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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

It is known that the antimalarial drug mefloquine may cause neurological side-effects. Only few cases of encephalitis ascribed to mefloquine treatment have been reported. We here describe a 34 year-old female patient with symptoms of acute brain syndrome. The patient was initially treated with mefloquine for infection with P. falciparum. She was rehospitalized 12 days after mefloquine treatment with fever, nausea, dizziness and headache. Her condition worsened and her temperature rose and 15 days after treatment she had generalized convulsions and went into a coma. The EEG was severely abnormal. The patient was discharged 37 days after mefloquine treatment, but it was two months before the EEG was normal and the patient in her usual condition.
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PMID:[Acute brain syndrome after mefloquine treatment]. 799 50

The results of a retrospective review of the conventional radiographs performed on head injury patients are reported. Skull radiography findings were compared with clinical symptoms and CT results, when CT was performed, to investigate the presence of intracranial lesions. The radiographs of 2,285 adult patients of both sexes were evaluated: skull fractures were observed in 21/2,285 patients (0.9%) only. CT was positive for an intracranial lesion in 18 of 21 patients (85.71%). Clinical symptoms were divided into three groups according to lesion severity and to neurologic impairment. 979 patients were asymptomatic and 1,306 were symptomatic: 1,114 patients were included in group I, their symptoms being nausea, vomit and loss of consciousness for less than ten minutes, 124 were included in group II (epistaxis and loss of consciousness for more than 10 minutes) and 68 were included in group III (coma and focal neurologic signs). All the patients in groups II and III and 30 patients in group I were submitted to CT--222 CT exams on the whole. Thirty-five patients in group III and 9 in group II had an intracranial lesion on CT, while CT findings were normal in all group-I patients. Thus, we conclude that the presence of a skull fracture is not always correlated with the presence of intracranial lesions. The latter are more likely to be correlated with clinical symptoms, especially coma and neurologic impairement. Therefore, the higher value is confirmed of the clinical examination than of conventional radiographs in head injury patients.
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PMID:[Critical review of the diagnostic protocol in patients with head injury]. 814 57

We have evaluated the effects of nitrous oxide on recovery following laparoscopic cholecystectomy in a prospective, randomised, double-blind study with 42 otherwise healthy patients. All patients received meperidine 1 mg/kg and atropine 6 micrograms/kg im for premedication, and anaesthesia was induced with fentanyl 2 micrograms/kg and thiopental 4-6 mg/kg. Succinylcholine was used for the intubation and muscle relaxation was achieved using vecuronium. Isoflurane with 70% nitrous oxide in oxygen and fentanyl was used for maintenance of anaesthesia in group I (n = 19), and isoflurane in air/oxygen and fentanyl in group II (n = 23). The postoperative ward staff and the surgeon evaluating the postoperative recovery were blinded to the anaesthetic technique. No differences were found in duration of operation and anaesthesia, need for postoperative analgesia or postoperative nausea treated medically. Recovery, judged by the Steward Coma Score, comprehension and collaboration, degree of sedation and orientation in time and space, was similar in the two groups. Postoperative hospital stay was 1 (1-4) day in the nitrous oxide group (median (10-90th percentiles) versus 2 (1-4) days in the air group. The time until patients were recovered, as judged by return to work and normal daily activities, was the same in the two groups: 8 (4-11) days in the nitrous oxide group and 8 (4-11) days in the air group. We conclude that nitrous oxide has no influence on recovery after laparoscopic cholecystectomy.
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PMID:Peroperative nitrous oxide does not influence recovery after laparoscopic cholecystectomy. 824 58

Propionitrile, a substituted aliphatic nitrile commonly used in the chemical manufacturing industry, is capable of generating cyanide. However, there are few reports of human intoxication involving propionitrile. We report two workers at an organic chemical manufacturing plant who were overcome by fumes while treating a waste slurry into which unreacted propionitrile was discharged by mistake. One victim was comatose, acidotic, and hypotensive; his blood cyanide level was later measured at 5.0 micrograms/ml. He responded to sodium nitrite/sodium thiosulfate therapy by regaining consciousness. Continued symptoms were treated with hyperbaric oxygen at 2 atmospheres for a total of 4 hours. The second victim, who complained only of nausea, dizziness, and headache and who never lost consciousness, was treated with sodium nitrite/sodium thiosulfate. His measured blood cyanide concentration was 3.5 micrograms/ml. The ambient concentration of propionitrile in air samples at the work site shortly after the exposure was 77.5 mg/m3. In occupational situations in which workers exhibit rapidly progressive symptoms of headache, dizziness, collapse, and coma, and where substituted nitriles are known to be on site, acute cyanide poisoning should be strongly considered. Because of continued endogenous generation of cyanide from the metabolism of the parent compound, hyperbaric oxygen may be a valuable adjunctive therapy to consider, in addition to the immediate use of the cyanide antidote kit, in cases of poisoning by propionitrile or other substituted nitrile compounds. We urge the Occupational Safety and Health Administration to adopt workplace standards for the maximum ambient air concentrations for propionitrile.
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PMID:Successful treatment of life-threatening propionitrile exposure with sodium nitrite/sodium thiosulfate followed by hyperbaric oxygen. 788 67

