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

Infusion-therapy with antidepressants has been of value in severe as well as therapy resistant depressive states. In addition to doses lower than those used for oral treatment, a more rapid onset of therapeutic effect and a better tolerance, the beneficial effect seems also to depend on the setting in which the treatment takes place. Infusion-therapy is a combined pharmacopsychotherapeutic procedure. Next to infusion-treatment a pretreatment with neuroleptics is advised either via the oral or parenteral route. In extremely refractory depression the infusion-therapy can be applied twice a day; in some cases we resort to continuous infusion for a few days. Infusion-therapy is not applicable in patients prone to epileptic seizures or with serious cerebral dysfunction with a risk of delirium. In case of doubt an EEG is mandatory. Tricyclic antidepressants may not be used in cardiac diseases especially those with troubles of the conduction propagation or repolarization.
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PMID:[The treatment of severe, therapy-resistant depression using infusions of antidepressants]. 292 14

The neurologic evaluation of an individual cardiac transplant recipient often does not lead to a succinct bedside diagnosis. There are few consistent clinical observations. The onset of seizures in the early postoperative period is associated with embolic cerebral infarction. Seizures occur most commonly, however, as a neurotoxic manifestation of cyclosporine. The onset of an acute delirium or psychosis in the first week after cardiac transplantation usually has multiple causative factors and is reversible. A postoperative brachial plexopathy or mononeuropathy can be identified with a neurologic examination, confirmed by appropriate electrophysiologic testing and is usually reversible. The onset of periorbital inflammation, ophthalmoplegia, and nasal turbinate or sinus invasion and necrosis is consistent with phycomycosis. Most patients, however, present with nonspecific findings of impaired mentation with or without focal neurologic signs. These patients require a fairly systematic search for potentially treatable neurologic complications (see Table 3). In a medically stable patient an aggressive diagnostic approach, at times including stereotaxic brain aspirate or biopsy, is indicated. In the severely ill patient with multiple organ failure, empirical therapy for the most probable treatable disorder is justified.
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PMID:Neurologic complications of cardiac transplantation. 304 45

A patient who developed neuroleptic malignant syndrome (NMS) from the use of several neuroleptic agents and the therapeutic interventions used to reverse the syndrome are described, and the clinical presentation and treatment of NMS are reviewed. Fever, leukocytosis, seizures, delirium, and elevated serum creatine phosphokinase levels developed in a 17-year-old girl who was receiving perphenazine and haloperidol. The patient was admitted to a hospital for treatment of atypical psychosis and received haloperidol and, later, thioridazine. Autonomic disturbances, altered consciousness, and muscular rigidity developed. Thioridazine was discontinued in favor of perphenazine because of anticholinergic adverse effects. Symptoms persisted despite treatment with benztropine and diphenhydramine. After the diagnosis of NMS was made, all neuroleptics were discontinued, and the patient began therapy with dantrolene sodium and bromocriptine. Dramatic improvement in the patient's condition followed. NMS has four characteristic signs: hyperthermia, muscular rigidity, altered consciousness, and autonomic dysfunction. Mechanisms believed to cause NMS include alteration of central neuoregulatory mechanisms and neuroleptic-induced imbalance between central dopaminergic and gamma-aminobutyric acid neurotransmitter systems. Bromocriptine, amantadine, dantrolene sodium, and electroconvulsive therapy have been used effectively in the treatment of NMS. NMS is a rare but potentially fatal adverse drug reaction that occurs in situations that make diagnosis difficult. Dramatic, favorable responses can be achieved with early diagnosis and appropriate treatment.
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PMID:Diagnosis and treatment of neuroleptic malignant syndrome. 324 Jun 62

Several anecdotal reports and two retrospective chart reviews have examined complications of concurrent lithium and electroconvulsive treatment. Discussions have generally been contradictory or confusing. This article reviews the literature and particularly emphasizes theoretical considerations and mechanisms, concluding (A) that lithium may act synergistically with neuromuscular blockers, but the effect is not clinically significant, and (B) that repeated electroconvulsive seizures may cause a toxic delirium in patients concurrently taking lithium.
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PMID:Complications of concurrent lithium and electroconvulsive therapy: a review of clinical material and theoretical considerations. 328 16

