Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0027497 (nausea)
 23,468 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Among 2,391 recipients of plain aspirin tablets, 121 (5.1%) were reported to have adverse reactions. Minor gastrointestinal disturbances, particularly heartburn and nausea, were most common (2.1%). Central nervous system effects were second (1.2%). Among these, tinnitus was reported most often (0.8%); deafness occurred in eight patients (0.3%). Gastrointestinal bleeding, the third major category of adverse reactions, occurred in 1.0% of recipients; it was not considered serious in any of the patients with reactions judged "definitely" or "probably" related to aspirin. The frequency of all adverse reactions increased as the unit dose, daily dose and total dose became larger. Deafness occurred only at high doses. Reactions were more common in females.
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PMID:Acute toxicity of aspirin in hospitalized medical patients. 30 23

Twenty-two patients with a complaint of sudden deafness were treated with one of the other of two radiopaque contrast media, 9 received daily doses of sodium iothalamate, and 13 were treated similarly with methylglucamine and sodium iodamide. Four of the first group and eight of the second demonstrated either an effective partial or a complete recovery of hearing function. Those failing to respond were generally classified completely deaf at admission and report nausea, vomiting, or vertigo at onset of sudden deafness. Treatment with sodium salts of triiodobenzoic acid derivatives, i.e., sodium iothalamate and methylglucamine and sodium iodamide, is judged to be effective in selected cases of sudden deafness.
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PMID:Treatment of sudden deafness with sodium salts of triiodobenzoic acid derivatives. 62 15

This report is a case of intracranial neurinoma of the jugular foramen. A 21-year-old woman was admitted to our hospital with complaints of headache, nausea, tinnitus on the left and deafness on the left. The neurological examination revelaed bilateral choked disc, Bruns Cushing nystagmus, hearing disturbance on the left, slight disturbance of vestibular function on the left, diminished gag reflex on the left, curtain sign on the left, loss of taste on the posterior third of the left side of the tongue, and deviation of the tongue to the left on protrusion, accompanied with atrophy and fasciculation on the left. Skull-XP showed the enlargement of the jugular foramen. Pneumoencephalogram showed the enlargement of the fourth ventricle combined with the superior, posterior displacement of it's floor. We confirmed the diagnosis of the jugular foramen neurinoma on the left. By suboccipital craniectomy a walnutsized tumor was disclosed at the jugular foramen. The tumor was encapsuled with smooth, thick capsule and was colored in dark rouge. This tumor was removed totally and the postoperative course was uneventful. The pathological diagnosis was neurinoma. We consider that this tumor originated in the ninth or tenth cranial nerve.
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PMID:[Intracranial neurinoma of the jugular foramen-a case report (author's transl)]. 124 Nov 11

Eighty patients with idiopathic sudden deafness existing no longer than 10 days were included in a prospective randomized double-blind study. Patients were treated for 10 days with infusions of either 10% low-molecular weight dextran or the combination of low-molecular weight dextran with naftidrofuryl. Before treatment and after 10 days hearing loss in the affected ear was determined at 0.5, 1, 2, 3, 4 and 6 kHz. The mean hearing loss was then calculated as the average from these values. During monotherapy with low-molecular weight dextran the mean hearing loss decreased from 40 to 27 dB compared to 38 to 17 dB when naftidrofuryl treatment was added (p < 0.01 between groups). A significant benefit of naftidrofuryl on hearing loss was also found at frequencies between 0.5 and 3 kHz. Furthermore, patients reported better improvement of tinnitus when naftidrofuryl was combined with dextran. Two patients receiving dextran alone developed side effects: one had an allergic reaction causing withdrawal of treatment, which the other case had vertigo, nausea and headache with spontaneous recovery. The results of the study showed that treatment with naftidrofuryl in addition to hemodilution with low-molecular weight dextran was of therapeutic benefit in the therapy of sudden deafness without increasing the rate of side effects.
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PMID:[Randomized double-blind study of therapy of sudden deafness. Low molecular weight dextran + naftidrofuryl vs. low molecular weight dextran + placebo]. 138 72

A case of acoustic neurinoma with multiple intratumoral hemorrhages is reported. A 56-year-old male noted sudden hearing reduction in his left ear in October of 1985. The diagnosis of a local physician was sudden deafness. About 10 months later, he had two episodes of severe headache without nausea or vomiting. The patient was hospitalized in October of 1986. Neurological examination cerebellar ataxia. cerebellar ataxia. Plain and enhanced computed tomography revealed only an unremarkable low-density area at the left cerebellopontine angle. In contrast, magnetic resonance imaging (MRI) clearly demonstrated a large (3 x 4 x 5 cm), multicystic tumor in the site. On exposure of the tumor at surgery, most of the cysts were found to be filled with a dark red or xanthochromic fluid. The tumor was completely removed following numerous cyst punctures to decrease its volume. There was no evidence of subarachnoid hemorrhage. Histological examination showed a typical acoustic neurinoma. The cyst wall contained numerous telangiectasia-like lesions. The initial symptom of this patient was sudden hearing loss, which is an atypical manifestation of acoustic neurinoma. The massive intratumoral hemorrhage was thought to be caused by telangiectatic lesions in the cyst wall. MRI clearly demonstrated the hemorrhagic cysts within the tumor, especially in the posterior fossa.
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PMID:[Acoustic neurinoma presenting with repeated intratumoral hemorrhage. Case report]. 247 16

