyte count (35.5% of leukocytes) in peripheral blood and splenomegaly; he was admitted to the hematology service of our hospital. He was diagnosed as having chronic myelomonocytic leukemia after bone marrow examination. He was treated with radiation therapy with improvement in splenomegaly. In May of 1995, he had fever, anemia, and thrombocytopenia for which he needed daily blood transfusion. In November of 1995, he had an onset of weakness in his right hand, and neurologic consultation was asked for in November 27, 1995. Neurologic examination revealed a chronically ill japanese man in no acute distress. He was alert and not demented. Higher cerebral functions were intact. Cranial nerve examination revealed right facial paresis of the central type. Motor-wise, he was right hemiparetic. Generalized muscle wasting was noted apparently due to the chronic debilitating disease. Deep tendon reflexes were within normal range in the right upper extremity, but were diminished in other areas. Sensation was intact, and no meningeal signs were noted. Pertinent laboratory findings were as follows: Hb 8 g/dl, RBC 238 x 10(4)/microliter, WBC 2,900/microliter (band 1.0%, seg 18.5%, lym 28.0%, mono 44.0%, Baso 2.5%), Plt 13 x 10(4)/microliter, PT 16.6"/10.9", APTT 44.7"/35.0". CSF contained 87 mg/dl of protein, 155 mg/dl of glucose and 2 mononuclear cells/microliter. Bone marrow was slightly hypercellular with mild increase in blast forms. No chromosome abnormality was found. CT and MRI revealed a large mass in the left fronto-parietal region and the meninges showed marked thickening with enhancement after gadolinium-DTPA in MRI. The patient was treated with glycerol and steroid, but the subsequent course was complicated by a seizure, agitation, and pneumonia. He died from respiratory failure on January 13, 1996. The patient was discussed in a neurologic CPC and the chief discussant arrived at the conclusion that the patient had chronic myelomonocytic leukemia with infiltration of leukemic cells into meninges and the parenchyme of the cerebrum. Thickening of the dura was thought to be in part a reaction to the subdural hematoma as well as to leukemic cells along the meninges. Postmortem examination revealed hypercellular bone marrow with increase in monocytic cells (more than 20%). The lungs showed pneumonia with scattered old tuberculous lesions. The heart showed an old myocardial infarction in the posterior wall of the left ventricle. The brain showed an old chronic subdural hematoma in the left fronto-temporal region and a cystic mass lesion in the left frontoparietal region. The mass was hypercellular and most of them were monocytes. The dura mater showed reactive thickening without leukemic cell infiltration. It was concluded that this patient had chronic myelomonocytic leukemia with a formation of leukemic mass in the brain. Pathologists thought that the mass was a hematogenous spread. It is rare for chronic myelomonocytic leukemia to form a mass lesion in the brain.
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PMID:[A 45-year-old man with peripheral monocytosis and right hemiparesis]. 962 75

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


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