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

Patients with alcohol dependence commonly experience symptoms of anxiety, depression, and insomnia. It is essential that clinicians recognize and treat anxiety disorders in alcoholic patients. Panic attacks with and without agoraphobia are especially prevalent among alcoholics and their families. Treatments of choice for panic disorder are the monoamine oxidase inhibitors, as well as tricyclic antidepressants and the benzodiazepine alprazolam. Benzodiazepines seem to be effective in controlling two pathophysiologic characteristics of alcohol withdrawal--noradrenergic and hypothalamic-pituitary-adrenocortical overactivity. They also can be used to prevent and treat withdrawal seizures and delirium tremens. They are not indicated for the treatment of alcohol dependence per se.
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PMID:Anxiety and alcoholism. 268 Nov 71

Seizures remain among the most serious side effects of psychotropic drugs. The authors review the literature associating neuroleptic and antidepressant medications with seizures, discussing the relative "seizurogenicity" of different medications, risk factors for seizures, and drugs of choice for high-risk patients. Case histories are presented. Available evidence suggests that molindone, fluphenazine, and haloperidol are among the least seizurogenic neuroleptics and that doxepin, monoamine oxidase inhibitors, or electroconvulsive therapy may be safest in treating the depressed patient at risk for seizures.
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PMID:Seizures with neuroleptics and antidepressants. 288 85

Wistar rats of a strain displaying spontaneous petit mal-like seizures and spike-wave EEG discharged (SWD) were injected i.p. with drugs affecting noradrenergic neurotransmission. The EEG and behavior were recorded. Drugs which decrease alpha-noradrenergic neurotransmission, prazosin (alpha 1-antagonist) and clonidine (alpha 2-agonist), increased SWD and were sedative in a dose-dependent manner. Drugs which increase alpha-noradrenergic neurotransmission, ST 587, cirazoline (alpha 1-agonists) and yohimbine (alpha 2-antagonist), reduced SWD and the latter two caused agitation. Drugs which interact with beta-noradrenergic transmission (salbutamol, isoprenaline and propranolol), monoamine oxidase inhibitors (nialamide and iproniazid), and a noradrenaline reuptake inhibitor (desipramine), did not affect SWD. These findings suggest that noradrenaline participates in the control of petit mal-like seizures in the rat, as in other types of seizures and other animal models.
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PMID:Effects of drugs affecting noradrenergic neurotransmission in rats with spontaneous petit mal-like seizures. 303 36

'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

Kinetic parameters of monoamine deamination processes in the rat brain and heart after hyperbaric oxygenation (HBO) in toxic conditions (6 ata) were studied. HBO was shown to cause a substantial reduction in MAO affinity to serotonin in the brain, but not in the heart. Contrastingly, MAO affinity to dopamine was found to decrease in the heart, but not in the brain in response to HBO. Differences of tyramine and 2-phenylethylamine deamination in the rat brain and heart were also reciprocal following toxic HBO. In the initial phase of seizure episode MAO activity in the brain and heart was also different. Distinct mechanisms of adaptation to toxic oxygen in the central nervous system and cardiovascular system are discussed.
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PMID:[Reaction of deamination of monoamines in the brain and heart of rats under the toxic action of hyperbaric oxygenation]. 340 82

Cold adaptation of white rats (45 days, 2 degrees C) considerably increased their resistance against hypoxic hypoxia as indicated by an increase of life duration under hypoxia, a decrease in seizure frequency, and the absence of changes in monoamine oxidase catalytic properties typical for hypoxia. Cold stress, however, reduced the animals resistance against hypoxic hypoxia.
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PMID:[Effect of cold adaptation and brief exposure to cold on the resistance of animals to hypoxic hypoxia]. 360 80

The reversible MAO-A inhibitor moclobemide (5 mg/kg) was shown to prevent seizures in rats during exposure to toxic oxygen (6 ata). Benzamide derivatives increased the latent period of oxygen seizures and decreased the lethality following hyperbaric oxygenation. The range of anti-MAO activity of moclobemide and clorgyline in the rat brain and heart after toxic oxygenation was studied. It was distinct from those in control animals. Clorgyline was found to be more active in inhibiting MAO during toxic oxygenation in the heart and moclobemide-in the brain. The possibility is shown to prevent oxygen seizures not only with irreversible MAO-A inhibitors (clorgyline), but also with reversible ones (moclobemide).
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PMID:[Effect of benzamide derivatives on convulsions induced by the toxic action of oxygen in rats]. 367 73

Chronic daily administration of electroconvulsive shock (ECS) to cats resulted in a progressive elevation of seizure threshold which was accompanied by a sustained elevation in the activity of an endogenous monoamine oxidase inhibitor (EMAOI) present in cerebrospinal fluid (CSF). The increase in EMAOI activity in CSF following chronic ECS was observed maximally at 24-48 h. In rats, a single application of ECS resulted in a rapid but short-lasting increase in EMAOI activity present in the crude membrane fraction from brain. These findings demonstrate that both acute and chronic ECS modify the activity of an EMAOI in brain and CSF which may contribute to both the antidepressant and anticonvulsant effects of ECS treatment.
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PMID:Electroconvulsive shock increases endogenous monoamine oxidase inhibitor activity in brain and cerebrospinal fluid. 372 91

During hyperoxia monoamine oxidase type A acquires the ability to deaminate polyamines and histamine. A preliminary injection of clorgyline (a monoamine oxidase type A inhibitor) before hyperoxic exposure leads to a significant removal of oxygen seizures and prevents changes in the cerebral spermidine and histamine content observed in the unprotected animals. The data confirm the important role of modification of catalytic properties in monoamine oxidase in the mechanism of oxygen intoxication.
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PMID:[Monoamine oxidase activity and effect of clorgyline on the polyamine level during hyperoxia in rats]. 372 40

The details of 88 cases involving trazodone overdose, either alone or in combination with other drugs, have been forwarded to the manufacturer by reporting physicians since trazodone was made available in March 1982. In 73 of these cases, recovery was uneventful; in 6 cases unexpected complications developed. Nine deaths occurred in patients who had taken trazodone in combination with other drugs and/or alcohol. These case reports are supplemented by data from the American Association of Poison Control Centers and the National Institute on Drug Abuse. Of 206 reported overdose exposures to trazodone, no deaths were recorded. For comparison, 2263 reported tricyclic and tetracyclic overdoses resulted in 16 deaths, and 125 reported monoamine oxidase inhibitor overdoses produced 3 fatalities. When taken alone in overdose, trazodone appears to have limited toxicity. Nevertheless, treatment should be monitored closely in patients who present with a history of seizures or who suffer from cardiovascular or respiratory disease.
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PMID:Trazodone overdose: four years of experience from voluntary reports. 377 99


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