Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of cryptococcal granulomatous arachnitis of the spinal cord was reported. A 12-year-old boy suffered from sudden occipitalgia and left hemiparesis. The symptoms disappeared spontaneously in about a half year. The next year, he consulted an orthopedist because of lumbago and gait disturbance. Myelography through the cisternal route showed complete block at the level of L1. Exploratory laminectomy of D12 and L1 revealed adhesive arachnitis. Symptoms were improved immediately after the operation. At the age of 15, he was admitted to our clinic, because of sudden onset of headache and vomiting. Computed tomography showed marked hydrocephalus. He recovered by ventriculoperitoneal shunt, and was discharged. The next year, sudden back pain occurred. Gait disturbance, sensory disturbance of the legs and trunks below the mamilla, and dysuria appeared gradually. He was readmitted and laminectomy of D2-4 was performed. The arachnoid membrane was white and 2 mm in thickness diffusely. Thickened arachnoid membrane was removed at the level of D2-4. Histological diagnosis was granulomatous arachnitis. Cryptococcus was seen in the removed tissue. Symptoms were improved after operation. One thousand milligrams of amphoterisin B was injected intermittently. He was discharged on food. Spinal symptoms in cryptococcosis are rare. Operative procedures were effective before the administration of amphoterisin B.
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PMID:[Cryptococcal granulomatous arachnitis of the spinal cord--a case report (author's transl)]. 49 61

An eight year old boy was admitted to our ward with a history of abrupt onset of rapidly progressive gait disorder, nausea, vertigo and vomiting. The clinical as well as the laboratory findings suggested the diagnosis of acute cerebellar ataxia. Magnetic resonance imaging (MRI), however, showed marked demyelinisation in the cerebellar region and visual evoked potentials were pathologic. After immunosuppression the patient promptly improved clinically and the lesions depicted by MRI disappeared almost completely.
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PMID:Transient cerebellopontine demyelinisation revealed by MRI in acute cerebellar ataxia. 225 Oct 8

The use of high doses of cisplatin in treating cancers has been limited by two major adverse effects--emesis and peripheral neuropathies. The emesis has become largely controlled by the introduction of a new class of drugs--the 5-HT3 receptor antagonists. The current study was undertaken to determine if these drugs would also prevent cisplatin-induced neuropathy. We have used a developing rat as an animal model and determined the effects of cisplatin on morphology (loss of spinal cord calcitonin gene-related peptide (CGRP)-containing neurons) and behavior (gait abnormalities and pain perception). Rat pups from the age of 5 days were treated twice weekly for 4 weeks with cisplatin (1 mg/kg), the 5-HT3 antagonist MDL 72222 (3 mg/kg) or both. The animals were tested for pain perception (using tail-flick latencies) at 17 and 21 days of age and for a gait abnormality at 24 days of age. At 34 days of age, the animals were perfused and the lumbar region of the spinal cords stained immunocytochemically for CGRP. Our results show that cisplatin treatment resulted in a dramatic loss of CGRP neurons in the dorsal horn of the spinal cord and a corresponding increase in the animals' threshold for pain. In addition, the animals showed a pronounced gait abnormality, characterized by 'toeing-in'. Treatment with MDL 72222 not only failed to protect against the loss of CGRP neurons but also worsened the gait abnormalities seen after cisplatin treatment alone. These studies confirm and extend the list of morphological and functional adverse effects of cisplatin treatment.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:A 5-HT3 receptor antagonist fails to prevent cisplatin-induced toxicity in immature rat spinal cord. 779 48

A 50-year-old male developed gait disturbance and bilateral sensory disturbance in territories below Th 11 level in February, 1990. On February 26, 1990, an intradural tumor was partially removed at Th 11-12 levels, which was histologically diagnosed as glioblastoma multiforme; followed by post-operative radiotherapy (40Gy to the tumor area). CT scan of the brain was unremarkable and he was discharged home as ambulatory in July, 1990. Gait disturbance, occasional headache and vomiting developed in June, 1991. MRI revealed multiple spinal cord tumors at Th 11-12 and L 2-3 levels, as well as multiple intracranial tumors in the cerebellum, cingulate gyrus, and sylvian fissure, all of which were thought to be located in the cerebrospinal fluid (CSF) space. VP shunt was performed for hydrocephalus. MRI taken 2 months after operation demonstrated diffuse subarachnoid dissemination and new spinal cord tumors at C 3-4 and Th 3-10 levels. Although pathology of the intracranial tumors was not confirmed, dissemination from the spinal tumor was strongly suggested by the evidence including the long interval after the spinal cord operation, the location of the multiple tumors in the CSF space, and the simultaneous intraspinal dissemination. Only 31 cases with intracranial dissemination from malignant spinal astrocytoma or glioblastoma have been reported, and, of these, most were located around the brainstem, cerebellum, and other regions bordering the CSF space. In malignant spinal cord tumor, every effort should be made to prevent CSF dissemination at operation or to detect it as early as possible thereafter. MRI was found to be the most effective method for evaluating CSF dissemination.
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PMID:[A case of spinal glioblastoma with intracranial dissemination]. 825 21

