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Query: UMLS:C0085631 (agitation)
 12,064 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ever since the introduction of the alkaloid ephedrine as an anti-asthmatic, the CNS stimulatory effects of this sympathomimetic have been a problem in therapy. Indeed, the use of ephedrine is not only limited by its cardiovascular effects, but also by the occurrence of insomnia, restlessness and anxiety. Exceptionally, ephedrine may even induce toxic psychosis, and the possibility of this side effect has recently received renewed attention. Besides ephedrine, the ephedra plant contains some norpseudoephedrine. This substance is also called cathine, because it is a major alkaloid of Catha edulis or khat, a plant that is widely used as a stimulant in certain countries of East Africa and of the Arab Peninsula. The effects of khat have been explained formerly by those of cathine; some time ago, however, the labile alkaloid cathinone was discovered in khat. This substance is the keto-analog of cathine; it is therefore more lipophilic and penetrates easily to its sites of action in the central nervous system. Indeed, cathinone has been found to be a highly potent CNS stimulant and it is now known to be the main psychoactive constituent of khat; the results of various in vitro and in vivo studies indicate that cathinone must be considered a natural amphetamine. In confirmation of this view, it has recently been demonstrated that cathinone has in humans marked euphorigenic and psychostimulant effects. As the case may be, these findings may lead, together with epidemiological data, to a reconsideration of the use of khat as a stimulant and social drug.
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PMID:The pharmacology of psychoactive alkaloids from ephedra and catha. 188 Nov 58

A case of amphetamine abuse in late pregnancy is reported. The presenting features of convulsions, confusion, agitation with hypertension and proteinuria led to a diagnosis of eclampsia for which a caesarean section was performed. Investigations and differential diagnosis of convulsions in late pregnancy are reviewed. A general urinary drug screen gives results after 24 hr whereas, if amphetamine abuse is suspected, this can be confirmed within three hr if a specific test for urinary amphetamines is performed. The sympathomimetic effects of a single dose of amphetamine are contrasted with the depression of the sympathetic nervous system which occurs after long-term use. Implications for anaesthesia are discussed.
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PMID:Amphetamine ingestion presenting as eclampsia. 229 97

'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

Over-the-counter stimulants (phenylpropanolamine hydrochloride, ephedrine, pseudoephedrine, caffeine) are used widely as decongestants, anorectic agents, amphetamine substitutes, and "legal stimulants." Toxic effects may result from overdose, drug interactions, or diseases that increase sensitivity to sympathomimetic agents. The most important toxic effect of the alpha-adrenergic agonist phenylpropanolamine is hypertension, which may result in hypertensive encephalopathy or intracerebral hemorrhage. The therapeutic index of phenylpropanolamine is low, and severe hypertension may occur after ingestion of less than three times the therapeutic dose. Ephedrine and pseudoephedrine may also cause hypertension, as well as tachyarrhythmias due to beta-adrenergic stimulation. Toxic reactions from caffeine are characterized by agitation, seizures, tachyarrhythmias, and hypotension. Management of toxic reactions to over-the-counter stimulants includes control of hypertension with a rapidly acting vasodilator, beta-blockers for tachyarrhythmias, and control of seizures.
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PMID:Toxicity of over-the-counter stimulants. 647 21

Phencyclidine (PCP), a widely abused drug currently, has multiple pharmacological actions, including psychotomimetic [1], anesthetic [2], sympathomimetic [2], anticholinergic [3-7], and dopaminergic [8-10]. Similarly, PCP intoxication in man can present with diverse symptoms: schizophrenia-like delusions and hallucinations; mania; violence, dyskinetic, catatonic, or stereotyped movements; hypertension; and coma [11, 12]. There is general agreement that the treatment of PCP intoxication includes support of vital functions and acidification of the urine [13]. However, there is no known specific antidote for PCP toxicity. Although diazepam [13], haloperidol [14, 15], and chlorpromazine [16] have been reported to improve the agitation and psychotic symptoms caused by PCP, the therapeutic efficacy of these agents has rarely been documented with objective clinical measures. Recently we found that intramuscular physostigmine and haloperidol [17, 18] improved several symptoms of acute PCP intoxication as measured by the Brief Psychiatric Rating Scale (BPRS) [19].
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PMID:Phencyclidine intoxication: assessment of possible antidotes. 713 17

A case of tranylcypromine (Parnate) overdose is presented in which the main toxic effects were headache, obtundation, hypertension, and diffusely peaked T-waves on ECG. The latter effect, which occurred in the absence of hyperkalemia, has not been previously associated with monoamine oxidase inhibitors (MAOI). Recent case reports of tranylcypromine toxicity are briefly reviewed, confirming the potential for hypertension, hypotension, shock, hyperpyrexia, intracranial hemorrhage, agitation, hyperkinesis, coma and death in association with overdosage, or concomitant ingestion of sympathomimetic substances or other drugs. These ECG changes add to the worrisome list of potential toxicities in an era in which MAOI are finding increased clinical use.
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PMID:Peaked "T" waves with tranylcypromine (parnate) overdose. 726 32

Phenylpropanolamine hydrochloride is an amphetamine-like substance that is found in 64 different over-the-counter preparations for colds and appetite suppression. It is also found in numerous prescription drugs. Recently, it has been reported to cause symptoms of sympathomimetic-like effects, such as severe hypertension, hypertensive crisis, and possible renal failure. Also, several cases of psychotic episodes while taking phenylpropanolamine have been reported. This is the report of seven patients who have experienced acute CNS effects. These effects range from stimulation of the medullary respiratory center to tremor, restlessness, increased motor activity, agitation, and hallucinations.
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PMID:Amphetamine-like reactions to phenylpropanolamine. 745 88

