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

Anticholinergics (in particular, ipratropium bromide [Atrovent]) are first-line therapy in patients with chronic obstructive pulmonary disease (COPD). Although more studies are needed to support the use of combination therapy, adding an inhaled beta agonist to the therapeutic regimen is reasonable in patients who remain symptomatic and need quick relief. Patients frequently receive inadequate amounts of drug with standard doses delivered by metered-dose inhalers, often as the result of improper technique, so symptomatic patients may require higher doses. Caution is recommended when the dose of inhaled sympathomimetics is increased in COPD patients with ischemic heart disease or tachyarrhythmias. The addition of an oral sympathomimetic is seldom necessary. Theophylline may be considered in outpatients who remain symptomatic despite their use of inhaled bronchodilators, but heart disease, seizure disorders, and gastroesophageal reflux are contraindications. Corticosteroid therapy remains controversial but can be helpful in patients who still have severe disease despite maximum bronchodilator therapy. Antibiotics can be of benefit in COPD patients undergoing an exacerbation who have increasing dyspnea, cough, and phlegm production.
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PMID:Drug treatment of COPD. Controversies about agents and how to deliver them. 134 54

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

We present two cases of severe headache associated with the use of bromocriptine for lactation suppression in otherwise healthy women. In each case, the additional use of a therapeutic sympathomimetic agent resulted in extreme worsening of symptoms with development of hypertension and life-threatening complications (ventricular tachycardia and cardiac dysfunction in one case, seizures and cerebral vasospasm in the other). Sympathomimetics in combination with bromocriptine in patients with a bromocriptine-associated headache during the puerperium may be dangerous.
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PMID:Bromocriptine-associated headache: possible life-threatening sympathomimetic interaction. 192 36

Cocaine is a potent sympathomimetic drug, and has been implicated as a causative factor in cardiac seizures. However, little is known about the effect of the drug on myocardial substrate utilization. In the present study, rats were injected intravenously with saline solution or one of three doses of cocaine-HCl (1.25, 5.0, 10.0 mg/kg) and subsequently rested or exercised (22 m/min at 15% grade) for 20 minutes. Hearts were removed and frozen within 30 seconds after the injection of anesthetic and within 10 seconds after opening the thoracic cavity. The mean values for resting glycogen content ranged from 24.9 to 27.0 mumol/g, and for glucose-6-phosphate, from 0.27 to 0.30 mumol/g across groups. These values were unaffected by cocaine or exercise. We conclude, based on the conditions of this study, that cocaine has no direct or indirect effect on glycogen storage of the myocardium at rest or during exercise.
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PMID:Cocaine does not alter cardiac glycogen content at rest or during exercise. 281 77

The influence of various substances modulating the activity of central noradrenergic, serotonergic or dopaminergic neurotransmission systems on the anticonvulsant effectiveness of phenobarbital (phenytoin, carbamazepine) was investigated in mice using the maximal electroshock seizure test (MES). The results demonstrated that especially the noradrenergic system might play a predominant role in modulating the efficiency of the standard antiepileptics tested. In general, pharmacological stimulation with different sympathomimetic drugs (e.g. methamphetamine, maprotiline, tranylcypromine, yohimbine) increased the anticonvulsant activity significantly. Conversely, pharmacological suppression of the noradrenergic system (e.g. 6-OHDA, phenoxybenzamine) reduced the activity of the antiepileptics. In contrast, some beta-receptor blockers with local anesthetic properties (e.g. propranolol, alprenolol, pindolol) were also able to enhance the protective effect of phenobarbital in higher concentrations. The influence of manipulations of serotonergic mechanisms was not so pronounced. However, substances such as 5-HTP, clomipramine, citalopram, zimelidine, showed also additive anticonvulsive effects. On the other hand, the dopaminergic system seemed to exert no significant influence in this respect. These findings give further support to the view that the noradrenergic system may play a remarkable role via the inhibitory function of noradrenaline in the CNS in suppression of epileptic activity and reveal also interesting aspects for a possible comedication in convulsive disorders.
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PMID:Pharmacological modulation of central monoaminergic systems and influence on the anticonvulsant effectiveness of standard antiepileptics in maximal electroshock seizure. 284 28

Exposure of rats to one injection of cocaine (35 mg/kg, i.p.) or a single four-hour period of immobilization protected them from the virtually instantaneous death but not from the later, seizure-related death seen in untreated controls following administration of the local anesthetic, tetracaine, 1-4 weeks later. These data suggest that when appropriately timed, strong sympathomimetic stimulation--whether generated by an environmental stressor or a drug--can provide long-lasting protection against the sudden cardiac death potential of local anesthetics. As such, they provide a means for understanding why the incidence of sudden cardiac arrest from one such agent--cocaine itself--is not higher and suggest that an individual's stress history may play a key role in determining vulnerability to the cardiotoxic effect of this compound.
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PMID:A single exposure to cocaine or immobilization stress provides extremely long-lasting, selective protection against sudden cardiac death from tetracaine. 291 99