Single-dose toxicity studies of prulifloxacin, a new antibacterial agent, were conducted in mice, rats and dogs. In addition, a single-dose toxicity study of (+/-)-6-fluoro-1-methyl-4-oxo-7- (1-piperazinyl)-4H-[1,3]thiazeto[3,2-a]quinoline- 3-carboxylic acid (NM394), an active metabolite of prulifloxacin, was performed in rats. Prulifloxacin was administered orally, intraperitoneally (i.p.) or subcutaneously (s.c.) to mice and rats, and orally to dogs. NM394 was administered intravenously (i.v.) to rats. When prulifloxacin was administered orally or s.c., LD50 values were more than 5000 mg/kg in both sexes of mice and rats; when it was administered i.p., LD50 values were 1757 mg/kg in male mice, 1652 mg/kg in female mice, 915 mg/kg in male rats, and 1076 mg/kg in female rats. The lethal doses of this drug were more than 5000 mg/kg in both sexes of dogs by the oral route. The LD50 values of NM394 were 226 mg/kg in male rats and 238 mg/kg in female rats by the i.v. route. In mice, the major clinical signs observed following the administration of prulifloxacin were sedation, oligopnea, abnormal gait, piloerection, closed eye and tremor by the i.p. route and a scab at the site of injection by the s.c. route; in rats, decreased spontaneous locomotor activity by any of the three routes, oligopnea, lacrimation, hypothermia, piloerection and abnormal gait by the i.p. route, and a scab at the site of injection by the s.c. route; and in dogs, vomiting, reddening of the skin, and loose stool by the oral route. When NM394 was administered i.v., rats showed clonic convulsion and dyspnea. The site of injection was hyperemic, swollen and necrotic. Mice showed a decrease in body weight or an inhibition in weight gain when prulifloxacin was administered i.p. and rats showed the same effects when prulifloxacin or NM394 was administered by any of the above-mentioned routes. Macroscopic findings detected following the i.p. administration of prulifloxacin in mice were pale color of the liver and spleen, thickening of the liver, and adhesion of intra-abdominal organs; and in rats, hydrothorax, congestion and edema of the lung, adhesion of intra-abdominal organs, swelling of the kidney accompanied by fine yellowish-white foci, and atrophy of the testis. When NM394 was administered i.v. to rats, congestion of the lung was macroscopically observed.
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PMID:[Single-dose toxicity studies of prulifloxacin (NM441) in mice, rats and dogs and the active metabolite (NM394) in rats]. 870 68

A single dose toxicity of calcipotriol (MC903), an anti-psoriasic agent, administered subcutaneously (s.c.) and percutaneously (p.c.) was studied in Slc:SD rats (s.c. and p.c.) and beagle dogs (s.c.). The LD50 values of MC903 were as follows: rats, 2.19 mg/kg in males and 2.51 mg/kg in females by s.c., and more than 15 mg/kg in both sexes by p.c.; dogs, more than 1.5 mg/kg in males by p.c. No sexual difference was noted in LD50 values of rats. Death of rats was observed from 1 to 3 days after administration by both routes. Dead animals showed decreases in body weight and locomotor activity, reddish tear, abnormal gait and dirty hair by both routes. Furthermore, dead animals administered by s.c. showed salivation, nasal discharge, piloerection, ptosis, diarrhea, urorrhea, nasal and vaginal bleeding, subnormal temperature, loose stool, cyanosis, irregular and deep respirations, clonic and tonic convulsions. Survival of rats showed similar signs to those of dead animals except for nasal discharge, nasal and vaginal bleeding, cyanosis, agonal respiration and convulsion. Discoloration of the kidney, white patch of the heart and a dilatation of the stomach wall were observed on macroscopic examinations. No mortalities were observed in dogs which showed vomiting, conjunctival congestion, circumoral and auricular reddenings, periblepharal purplish reddening, decreases in locomotor activity and defecation, emaciation, eye discharge, skin desquamation of treated area and an increase in respiration. On macroscopic examination, desquamation of the skin, reddening of the circumoral mucosa, pale gray yellow striations in renal tubules of the cortex and discoloration of the thyroid were observed. Histopathological findings revealed epidermal thickening with parakeratosis, fibrocytes, hypertrophy and hypersecretion of the sebaceous and sweat glands, formation of epitheloid glanulomas and infiltration of neutrophils in the subcutaneous tissues. Furthermore, moderate calcium deposits in the renal tubules, fatty cells and slight calcium deposits in interstitial tissues of the thyroid, and a cystic nest of an ectopic intestinal epithelium between muscle layers of the duodenum were observed at the highest dose. On the basis of results obtained in the present study, rats administered MC903 by s.c. or p.c. died probably due to the circulatory and renal disturbance resulted from effects of this drug on the heart and kidney.
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PMID:[Single dose toxicity studies of calcipotriol (MC903) in rats and dogs]. 874 15

