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)

The patient arriving at the emergency department with somnolence must be evaluated quickly, efficiently, and with a definite goal in mind. Head and neck trauma should always be suspected and protective steps taken in the unconscious patient. The coma mnemonic, AEIOU TIPS, (alcohol, epilepsy, insulin, overdose, uremia, trauma, infection, psychiatric, stroke) provides an excellent memory tool for the evaluation of decreased level of consciousness in the emergency setting. Interventions that provide diagnostic and therapeutic results (naloxone and 50% dextrose) should be initiated immediately while blood samples are drawn for pretreatment documentation. Each of the possible causes of lethargy or somnolence needs to be evaluated with the understanding that a multitude of factors may be present in the patient whose condition precludes a thorough history; the depressed diabetic may have taken an overdose of medications in addition to his insulin. Social preconceptions may also effect the outcome. The intoxicated patient described herein was allowed to "sleep it off" in the emergency department under the watchful eyes (and ears) of a nursing staff who faithfully recorded vital signs and pupil reactivity as the patient's blood gas values deteriorated.
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PMID:Sleeping beauty: a case of pickwickian syndrome. 266 15

The widespread use of phenytoin results in frequent accidental and intentional toxicity. Metabolism is enzymatic and can be described by Michaelis-Menten kinetics. This results in an increased half-life in overdose situations and a protracted clinical course which may last a week or more. The primary toxicity is on the central nervous system. The most common initial finding in mild toxicity is nystagmus. As concentrations increase ataxia, decreased coordination, hyper-reflexia, slurred speech and diplopia may develop. Progressive increases result in confusion, lethargy and coma. Various methods tried to increase elimination including dialysis, haemoperfusion, diuresis and plasmaphoresis have been ineffective and are not without risk. Meticulous supportive care including ventilation if necessary should provide a good clinical outcome. Multiple-dose activated charcoal may be helpful in shortening the duration of symptoms.
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PMID:Clinical features and management of poisoning due to phenytoin. 267 94

We determined the horizontal and vertical components of brain displacement on coronal MRIs in 10 patients with acute supratentorial masses. The vertical distances from the superior sagittal sinus to the pontomesencephalic junction (PMJ) and from the vertical midline of the brain to the PMJ did not differ from measurements in 30 patients without masses. Horizontal displacement of the 3rd ventricle (mean, 5.2 mm) exceeded vertical displacement of the PMJ (mean, 1.2 mm) in all but 1 patient. Total brain displacement near the incisura increased from 3 mm in awake patients to 6 to 13 mm in stuporous and comatose patients and remained predominantly horizontal. Uncal herniation, seen only in a patient who was imaged a day after the onset of coma, did not appear to be the immediate cause of brainstem compression but was accompanied by prominent lateral distortion above the tentorium. This preliminary study suggests that most patients with acute unilateral masses have upper brainstem distortion due predominantly to horizontal shift at or above the tentorium.
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PMID:A preliminary MRI study of the geometry of brain displacement and level of consciousness with acute intracranial masses. 271 Mar 50

At necropsy, two patients with sickle cell trait and progressive motor and visual deficits, lethargy and coma showed infarctions of the deep cerebral white matter and brain stem. The findings in these patients and another reported in the literature suggest that subcortical infarctions may be more common in sickle cell trait than has been recognised and should be suspected in any patient with sickle cell trait who presents with an unusual neurological illness.
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PMID:Subcortical cerebral infarctions in sickle cell trait. 273 95

Inverse ocular bobbing (IOB) is an uncommon abnormal eye movement. Its characteristics are slow downward eye movement with rapid upward return, a nadir at the extreme of downgaze position and horizontal roving eye movement. We present a case of IOB associated with cerebral embolism and diabetes insipidus. A 69 year-old right-handed woman was admitted because of a consciousness disturbance. She had been well until November 10, 1983, when she was found dysarthric and left hemiplegic. On admission, she was stuporous. There were conjugate deviation to the right, central left facial and hypoglossal palsy, left hemiplegia with spasticity, left hyperreflexia with positive pathologic reflex and anosognosia. A CT scan performed on November 11 showed extensive hypodense area in the region supplied by the right middle cerebral artery. A right carotid angiography revealed multiple occlusions in the top of the right internal carotid artery with poor collateral circulation. After admission, the level of consciousness gradually deteriorated and became comatose on November 18, when the following abnormal eye movements were observed. Following spontaneous horizontal roving eye movement, both eyes deviated downward slowly from midposition, taking 1 to 2 seconds to reach the nadir. The eyes then remained in the position for 1 to 15 seconds, followed by a rapid return to the midposition. These abnormal eye movements are compatible with inverse ocular bobbing (IOB) described by Knobler. Electronystagmography detected typical IOB and spontaneous upward nystagmus. There was no evidence of hypoxia when these abnormal eye movements were present.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Inverse ocular bobbing associated with cerebral embolism and diabetes insipidus--a case report]. 274 84

D-Lactate-associated encephalopathy is a rare clinical syndrome characterized by dizziness, ataxia, confusion, headaches, memory loss, lethargy, and aggressiveness which may progress to frank but reversible coma. It occurs in patients with profound dysfunction of the short-bowel syndrome and is believed to result from massive carbohydrate malabsorption with resultant over-production of D-lactate and other organic anions by the colonic flora. Extremely elevated serum levels of D-lactate (but not L-lactate) confirm the diagnosis, but currently D-lactate is not clearly established as the putative neurotoxin. We describe a patient who repeatedly developed D-lactate encephalopathy after surgical removal of nearly the entire jejunum and ileum. Markedly elevated D-lactate serum levels were documented during an encephalopathic episode. Potential pathophysiologic mechanisms and the treatment rationale are discussed.
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PMID:D-lactate-associated encephalopathy after massive small-bowel resection. 276 Apr 34

