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 74-year-old female who complained of severe attacks of pain in the throat and neck on the left side was first admitted to our hospital in 1971. Carbamazepine was effective at this time, and so she could be discharged. She was readmitted to the hospital in 1974 because of severe stabbing paroxysms of pain in the left throat, radiating into the auricular region as frequent as more than ten times a day. Paroxysms could not be alleviated by large doses of Carbamazepine, and side effects of the drug ensued. The pain could be easily elicited by talking, laughing, swallowing, pulling the left ear and pushing the left tragus. Block of the left 9th nerve with xylocaine produced complete relief of pain for 30 minutes to 1 hour; Plain skull X-rays and veretebral angiograms were normal. The patient was operated under general anesthesia in the sitting position. With the left suboccipital craniectomy, the left 9th nerve was cut without any change on ECG. Pulse rate, and blood pressure. Upon touching vagus nerve, the ventricular extrasystole and hypotension occurred. After the blood pressure restored to normal level and the extrasystole disappeared with administration of atropine and carnigen, the uppermost rootlet of the vagus nerve was cut. The blood pressure dropped abruptly again followed by the right bundle-branch block on ECG for approximately 20 minutes. Postoperatively, she was lethargic and had disorientation, delusion and disorientation. We attributed these symptoms to the hypoxia in operative procedure. The symptoms completely disappeared on the fifth postoperative day. The patient has been perfectly free from pain at the 15 month's follow-up without neurological or mental deficit except diminished gag reflex on the left side. We reported this our experienced case and discussed about the mechanism of the hypotension on sectioning a rootlet of the vagus nerve with literatures.
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PMID:[Glossopharyngeal neuralgia associated with the right-bundle branch block and hypotension on sectioning a rootlet of the vagus nerve--case report (author's transl)]. 55 84

A 56 year-old man presented with vertigo and the right sided weakness. Neurological examination revealed a lethargic man with good orientation to three spheres. His neck was supple. He had anisocoria, the right pupil being larger than the left by 1.5 mm with sluggish light reaction bilaterally. He had exotropia of the right eye in primary gaze. The abduction of both eyes were full with terminal horizontal nystagmus. The adduction of both eyes were quite limited in each eye. He had a limited upward gaze with poor convergence. These were interpreted as the syndrome of the medial longitudinal fasciculus (MLF) bilaterally. He had a depressed gag reflex on the right side with tongue deviation to the right. He had a mild weakness of the right side limb and also had the right sided hemihyperesthesia including his face to pain and temperature. Twenty four hours after the onset, the left brachial angiography revealed a complete occlusion of the rostral portion of the basilar artery without visualization of the posterior cerebral and superior cerebellar arteries bilaterally. CT scans three days after the onset revealed a low density area in the mid pons with extension rostrally up to the mesencephalon. Four days later he became quadriplegic with bilateral horizontal gaze palsy. No more internuclear ophthalmoplegia is noted on both sides. The midline location of the MLF in the pons, and the separate blood supplies by different paramedian branches of the basilar artery, form the anatomical explanation for the frequent unilaterality of vascular and bilaterality of demyelinating lesions. Bilateral MLF syndrome has been considered almost pathognomonic of multiple sclerosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Bilateral internuclear ophthalmoplegia in association with basilar artery occlusive disease]. 235 Sep 28

Maple syrup urine disease (MSUD) is a rare heritable enzyme defect associated with mental retardation. A diet deficient in the branched-chain amino acids is essential for survival. Patients with MSUD are at risk of ketoacidotic metabolic crises brought on by catabolic states, including simple infection or fasting. Delayed diagnosis and therapy can predispose these patients to loss of the gag reflex, lethargy, seizures, and feeding problems. Ultimately, this may result in aspiration and respiratory arrest, which, in turn, can cause cerebral palsy. Of seven cases of MSUD reviewed at The Hospital for Sick Children, two developed spastic diplegic cerebral palsy because of these sequelae. These two patients are similar to other patients with cerebral palsy. Despite special diet, healing of surgical wounds and fractures in patients with MSUD is normal. Simple precautions allow uncomplicated surgery and recovery, even though catabolic states can easily trigger acute ketoacidotic metabolic crises in these patients. The patients with MSUD discussed did not have an increased risk of infection.
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PMID:Cerebral palsy associated with maple syrup urine disease. 710 73

Between March 1980 and March 1989 there were six identified cases of infant botulism. The presenting symptoms were predominantly poor feeding, lethargy and constipation, and the presenting signs were predominantly hypotonia, weak gag reflex and respiratory difficulty. All required intensive care and prolonged hospital stays. Recovery was eventually complete in all cases. Infant botulism is an uncommon condition but early recognition with adequate intensive care usually results in complete recovery.
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PMID:Infant botulism: a review in South Australia (1980-89). 846 Nov 74

An 11-mo-old captive-bred male neutered bobcat (Felis rufus) presented with lethargy, anorexia, leukopenia, neutropenia, lymphopenia, and nonregenerative anemia. The animal was diagnosed as feline leukemia virus (FeLV) positive by immunofluorescent antibody and enzyme-linked immunosorbant assay (ELISA) testing. It died despite supportive care. Pathologic examination revealed multifocal non-suppurative encephalitis, diffuse interstitial pneumonia, multifocal hepatocellular necrosis, non-suppurative peritonitis, and lymphoid depletion. FeLV was isolated from peripheral blood mononuclear cells, bone marrow, spleen, and lymph node. FeLV-specific gag sequences were amplified by DNA polymerase chain reaction (PCR) and aligned with known domestic cat FeLV's. The source of the virus was speculated to be a domestic cat that was a surrogate nurse. Case reports of FeLV in nondomestic felids are few, and FeLV does not appear to be enzootic in wild felids, except European wildcats (Felis silvestris) in France and Scotland. Introduction of FeLV into free-living and captive nondomestic felid populations could have serious consequences for their health and survival. Measures to prevent the introduction of this virus to nondomestic felids are warranted.
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PMID:Feline leukemia virus in a captive bobcat. 1127 97

An 8-month old girl, weighing 9 kg, was brought by her parents at 8.15 am to the Emergency Department (ED) for a progressive worsening of weakness and acute respiratory failure. On admission, the baby presented with poor oral intake, a weak cry and extremely weak muscular body control. Poor gag and suck, unreactive mydriasis, hypotonia, lethargy and absence of peristalsis were noted. Laboratory data showed severe respiratory acidosis. Chest X-ray, electroencephalography, encephalic CT scan and MRI were all normal, as were cerebrospinal fluid analysis and viral tests. Orotracheal intubation and continuous mechanical ventilation were applied. The patient received fluids, corticosteroids, aerosol therapy, large-spectrum antibiotics and enteral-nutrition. Further investigation revealed ingestion of an improperly prepared home-canned homogenized turkey meal. Type A botulinum neurotoxin was identified. Trivalent botulinum antitoxin, prostigmine and oral activated charcoal were administered. Generalized flaccid paralysis, areflexic bilateral mydriasis, gastric stasis and deep coma persisted for the duration of the hospital stay, and the patient died of severe respiratory failure and cardiac arrest 12 days after ED admission. Botulism poisoning should be suspected in any infant presenting with feeding difficulties, constipation, descendent paralysis or acute respiratory failure. Supportive treatment and antidotal therapy should be performed as soon as a clinical diagnosis is made. We describe a case of foodborne botulism in an 8-month old infant caused by ingestion of an improperly prepared home-canned homogenized turkey meal, representing the youngest fatal case reported in medical literature.
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PMID:Fatal course of foodborne botulism in an eight-month old infant. 2235 16