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Query: UMLS:C0023380 (lethargy)
 5,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This review of studies on the prevalence of mental disorders in adults with mental retardation comes to the following principal conclusions: Mainly due to research problems and psychiatry's disinterest there continues to be limited epidemiological findings; compared with people of normal intelligence the prevalence rate of mental disorders is about 50% higher in mild mental retardation and 2-3 fold higher in severe mental retardation; substance abuse or -dependence as well as neurotic disturbances may be less prevalent while self-injurious behaviour seems to be rather specific for subjects with mental retardation. As far as factor analytic studies are concerned the two syndromes of irritability and lethargy may play a major role in the psychopathology of severe mental retardation.
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PMID:[Psychological disorders in mental handicap--prevalence and psychopathologic characteristics]. 794 46

Thirty adults with Prader-Willi syndrome (PWS) were compared with 30 adults with non-specific learning disability matched for age, sex and severity of mental retardation. Maladaptive behaviour was assessed with the Aberrant Behavior Checklist (ABC), a 58-item structured interview which rates behaviours from 0 (not a problem) to 3 (severe problem) and which yields five factors (I) irritability, agitation; (II) lethargy, withdrawal; (III) stereotypic behavior; (IV) hyperactivity, non-compliance; and (V) inappropriate speech). The PWS sample had significantly higher factor I (P < 0.001) and factor V (P < 0.05) scores. The PWS sample had mean scores above 1 for 17 ABC items; the contrast subjects had no mean scores above 1. The factor I scores for the PWS sample were similar to those of inpatients in hospital facilities for adults with mental retardation and mental illness or severely challenging behaviour. The results support previous work, and extend it by suggesting that temper tantrums, self-injury, impulsiveness, lability of mood, inactivity and repetitive speech are characteristic behaviours in PWS in adult life. Studies of the reasons for heterogeneity in behaviour are now needed.
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PMID:Maladaptive behaviour in Prader-Willi syndrome in adult life. 873 73

Kernicterus is a preventable life-long neurologic syndrome caused by severe and untreated hyperbilirubinemia during the neonatal period. High levels of bilirubin are toxic to the developing newborn. In full-term infants, hyperbilirubinemia symptoms include severe jaundice, lethargy, and poorfeeding. Features of kernicterus may include choreoathetoid cerebral palsy, mental retardation, sensorineural hearing loss, and gaze paresis. Kernicterus is not a reportable condition in the United States, and its prevalence is unknown; however, a pilot registry at a Pennsylvania hospital documented 90 cases in 21 states from 1984 to June 2001 (L. Johnson, Pennsylvania Hospital, Philadelphia, personal communication, 2001). This report summarizes case histories of four full-term, healthy infants who developed kernicterus and underscores that to prevent kernicterus, newborns must be screened and promptly treated for hyperbilirubinemia.
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PMID:Kernicterus in full-term infants--United States, 1994-1998. 1142 29

Profound hypothermia (core temperature of less than 28 degrees C) is a life threatening state and a medical emergency associated with a high mortality rate. The prognosis depends on underlying diseases, advanced or very early age, the duration prior to treatment, the degree of hemodynamic deterioration, and especially, the methods of treatment, including active external or internal rewarming. This is a case study of an 80-year-old female patient with severe accidental hypothermia (core temperature 27 degrees C). She was found in her home lying immobile on the cold floor after a fall. The patient was in a profound coma with cardiocirculatory collapse, and the medical staff treating her was inclined to pronounce her deceased. On her arrival at the hospital, she was resuscitated, put on a respirator and actively warmed. Very severe metabolic disorders were found, including a marked metabolic acidosis composed of diabetic ketoacidosis (she had suffered from insulin treated type 2 diabetes mellitus) and lactic acidosis with a very high anion gap (42) and a hyperosmotic state (blood glucose 1202 mg/dl). There were pathognomonic electrocardiographic abnormalities, J-wave of Osborn and prolonged repolarization. Slow atrial fibrillation with a ventricular response of 30 bpm followed by a nodal rhythm of 12 bpm and reversible cardiac arrest were recorded. The pulse and blood pressure were unobtainable. Despite the successful resuscitation and hemodynamic and cognitive improvement, rhabdomyolysis (CKP 6580 u/L), renal failure and hepatic damage developed. She was extubated and treated with intravenous fluids containing dopamine, bicarbonate, insulin and antibiotics. Her medical condition gradually improved, and she was discharged clear minded, functioning very well and independent. Renal and liver tests returned eventually to normal limits. Progressive bradycardia, hypotension and death due to ventricular fibrillation or asystole commonly occur during severe hypothermia. Respiratory and metabolic, sometimes lactic, acidosis, lethargy and coma, hypercoagulopathy, hyperosmolar state, acute pancreatitis and renal and hepatic failure are frequent complications of hypothermia. Underlying predisposing causes of hypothermia are diabetic ketoacidosis, cerebrovascular disease, mental retardation, hypothyroidism, pituitary and adrenal insufficiency, malnutrition, acute alcoholism, liver damage, hypoglycemia, sepsis, hypothalamic dysfunction, sepsis and polypharmacy, and especially, the use of sedative and narcotic drugs. Our case demonstrates once again that CPR once begun should continue until the successful rewarming because "no one is dead until warm and dead".
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PMID:[Severe accidental hypothermia in an elderly woman]. 1175 73

