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)

A 52-year-old man with myxedema was evaluated for anterior chest pain that was considered to be compatible with myocardial ischemia. The night after admission he developed extreme bradycardia, hypotension, and apneic episodes lasting up to 25 s. Continuous positive airway pressure and administration of medroxyprogesterone acetate prevented further episodes and relieved much of the somnolence and lethargy that had contributed to the evidence for myxedema. Alveolar hypoventilation caused by decreased sensitivity to carbon dioxide, inadequate central neural drive, peripheral muscle force, and obesity all may have contributed to the apnea. Chest pain has not recurred, and results of electrocardiography have remained normal following full thyroid hormone replacement. The early recognition of myxedema causing sleep apnea will allow specific treatment to avoid the cardiovascular risks related to prolonged apnea and will help avoid confusion with other etiologies of cardiovascular abnormalities.
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PMID:Extreme bradycardia during sleep apnea caused by myxedema. 363 55

Sixteen patients with advanced malignancy were treated with rDNA alpha-2b interferon using a continuous 6-week i.v. schedule. Patients received 1 microgram, 3 mu [corrected], 5 mu and 7 mu/m2/day via a portable infusion pump system, all therapy being on an outpatient basis. The dose-limiting toxicity occurring at 7 mu/m2/day [corrected] was lethargy and somnolence. Five million units (mu) was the maximum tolerated dose but significant nausea, anorexia and lethargy affected 4/5 patients at this level. A dose of 3 mu/m2/day was well tolerated, producing little disturbance of normal activity in the majority of patients. Suppression of WBC and platelets was seen at all doses but was not dose-limiting. There was increasing severity of derangement of hepatic transaminases with increasing dose, and the occurrence of liver toxicity appeared to correlate with nausea, anorexia and lethargy. Assay of serum interferon during the infusion showed that this system maintained a constant level of interferon in the blood. However, the increase did not show a linear pattern with increasing dose, suggesting saturation of metabolic inactivation at 7 mu/m2/day. We recommend that a dose of 3 mu/m2/day be used in future studies of prolonged infusions of alpha-2 interferon.
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PMID:A phase I study of rDNA alpha-2b interferon as a 6-week continuous intravenous infusion. 369 Aug 6

Two adolescent boys with Kearns-Sayre syndrome (progressive external ophthalmoplegia, heart block, elevated CSF protein, and ragged-red muscle fibers) developed lethargy, increasing somnolence, polydipsia, polyphagia, and polyuria after a brief course of steroid therapy. Both had hyperglycemia and acidosis. Nonketotic, lactic acidosis was present in one and ketosis in the other. Severe respiratory failure developed, and both patients died. Postmortem revealed fatty infiltration of the pancreas in addition to a diffuse spongiform encephalopathy.
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PMID:Fatal metabolic acidosis, hyperglycemia, and coma after steroid therapy for Kearns-Sayre syndrome. 370 1

This paper presents the clinical and metabolic findings in two young boys with long-standing Kearns-Sayre syndrome. Following short exposure to oral prednisone, both boys developed lethargy, increasing somnolence, polydipsia, polyphagia, and polyuria. Both presented in the emergency room with profound coma, hypotension, severe hyperglycemia, and acidosis. Nonketotic lactic acidosis was present in one and ketosis without a known serum lactate level was present in the other. Respiratory failure rapidly ensued and both patients expired in spite of efforts at resuscitation. We believe these two cases represent a newly described and catastrophic metabolic-endocrine failure in the Kearns-Sayre syndrome.
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PMID:Hyperglycemic acidotic coma and death in Kearns-Sayre syndrome. 370 9

This is the first report in which a marine mollusc, Oliva vidua fulminans (olives), generally not known to be poisonous, was responsible for death in five children after consuming boiled olives with tamarind. The onset of symptoms was rapid 10 to 20 min after consumption of the olives. Signs and symptoms included nausea, vomiting, abdominal pain, tingling sensation around the lips, numbness around the mouth, drowsiness, lethargy and generalized weakness with paraesthesia in the limbs. The five deaths occurred within 3 to 4 hours after eating the poisoned olives and resulted from respiratory failure. Left-over olives from the affected household and freshly collected live olives had a toxicity of 14,200 mouse units (M.U.) and 15,000 M.U. per 100 g meat respectively. No other common chemical poison and organophosphorus insecticides were detected. The neurotoxic agent was acid and heat stable and was toxic at pH less than 4. Its action was similar to that of paralytic shellfish poisoning which was caused by toxins from certain dinoflagellates.
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PMID:Oliva vidua fulminans, a marine mollusc, responsible for five fatal cases of neurotoxic food poisoning in Sabah, Malaysia. 372

The centrally active, alpha-2 adrenergic receptor agonist clonidine was given to 12 spinal cord injury patients with problematic spasticity not adequately controlled by recognized spasmolytic drug therapy. Five patients had an excellent reduction and 2 patients had some reduction in clinical spasticity (average dose 0.39 mg daily). Four of the 7 responders discontinued clonidine because of adverse reactions after an average of ten weeks of therapy. Three responders have continued to tolerate the drug well with excellent control of spasticity for 18 to 34 months. Five patients had no change in clinical spasticity (average dose of 0.24 mg daily). Three of the non-responders discontinued clonidine because of adverse reactions after an average of three weeks of therapy. Significant associated adverse reactions included syncopal seizures (3), cerebrovascular accident (1), deep vein thrombosis (1), autonomic hyperreflexia (3), lethargy/drowsiness (3), and nausea/vomiting (1). Possible mechanisms of action for clonidine to affect spasticity and the unstable cardiovascular system of quadriplegics is discussed. While spinal cord injured patients with severe spasticity may benefit from clonidine, great caution is recommended during its use until further study establishes safe parameters of administration and efficacy is confirmed on controlled studies.
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PMID:Early clinical experience with clonidine in spinal spasticity. 374 98

