Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cyclobenzaprine (CBP) has a cyclic structure similar to amitriptyline. In overdose, CBP has been suggested to produce the cardiovascular and neurologic toxicity found with the cyclic antidepressants. To examine this possibility, a retrospective chart review of all cases of CBP exposure reported to five regional poison centers was performed for the years 1989-93. There were a total of 750 charts identified for CBP exposure, of which 523 had data sufficient for evaluation. There were 121 polydrug ingestions leaving 402 pure CBP ingestions. Ages ranged from 7 mo to 77 yrs, with a mean of 20 yrs; 26% were 6 yrs or less. Females comprised 63% of the patient group. No deaths occurred. Dysrhythmias beyond sinus tachycardia were infrequent, and none were life-threatening. No seizures occurred. Common effects were lethargy, sinus tachycardia, and agitation, and both hypertension and hypotension were seen. All symptomatic cases with a known time of ingestion were symptomatic within 4 h of ingestion. Doses ingested ranged from 5-1000 mg, with a mean of 133 mg. Asymptomatic and symptomatic patients had a mean dose ingested of 45 mg and 183 mg, respectively. Treatment was primarily gastrointestinal (GI) decontamination and supportive care. Other therapies required were mechanical ventilation, dopamine, fluid bolus, sedation, and foley catheter. Symptoms requiring treatment beyond GI decontamination did not occur with ingestions less than 100 mg. In conclusion, cyclobenzaprine does not appear to produce the life-threatening cardiovascular or neurologic effects of the cyclic antidepressants in doses less than 1 g. Lethargy and anticholinergic effects are prominent, though serious toxicity is infrequent.
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PMID:Five-year multicenter retrospective review of cyclobenzaprine toxicity. 874 27

Traditional centrally acting antihypertensives have been associated with a high incidence of adverse effects and are no longer recommended as first-line therapy. The newer imidazoline receptor agonists must overcome this reputation if they are to gain recognition as potential first-line agents for hypertension. Methyldopa, a centrally acting alpha(2)-agonist, is characterized by a number of serious adverse reactions that limit its use. Although unpredictable idiosyncratic or hypersensitivity reactions are uncommon, these include hepatitis, myocarditis, and hemolytic anaemia. Less serious problems such as abnormal liver function tests, positive Coombs test, drug-induced fever, and pancreatitis also occur. Central side effects include drowsiness, fatigue, lethargy, sedation, depression, psychotic reactions, nasal stuffiness, impotence, and exacerbation of Parkinsonism. In hypertensive men, methyldopa is less well tolerated than either captopril or propranolol, and up to 20% of patients discontinue therapy because of adverse effects. Clonidine acts primarily as an alpha(2)-agonist but also acts as an agonist at imidazoline receptors in the rostroventrolateral medulla. It is equipotent to most other antihypertensives but is considerably less well-tolerated in comparative trials. The principal adverse effects of clonidine are drowsiness, sedation, lethargy and dry mouth. Reserpine acts primarily by depleting central catecholamine neurotransmitter stores. It was very extensively used in early hypertension trials, but its central side effects of sedation, nasal stuffiness, and severe depression are now considered so undesirable that the drug is seldom prescribed. The imidazoline (I1) agonists moxonidine and rilmenidine act selectively and have very little central alpha(2)-agonist activity. In comparative studies against placebo and other reference antihypertensives, the only adverse effect consistently associated with these drugs was dry mouth (approximate placebo-corrected incidence 10%). Sedation was not pronounced. Withdrawal syndromes are complex pathophysiologic processes and occur with a variety of antihypertensive drugs. Cessation of therapy with clonidine and, to a lesser extent, methyldopa may result in a severe withdrawal syndrome characterized by restlessness, sweating, anxiety, tremor, palpitations, and headache. There may be a rapid rise in blood pressure, often with a true "rebound" to higher than pretreatment levels. Plasma and urinary catecholamine levels are increased, and fatalities have been reported. It is important to stress that such a syndrome has not been recorded, in animal or human studies, with either moxonidine or rilmenidine.
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PMID:Aspects of tolerability of centrally acting antihypertensive drugs. 887 99