A 42-year-old woman suddenly developed headache and nausea on July 26, 1991, and the computed tomography (CT) scan showed a moderate-sized hematoma in the left occipital lobe. After one month's conservative treatment, she had recovered to a neurologically intact state. Cerebral angiography demonstrated a giant arteriovenous malformation fed by enlarged branches of the left posterior cerebral artery as well as small branches arising from the middle cerebral artery, anterior cerebral artery and the meningeal branches of the middle meningeal artery and the occipital artery. Preoperative embolization was planned on February 24, 1992. During an attempt at catheterization of the basilar artery and the left posterior cerebral artery with a balloon catheter and a Tracker-18 catheter, the patient complained of an intensification of her headache, nausea and vomiting. So the embolization procedure was stopped. The CT scan taken immediately at that time showed a severe subarachnoid hemorrhage (SAH). She became comatose about 40 minutes later. CT scan taken next day revealed also a complication of the pontine hemorrhage. Neurologically, she had gradually recovered and could communicate with some simple words 3 months after SAH. The total removal of the AVM was performed on May 26, 1992. Postoperative course was uneventful. She showed rapid and remarkable improvement in her neurological state suggesting that the blood flow in the surrounding brain area had been corrected. A blood deficit had no doubt been caused when blood had been stolen by the giant AVM.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Subarachnoid hemorrhage and pontine hemorrhage followed by an embolization procedure of left occipital giant arteriovenous malformation: a case report]. 841 9

A 58-year-old man was admitted to our hospital with suspicion of aseptic meningitis. He had been well until the day before admission, when he became suffering from headache and nausea. Cerebral spinal fluid (CSF) analysis on admission revealed Cryptococcus neoformans. Neurological examination and brain CT scan showed no abnormality. On the 5th hospital day, he noticed ataxia and weakness in his right extremities and soon fell into drowsy to comatose state. CSF study revealed marked elevation of pleocytosis and oligoclonal IgG bands. The T2 weighted image of brain MRI showed multiple high intensity areas, mainly in the white matter, in cerebellar hemisphere, vermis, left medulla oblongata, left occipital lobe and parieto-occipital lobe. Steroid pulse therapy remarkably improved neurological deficit as well as MRI abnormalities. He became alert at the next day. Ataxia and motor weakness disappeared in a week. Laboratory examination before the pulse therapy revealed impairment of T cell response to mitogens and reduced number of CD8-positive cells. These abnormalities in the cell-mediated immunity were completely corrected by the steroid pulse therapy. It was hypothesized that cryptococcus infection induced the autoimmune mechanism which resulted in the ADEM-like exacerbation.
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PMID:[Acute disseminated encephalomyelitis (ADEM)-like exacerbation in the patients with cryptococcus meningitis treated successfully by steroid pulse therapy]. 866 39

Described here is a fatal case of accidental aconitine poisoning following the ingestion of aconite, Torikabuto, mistaken for an edible grass, Momijigasa. A 61-year-old man developed symptoms of nausea, diarrhea, and discomfort of the body about 2 h after the ingestion and was taken to an emergency room. Resuscitation and antiarrhythmic drugs were ineffective, and ventricular tachycardia and fibrillation developed and lasted for 6 h. He was transferred to a coronary care unit and complete sinus rhythm was obtained on an electrocardiogram 30 h after his admission. The patient fell into a coma and died of brain edema diagnosed by CT on the 6th day. Consent for autopsy was denied by the family but was given for gas chromatography/selected ion monitoring (GC/SIM) to analyze the toxicity of aconitine alkaloids in the blood and the urine. Only a faint amount of jesaconitine was detected, while aconitine, mesaconitine and hypaconitine were not detectable in the blood 24 h after ingestion. On the other hand, aconitine and its related alkaloids such as mesaconitine, jesaconitine, and hypaconitine were clearly detected in the urine.
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PMID:A case of aconitine poisoning with analysis of aconitine alkaloids by GC/SIM. 883 86

We have performed a prospective randomised trial of 30 patients undergoing craniotomy to compare intramuscular codeine phosphate with patient-controlled analgesia using morphine 1 mg bolus with a 10-min lockout and no background infusion. For 24 h postoperatively, pain, nausea, Glasgow coma score, respiratory rate and sedation score were assessed. There was a wide variation in the amounts of morphine requested by the patients in the patient-controlled analgesia group in the first 24 h postoperatively (range 2-79 mg, median 17 mg). There was a small, but non-significant, reduction in pain scores in the patient-controlled analgesia group. There were no significant differences between the two groups in respect of nausea and vomiting, sedation score or respiratory rate. No major adverse effects were noted in either group. Patient-controlled analgesia with morphine is an alternative to intramuscular codeine phosphate in neurosurgical patients which merits further investigation.
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PMID:Pain following craniotomy: a preliminary study comparing PCA morphine with intramuscular codeine phosphate. 920 94

