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)

Alterations of consciousness with impaired perception and drive persisting over hours to days can be due to a nonconvulsive status epilepticus. This possibility has to be considered not only in patients with already known epilepsy, but also in those with a negative history for seizure disorders. The immediately recorded electroencephalogram (EEG) provides decisive clues. In the case of petit mal status most frequently appear tiredness, reduced vigilance and lack of drive. The EEG shows a generalized spike-wave activity. In status psychomotoricus, the clinical symptomatology varies from case to case. It can be characterized by anxiety, dreamy states or productive-psychotic states with agitation, automatisms and hallucinations. In the EEG a temporal or temporally-accentuated epileptic activity will be recorded. Transitional and mixed forms of petit mal status and status psychomotoricus can also be found. I.v. injections of benzodiazepines (clonazepam, diazepam) are an appropriate therapy for any type of nonconvulsive status epilepticus. Phenytoin is indicated in status psychomotoricus, but contra-indicated in the case of petit mal status.
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PMID:[Epileptic impaired consciousness in adults]. 250 9

Teething does not appear to cause diarrhea, fever, rashes, seizures or bronchitis. It may be associated with some daytime restlessness, thumb sucking, gum rubbing, drooling and temporary loss of appetite. It is not clear whether these signs are developmental in origin or are actually related to tooth eruption. Illness occurring with teething should be thoroughly evaluated so that a serious systemic disturbance is not overlooked.
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PMID:Teething. 281 81

Primary care physicians have a vital role to play in identifying depression in their elderly patients. Diagnosis may be difficult, because symptoms are atypical and frequently include psychomotor agitation, somatic symptoms, and complaints of memory loss. Patients with medical illnesses, such as cancer, postmyocardial infarction, stroke, Parkinson's disease, and early Alzheimer's disease are particularly vulnerable to depression. Drugs that may cause depressive symptoms are digitalis at toxic levels, beta-blockers, centrally acting antihypertensives, immunosuppressants, and nonsteroidal anti-inflammatory agents. Cyclic antidepressants are the drugs of first choice. Selection depends on the patient's physical health and current medications and the side effect profile of the drug. Side effects are more pronounced in old age because of drug accumulation owing to slowed clearance. Troublesome side effects are anticholinergic effects, orthostatic hypotension, sedation, cardiotoxicity, and weight gain. The most useful antidepressants for geriatric patients are the secondary amines, desipramine and nortriptyline. The second-generation drug trazodone has the advantage of causing the least anticholinergic effects, but it is very sedating. Before treatment, the patient should have an electrocardiogram, liver function tests, tonometry, sitting and standing blood pressures, evaluation of urinary symptoms for outflow obstruction, review of current medications, and estimation of suicide risk. Cyclic antidepressants are contraindicated during recovery from myocardial infarction, in heart disease when there is severe impairment of myocardial performance, in seizure disorders, and in the presence of glaucoma or a large prostate. Drug interactions that may cause trouble can occur with epinephrine, MAO inhibitors, thyroid hormone, cimetidine, and centrally acting antihypertensives. Dosage should start low, increasing usually by 25 mg every 4 to 5 days until a therapeutic level is reached. Failure of a noradrenergic antidepressant after 4 to 5 weeks can be followed by a trial of a serotonergic drug. Drug serum level monitoring is useful for imipramine, desipramine, and nortriptyline. Monoamine oxidase inhibitors are effective in many elderly patients who are resistant to TCAs. Sympathomimetic drugs must be avoided with MAOIs. Elderly patients are at high risk of toxicity and drug interactions with lithium. Electroconvulsive therapy is useful for patients who do not respond to drug treatment, but medical complications, particularly cardiovascular, often occur in patients 75 or older. Many patients relapse after ECT. Psychotherapy together with pharmacotherapy may be the optimal treatment for elderly depressives. Older patients are more likely to become chronically depressed than younger patients. The risk of suicide in depressed elderly males is high, particularly in those with psychosocial problems, and depression rises with age.
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PMID:Management of depression in the elderly. 266 41

