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)

Nine children, hospitalized for severe respiratory failure following scorpion envenomation, were a part of a group of 61 youngsters and infants admitted to the Pediatric Intensive Care Unit of the Soroka Medical Center, Beer-Sheva during the years 1983-87 because of scorpion venom intoxication. Four out of the nine had cardiogenic shock, three had severe systemic hypertension and one had severe airway obstruction. All nine patients had central nervous system manifestations, including lethargy, confusion and agitation (three cases), and markedly reduced level of consciousness (six cases). Hemodynamic studies performed in two patients showed 'high pressure' (cardiogenic) pulmonary edema. Seven patients recovered completely, one died and another one was left severely handicapped. Hydralazine i.v. showed a remarkable effect on the systemic blood pressure and central nervous system disturbances in addition to mechanical ventilation. Based on our own experience and previous clinical and experimental studies, the possible pathogenetic mechanisms underlying the respiratory and central nervous system dysfunction following scorpion sting are discussed.
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PMID:Respiratory failure in children following envenomation by the scorpion Leiurus quinquestriatus: hemodynamic and neurological aspects. 320 82

A prospective review of 51 cases of tobacco ingestion and 5 cases of nicotine resin chewing gum exposure was conducted to evaluate the incidence and degree of toxicity caused by these products in children. A dose-response relationship was observed for cigarette exposures. Nine of 10 children ingesting more than one cigarette or three cigarette butts developed signs or symptoms, while 12 of 24 ingesting lesser amounts became symptomatic (P less than 0.01). Severe symptoms (e.g. limb jerking and unresponsiveness) were only seen with the larger amounts. Nicotine resin gum produced toxicity in 4 of 5 children who chewed 1/2 to 4 pieces. Agitation, lethargy, tachycardia, hypotension, abdominal pain, and vomiting were seen within 30 min of exposure to the gum.
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PMID:Cigarette and nicotine chewing gum toxicity in children. 334 35

The case of a 3-week-old male infant is described. After receiving an iatrogenic overdose of metoclopramide (1.0 mg/kg every six hours) throughout a 36-hour period for the treatment of suspected gastroesophageal reflux, he became cyanotic, lethargic, and irritable, he fed poorly, and he had diarrhea and respiratory distress. Methemoglobinemia (20.5%) and reduced oxyhemoglobin saturation (79%) were identified. The patient had an excellent clinical response following a single IV dose of methylene blue. Subsequently, methemoglobin reductase activity was normal and there was no measurable hemoglobin M. The diagnosis of methemoglobinemia should be considered in any infant receiving large doses of metoclopramide who has clinical findings of cyanosis, ashen color, or a history of lethargy and/or motor restlessness.
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PMID:Metoclopramide-induced methemoglobinemia. 340 65

The epidemiology and incidence, etiology, pathogenesis and pathophysiology, clinical presentation, diagnosis, principles of therapy, and treatment of bacterial meningitis in infants and children are reviewed. Bacterial meningitis is a major cause of morbidity and mortality, and most cases occur in children less than five years old. Haemophilus influenzae type b, Neisseria meningitidis, and Streptococcus pneumoniae are the major pathogens involved. Bacteremia or colonization of the upper-respiratory-tract epithelium often precedes meningitis. Defense mechanisms are poor in the cerebrospinal fluid; once an organism penetrates the blood-brain barrier, infection may follow quickly. Clinical signs and symptoms are somewhat nonspecific, with lethargy, restlessness, and poor feeding prominent; diagnosis often relies on the patient history along with preliminary results of lumbar punctures. Therapy is based on pharmacologic and pharmacodynamic principles concerning the available antimicrobial agents, the blood-brain barrier, and supportive therapy. Effective antimicrobial therapy requires attainment of adequate bactericidal activity in the cerebrospinal fluid; penetration of agents into the brain depends on their physico-chemical characteristics. Antibiotic therapy must generally be started before culture results are available, making empiric therapy based on the child's age, history, and underlying conditions important. Established therapeutic agents include penicillins, aminoglycosides, and chloramphenicol, though newer expanded-spectrum cephalosporins such as cefuroxime, ceftriaxone, and cefotaxime are being used with increasing frequency. However, the use of these newer, more potent antimicrobial agents have not appreciably altered associated morbidity and mortality. Aggressive supportive care and evaluation of newer nonantibiotic treatments should be addressed in future studies of bacterial meningitis in infants and children.
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PMID:Current concepts in clinical therapeutics: bacterial meningitis in infants and children. 353 67

