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)

Apoplexy of the heart can be responsible for sudden and for recurring instability of cardiac rhythm and conduction, and for the clinical counterparts of syncope and sudden death. Every pathophysiological mechanism which produces cerebral apoplexy has its counterpart in apoplexy of the heart. Among the mechanisms documented are thrombosis, embolism and rupture of those special vessels supplying the sinus node, atrioventicular (A-V) node and His bundle. Apoplexy of the heart can occur either with or without significant or recognizable ventricular myocardial infarction. Acute vascular accidents within the critical centers of cardiac impulse formation and conduction deserve more frequent consideration in the explanation of unusual cases of "epilepsy", of seizure disorders of the elderly, of neurologic manifestations (which may be secondary as well as primary) of systemic diseases such as lupus erythematosus or thrombotic thrombocytopenic purpura, and indeed of every case of otherwise unexplanined syncope or sudded death at any age.
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PMID:De subitaneis mortibus. XXVIII. Apoplexy of the heart. 61 31

A patient with an acute anterior wall myocardial infarction complicated by bilateral bundle branch block and paroxysmal AV block is presented. The following new, uncommon or unreported phenomena were documented: the simultaneous occurrence of phase-3 block in the right bundle branch and phase-4 block in the left bundle branch; the simultaneous occurrence of phase-4 block in both main bundle branches; phase-4 left posterior hemiblock associated with escape beats arising from the injured posterior division of the left bundle branch; supernormal conduction in the right bundle branck and 2:1 right bundle branch block related to supernormality. Most of these changes were, of course, not simultaneous, and their successive appearance was related to day-to-day and sometimes hour-to-hour variations in the degree and quality of the multifascicular injury caused by the infarct. In addition, the actions of several drugs upon automaticity and conduction were tested. The effects of amiodarone, lidocaine and isoproterenol were similar to those previously reported under comparable circumstances. At a moment when the patient had repeated episodes of paroxysmal AV block with severe Adams-Stokes seizures, the administration of a single i.v. dose of 0.25 mg of strophanthin suppressed totally the Adams-Stokes attacks through a significant enhancement of ventricular automaticity. If rapid implantation of an artifical pacemaker is not at hand, strophanthin may be life-saving in patients with acute paroxysmal AV block.
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PMID:Electrophysiologic and pharmacologic studies in a patient with acute myocardial infarction complicated by intraventricular and atrioventricular block. 119 12

In a retrospective survey of mortality among the first 1000 unselected patients referred to the Epilepsy Research Unit at the Western Infirmary in Glasgow between 1985 and 1990, a total of 18 deaths were identified. Three patients had committed suicide and one each had died of status epilepticus in hospital, a subdural haematoma and a myocardial infarction. The remaining 12 deaths (67%) were sudden (median age 32 years; range 22-68 years). Poor seizure control and poor compliance with antiepileptic drug therapy were recorded in only three (25%) of these patients. There was a change in antiepileptic drug regimen in five (28%) in the month before death. Only two (17%) underwent postmortem examination. In nine of the 12 patients dying suddenly, the primary cause of death was not listed as epilepsy but as asphyxia (3), aspiration (2) and one each of ischaemic heart disease, myocardial infarction, asystole and drowning (in the bath). 'Status epilepticus' was assumed to have been responsible for the other three deaths, two of which were unwitnessed. Sudden death in people with epilepsy is an entity of great concern. Appropriate death certification and mandatory postmortem examination are essential to provide a truer picture of this neglected phenomenon.
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PMID:Sudden death in epilepsy: an avoidable outcome? 143 37

