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 17 year old high school boy experienced fever and diarrhea, which subsided within 4 days by appropriate medications. Six days later, however, he developed unsteadiness and limb spasm. On the morning of admission, he was found to have drowsiness, dysarthria, gait disturbance and involuntary jerks. When he was brought to the hospital, he was lethargic but could follow simple verbal commands. Frequent involuntary movements manifested by facial grimacings, limb spasms and twitchings with dystonic features were seen. Decorticate posturing was readily elicited by painful stimuli. There was no meningeal irritation sign or gross sensory impairment. The deep tendon reflexes were symmetrically exaggerated with bilateral Babinski signs. Bilateral lateral rectus muscle weakness was found together with mild ptosis and upward gaze limitation. Nystagmus was not present and the funduscopic examination was normal. Immediately he was placed on anticonvulsants, steroid hormone, gamma-globulin and antibiotics as well. A brain CT scan and a CSF examination revealed no abnormality. Meanwhile he continued to show a progressive deterioration associated with fever and status epilepticus, and within 24 hours he lapsed into coma in decorticate posture. An EEG obtained at the 3rd hospital day was compatible with spindle coma. In spite of aggressive treatment he remained febrile and comatous. Therefore, vidarabine (adenine arabinoside) was initiated from the 3rd hospital day for 5 days. Then he began to groan and show frequent choreic movements. For the subsequent 2 weeks he made a slow recovery.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of brain stem encephalitis with complete recovery (Bickerstaff's encephalitis)]. 620 73

Blood concentrations and clinical findings in 25 cases of overdose involving chlordiazepoxide (CDZ) alone ("pure") were compared with those in 23 cases of overdose involving ethanol in addition to CDZ ("mixed"). Both groups consisted predominantly of men who were chronic alcoholics. The mean blood CDZ concentrations did not show statistically significant difference between the two groups ("pure," 5 mg/L; "mixed," 6 mg/L). Following "pure" ingestion, patients were usually alert, and the level of consciousness showed no statistically significant correlation with the blood CDZ concentration. In contrast, after "mixed" ingestion patients were usually lethargic, and the level of consciousness correlated significantly with the blood CDZ concentration (P less than 0.05) but not with the blood ethanol concentration. In neither group was coma noted. For both groups the most common physical findings were tachycardia and dysarthria. Nystagmus was much more common following "mixed" ingestion while seizures, hyperreflexia, and hypertension were more frequent after CDZ overdose alone. Most patients were seen only in the emergency room and were discharged. The implications of these findings are discussed.
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PMID:Blood concentrations and clinical findings following overdose of chlordiazepoxide alone and chlordiazepoxide plus ethanol. 653 Jul 1

Primary amebic meningoencephalitis and granulomatous amebic encephalitis are well recognized clinicopathological entities caused by free-living amebas. Associated arteritis and "mycotic aneurysms" with infiltration of intracranial arteries by lymphocytes, amebic trophozoites and cysts have not been previously reported. A 26-month-old girl had a 3-week history of encephalitis, characterized, initially, by vomiting and low-grade fever. Subsequently, she developed ataxia, generalized weakness, lethargy, and esotropia. The first CSF showed 490 RBC/microliters, 705 WBC/microliters with 90% mononuclears. Her pupils reacted briskly to light. Moderate nuchal rigidity, nystagmus, fixed downward gaze, anisocoria, bilateral 6th nerve palsy, left arm monoparesis and left Babinski were present. CAT scan revealed slight symmetrical dilatation of anterior horns of lateral ventricles and an area of abnormal enhancement above the 3rd ventricle. She died 14 days after admission, 5 weeks after onset of symptoms. The brain showed focal necrotizing encephalopathy, involving thalami, cerebellum, brain stem, and cervical and upper thoracic spinal cord. Numerous free-living amebic trophozoites and cysts were present within a chronic granulomatous encephalitis. There were trombosis of basilar, posterior cerebral, and vertebral arteries with profuse chronic panarteritis, fibrinoid necrosis, and mycotic aneurysms.
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PMID:Granulomatous encephalitis, intracranial arteritis, and mycotic aneurysm due to a free-living ameba. 689 86

In 1,000 cases of phencyclidine (PCP) intoxication evaluated at the time of first examination in an emergency department, the incidence of "typical" findings was found to be lower than has been reported previously. Nystagmus and hypertension occurred in only 57% of our cases; some patients had only one of these findings and many had neither. The incidence of violence was 35%; bizarre behavior, 29%; and agitation, 34%. Changes in sensorium consisted of coma, lethargy/stupor, and acute brain syndrome; however, 46% of patients were alert and oriented. Motor signs included grand mal seizures, generalized rigidity, localized dystonias, catalepsy, and athetosis. Profuse diaphoresis, hypersalivation, bronchospasm, and urinary retention occurred in less than 5%. A small percentage had severe disturbances in vital signs, including three cases (0.3%) of cardiac arrest and 28 cases (2.8%) of apnea. Hypoglycemia and elevated serum CPK, uric acid, and SGOT/SPGT were common. Urine PCP levels did not correlate with the severity of the clinical findings.
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PMID:Acute phencyclidine intoxication: incidence of clinical findings in 1,000 cases. 722 71