A single dose toxicity study of magnesium sulfate by intravenous administration was conducted in rats and dogs. The results are summarized in the following. Magnesium sulfate was administered once at dose levels of 90, 130, 200, 300 and 450 mg/kg to Crj:CD(SD) rats at 6 weeks of age. Deaths occurred in the 200 mg/kg and above groups in both sexes. The LD50 values were 206 mg/kg for males and 174 mg/kg for females. In the surviving animals, in the 130 mg/kg and above groups, tonic convulsions, abnormal gait and tachypnea were seen. However, these signs disappeared gradually and all animals returned to a normal state by 15 min after dosing. There were no treatment-related changes in the body weight or gross pathology. Magnesium sulfate was infused for 6 hr at dose levels of 75, 300 and 1200 mg/kg (12.5, 50 and 200 mg/kg/hr) to female beagle dogs at 6 months of age. No deaths were observed in any of the dose groups and it was considered that the lethal dose level would be higher than 1200 mg/kg(200 mg/kg/hr). In the 1200 mg/kg group, vomiting, decreased spontaneous movement, staggering gait, prone position and flush of the conjunctiva and ear auricles were seen. However, these signs disappeared gradually and animals returned to a normal state by 1 hr after dosing. There were no treatment-related changes in the body weight, food consumption or gross pathology.
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PMID:[A single dose toxicity study of magnesium sulfate in rats and dogs]. 961 34

A colloid cyst, also called a neuroepithelial cyst, is a slow-growing, benign tumor that occurs in the anterior third ventricle. The cyst typically blocks the foramen of Monro, causing obstructive hydrocephalus involving only the lateral ventricles. The most common presenting sign and symptom of a colloid cyst is headache. Less common presenting signs and symptoms include nausea, vomiting, memory loss, mental status changes, gait disorder, and visual disturbances. Surgical resection is the recommended treatment. Meticulous baseline and ongoing neurological assessments are of paramount importance in the care of a patient with a colloid cyst to promote optimal patient outcomes.
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PMID:Colloid cyst: a case study. 1848 40

Ziconotide is a conopeptide intrathecal (IT) analgesic which is approved by the US Food and Drug Administration (FDA) for the management of severe chronic pain. It is a synthetic equivalent of a naturally occurring conopeptide found in the venom of the fish-eating marine cone snail and provides analgesia via binding to N-type voltage-sensitive calcium channels in the spinal cord. As ziconotide is a peptide, it is expected to be completely degraded by endopeptidases and exopeptidases (Phase I hydrolytic enzymes) widely located throughout the body, and not by other Phase I biotransformation processes (including the cytochrome P450 system) or by Phase II conjugation reactions. Thus, IT administration, low plasma ziconotide concentrations, and metabolism by ubiquitous peptidases make metabolic interactions of other drugs with ziconotide unlikely. Side effects of ziconotide which tend to occur more commonly at higher doses may include: nausea, vomiting, confusion, postural hypotension, abnormal gait, urinary retention, nystagmus/amblyopia, drowsiness/somnolence (reduced level of consciousness), dizziness or lightheadedness, weakness, visual problems (eg, double vision), elevation of serum creatine kinase, or vestibular side effects. Initially, when ziconotide was first administered to human subjects, titration schedules were overly aggressive and led to an abundance of adverse effects. Subsequently, clinicians have gained appreciation for ziconotide's relatively narrow therapeutic window. With appropriate usage multiple studies have shown ziconotide to be a safe and effective intrathecal analgesic alone or in combination with other intrathecal analgesics.
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PMID:Safety and efficacy of intrathecal ziconotide in the management of severe chronic pain. 1970 62

Fourth ventricle meningiomas (FVMs) are rare, often misdiagnosed, lesions. To the best of our knowledge, 47 cases have been reported in the literature: we describe our series of three cases treated at our Institution, focusing on some diagnostic tips and intraoperative features of these tumours. Our three patients have a history of headache. Gait disturbances, vomiting and/or diplopia complicated the clinical picture before the referral at our Department. The operations were uneventful, and the patients fully recovered from neurological symptoms. They are free of recurrence at a median follow-up of 19 years. FVMs are rare lesions, which are difficult to differentiate preoperatively from the much more common ependymomas. A preoperative distinction would be extremely advantageous: indeed, although both tumours share similar radiological and clinical patterns, they clearly differ as to surgical difficulty and outcome. In fact, meningiomas are comparatively easier to remove, granting better clinical results.
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PMID:Fourth ventricle meningiomas: a rare entity. 2170 37


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