Some patients fail to respond to antiepileptic drugs (AEDs) or their response varies over time. Unexpected fluctuations in AED concentrations can cause loss of seizure control or side effects. Recent advances in AED clinical pharmacology have characterized a number of factors that alter AED concentrations. Storage of carbamazepine (CBZ) and phenytoin (PHT) formulations in hot, humid conditions alters the dosage form and reduces bioavailability up to 50%. Diurnal changes in gastrointestinal physiology affect disintegration of valproate (VPA) enteric-coated tablets, reducing nighttime drug concentrations 30 to 40% compared with daytime values. Drug-drug interactions or pathophysiologic conditions (e.g., hypoalbuminemia) may displace AEDs from protein-binding sites reducing total but not unbound drug concentrations decrease. VPA not only displaces PHT from protein-binding sites but inhibits its metabolism, causing a decrease in total concentration and an increase in the unbound concentration, occasionally necessitating a reduction in PHT dosage. Alterations in drug metabolism can cause fluctuations in the concentrations of AEDs and active metabolites. Enzyme inhibitors such as cimetidine or VPA can increase concentrations of both CBZ and CBZ epoxide (CBZE). Enzyme inducers such as ethanol, PHT, CBZ, and phenobarbital accelerate the metabolism of other AEDs. Some forms of physiologic stress increase binding to alpha 1-acid glycoprotein (AAG), which is stimulated within hours of a myocardial infarction or major surgery. Total CBZ and CBZE, both of which bind to AAG, increase over the same period. Stress may also activate hepatic drug metabolism. Unbound PHT clearance increases 7 to 21 days following head trauma, necessitating larger maintenance doses. Age greater than 65 years is associated with decreases in protein binding and drug clearance and longer elimination half-lives. In elderly patients, AED dosage may need to be reduced and the dosing interval extended. Knowledge of these factors permits prospective assessment of risk and the design of treatment plans that minimize fluctuations in response.
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PMID:Pharmacokinetic pitfalls of present antiepileptic medications. 174 71

Intravenous fluorescein angiography is a commonly performed and extraordinarily valuable diagnostic procedure. The frequency of adverse reactions after angiography has varied considerably in previous reports. In a prospective study of 2789 angiographic procedures in 2025 patients, the authors found that the percentage of adverse reactions depended strongly on the patient's angiographic history. Overall, adverse reactions followed 4.8% of the angiographic procedures. These reactions included nausea (2.9%), vomiting (1.2%), flushing/itching/hives (0.5%), and other reactions (dyspnea, syncope, excessive sneezing) (0.2%). No cases of anaphylaxis, myocardial infarction, pulmonary edema, or seizures occurred. The percentage of reactions was 1.8% for patients who had had previous angiography without ever having had an adverse reaction. In contrast, the percentage of reactions was 48.6% for patients who had had an adverse reaction to angiography previously.
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PMID:Frequency of adverse systemic reactions after fluorescein angiography. Results of a prospective study. 189 Dec 25

Cocaine is increasingly used by drug addicts. It is considered harmless, but numerous, varied and often serious complications due to its abuse have been published. Among these, neurological complications are in the forefront. They include generalized or partial epileptic seizures, ischaemic or haemorrhagic cerebral vascular accidents, visual loss caused by optic neuropathy or by retinal artery occlusion, headaches and exacerbation of tics. Infections of the central nervous system are possible via endocarditis or septicaemia of venous or nasal origin. Neurological disorders may also occur as a consequence of a major cardiovascular complication induced by cocaine (myocardial infarction and/or dysrhythmia, aortic dissection). These neurological complications are unpredictable, and they weigh heavily on the functional and sometimes vital prognosis in habitual or occasional cocaine abusers.
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PMID:[Neurologic complications of cocaine abuse]. 214 Nov 59

Carbamazepine is being used more frequently in the U.S. as an initial agent of choice to treat generalized tonic-clonic, mixed, and partial seizures with complex symptomatology. Carbamazepine is extensively metabolized in the liver; however, there is little information available on its pharmacokinetics in patients following surgery or myocardial infarction, or in those with liver disease. We report a case of a patient who attained toxic carbamazepine serum concentrations (ranging from 18.2 to 21.5 micrograms/mL) two days after cardiothoracic surgery and an intraoperative myocardial infarction, and experienced lethargy, diplopia, dysarthria, diaphoresis, and horizontal and downgaze nystagmus. These alterations in serum carbamazepine concentration normalized ten days after surgery. They may have been due to a combination of changes in protein binding and decreased elimination due to altered intrinsic hepatic clearance. With carbamazepine achieving a more prominent place in anticonvulsant therapy, the influence of various procedures and disease processes on the pharmacokinetics and pharmacodynamics of carbamazepine, as well as the clinical consequences of such changes, need further investigation.
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PMID:Toxic carbamazepine concentrations following cardiothoracic surgery and myocardial infarction. 226 Mar 36