Many of the drugs used in anesthesia and intensive care may cause blockade of the central cholinergic neurotransmission. Acetylcholine is of significance in modulation of the interaction among most other central transmitters. The clinical picture of the central cholinergic blockade, known as the central anticholinergic syndrome (CAS), is identical with the central symptoms of atropine intoxication. This behaviour consists of agitation including seizures, restlessness, hallucinations, disorientation or signs of depression such as stupor, coma and respiratory depression. Such disturbances may be induced by opiates, benzodiazepines, phenothiazines, butyrophenones, ketamine, etomidate, propofol, nitrous oxide, and halogenated inhalation anesthetics as well as by H2-blocking agents such as cimetidine. There is an individual predisposition for CAS--but unpredictable from laboratory findings or other signs. Reports of postanesthetic occurrence of the CAS requiring treatment are not unanimous, varying between 1 and 40%. Differential diagnosis of the CAS includes disorders of glucose and electrolyte metabolism, severe hormonal imbalance, respiratory disorders (hypoxia, hypercarbia), hypothermia, hyperthermia and neuropsychiatric diseases (cerebral hypoxia, stroke, catatony, acute psychosis). The CAS may considerably impair the postanesthetic period especially when agitation is prevalent, which may endanger the patient or the surgical results. The diagnosis is confirmed ex iuvantibus by the sudden increase in the acetylcholine level in the brain. This is achieved with physostigmine, a cholinesterase inhibitor able to easily cross the blood-brain barrier. Its peripheral muscarinic effects are minimal. Postanesthetic CAS can be prevented by administration of physostigmine during the anesthesia procedure. During intensive care (IC), agitated forms of CAS may occur in patients undergoing mechanical ventilation, particularly during prolonged high-dose sedation. Artificial ventilation of such patients becomes very difficult and muscle relaxation may be necessary. In these cases of IC-CAS, physostigmine is of value and has proven beneficial during weaning from mechanical ventilation. Dealing with the CAS for more than a decade has improved knowledge of the central cholinergic transmission. For example, it can be said that CAS occurs alongside general anesthesia, being no more than a frequent side-effect. Furthermore, acetylcholine is involved in nociception through the endorphinergic and the serotoninergic systems. There is a close relation between the central cholinergic transmission and actions of nitrous oxide. Moreover, cholinergic transmission is involved in withdrawal from (among others) alcohol, opiates, hallucinogens and nitrous oxide. In some intoxications with psychoactive agents, physostigmine is useful for reversal of the central nervous symptoms of the acute intoxication itself. In addition it can be used for prevention of some withdrawal states. In
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PMID:Central anticholinergic syndrome (CAS) in anesthesia and intensive care. 268 49

We conducted a study to determine the type, incidence, and timing of complications that occur in patients who have a carbon monoxide (CO) exposure serious enough to require hyperbaric oxygen therapy (HBOT). Complication data were retrospectively collected from a ten-year period for 297 consecutive CO-poisoned emergency department patients who received HBOT. HBOT was indicated for 41% of the patients because of an elevated carboxyhemoglobin (COHb) level alone. Central nervous system dysfunction, including loss of consciousness, and/or cardiovascular dysfunction, was the criteria for HBOT in 59% of patients, regardless of their COHb level. The mean peak COHb level was 38 mg%, with 88% of patients having a peak COHb level greater than 25 mg%. The mortality rate was 6% in this case series. Cardiac arrest occurred in 8% of patients; all experienced their first arrest prior to HBOT. The 3% of patients who sustained an isolated respiratory arrest and those who had a myocardial infarction did so prior to HBOT. Several complications, however, occurred for the first time or as a recurrent event during HBOT. These included emesis (6%), seizures (5%), agitation requiring restraints or sedation (2%), cardiac dysrhythmias or arrests (2%), and arterial hypotension (2%). No patient's level of consciousness deteriorated subsequent to the initial resuscitation except for those who later had a generalized seizure. The most significant complication attributable to HBOT was tension pneumothorax, noted in three patients (1%).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Complications and protocol considerations in carbon monoxide-poisoned patients who require hyperbaric oxygen therapy: report from a ten-year experience. 224 Jul 43