To minimize the symptoms of antidepressant discontinuation, gradual tapering is necessary for all serotonin reuptake inhibitors (SRIs) except fluoxetine, which has an extended half-life. Agents with shorter half-lives such as venlafaxine, fluvoxamine, and paroxetine should be tapered gradually. Discontinuation symptoms, which frequently emerge after abrupt discontinuation or intermittent non-compliance and, less frequently, during dose reduction, are generally mild, short-lived, and self-limiting but can be distressing and may lead to missed work days and decreased productivity. The symptoms may be somatic (e.g., dizziness and light-headedness; nausea and vomiting; fatigue, lethargy, myalgia, chills, and other flu-like symptoms; sensory and sleep disturbances) or psychological (anxiety and/or agitation, crying spells, irritability). Mild symptoms can often be treated by simply reassuring the patient that they are usually transient, but for more severe symptoms, it may be necessary to reinstitute the dosage of the original antidepressant and slow the rate of taper. Symptoms of discontinuation may be mistaken for physical illness or relapse into depression; misdiagnosing the symptoms may lead to unnecessary, costly tests and treatment. Thus, health care professionals need to be educated about the potential adverse effects of SRI discontinuation.
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PMID:Clinical management of antidepressant discontinuation. 981 35

Although clinicians have observed for centuries that som depressed patients become worse in the winter, it was first in 1984 that Norman Rosenthal and co-workers described a syndrome which they called seasonal affective disorder (SAD), characterised by winter depression, lethargy and a craving for carbohydrate. Phototherapy was proved to be an effective treatment right from the start. Recently it has been reported that not only depression, but also panic disorder and obsessive compulsive disorders may exhibit a seasonal pattern and thus benefit from phototherapy. Phototherapy may also benefit patients suffering from "sun-downing", a syndrome of confusion and agitation in the evening in persons with Alzheimer's disease. Based on the observation that bright light may both elevate brain serotonin and ameliorate sleep abnormalities, the authors report the results of phototherapy for treatment of non-seasonal depressions, either alone or in combination with antidepressants or sleep deprivation.
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PMID:[Phototherapy. An alternative for seasonal affective disorders or sleep disorders]. 926 11

Cases involving ingestion of a dextromethorphan-containing product recorded at a poison control center were studied. A retrospective review of all consultations involving the ingestion of Coricidin HBP Cough & Cold tablets recorded by the California Poison Control System was conducted for the period from January 1 to October 1, 2000. Computerized charts on the consultations were reviewed to obtain data on patient age and sex, number of tablets taken, reason for tablet ingestion, symptoms, treatment, disposition, and outcome. A total of 92 charts (for 92 patients) documenting Coricidin HBP Cough & Cold tablet ingestion were reviewed. The reason for tablet ingestion was classified as abuse in 65 patients (71%), a suicide attempt in 8 (9%), misuse in 1 (1%), malicious administration in 1 (1%), and normal use (but with an adverse drug reaction) in 1 (1%); 16 patients (17%) consumed the tablets for an unknown reason. The 92 patients comprised 42 males and 50 females. Among all patients, 78 (85%) were 13-17 years old, and among those classified as having abusive intent, 58 (89%) were in the same age range. The most commonly reported signs and symptoms associated with ingestion were tachycardia (50 patients), hypertension (29), lethargy (40), mydriasis (20), agitation (15), ataxia or dizziness (20), and vomiting (9). Sixty-one patients (66%) had some alteration in mental status. Fifty-six (61%) were treated in the emergency department; 11 (12%) were admitted. All patients recovered completely. Information on the ingestion of Coricidin HBP Cough & Cold tablets recorded at a poison control center indicated a high rate of abuse of the product among teenagers.
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PMID:Abuse of Coricidin HBP cough & cold tablets: episodes recorded by a poison center. 1159 95

The therapeutic use of methylphenidate for the management of attention-deficit hyperactivity disorder in children is increasing. As therapeutic use increases, the risk increases of unintentional overdoses, medication errors, and intentional overdoses caused by abuse, misuse, or suicide gestures and attempts. Side effects during therapy, which include nervousness, headache, insomnia, anorexia, and tachycardia, increase linearly with dose. Clinical manifestations of overdoses include agitation, hallucinations, psychosis, lethargy, seizures, tachycardia, dysrhythmias, hypertension, and hyperthermia. Methylphenidate tablets can be abused orally, or they can be crushed and the powder injected or snorted. Despite its abuse potential, there is disagreement regarding the extent to which methylphenidate is being diverted from legitimate use to abuse in preteens and adolescents.
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PMID:Abuse and toxicity of methylphenidate. 1198 Dec 94