A healthy 19-year-old recruit in a French artillery regiment drank 250 mL of a mixture of beer and wine that had rinsed in a hot 155-mm gun-barrel. Fifteen minutes later, he complained of nausea followed by seizures. He was comatose for 24 h, presenting signs of encephalopathy. A moderate renal failure was noted initially and worsened to an extensive tubular necrosis with anuria on the day after the incident. The first toxicological investigations only showed a 0.31 g/L blood ethanol. Then inductively-coupled plasma (ICP) emission-spectrometry revealed very high concentrations of tungsten in the "beverage" as well as in gastric content, blood and urine (1540 mg/L, 8 mg/L, 5 mg/L, and 101 mg/L, respectively). The nature of the metal was confirmed by ICP coupled to mass spectrometry. A simple and reliable ICP quantitative assay of tungsten in biological fluids, hair and nails was then developed. It showed high blood levels (> 0.005 mg/L) until day 13 in spite of six hemodialyses, and in urine until D33. Tungsten was also incorporated in hair and nails. To the best of our knowledge, such an intoxication has never been reported before though this drinking seems to be traditional in the French Artillery. It has probably been favored by the unusually high volume of beverage absorbed and by the new alloy of the gun, containing tungsten. The clinical evolution was satisfactory over weeks and the patient was declared totally cured after five months.
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PMID:Tungsten determination in biological fluids, hair and nails by plasma emission spectrometry in a case of severe acute intoxication in man. 914 46

We report a 64-year-old woman who developed nausea, headache, and consciousness disturbance. She was well until four years before the onset of her neurologic illness when (April of 1990 at her 59 years of the age) she was found to have an early cancer in her anterior wall of the lower stomach. Subtotal gastrectomy was performed and the operative result was reported as curative. Four years after the surgery (December of 1994 at her 64 years of the age), she noted suboccipital headache and nausea which had become progressively worse and she was admitted to our service on May 24, 1995. On admission, she appeared chronically ill but general physical examination was unremarkable with normal vital signs. Neurologically she was alert and not demented, and the higher cerebral functions were intact. Cranial nerves were also unremarkable. She was able to walk in tandem and on heels. No motor weakness or ataxia was noted. Deep tendon reflexes were moderately increased, however, no Babinski sign was noted. Although she had headache, no meningeal signs were seen. Slight superficial and vibratory sensory loss was noted in both feet. Routine blood work was again unremarkable except for slight increase in CEA to 8.3 ng/dl (N < 5 ng/dl). The opening pressure of lumbar CSF was 180 mm H2O and the CSF contained 39 cells/microliter, 79 mg of protein, and 10 mg/dl of glucose. Approximately half of the cells were atypical malignant cells. Plain CT was unremarkable, however, tentorial border showed enhancement after contrast infusion. FGS showed no malignant tumors in the stomach. She was treated with intravenous glycerol and whole brain radiation, however, she continued to complain of severe headache, and her sensorium started to be disturbed one month after the admission. Follow-up cranial CT scan revealed enlargement of the lateral and the third ventricles. Her consciousness progressively deteriorated and she became comatose three months after the admission. Repeated cranial CT scan showed enlargement of the ventricles, but no mass lesions were seen within the brain. She developed respiratory arrest on September 25 of the same year. She was discussed in a neurological CPC and the chief discussant arrived at the conclusion that the patient had a gastric cancer with meningeal seeding developing meningeal carcinomatosis. The cause of deep coma was ascribed to damage of cerebral cortical areas secondary to metastatic carcinoma cells and fibrinous materials in the surface of the brain. Postmortem examination revealed thickening and clouding of leptomeninges of the cerebral convexity. On histologic observation, patchy areas of fibrous thickening were seen in the cerebral leptomeninges; in such areas, adenocarcinomatous cells were seen scattered. The basal meninges were free of carcinoma cells, however, leptomeninges of the cerebellum and brain stem tegmentum contained scattered carcinoma cells. The lateral and the third ventricles were enlarged, however, insides of the brain were free of pathologies; the ependymal layer were intact. In the stomach no carcinoma cells were remaining. Pneumonic changes were seen in the right upper and the left lower lobes which appeared to be the direct cause of her death. No evidence of tentorial herniation was noted. The cause of her deep coma was not clearly determined, however, combination of hydrocephalus and cortical malfunction due to leptomeningeal carcinoma cell infiltration and fibrinous material accumulation appeared to have played a role.
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PMID:[A 64-year-old woman with severe headache and progressive disturbance of consciousness]. 919 1


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