A mixture containing 3 g of boric acid and 300 mg of cinchocaine chloride prescribed due to painful dental protrusion was accidentally ingested by a 12-month-old girl. She developed violent vomiting and coughing. Irritability, tremor, seizures and a delirious reaction. She was treated with diazepam, intubated, sedated and ventilated. Her diuresis was stimulated with furosemide and fluid. Within the first 24 h she was treated with haemodialysis twice on femoral catheters. Her renal function was unaffected. In two days she fully recovered. The maximum measured levels of boric acid and cinchocaine chloride approximately 6 h after ingestion were 26 micrograms/ml and 71 ng/ml respectively. The plasma half-life of boric acid was 7.0 h and decreased to 3.6 and 4.4 h during the two haemodialyses. The total body clearance of boric acid increased correspondingly from 21 ml/min to 41 and 34 ml/min. The in vitro clearance of boric acid of the dialyser was later determined to be 18 ml/min. It is concluded that haemodialysis is valuable in the treatment of boric acid intoxication because it increases the elimination of the drug even in patients without any sign of renal toxicity.
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PMID:Combined boric acid and cinchocaine chloride poisoning in a 12-month-old infant: evaluation of haemodialysis. 337 4

We report a case of prolonged coma (7 days) which arose as a complication of the treatment of alcohol withdrawal seizures and delirium with intravenous phenobarbital and diazepam. In an attempt to enhance the elimination of diazepam and its active metabolites, as well as phenobarbital, 40 grams activated charcoal was given every 4 hours (6 doses). Coma was completely reversed within 12 hours; serum half life (t1/2) of diazepam was reduced from 195 to 18 hours during charcoal administration. We postulate that higher free (unbound) diazepam concentrations secondary to hypoalbuminemia, occurring as a result of liver disease, may have increased the depth of our patient's coma, but paradoxically, by making more drug available for diffusion across the gastrointestinal membrane barrier, may have enhanced the ability of activated charcoal to adsorb diazepam and, therefore, decrease its t1/2.
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PMID:Reduction of diazepam serum half life and reversal of coma by activated charcoal in a patient with severe liver disease. 374 88

Patients with the barbiturate abstinence syndrome require pharmacotherapy (and hospitalization) when there is a history of the ingestion of greater than 0.4 g of secobarbital or its equivalent for 90 or more days, or of 0.6 g for 30 or more days, or a previous history of barbiturate withdrawal seizures or delirium. The pharmacological management of withdrawal, which is rational, safe, efficacious and relatively simple, is described and recommended. This treatment relies on a phenobarbital loading-dose technique which is titrated to clinical end-points. The prolonged elimination of phenobarbital prevents the reappearance of withdrawal symptoms and, since repeated doses are not required, results in less manipulative drug-seeking behaviour.
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PMID:Treatment of the barbiturate abstinence syndrome. 377 32

From January 1974 to June 1983, the Paris Poison Control Centre collected 84 cases of overdosage with orphenadrine alone or in combination. Prior papers emphasized fatalities related to orphenadrine poisoning. This retrospective study suggests an underestimated incidence of anticholinergic drugs abuse in our country. The clinical picture of orphenadrine poisoning associates drowsiness, agitation, confusion, delirium and seizures. Anticholinergic symptoms are often noted: mydriasis, sinus tachycardia, dryness of the mouth and urinary retention. No severe cardiac disturbance was found in these patients.
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PMID:[Acute poisoning by orphenadrine]. 383 10

In 19 chronic alcoholics with rhabdomyolysis the clinical picture demonstrated markedly different degrees of severity of myolysis. Muscle pain, muscle swellings and brown-coloured urine were rare. But symptoms of delirium, at times with cerebral seizures, were frequent at the onset. Renal failure of different degrees was common; five patients had to be dialysed. Two patients died in irreversible shock. Respiratory insufficiency and hypercalcaemia were other complications. Early recognition of the disease is important, because early treatment can prevent acute "myoglobinuric" renal failure.
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PMID:[Rhabdomyolysis as a complication of chronic alcoholism. Observations in 19 cases]. 394 97

A report is given on the clinical trial of the ultra-short-acting hypnotic etomidate for treatment of withdrawal delirium with special reference to delirium tremens. Severe and disturbing side-effects such as myoclonic movements or seizures with equivalent EEG changes compelled discontinuance of the therapy in five of seven patients. The activation of epileptogenic activity in the treatment of delirium tremens by etomidate long-term-infusions and the lack of international experience in this field do not support the use of etomidate as an anticonvulsive agent.
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PMID:[Increased tendency to seizures as affected by long-term infusions of etomidate in delirium tremens]. 408 68


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