A double-blind crossover study was carried out in general practice in 88 patients with peripheral vertigo of unknown origin to compare the efficacy and tolerance of 12 mg betahistine dihydrochloride and 15 mg cinnarizine. Patients were allocated at random to receive 2 tablets 3-times daily of one or other drug for 3 consecutive months before being crossed over to the alternative medication for a further 3 months. Severity of symptoms was assessed at 4-week intervals using the Clinical Global Impression scale and patients kept a record in a daily diary of the frequency and duration of attacks. Details were also recorded of any side-effects reported. The results were analyzed for 46 patients who completed the 6-month study period. Both drugs were shown to be equally effective in reducing the duration and severity of symptoms. Significantly fewer attacks of vertigo, however, occurred during betahistine therapy. Side-effects were the most common reason for dropping out whilst on cinnarizine (9 patients) and were complained of by 38 patients during the study (16 only when on betahistine, 19 only on cinnarizine, 3 whilst on both drugs). The most frequently reported were drowsiness or lethargy affecting 16 patients on cinnarizine and 7 on betahistine.
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PMID:A double-blind crossover study comparing betahistine and cinnarizine in the treatment of recurrent vertigo in patients in general practice. 378 Feb 84

Forty-eight sequential narcoleptic patients were treated with propranolol (80-240 mg/day) for an average period of 18.4 months. Initially all patients received single drug therapy; after 10 days or longer, however, 50% of patients also received tricyclics or stimulants because propranolol alone did not sufficiently suppress the narcoleptic symptoms. Fifty percent of patients judged the initial effectiveness of propranolol on daytime sleepiness to be good to very good; in these patients the effects seemed comparable to that of pemoline. Within 6 months, however, the effectiveness started to decrease, and after 26 months only 8% (2 out of 24) of those patients taking the single drug were satisfied with propranolol therapy alone. Side effects included disturbed night sleep, decreased blood pressure, increased lethargy, allergic skin rash, and asthma; 58% of the patients dropped out of the study after 26 months. Vigilance tests during the first 4 months (16 patients) showed significant improvements in all test criteria, including a shorter reaction time. All-night polygraphic electroencephalogram recordings of 14 patients on the eighth and ninth day of medication showed that average total sleep time decreased by 5.7%, but other sleep characteristics did not change significantly.
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PMID:Propranolol: long-term treatment in narcolepsy-cataplexy. 392 25

Brain-tissue shifts associated with drowsiness, stupor, and coma were studied by clinical examination and CT scanning in 24 patients with acute unilateral cerebral masses. Studies were performed soon after the appearance of the mass to detect the earliest CT changes associated with depression of consciousness. Contrary to traditional concepts, early depression of the level of alertness corresponded to distortion of the brain by horizontal displacement rather than transtentorial herniation with brain-stem compression. Horizontal displacement of the pineal body of 0 to 3 mm from the midline was associated with alertness, 3 to 4 mm with drowsiness, 6 to 8.5 mm with stupor, and 8 to 13 mm with coma. Moreover, drowsy or stuporous patients and some comatose patients had widened cisterns between the tentorial edge and the midbrain on the side of the mass, suggesting that the space was not filled by herniated medial temporal lobe. Downward displacement of the pineal body, indicating central transtentorial herniation, did not occur. Compression of one hemisphere by the other anteriorly (transfalcial herniation) was inconsistently related to alertness, though very large anterior displacements may have caused stupor in some patients. Current concepts of the pathoanatomical nature of depressed consciousness, based on pathological material obtained well after clinical examinations, may require revision, because they do not reflect early brain-tissue distortions.
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PMID:Lateral displacement of the brain and level of consciousness in patients with an acute hemispheral mass. 396 59

A transient cerebral disturbance characterized by somnolence of varying degree is described in children after cranial irradiation given as part of central nervous system (C.N.S.) prophylaxis for acute lymphoblastic leukaemia in remission.Out of 28 such children receiving cranial irradiation as part of the Medical Research Council protocol for C.N.S. prophylaxis 11 (39%) developed pronounced symptoms of somnolence, anorexia, and lethargy some six weeks after the completion of cranial irradiation, and a further 11 (39%) developed these features in mild form. In all cases the symptoms were transient, no focal neurological abnormality was detected, and all children made a spontaneous and complete recovery. E.E.G. studies on five somnolent children showed similar abnormal activity of diffuse and patchy distribution over both hemispheres. Indirect evidence is presented to support the concept that this syndrome represents a transient radiation encephalopathy, analogous to acute transient radiation myelopathy, caused by temporary disturbance of myelin synthesis.
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PMID:Somnolence after prophylactic cranial irradiation in children with acute lymphoblastic leukaemia. 451 11


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