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

Alzheimer's disease is a slowly progressive disorder involving deterioration of both intellect and personality. The neuropathological features of Alzheimer's disease include abundant neurocortical senile plaques and neurofibrillary tangles. Drug therapies of Alzheimer's disease have been based on empirical observations of the signs and symptoms of the disease and have included the use of hypnotics to reverse insomnia or inverse sleep rhythms; anxiolytics to relieve anxiety, tension and restlessness antipsychotics to "tranquilize" or control psychotic symptoms, such as delusions and hallucinations; stimulants to overcome withdrawn behavior or lethargy; and lastly, antidepressants to control depression. Our growing knowledge of neuropathological and neurochemical changes associated with normal aging and Alzheimer's disease has made it possible to explore and develop pharmacologically-based therapies in Alzheimer's disease. Recent research has revealed behavioral symptoms associated with underlying biochemical changes in either the cholinergic, dopaminergic/ GABAergic (gama-aminobutyric acid) noradrenergic, serotoninergic, neurochemical and/or neuropeptidergic systems. Pharmacological strategies involving manipulation of these systems as a means of relieving Alzheimer's disease symptoms will be reviewed from several perspectives, e.g., those involving transmitter substitution, enzyme inhibition and direct specific receptor stimulation.
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PMID:Pharmacotherapy in Alzheimer's disease: basis and rationale. 354 Oct 49

Delirium (acute confusional states), a common and often overlooked psychiatric disorder, can occur at any age, but elderly persons are especially prone to develop it. In later life, it is often a conspicuous feature of systemic or cerebral disease and drug (notably anticholinergic) toxicity, and it may constitute a grave prognostic sign. Its development in a hospitalized patient may interfere with his or her management, disrupt ward routine, and cause medicolegal complications as a result of patient injury. Acute onset of a fluctuating level of awareness, accompanied by sleep-wake cycle disruption, lethargy or agitation, and nocturnal worsening of symptoms, are diagnostic. Early recognition of delirium and treatment of its underlying cause are essential.
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PMID:Delirium (acute confusional states). 362 89

Lethargy, hyperpyrexia, tremor, and rigidity associated with leukocytosis and elevation of the creatine kinase level occurred in a patient with a closed head injury who was being treated with haloperidol for control of agitation. This constellation of symptoms, known as the neuroleptic malignant syndrome (NMS), partially improved when the neuroleptic medication was stopped, but complete resolution of the syndrome did not occur until the patient was treated with bromocriptine. Because haloperidol is the most widely used medication for the agitation that develops in patients with significant closed head injuries, neurosurgeons should be aware of the NMS. The NMS is caused by neuroleptic medications and may initially present with unexplained hyperpyrexia, leukocytosis, and elevated creatine kinase levels. Halting the neuroleptic, supportive care, and the use of dantrolene sodium and bromocriptine are the treatment modalities of choice for this syndrome, which has a mortality rate of 20 to 30% and may be linked to malignant hyperthermia.
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PMID:Neuroleptic malignant syndrome complicating closed head injury. 396 Feb 97

The development of a scale to assess drug and other treatment effects on severely mentally retarded individuals was described. In the first stage of the project, an initial scale encompassing a large number of behavior problems was used to rate 418 residents. The scale was then reduced to an intermediate version, and in the second stage, 509 moderately to profoundly retarded individuals were rated. Separate factor analyses of the data from the two samples resulted in a five-factor scale comprising 58 items. The factors of the Aberrant Behavior Checklist have been labeled as follows: (I) Irritability, Agitation, Crying; (II) Lethargy, Social Withdrawal; (III) Stereotypic Behavior; (IV) Hyperactivity, Noncompliance; and (V) Inappropriate Speech. Average subscale scores were presented for the instrument, and the results were compared with empirically derived rating scales of childhood psychopathology and with factor analytic work in the field of mental retardation.
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PMID:The aberrant behavior checklist: a behavior rating scale for the assessment of treatment effects. 399 94

This article presents causes of poor motor performance in children other than intrinsic physical disabilities and describes treatment of those problems involving behavioral barriers. Chief among these are motivational-emotional handicaps in the form of lack of confidence, dependence ("learned helplessness"), impulsivity, restlessness, and lethargy. An observational check list for the identification of these nonphysical sources of failure has recently been published as part of the revision of the Stott-Moyes-Henderson Test of Motor Impairment (TOMI-R). The affected children erect defenses against motor challenges by either a frightened refusal to attempt a task (inhibition) or unconscious avoidance strategies such as distractibility, or defeatism. We give guidelines for helping children overcome each of these drawbacks and illustrate in detail the procedures for four of the tasks used in the TOMI-R.
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PMID:Treatment strategies for emotional-motivational blocks to motor functioning in children. 400 Nov 71


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