Electromechanical dissociation (EMD) is the presenting rhythm in approximately 17% of all prehospital cardiorespiratory arrests. Yet, we know comparatively little about the demographic profile of these patients. The purpose of this study was to review historical and resuscitative parameters to help create a demographic profile. For a 6-year period of time from January 1st, 1980 to December 31st, 1985, 503 adult patients presented to a prehospital system in non-traumatic, nonpoisoned, cardiorespiratory arrest with an initial rhythm of electromechanical dissociation. The overall average response time was 6.1 +/- 3.2 min. Sixty percent of the patients were witnessed arrests and 65% had bystander initiated CPR. Forty-six percent of the patients had a cardiac history: myocardial infarction 13%, CHF 11% and other 21%. Other pertinent past medical history included diabetes 15%, COPD 10% and seizures 3%. The average age was 69.8 +/- 13.7 years. Fifty-seven percent were male. Forty-three percent were on cardiac medication including: digoxin, 24%; nitroglycerin, 12%; potassium supplements, 9%; propranolol, 8%; isordil, 6%; quinidine, 3%; nitropaste, 3%; and other cardiac medications, 15%. One hundred forty-eight (29%) patients developed a pulse at some time during resuscitative efforts, of these 17 (3.4%) patients responded with a pulse immediately after intubation. The mean time of resuscitation to sustaining pulse was 20 +/- 11 min and the mean resuscitation time to sustaining pressure was 22 +/- 11 min. Nineteen percent were successfully resuscitated, defined as a conveyance of a patient with a pulse and a rhythm to an emergency department. Four point four percent were saved, defined as a patient discharged alive from the hospital. Approximately 53% of the successfully resuscitated patients and 45% of the save patients were determined to have a probable respiratory event as the primary etiology of their arrest. This study attempts to provide some insight into the demographic profile of the patients in EMD.
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PMID:Electromechanical dissociation: six years prehospital experience. 254 33

Twenty-nine patients with late-onset epilepsy were followed prospectively for a mean period of 4.9 years; 14 had CT evidence of occult cerebral infarction and 15 had normal scans. The prognosis was similar in the 2 groups; 57% and 53% respectively became seizure-free. One patient in each group had a myocardial infarction and one patient with occult cerebrovascular disease had a stroke. A separate study was made of the prognosis of 24 patients with epilepsy following stroke (mean follow-up 5.9 years). Twelve of 12 patients with seizure onset within 2 weeks of the stroke became seizure-free, compared with 7/12 with more delayed onset. Late-onset epilepsy has a favourable prognosis, and excellent control should be expected if seizures commence within 2 weeks of stroke.
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PMID:The natural history of late-onset epilepsy secondary to vascular disease. 261 79

The chemistry, pharmacology, and pharmacokinetics of cocaine are described, and the medical complications of illicit cocaine use are reviewed. Cocaine is readily absorbed from mucous membranes, the gastrointestinal tract, and the vascular beds of the lungs. Thus there are a number of routes for illicit cocaine administration, with the most popular one being intranasal. The most prevalent problems associated with the use of cocaine appear to be route and dose independent and are cardiovascular in nature; they include myocardial infarction and ischemia, sudden death, cardiac arrhythmias, and hypertension. Seizures, cerebrovascular accidents, hepatotoxicity, rhabdomyolysis, pulmonary complications, and obstetrical complications have also been reported. Gastrointestinal complications and acute toxicity may occur in cocaine smugglers who ingest cocaine-filled packets. Route-dependent complications of cocaine use are also of concern. The mechanism underlying the medical complications has not been fully elucidated but appears to be an extension of the drug's pharmacological properties. The treatment of cocaine-related toxicities is supportive and is based on the organ system affected. Drugs such as propranolol, labetalol, and nitrendipine have been advocated for treating the cardiovascular complications, and measures such as maintaining arterial blood pH, monitoring core body temperature, and diazepam therapy have been used to manage seizures. As the number of case reports of cocaine toxicity increases and the underlying mechanism is conclusively defined, management of the medical complications will improve.
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PMID:Medical complications of illicit cocaine use. 266 29


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