Although the standard tricyclic antidepressants (TCAs) are generally effective in the treatment of depression, they can cause several troublesome adverse effects. Chief among these are their anticholinergic actions, which range from annoying dryness of the mouth and constipation to potentially dangerous urinary retention and confusion or delirium in the ill and elderly. Cardiovascular effects of TCAs include orthostatic hypotension, tachycardia and cardiac conduction slowing. Many TCAs are sedating and promote weight gain. Also problematic is the potential lethality of TCAs in overdose. The continual introduction of a host of new antidepressants over the past 15 years has provided an opportunity to improve the benefit-risk ratio for many patients by reducing medication-related toxicity. Selective serotonin reuptake inhibitors (SSRIs) and amfebutamone (bupropion), among others, are examples of effective antidepressants free of tricyclic-like anticholinergic, cardiovascular, sedating and appetite/weight-increasing effects. However, the new-generation drugs also present adverse effects of their own, including gastrointestinal distress, agitation and drug-drug interactions in the case of the SSRIs, and the risk of seizures or psychosis in amfebutamone recipients. Monoamine oxidase (MAO) inhibitors have also been refined; reversible inhibitors of MAO-type A afford protection against the usually feared hypertensive reaction to indirect sympathomimetic substances. The availability of new-generation antidepressants thus increases the likelihood of clinical response with a reduction in unwanted toxicity.
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PMID:Comparative tolerability profiles of the newer versus older antidepressants. 813 85

Pharmacological praemedication. In patients receiving regional anaesthetics induction of deep sedation prior to the performance of the block should be avoided because during the installation of the nerve block it is an advantage to have a cooperative patient. Adequate anxiolytic effects are achieved by oral administration of chloracepate (0.3-0.5 mg/kg body weight). Intraoperative sedation. Once regional anaesthesia is established deep sedation or even a light sleep might be appropriate to improve the patient's comfort. Short acting i.v. substances are the agents of choice. Propofol (1.5-5 mg/kg per h) and midazolam (0.03-0.09 mg/kg per h) are recommended. Both substances should be titrated as needed. Since respiratory depression or loss of airway patency may occur, close observation and pulse oxymetric monitoring are mandatory. Intraoperative analgesia. Restlessness due to pain is not an indication for sedatives and/or hypnotics. Pain can be caused not only by incomplete regional anaesthesia, but also by a tourniquet or uncomfortable body positions, for example, and it should be treated in different ways according to its cause. In the case of an incomplete block, a catheter technique makes a top-up dose for augmentation possible; additional peripheral nerve blocks can also be used to complete the analgesia. If these attempts are unsuccessful, systemic analgesics (preferable narcotics) or even anaesthetics must be given. Opioids are recommended only in mild to moderate pain or discomfort. The risk of respiratory depression should be considered. The administration of oxygen by mask and pulse oxymetric monitoring are useful. Ketamine is a common drug with a potent analgesic effect, which possesses the advantages of good support for the cardiovascular system, because of its sympathomimetic action, and minimal depression of the ventilatory drive. However, with the exception of a few specific indications, Ketamine is not a drug that is initially an integral part of planned regional anaesthetic procedures. In case of incomplete regional blocks administration of ketamine is more frequently the "ultima ratio" following a number of previous, unsuccessful attempts-primarily with sedatives and/or opioids-to achieve a condition that will permit surgical procedures; as a result, the hypnotic and respiratory depressant effects of subsequently administered drugs are enhanced and potentiated. An important consequence of this complex pharmacodynamic interaction scenario is a potential loss of the advantages that would otherwise be gained by using "subanaesthetic" ketamine doses (< 0.5 mg/kg), namely: a cooperative patient who is breathing spontaneously and has an intact laryngopharyngeal reflex response and, therefore, an uncompromised airway competence. Pulse oxymetric monitoring of the potentially endangered respiratory function is obligatory. The individual transition to general anaesthesia is not easy to determine. Therefore, it is essential that, whenever the need arises, intubation and mechanical ventilation intervention procedures be carried out immediately.
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PMID:[Analgesia and sedation to supplement incomplete regional anesthesia]. 859 70

A 3-year-old German Short-haired Pointer was examined because of extreme agitation, hyperactivity, and vomiting that began within 24 hours after ingestion of approximately 750 mg of pemoline, a CNS stimulant. On physical examination, the dog was agitated, tachycardic, hyper-responsive, pyrectic, disoriented, and had mydriasis. These signs were consistent with excessive stimulation of the CNS and sympathomimetic effects resulting from pemoline toxicosis. Serial blood and urine samples were obtained, and toxicologic analyses were performed. Extrapolation of the plasma pemoline concentration 32 hours after ingestion provided an estimated peak plasma concentration of 368 micrograms/ml, dramatically higher than a therapeutic concentration of 1.7 to 7.0 micrograms/ml reported for children. Several sedatives were administered intravenously to alleviate clinical signs and to allow administration of activated charcoal (PO) and fluids (IV). Clinical signs resolved approximately 72 hours after ingestion of pemoline.
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PMID:Pemoline toxicosis in a dog. 942 82


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