Triphasic waves (TWs) are a distinctive, but nonspecific, EEG pattern found in metabolic encephalopathies and a variety of other neurologic conditions. The prognostic value of TWs was studied in 30 patients with altered state of consciousness. Patients were either comatose (18 patients) or very lethargic (12 patients). Triphasic waves were the dominant EEG pattern, present for at least 35% of the tracing. The etiology of their underlying encephalopathy was multiple metabolic derangements (12 patients), hepatorenal syndrome (5 patients), renal failure (4 patients), hypoxic encephalopathy (4 patients), hepatic failure (3 patients), hyponatremia (1 patient), and hypoglycemia (1 patient). Patients were followed up to 22 months. Fifty percent of the subjects died within 30 days of recording TWs. The overall mortality was 77%. Seven patients (23%) have survived, but only three patients (10%) are neurologically normal. In conclusion, TWs occur most often in patients with metabolic encephalopathies, cannot be used to distinguish different diagnostic entities, and indicate a poor prognosis for survival.
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PMID:Prognostic significance of EEG triphasic waves in patients with altered state of consciousness. 279 20

Recently, Ropper reported that horizontal brain shift caused by acute unilateral mass lesions correlated closely with consciousness, and suggested that recovery of consciousness was unlikely to occur after surgical evacuation if the shift was insufficient to explain the observed diminution of consciousness. The authors have sought to confirm the correlation of pineal shift with level of consciousness and to assess the prognostic value of brain shift measurements in a prospective study. Forty-six patients (19 with subdural hematoma, 14 with intracerebral hematoma, and 13 with epidural hematoma) were accrued to the study group consecutively. A correlation was found between a decrease in the level of consciousness and a significant increase in the mean lateral brain displacement at the pineal gland (from 3.8 to 7.0 mm) and septum (5.4 to 12.2 mm). When outcome was examined in patients who were stuporous or comatose on admission, a significant increase in septal shift was found among patients with a poor outcome, but there was no significant relationship between outcome and degree of pineal or aqueductal shift. A poor outcome was more likely with effacement of both perimesencephalic cisterns or the ipsilateral cistern, but not the contralateral cistern, although this difference did not reach statistical significance. These results do not substantiate the value of brain shift as an independent prognostic factor after evacuation of an acute unilateral mass lesion. The decision to operate and the determination of prognosis should be based rather on established criteria such as the clinical examination, age of the patient, and the mechanism of injury.
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PMID:Brain shift, level of consciousness, and restoration of consciousness in patients with acute intracranial hematoma. 279 68

To better assess the role of hyperammonemia versus hypoosmolarity versus hyponatremia in the TUR syndrome, we developed a rat model. Sprague-Dawley female rats received an intraperitoneal injection (250 cc/kg body weight) of either 1.5% glycine, 2.0% glycine, 2.0% glycine plus 1.5% mannitol, 3.0% mannitol, 5.0% mannitol, or 2.0% glycine plus 0.25% saline. Arterial blood samples were obtained prior to injection, at 2, 8, 16, and 24 hr and analyzed for osmolarity, sodium, and ammonia. Those animals receiving 2.0% glycine, 2.0% glycine plus 1.5% mannitol, and 5.0% mannitol all died within 24 hr with lethargy, convulsions, and coma. Hyponatremia developed in all animals; death, however, occurred only when the sodium concentration declined to 90-95 meq/dl. Mannitol maintained serum osmolarity but did not prevent coma and death. Including 0.25% saline in the initial injection, or an iv injection of 5.0% saline delayed 8 hr achieved 100% survival. Ammonia concentrations increased 15-fold by 8 hr in groups receiving 2.0% glycine; it rapidly decreased to near normal by 24 hr. Decreasing the rise in ammonia by 50% with iv arginine had no effect on survival. Our results suggest that hyponatremia rather than hyperammonemia or hypoosmolarity accounts for the major morbidity and mortality secondary to the TUR syndrome.
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PMID:The physiologic basis of the TUR syndrome. 291 15

The role of spinal cord injury in the pathogenesis of abnormal motor signs (depressed tone and reflexes) following severe perinatal hypoxia-ischemia was prospectively evaluated by clinical, electrophysiological, and neuropathological examinations in 18 asphyxiated neonates. All infants had an abnormal mental status (lethargy or coma), and seizures were present in 12. Neuromuscular examinations revealed hypotonia or flaccidity and hyporeflexia or areflexia in all infants. Neuropathological examinations of the cerebrum and spinal cord were conducted in the 12 neonates who expired. Cerebral pathological findings included cortical neuronal necrosis in 10 of 12 and subcortical white matter injury in 5 of 12. All infants with coma or seizures displayed diffuse cortical injury, but no injury conformed to a parasagittal "watershed" distribution. Spinal cord gray matter displayed prominent ischemic necrosis in 5 patients who were typically flaccid and areflexic. Electromyographic examinations of all 6 survivors were abnormal, consistent with recent injury to the lower motor neuron above the level of the dorsal root ganglion. We conclude that ischemic injury to anterior horn cells within spinal cord gray matter is relatively common among hypotonic-hyporeflexic neonates following severe perinatal hypoxia-ischemia. Although the acute neurological syndrome of neonatal asphyxia is often overshadowed by prominent cerebral signs such as coma and seizures, the motor abnormalities may be partially attributed to concurrent spinal cord injury.
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PMID:Hypoxic-ischemic spinal cord injury following perinatal asphyxia. 291 67


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