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

Shock, seizures, cardiac arrhythmias, and respiratory and cardiac arrests developed in a patient who ingested 8.5 g of theophylline. Her condition improved and her serum theophylline concentration decreased from 170 to 20 mg/ml during six hours of charcoal hemoperfusion. Theophylline was removed from the serum by the uncoated charcoal column, as shown by an extraction efficiency approaching 100%. The maximum charcoal clearance of theophylline was 163 ml/kg/hr. The average endogenous theophylline clearance in adults is 50 ml/kg/hr and that achieved with hemodialysis is only 24.3 ml/kg/hr. Uncoated charcoal efficiently removes theophylline from the serum; charcoal hemoperfusion should be considered in severe theophylline toxic reactions.
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PMID:Massive theophylline overdose. Rapid elimination by charcoal hemoperfusion. 9 82

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

Aminophylline, 285.7 +/- 2.19 mg/kg infused intravenously in unanaesthetized rats produced onset of seizures within 3.2 +/- 0.99 minutes. Seizures were repetitive and death occurred in 10.5 +/- 1.75 minutes. Pretreatment of rats with carbamazepine, sodium valproate and diazepam at doses that prevented electroshock induced seizures were effective in significantly postponing seizures and death, but did not reduce mortality. Concomitant EEG studies in aminophylline infused rats showed that cortical excitability evidenced by initial cortical spiking occurred at 42 secs and polyspiking at 165 seconds. Following diazepam, the initial cortical spike was delayed 50 fold, appearing after 36 minutes. Antiepileptic drugs and EEG monitoring may prove useful in patients with status asthmaticus receiving intravenous aminophylline.
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PMID:Antiepileptic drugs delay the onset of seizures induced by aminophylline in conscious rats. 159 41

The patient with theophylline overdose commonly presents with gastrointestinal, cardiovascular, neurologic, and electrolyte abnormalities. Respiratory alkalosis is the most common acid-base alteration, but mild metabolic acidosis has been reported. Two cases of severe lactic acidosis (pH 6.67 and 6.63) in patients without hypoxemia, shock, or prolonged seizure activity are reported. Possible causative mechanisms and aspects of therapy are discussed. Theophylline toxicity should be considered when an unconscious patient with concurrent severe metabolic acidosis presents to the emergency department.
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PMID:Severe lactic acidosis following theophylline overdose. 165 19

Theophylline overdoses are frequent conditions that may require emergency treatment. Clinical features common to severe theophylline toxicity include nausea and vomiting, tachydysrhythmias, metabolic disturbances, seizures, and cardiovascular collapse. Several reports have described these manifestations and their treatments. We report the case of a patient suffering from an acute, intentional theophylline overdose who exhibited the classic features of a toxic ingestion and describe the first reported use of IV esmolol in the treatment of accompanying cardiovascular manifestations.
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PMID:Acute theophylline toxicity and the use of esmolol to reverse cardiovascular instability. 197 2

Focal injection of 2-chloroadenosine into the substantia nigra protects Sprague-Dawley rats against electroshock seizures (50 mA. 60 Hz, 0.2 s) and genetically epilepsy prone rats against audiogenic seizures. 2-Chloroadenosine infusion into the substantia nigra pars reticulata provided significant protection against electroshock seizures (1.66, 8.33 and 25 nmol) and audiogenic seizures (66, 331 pmol and 1.66 nmol). High doses of 2-chloroadenosine injected into the substantia nigra pars compacta resulted in a similar suppression of electroshock seizure activity (8.33 nmol) and audiogenic seizures (1.66 nmol). No anticonvulsant activity was observed when 2-chloroadenosine was infused into the entopeduncolar nucleus. Lower doses of 2-chloroadenosine provided significant protection against audiogenic seizures (66 and 331 pmol) when injected into the inferior colliculus. Aminophylline antagonised these effects, indicating that purinergic mechanisms are involved in both audiogenic and electroshock seizures. In addition, the similarity of these effects to those elicited by excitatory amino acid antagonists in the inferior colliculus and substantia nigra pars reticulata is consistent with 2-chloroadenosine acting by reducing excitatory transmission.
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PMID:Anticonvulsant action of 2-chloroadenosine injected focally into the inferior colliculus and substantia nigra. 206 May 98