'Designer drugs' are substances intended for recreational use which are derivatives of approved drugs so as to circumvent existing legal restrictions. The term as popularised by the lay press lacks precision. Contrary to the popular belief that 'designer drugs' are original creations, the majority of these agents are 'borrowed' from legitimate pharmaceutical research. They merely represent the most recent developments in the evolution of mind-altering chemicals. The most extensively studied class of psychoactive compounds is the phenylethylamines (mescaline analogues). This class includes catecholamines, therapeutic agents and numerous illicit derivatives. Subtle alterations of the phenylethylamine molecule give rise to a spectrum of pharmacological properties ranging from pure sympathomimetic stimulation to primarily psychoactive effects. Although most of these compounds are only of historical interest, amphetamine, methamphetamine, 3,4-methylenedioxyamphetamine (MDA), and 3,4-methylenedioxymethamphetamine (MDMA) continue to be used recreationally. Many deaths have been ascribed to this class of compounds. In overdose the differences between these compounds blur and the clinical presentation is similar to that of amphetamine overdose characterised by tachycardia, hypertension, hyperthermia, diaphoresis, mydriasis, agitation, muscle rigidity, and hyper-reflexia. Death usually results from arrhythmias, hyperthermia or intracerebral haemorrhage. Treatment is aggressive and supportive with careful attention to temperature, blood pressure and seizure control. Synthetic opioid derivatives, which represent the second major class of 'designer drugs', are derivatives of fentanyl (e.g. alpha-methylfentanyl, 3-methylfentanyl) or pethidine (meperidine) and are extremely potent compounds responsible for numerous overdose deaths. Attempts to synthesise pethidine have resulted in the accidental production of MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), a compound which is metabolised in the brain by the monoamine oxidase system to a toxic intermediate (MPP+) which selectively destroys the sustantia nigra, resulting in the rapid onset of severe Parkinsonian symptoms. Naloxone will antagonise the opiate effects of this drug class, although high doses may be required. Arylhexylamines constitute the third class of 'designer drugs'. The predominant member of this class is phencyclidine (PCP), a derivative of the anaesthetic ketamine. This unique class of psychoactive agents exhibits broad and complex pharmacological effects.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:'Designer drugs'. A problem in clinical toxicology. 328 24

Antiasthma drug development, for the most part, seems based on three classes of therapeutic agents. Many new sympathomimetic and corticosteroid drugs with increased specificity for the lung have been introduced. The third class of drugs, the xanthines, is still best represented by the prototype drug theophylline. After a brief review of the chemical history of antiasthma xanthines (the first limited attempts to develop novel derivatives 30 to 40 years ago), and some recent structure-activity findings, this article discusses the pharmacology of a selected xanthine derivative, enprofylline (3-propylxanthine). In various experimental systems and in patients, enprofylline shares antiasthmatic effects with theophylline; however, enprofylline is the more potent of the two (greater than 1 to 2 micrograms/ml plasma are effective concentrations of enprofylline). At present, enprofylline, which lacks diaphragmatic and central nervous system stimulatory actions, has been shown to be at least as clinically efficacious as theophylline in obstructive lung disease. Further work is needed to elucidate the target cells and mechanism(s) of action involved in bronchodilatory and anti-inflammatory effects of the xanthines. Growing numbers of animal and human pharmacologic studies show that enprofylline is without many of theophylline's extrapulmonary effects--in particular the excitatory ones. Perhaps most significantly, enprofylline does not produce central nervous system stimulant behavioral effects, including seizures. If and when enprofylline becomes available as an alternative drug, increased attention will probably be focused on the significance of other theophylline actions (gastric secretion, release of free fatty acids, vasoconstriction, diuresis, etc.) that are not shared by enprofylline.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Development of safer xanthine drugs for treatment of obstructive airways disease. 353 62

A historical cohort study was undertaken to determine the risk of epilepsy in a population of 18 newborns with neonatal hypoglycemia due to insulin excess. Follow-up was 3 years 8 months (range 7 years-1 year 3 months). Insulin excess was associated with maternal diabetes in 13 infants, with an isolated macrosomia in 2 infants, in one case with probable Langerhans hyperplasia, and in 2 newborns only prolonged beta-sympathomimetic therapy was the possible cause of insulin excess. Newborns with anoxia, brain malformation or small for date were excluded. Two newborns had hypoglycemia with epileptic clonic seizures, but only one was later epileptic. In this case, hypoglycemia was severe and persistent (16 hours). Hyperinsulinism was related to Langerhans hyperplasia. CT scan made at ages one and 6 months showed large hypodensity of the frontal and occipital white matter. Visual evoked responses were also abnormal. Visual evoked responses and CT scan normalized at 1 year. In other children, asymptomatic hypoglycemia (n = 11) or symptomatic hypoglycemia without epileptic seizures (n = 5) did not increase the epileptic risk as none of them had epileptic seizure later on. Thus, seizures associated with neonatal hypoglycemia alone seem to increase the epileptic risk with duration and severity of hypoglycemia being also essential prognostic factors.
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PMID:[Neonatal hypoglycemia caused by hyperinsulinism and subsequent epilepsy]. 357 76

Phenylpropanolamine (PPA), a synthetic sympathomimetic that is structurally similar to amphetamine, is available over the counter in anorectics, nasal congestants, and cold preparations. Its prolonged use or overuse has been associated with seizures, intracerebral hemorrhage, neuropsychiatric symptoms, and nonhemorrhagic cerebral infarction. We report the case of a young woman who suffered a cerebral infarction after taking a single oral dose of PPA.
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PMID:Cerebral infarction with a single oral dose of phenylpropanolamine. 382 20


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