The records of 37 patients with systemic lupus erythematosus (SLE) followed at The Children's Hospital of Philadelphia between 1968 and 1978 were reviewed for evidence of central nervous system (CNS) involvement. Criteria for CNS involvement included evidence of organic brain syndrome, electroencephalographic abnormalities with symptoms referable to CNS, or objective neurologic signs. Sixteen of 37 children had CNS involvement (43%). Thirteen patients had CNS involvement at the onset of SLE. Three patients had late onset CNS manifestations 1 to 2 years after the diagnosis of SLE. The most frequently observed symptoms were headache, behavior disorder, lethargy, diplopia, blurred vision, memory alteration, dizziness, and alteration of consciousness. The most frequently observed neurologic signs were seizures, cranial nerve palsy, ataxia, papilledema, nystagmus, meningitis, tremor, rigidity, cortical blindness, and coma. Neuropsychiatric manifestations included organic brain syndrome, functional psychosis, and personality disorder. Laboratory tests showed elevated cerebrospinal fluid opening pressure and protein, negative cultures, and abnormal electroencephalograms and computerized axial tomography scans. Fourteen of 16 children with CNS manifestations are alive. Thirteen had a mean IQ of 89 by the Wechsler Intelligence Tests. Twelve are in educational programs. One required long-term psychiatric care. A residual neurologic abnormality, a seizure disorder, was present in 3. CNS involvement with SLE in children carries a favorable prognosis.
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PMID:Central nervous system involvement in childhood systemic lupus erythematosus. 731 16

Infection with rickettsiae of the spotted fever group was clinically and serologically diagnosed in four dogs from two households on Long Island. In two dogs, clinical signs included high fever (to 40.5 C), abdominal pain, lethargy, depression, anorexia, and nystagmus. One of these dogs had conjunctivitis and petechial hemorrhages in the oral mucous membranes. The third dog initially had high fever, evidence of abdominal pain, anorexia, and depression. The fourth dog appeared clinically normal. Clinical signs disappeared following treatment with tetracycline given orally.
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PMID:Rocky Mountain spotted fever in dogs. 738 Jul 21

Six cases of PCP intoxication in young children age 5 years and younger seen at UCLA Medical Center recently and 10 other cases from the literature are described and their clinical findings summarized. PCP intoxication should be suspected in young children and infants presenting with rapid onset of lethargy or coma, strange behavior, staring spells, ataxia, and nystagmus. Other findings less frequent but still suspect are opisthotonos, hypertension, tachypnea or hyperpnea, miosis, hyperreflexia, hypertonia, and rigidity. Once suspected, the diagnosis is most easily made by finding PCP in the urine. Proper diagnosis of PCP intoxication is important to ensure that rapid, appropriate treatment is given, costly diagnostic workups are avoided, and family evaluations are instituted. One case strongly suggests that intoxication in infants may result from accidental inhalation when near individuals who are smoking PCP.
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PMID:PCP intoxication in young children and infants. 738 38

A 32-year-old healthy man developed vomiting, blurred vision, and consciousness disturbance following cervical manipulation. Physical examination showed stuporous consciousness and spontaneous horizontal nystagmus. Computed tomography (CT) and magnetic resonance (MR) imaging of the brain revealed infarction in the territory of the basilar artery. Studies of MR angiography and vertebral angiography disclosed dissection of the right vertebral artery at the atlantoaxial segment. Antiedematous drugs were prescribed and the patient gradually improved. Neurologic examination six months later demonstrated mild cerebellar ataxia. Physicians and patients should be aware that vertebro-basilar dissection may follow cervical manipulation, and, more importantly, should attempt to prevent progressive infarction.
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PMID:Vertebral artery dissection complicated by cervical manipulation: a case report. 763 91

Thirty pediatric cases of carbamazepine overdoses were reviewed retrospectively for the frequency of toxic effects. Patients were divided into three groups, depending on the type of overdose: acute, acute-on-chronic, and chronic. Effects included lethargy in 93%, ataxia in 50%, nystagmus in 13%, and minor arrhythmias in 10%. Major effects included seizures in 20%, coma in 27%, and need for intubation in 20%. Higher serum carbamazepine levels were associated with these major effects in the acute and acute-on-chronic groups but not in the chronic group. Serum levels greater than 35 mg/L (147 mumol/L), were significantly associated with major toxicities.
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PMID:Pediatric carbamazepine overdoses. 784 50

Nonketotic hyperglycinemia (NKH) is an inborn error of glycine degradation causing muscular hypotonia, seizures, apnea, and lethargy; it has a poor prognosis. Accumulation of glycine in the brain is thought to cause excessive stimulation of the N-methyl-D-aspartate receptor. Dextromethorphan (DM), an N-methyl-D-aspartate receptor antagonist, in doses of 5 to 35 mg/kg per day has been shown to have beneficial therapeutic effects in some patients with NKH. We report the case of a 1-year-old infant with NKH, seizure disorder, and psychomotor delay who was clinically seizure free during treatment with sodium benzoate, arginine, benzodiazepam, and phenobarbital. Although sodium benzoate normalized serum glycine levels (103 to 125 mumol/L), cerebrospinal fluid glycine levels remained elevated (42 to 47 mumol/L), with epileptiform activity on electroencephalography. The addition of low-dose DM (0.25 mg/kg per day) to the treatment led to improvement of electroencephalographic activity, resolution of nystagmus with increased eye contact, and modest progression of developmental milestones. These data suggest that DM at doses significantly lower than previously reported may be beneficial in some patients with NKH. Treatment with low-dose DM needs further evaluation.
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PMID:Efficacy of low-dose dextromethorphan in the treatment of nonketotic hyperglycinemia. 865 42


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