Table salt can now be fortified with iodine and iron without interaction and without loss of potency. According to Levente Diosady, professor of Food Engineering at the University of Toronto, the amounts of the two micronutrients available to the human body have been significantly reduced when the two interacted. In the new technology, the iodine is covered with a dextrin (a water soluble starch) capsule that serves as a physical barrier to the iron. Micronutrient Initiative (an international secretariat based at IDRC that works to eliminate health problems resulting from iron, iodine, and vitamin A deficiencies) and IDRC supported the development of the technology. The efficiency of absorption of the two micronutrients in the new double fortified salt in the human body is being tested at the Hospital for Sick Children in Toronto. Later testing will be conducted by University of Ghana scientists in IDRC-funded trials that will focus on women and their families in areas of Ghana where these deficiencies are endemic. Iodine is part of thyroid hormone, which contributes to brain development in the fetus and regulates human metabolism; iodine deficiency is the most frequent cause of preventable mental retardation. Related disorders include lethargy, physical disabilities, goiter, stillbirth, and neonatal death. Iron deficiency, the most common nutritional problem in the world (particularly among women, infants, and children), is associated with anemia, fatigue, learning problems, pregnancy complications, premature births, and maternal mortality. The two deficiencies together affect more than one-third of the world's population. Approximately 1.6 billion people, in more than 100 countries, live in areas where iodine is not available in sufficient amounts; those most at risk include about one-third of China's population. It is also a severe problem in the Himalayas, the Andes, India, and West Africa.
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PMID:Micronutrient deficiencies. Reports from the field -- Africa. 1229 Mar 27

We reported three term or near-term infants with parasagittal infarcts. Their Apgar scores were low and the amniotic fluid was meconium-stained. Resuscitation was necessary immediately after birth, but they were not stuporous and no neurological abnormalities were recognized on admission. They showed metabolic acidosis and transient hypoglycemia, and two showed hematoemesis. Seizures were observed between 2 and 15 h of age in all of them. Electroencephalography demonstrated moderate or severe depression, and CT demonstrated bilateral abnormal low densities in the border zones of the middle and posterior cerebral arteries. Two of them had mental retardation and epilepsy, although the other exhibited normal development. Our infants suggest that neonatal seizures can also occur in infants with hypoxic ischemic encephalopathy without apparent neurological abnormalities.
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PMID:Hypoxic ischemic encephalopathy associated with neonatal seizures without other neurological abnormalities. 1268 4

This study evaluated the effects of lamotrigine as adjunctive therapy for refractory epilepsy in patients with mental retardation. Patients with epilepsy and mental retardation having uncontrolled seizures despite treatment with other antiepileptic drugs were eligible (n=67). The open-label study comprised a Baseline Phase, an Escalation Phase during which lamotrigine was titrated to a target dose, an 8-week Maintenance Phase during which doses of lamotrigine and concomitant antiepileptic drugs were maintained, and a 12-week Optimization Phase during which doses of lamotrigine and other antiepileptic drugs could be adjusted. Almost half (44%) of patients experienced a 50% reduction in seizure frequency during the Maintenance Phase after addition of lamotrigine; 15% of patients became seizure-free. A similar pattern of results was reported for the Optimization Phase. Investigator-rated clinical status was improved relative to baseline in 66 and 74% of patients at the end of the Maintenance and Optimization Phases, respectively. Most patients experienced improvements in seizure frequency, duration, and intensity during the Maintenance Phase (62 to 72%) and the Optimization Phase (65 to 74%). Many patients were rated as having improved social functioning during the Maintenance Phase (42%) and the Optimization Phase (46%). The Aberrant Behavior Checklist score for lethargy and the mean Habilitative Improvement Scale score were improved at the ends of the Maintenance and Optimization Phases relative to baseline (P< or =0.04). One limitation of this study is its open-label design, which limits the ability definitively to attribute the clinical improvements to lamotrigine. Adjunctive lamotrigine in patients with refractory epilepsy and mental retardation appears to decrease seizure frequency and improve behavior while permitting a reduction in dose of concomitant antiepileptic drugs.
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PMID:Lamotrigine as adjunctive therapy in patients with refractory epilepsy and mental retardation. 1289 58