We present a case of acute Quetiapine (SeroQuel) overdose in an 11-y-old girl who ingested 1,300 mg (22.2 mg/kg bw). Initial lethargy developed within I h followed by an episode of agitation and combativeness 3 h after ingestion. After treatment with lorazepam the patient experienced extended somnolence followed by return to normal mental status 16 h after ingestion. No cardiotoxic or laboratory abnormalities were found. This is the first report of acute Quetiapine overdose in an adolescent and suggests a relatively benign clinical course.
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PMID:Acute quetiapine overdose in an eleven-year-old girl. 1204 70

We used exchange transfusion as an alternative to hemodialysis in an infant with severe salicylism. A 4-mo old, 5 kg male was presented to a local hospital with acute vomiting, tachypnea, hyperpnea and intermittent agitation and lethargy. Shortly after a generalized tonic-clonic seizure he passed several tablets in his stool. Salicylate (ASA) level was 85 mg/dL. He was transferred to our institution for further management: i.v. fluids, activated charcoal, whole bowel irrigation and supplementation with sodium bicarbonate, potassium and calcium. The patient's mental status and gas exchange deteriorated and he was intubated. Despite large amounts of sodium bicarbonate and potassium, severe hypokalemia, anion gap metabolic acidosis and aciduria persisted for 10 h. The small size of the infant precluded use of hemodialysis. An exchange transfusion using 180 mL/kg packed red blood cells reconstituted in fresh frozen plasma was performed. The pre-exchange transfusion ASA level was 70.1 mg/dL; the post-exchange transfusion ASA level was 34.4 mg/dL. There was rebound elevation of ASA to 35.2 mg/dL at 6 h post-exchange transfusion. The 18, 36 and 48 h post-exchange transfusion ASA levels were 20.2, 6.8 and < 2 mg/dL respectively. The ASA level dropped 17.6% before, 41.9% in 8.5 h during, and 40.5% by 48 h after the exchange transfusion. There were no complications. The patient recovered completely to his pre-morbid state. Double volume exchange transfusion was used safely as an effective alternative to hemodialysis in this case of severe infant salicylate poisoning.
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PMID:Exchange transfusion in severe infant salicylism. 1213 72

Psychotropic medication-induced hyponatraemia is an uncommon but important clinical problem with potential serious consequences if not recognised and treated early. Several risk factors have been associated with the development of hyponatraemia. This article reviews reported cases of hyponatraemia associated with the use of psychotropic medications and evaluates possible risk factors and causes. The data were sourced by a search of Medline for reports of hyponatraemia associated with the use of psychotropic medication between January 1966 and December 2000 and a search of US Food and Drug Administration (FDA) spontaneous reporting system database between January 1966 and December 1999. All the reports were included in this review. In the case reports the following data were assessed: age, gender, daily dosage, days to onset, days to recovery, medical condition, concurrent medications. Several risk factors were identified: advanced age, female gender, use of other medications, medical comorbidity. The risk of hyponatraemia was found to be higher during the first 2 weeks of treatment. Administration of the dosage of the drug was not found to be related to the development of hyponatraemia. Hyponatraemia can cause confusion, agitation and lethargy. Any change in the course of illness should alert the physician to the possibility of hyponatraemia.
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PMID:Hyponatraemia associated with psychotropic medications. A review of the literature and spontaneous reports. 1214 Sep 5

Clinical data adequate for analysis were available in 386 laboratory-confirmed cases of arthropod-borne encephalitis - 38 St. Louis and 348 western equine. Consistently observed symptoms varied with the age of the patient. Symptoms that occurred in a high proportion of patients in each age group were:LESS THAN ONE YEAR OF AGE: Fever and convulsions. (None had the St. Louis disease.)ONE THROUGH FOUR YEARS: Fever, headache, vomiting, drowsiness, irritability, restlessness, nuchal rigidity, tremor, and sometimes convulsions. FIVE THROUGH FOURTEEN YEARS: Headache, fever, and drowsiness. Sometimes the disease progressed no further, but if it did, nausea, vomiting, muscular pain, photophobia and limitation of neck and back flexion often were noted; and sometimes convulsions and intention tremors. FIFTEEN YEARS AND OLDER: Drowsiness, lethargy, malaise, fever, stiffness at the back of the neck and, almost always, severe intractable occipital headache associated with nausea, disturbance of vision, photophobia and vertigo. The extreme difficulty of differential diagnosis on the basis of clinical observation was indicated by the wide range of diagnoses made in these cases before the invading organism was identified by laboratory studies.
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PMID:The 1952 outbreak of encephalitis in California; differential diagnosis. 1306 16


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