H2-antagonists such as cimetidine and ranitidine are metabolized by cytochrome P-450. In this way they may interfere with theophylline metabolism. Cimetidine is known to have this effect and frequently to induce a theophylline toxic effect, while data concerning ranitidine are more uncertain. In this paper, we report the case of a 67-year-old woman with non-insulin dependent diabetes. She was taking aminophylline for respiratory failure and after ranitidine infusion exhibited generalized convulsions. Theophylline values which were monitored within the therapeutic range, increased toxic levels after ranitidine therapy and epileptic episodes. The increase in theophylline levels was associated with a further reduction in the clearance rate of the bronchodilator. We think that ranitidine may combine with other clinical factors known to reduce theophylline metabolism mainly in the elderly and severely ill patients. Theophylline-induced seizures may occur when theophylline serum levels are slightly above the therapeutic range, as in our case report.
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PMID:Seizures during concomitant treatment with theophylline and ranitidine: a case report. 209 63

The mechanism of action of aminophylline in prolonging seizures was tested in amygdala-kindled rats. Aminophylline prolonged the afterdischarge duration of kindled seizures. This seizure-prolonging action of aminophylline was strongly antagonized by the adenosine A1 agonist cyclohexyladenosine and partially antagonized by the benzodiazepine partial agonist RO 15-1788. However, the specific benzodiazepine antagonist CGS 8216 did not affect the seizure-prolonging action of aminophylline. Also, the potent anticonvulsant effect of diazepam on kindled seizures, which was completely antagonized by CGS 8216, was unaffected by aminophylline. Furthermore, a range of benzodiazepine inverse agonists, GABA antagonists, phosphodiesterase inhibitors and xanthines did not prolong afterdischarge durations. These results demonstrate that the seizure-prolonging action of aminophylline is due to block of A1 adenosine receptors since it is prevented by adenosine A1 agonists.
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PMID:Adenosine receptor antagonism accounts for the seizure-prolonging effects of aminophylline. 221 1

Hippocampal and neocortical blood flows and tissue pO2 were investigated by mass spectrometry in unanaesthetized spontaneously breathing rats during kainic acid-induced seizures to determine whether adenosine is involved in the coupling of cerebral blood flow to metabolism during enhanced metabolic demand. The possible involvement of adenosine in the neuronal damage induced by seizures was also analyzed. The intrinsic effects of theophylline and the duration of the adenosine receptor blockade by this xanthine were first tested in 8 rats. Two groups of rats were then compared: one (n = 6) received kainic acid, and the other (n = 10) theophylline 15 min prior to kainic acid administration. An additional group of 10 rats was taken for classical histology 48 h after kainic acid treatment. Theophylline significantly reduced the hyperaemia observed during seizures, prevented any tissue hyperoxia and enhanced brain damage. This strongly suggests that adenosine is partly responsible for the increase in cerebral blood flow during kainic acid-induced seizures and has neuroprotective properties.
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PMID:Theophylline reduces cerebral hyperaemia and enhances brain damage induced by seizures. 233 48

Theophylline overdosage can cause life-threatening symptoms, that include seizures and cardiac arrhythmias, and can be fatal. Neither the onset of toxicity nor the severity of symptoms is well predicted by serum theophylline concentrations. Since depressed vitamin B6 plasma levels can occur in patients receiving theophylline, we explored a B6-theophylline interaction in a rabbit model. Administration of theophylline preparations intraperitoneally (aminophylline) or orally (sustained release anhydrous theophylline) resulted in a 47% depression of plasma pyridoxal 5'-phosphate (PLP) levels. The 87% increase in PLP with pyridoxine administration was only 18% when aminophylline was also given. The mechanism of the theophylline-B6 interaction is obscure. Ethylenediamine in some theophylline preparations binds directly to PLP, potentially increasing the less direct theophylline effect. Pyridoxine supplementation resulted in higher average PLP levels but did not prevent death in animals with profoundly low PLP levels. If these data apply to humans, B6 deficiency may contribute to chronic theophylline toxicity; however, pyridoxine administration in the dosage used may not prevent toxicity. Larger doses may prove beneficial after further investigation.
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PMID:Depression of vitamin B6 levels due to theophylline. 236 33


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