1. This study presents the results of the preliminary screening of vigabatrin as add-on therapy in an open, non-controlled multicentre study in children with refractory epilepsy. 2. There were 135 children, with an age range of 2 months-12 years. Main seizure type was partial in 42%, generalized in 29%, Lennox-Gastaut syndrome in 19% and West syndrome in 10%. 3. Vigabatrin was added onto current antiepileptic treatment in an initially recommended dose of 40-80 mg kg-1 day-1. However, the doses were frequently increased when tolerance allowed it, and the final mean dose used was 87 mg kg-1 day-1 (27-600). 4. A 75% to 100% reduction in seizure frequency was observed in 25% of patients (11 patients became seizure free) and 50 to 75% decrease in a further 13%. Efficacy was better in partial seizures, with good to excellent results in 49% of patients. The use of high doses, above 100 mg kg-1 day, was not associated with greater efficacy in this preliminary study. 5. No side effects were reported in 79% of patients. Agitation and insomnia were observed in 8.8% and somnolence in 6%. Other adverse events included ataxia (2.2%), nausea (2.2%) and increased appetite (1%). A moderate and transient decrease in haemoglobin was reported in six patients from the same centre; these patients were all receiving very high doses of vigabatrin (250 to 600 mg kg-1 day-1). 6. Vigabatrin thus appears to be a safe antiepileptic drug that may be effective in the treatment of severe epilepsy in children.
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PMID:Vigabatrin in the treatment of epilepsy in children. 275 1

Thirty-three patients, operated on between 1981 and 1986, and presenting post-operative confusion and restlessness are analyzed. Two groups are identified: group 1 are patients who regularly received BZD before their present hospitalization; in group 2 patients were given high-dose BZD in the early postoperative period. Symptoms were anxiousness in 15 patients, restlessness in 14, myoclonia in 14, delirium in 3, coma and seizures in 1. BZD withdrawal syndrome was considered after the other causes of post-operative agitation were eliminated and the diagnosis was confirmed by the administration of BZD that relieved the symptoms and by the plasmatic concentration of BZD. This syndrome appears 1 to 5 days after BZD withdrawal and severity of symptoms seems to be directly proportional to the doses and duration of BZD therapy. Propranolol was proposed to reduce the intensity of the symptoms. Nevertheless, progressive withdrawal of BZD remains the best way for managing such patients.
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PMID:[Postoperative agitation. A new cause]. 290 29

It is well established that at low and clinically relevant concentrations theophylline (and caffeine) exerts antagonism at cell surface receptor sites for adenosine. However, it is not known which actions of theophylline are due to adenosine antagonism, because theophylline apparently activates other cellular mechanisms at the same low concentrations. Investigations into the actions of xanthines and their structure activity relationships have identified xanthine compounds like enprofylline (3-propylxanthine) that only has some actions in common with theophylline and that has a negligible ability to antagonize adenosine. Enprofylline is a more potent smooth muscle relaxant and antiasthmatic drug than theophylline but does not produce, e.g., theophylline-like diuretic effects, CNS-stimulant behavioural effects (restlessness - seizures), gastric secretory effects and release of free fatty acids. It is proposed that pharmacodynamic dissimilarities between enprofylline and theophylline may indicate physiological roles of adenosine.
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PMID:Effects of enprofylline and theophylline may show the role of adenosine. 300 2

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

Blood pressure, which ist the product of cardiac output and peripheral vascular resistance is regulated by a complex feedback mechanism involving the sympathetic and parasympathetic systems and hormones. An acute disturbance of regulation may lead to a life-threatening increase in blood pressure. Diagnosis is based upon a careful measurement of blood pressure, which must be performed under internationally standardized conditions. Hypertensive crisis refers to a rapid blood pressure increase greater than 30 mmHg above the age-related 95th percentile. The main causes of hypertension in childhood are renal diseases, which may be aggravated by additional conditions either by the clinician himself (e.g. cyclosporin, steroids) or by the patient (lack of compliance). Crisis affects the brain (hypertensive encephalopathy), the heart (left ventricular insufficiency), the retina (visual disturbances) and the mucous membranes (epistaxis). Hypertensive encephalopathy is induced by a break-through of the autoregulation of brain flow, leading to hyperperfusion and, thus to cerebral oedema. The clinical manifestations are characterized by restlessness, severe and diffuse headache, vomiting, nystagmus, impaired vision, dizziness, paraesthesia, seizures and palsies, which may lead - if untreated - to coma and death. The course is usually prolonged and reversible by adequate treatment. The morphological consequences are purpura cerebri, fresh retinal haemorrhages and papillary oedema, apart from left ventricular dilatation and hypertrophy. The diagnostic procedure rests on the quick realization of essential anamnestic (blood pressure, renal disease, drugs), clinical (oedema, cardiac action, central nervous system, fundus) and laboratory parameters (serum creatinine, electrolytes, glucose, blood count, urine). Treatment should start before the manifestation of clinical signs (hypertensive emergency) with rapidly acting antihypertensive drugs.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The hypertensive crisis in childhood]. 305 87


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