We reported a 51-year-old male with ischemic disturbance of right inner ear resembling Meniere's disease. The patient had a sudden-onset episode of vertigo, right severe hearing disturbance, nausea, vomiting and gait disturbance. Two days after, he had hypersomnia, vertical gaze palsy, double vision, left Horner's sign, and sensory disturbance of pain and temperature of right half body involving face. Brain MRI disclosed high intensity area in T2-weighted image and proton density in bilateral paramedian thalamo-mesencephalic region and right cerebellum (area of the anterior inferior cerebellar artery). Cerebral angiography showed 90% or more stenosis of the right vertebral artery, 50% stenosis of the left vertebral artery before the posterior inferior cerebellar artery (PICA), and 60% stenosis of distal portion of the basilar artery. Furthermore, stem portion of the posterior cerebral artery, and the right anterior cerebellar artery and the left vertebral artery after the PICA were absent or occluded. Right deafness was evaluated to be Jerger type II, namely disturbance of inner ear. Caloric tests showed no response, and right auditory brainstem response showed no waves. Main cause of this vertigo and right deafness was considered to be disturbance of inner ear due to ischemia of right labyrinthine artery, though this patient was not a typical case of the anterior cerebellar artery syndrome. Ischemic disturbances of inner ear have been reported only in patients with the anterior cerebellar artery syndrome, therefore this patient who had only acute ischemic disturbance of inner ear and did not have disturbance of caudo-lateral portion of the pons was considered to be very rare.
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PMID:[A case of ischemic disturbance of inner ear]. 259 43

Facial nerve neurinomas are relatively rare and most of them appear at the vertical portion of the facial nerve. Facial nerve neurinoma originated from the cerebellopontine (c-p) angle portion is less frequently reported. A 51-year-old woman was admitted to our hospital complaining of severe headache and nausea. She had had dizziness and unsteady gait for the previous two weeks. She did not complain of hearing disturbance, but otological examination revealed sensorineural deafness. She had no facial palsy. Skull x-ray showed no erosion of the internal auditory canal. Plain CT-scan revealed a large, unenhanced, low-density mass in the right c-p angle cistern. At the time of the operation, this tumor originated from the right facial nerve. Histological diagnosis of this tumor was schwannoma. After the operation, right facial nerve palsy appeared but hardness of hearing was no worse than previously. This tumor seemed to be facial nerve neurinoma in the c-p angle cistern. To the present, 121 facial nerve neurinomas have been reported in the previous literature. Facial nerve neurinomas in the c-p angle cistern, however, have only been reported in 5 cases. The most frequent symptom of facial nerve neurinoma in the temporal bone is facial nerve palsy, but that of facial nerve neurinoma in the c-p angle cistern is hearing loss, as in an acoustic neurinoma. Preoperative diagnosis of facial neurinoma in the c-p angle cistern using neurological symptoms alone is difficult. Furthermore, differential diagnosis from acoustic neurinoma in the c-p angle cistern using only skull x-rays and CT-scanning is also difficult.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A case of facial nerve neurinoma originated from the cerebellopontine angle portion]. 268 11

The pharmacokinetic and dynamic interactions among 3 antimalarials, ie quinine, doxycycline and mefloquine was observed in a 26-year-old Thai male patient with falciparum malaria. During the acute episode of the infection, the patient was treated with an intravenous dose of quinine hydrochloride at 600 mg qid, together with an oral dose of doxycycline 100 mg bid. Due to nausea, tinnitus and the persistence of parasitemia in peripheral blood smears, the dose of quinine was reduced 2 days after the first treatment to 300 mg; concurrently oral mefloquine 750 mg was given as 2 divided doses at 24 hours apart. During the course of treatment, the patient developed hearing loss; deafness of the right ear lasted for one week after stopping quinine administration. Higher plasma quinine and lower whole blood mefloquine concentrations than would be expected from the simulation profiles were detected 4 days after the first treatment. However, the concentration of mefloquine was increased upon the cessation of quinine treatment.
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PMID:Quinine toxicity when given with doxycycline and mefloquine. 785 66

A 36-year-old man was admitted to our university hospital, complaining of acute hearing loss of the right ear, which was his only hearing ear. He had developed complete deafness due to mumps in the left ear at the age of 26. Before admission, he had been diagnosed as having rubella infection. He noticed hearing loss in the right ear two days after disappearance of macular rash. Headache, nausea and vertigo were not present. Three weeks after the onset of hearing loss, he was admitted to our university hospital. Pure tone audiometry revealed sensorineural hearing loss; a mild ascending audiometric curve with a marked loss at 4,000 Hz and 8,000 Hz. SISI test was positive. Caloric stimulation (ice water 10 ml/10 s) to the right ear demonstrated a normal response. Rubella hemagglutination antibody titer was 512. Specific IgG antibody was over 3,200. Specific IgM antibody was positive (7.01 Enzyme Immunoassay). The data indicated recent infection with rubella. He was given betamethasone for 14 days. Pure tone audiometry showed hearing improvement.
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PMID:Unilateral hearing loss following rubella infection in an adult. 807 85

Quinine poisoning typically results in a constellation of non-life threatening symptoms which include tinnitus, deafness, nausea, vomiting, vision changes, headache, and hypotension. Cardiac conduction defects, dysrhythmias, and cardiovascular collapse have all been reported after overdose and generally occur within 8 hours of ingestion. We report a unique case of delayed cardiotoxicity following quinine ingestion. Toxicity included marked ventricular conduction abnormalities for which serum alkalinization appeared to be therapeutically beneficial, and torsades de pointes requiring overdrive pacing for termination.
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PMID:Delayed cardiotoxicity following quinine overdose: a case report. 834 May 83


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