The Smith-Magenis syndrome is a rare, complex multisystemic disorder featuring, mental retardation and multiple congenital anomalies caused by a heterozygous interstitial deletion of chromosome 17p11.2. The phenotype of Smith-Magenis syndrome is characterized by a distinct pattern of features including infantile hypotonia, generalized complacency and lethargy in infancy, minor skeletal (brachycephaly, brachydactyly) and craniofacial features, ocular abnormalities, middle ear and laryngeal abnormalities including hoarse voice, as well as marked early expressive speech and language delays, psychomotor and growth retardation, and a 24-hour sleep disturbance. A striking neurobehavioral pattern of stereotypies, hyperactivity, polyembolokoilamania, onychotillomania, maladaptive and self-injurious and aggressive behavior is observed with increasing age. The diagnosis of Smith-Magenis syndrome is based upon the clinical recognition of a constellation of physical, developmental, and behavioral features in combination with a sleep disorder characterized by inverted circadian rhythm of melatonin secretion. Many of the features of Smith-Magenis syndrome are subtle in infancy and early childhood, and become more recognizable with advancing age. Infants are described as looking "cherubic" with a Down syndrome-like appearance, whereas with age the facial appearance is that of relative prognathism. Early diagnosis requires awareness of the often subtle clinical and neurobehavioral phenotype of the infant period. Speech delay with or without hearing loss is common. Most children are diagnosed in mid-childhood when the features of the disorder are most recognizable and striking. While improvements in cytogenetic analysis help to bring cases to clinical recognition at an earlier age, this review seeks to increase clinical awareness about Smith-Magenis syndrome by presenting the salient features observed at different ages including descriptions of the neurologic and behavioral features. Detailed review of the circadian rhythm disturbance unique to Smith-Magenis syndrome is presented. Suggestions for management of the behavioral and sleep difficulties are discussed in the context of the authors' personal experience in the setting of an ongoing Smith-Magenis syndrome natural history study.
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PMID:Neurologic and developmental features of the Smith-Magenis syndrome (del 17p11.2). 1664 92

Epileptic seizures during infancy have a wide variety of clinical presentations and the outcome differs according to the etiology. Among the benign and rare causes of infantile seizures, Vitamin B12 deficiency has been encountered. Common symptoms of Vitamin B12 deficiency in infants include megaloblastic anemia, feeding difficulties, developmental delay, microcephaly, failure to thrive, hypotonia, lethargy, irritability, involuntary movements, seizures and cerebral atrophy. Involuntary movements and seizures may rarely be the initial symptoms of Vitamin B12 deficiency. Involuntary movements have also been reported to appear after initiation of Vitamin B12 supplementation in isolated cases, whereas, no such information exits for seizures. In this paper, three infants with Vitamin B12 deficiency associated with motor and mental retardation are reported because of long-lasting focal/multifocal epileptic seizures following the initiation of intramuscular Vitamin B12 treatment. Antiepileptics were introduced in addition to Vitamin B12. Seizures disappeared within a few days or weeks; electroencephalographic findings were normalized in a few months. No relapses occurred during the follow-up period.
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PMID:Seizures during treatment of Vitamin B12 deficiency. 1855 Mar 91

Autism is an etiologic heterogeneous entity caused by many different diseases occurring in the central nervous system at an early stage in life. Several metabolic defects have been associated with autistic symptoms with a rate higher than that found in the general population. Inborn errors of metabolism can probably account for less than 5% of individuals. Selective metabolic testing should be done in the presence of suggestive clinical findings, including lethargy, cyclic vomiting, early seizures, dysmorphic features, and mental retardation. In some patients, early diagnosis of the metabolic disorders and proper therapeutic interventions may significantly improve the long-term cognitive and behavioral outcome.
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PMID:Autism and metabolic diseases. 1807 13


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