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Query: UMLS:C0042963 (vomiting)
 31,883 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Calea zacatechichi is a plant used by the Chontal Indians of Mexico to obtain divinatory messages during dreaming. At human doses, organic extracts of the plant produce the EEG and behavioral signs of somnolence and induce light sleep in cats. Large doses elicit salivation, ataxia, retching and occasional vomiting. The effects of the plant upon cingulum discharge frequency were significantly different from hallucinogenic-dissociative drugs (ketamine, quipazine, phencyclidine and SKF-10047). In human healthy volunteers, low doses of the extracts administered in a double-blind design against placebo increased reaction time and time-lapse estimation. A controlled nap sleep study in the same volunteers showed that Calea extracts increased the superficial stages of sleep and the number of spontaneous awakenings. The subjective reports of dreams were significantly higher than both placebo and diazepam, indicating an increase in hypnagogic imagery occurring during superficial sleep stages.
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PMID:Psychopharmacologic analysis of an alleged oneirogenic plant: Calea zacatechichi. 382 Nov 39

We reviewed the natural history and differential diagnosis of ornithine transcarbamylase deficiency (an X-linked inborn error of urea synthesis) in 13 symptomatic female heterozygotes. The patients presented as early as the first week of life or as late as the sixth year. The most common symptoms before diagnosis were nonspecific: episodic extreme irritability (100 percent), episodic vomiting and lethargy (100 percent), protein avoidance (92 percent), ataxia (77 percent), Stage II coma (46 percent), delayed physical growth (38 percent), developmental delay (38 percent), and seizures (23 percent). Including the proband, 42 percent of the female members of the 13 families studied had symptoms. The median interval between the onset of major symptoms (vomiting and lethargy, seizures, and coma) and diagnosis was 16 months (range, 1 to 142). Five patients had IQ scores below 70 at the time of diagnosis. We suggest that careful evaluation of the family history, the dietary history, the episodic nature of the nonspecific symptoms, the response of these symptoms to the withdrawal of protein, and their frequent onset at the time of weaning from breast milk will permit early diagnosis and might thereby reduce the risk of death or neurologic impairment in female patients with partial ornithine transcarbamylase deficiency.
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PMID:Natural history of symptomatic partial ornithine transcarbamylase deficiency. 394 92

A series of 12 patients with cerebellar infarcts diagnosed by computerized tomography are reviewed. The clinical features of cerebellar infarctions cover a wide spectrum, mimicking symptoms and signs from an acute labyrinthitis to a rapidly expanding posterior fossa mass lesion with brain stem and cerebral dysfunction. Two patients were asymptomatic and three showed signs of cerebellar dysfunction only. Three patients had evidence of brain stem dysfunction with cranial nerve palsies accompanying the cerebellar deficit. Two presented a pseudovestibular form with sudden onset of nausea, vomiting, rotary dizziness and ataxia. A pseudotumoral form with intracranial hypertension was found in two cases, in which softening tissue acts as a rapidly expanding posterior foss mass lesion. It is difficult to identify the exact artery involved in a cerebellar infarct because of the collateral circulation and connections between the three major arteries. Atherosclerosis and general decrease in blood flow can be regarded as the most likely factors precipitating focal cerebellar infarction. Surveillance is necessary during the first days with anti-edematous therapy. Rapid deterioration of consciousness should be considered a sign of increasing intracranial pressure progressing with the development of hydrocephalus. If necessary, surgical decompression by external drainage or by direct access to the posterior fossa can be carried out.
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PMID:[Cerebellar infarct. Clinical presentation and x-ray computed tomography of the brain]. 394 88

After reviewing the literature, a personal series of 10 adult patients with cerebellar infarction diagnosed by CT scan is described. The clinical picture in young adult men is characterized by rapid onset of headache, vomiting, vertigo, ataxia and blurred vision. After this sudden onset the patients may present a stable course or a rapid or delayed onset of brain stem compression, revealed by impairment of consciousness. CT scan is the diagnostic method of choice. The correlation between angiographic and CT localization of the infarction is not good. For therapy the following policy is suggested: in alert and clinically stable patients: medical treatment (mannitol, glycerol, dexamethason), ICP and serial CT monitoring; in alert patients with hydrocephalus or mass effect: medical treatment and monitoring as mentioned before; ventricular drainage if ICP surpasses 350 mm H2O; in patients with impaired consciousness and hydrocephalus or mass effect: immediate ventricular drainage. If it is not followed by prompt improvement of the level of consciousness, an emergency suboccipital craniectomy with removal of the infarcted tissue should be done.
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PMID:Surgical management of acute cerebellar infarction. 398 89

Seventeen patients with computed tomographic (CT) evidence of a solitary cerebellar metastasis were studied. In 11 of 17 cases, neurologic symptoms preceded systemic evidence of carcinoma. Initial neurologic symptoms included gait instability (13 cases) and headache and vomiting (four cases). All patients had evidence of gait or limb ataxia on neurologic examination. Fourteen patients underwent craniotomy and subsequent irradiation, and three had radiotherapy without initial surgical biopsy. One patient with lung carcinoma had clinical and CT evidence of intracranial recurrence 14 months later but no evidence of widespread systemic carcinoma. Fifteen patients later showed evidence of systemic carcinoma but then died without subsequent development of recurrent cerebellar dysfunction or other neurologic abnormalities. Furthermore, in six of these patients with widespread systemic carcinoma, scans taken two to six months after completion of surgery and/or radiation therapy for the solitary metastasis showed no evidence of recurrent intracranial disease.
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PMID:Solitary cerebellar metastases. Clinical and computed tomographic correlations. 398 9

A four-year old girl developed signs of increased intracranial pressure (head-ache, vomiting, ataxia, tremor, papilledema, cranial suture spread). Abacterial meningoencephalitis due to herpes virus was diagnosed, while the initially suspected brain tumor was ruled out. Without specific therapy the patient recovered completely; even the cranial suture spread disappeared. This case report demonstrates an unusual and more benign course of central nervous herpes virus infection.
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PMID:[High intracranial pressure with the spreading of the cranial sutures as a leading symptom of herpes simplex meningitis]. 403 18

Idiopathic feline vestibular syndrome, a peripheral vestibular deficit of unknown cause, was diagnosed in 75 cats at the New York State College of Veterinary Medicine Teaching Hospital from July 1975 to October 1984. Review of the medical records of these cats indicated that the syndrome was seen in more cats in July and August (P less than 0.001) than in other months. Clinical signs included head tilt, ataxia, rolling, rotatory or horizontal nystagmus, and occasional vomiting.
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PMID:Review of idiopathic feline vestibular syndrome in 75 cats. 405 20

Animal studies have indicated a "vomiting center" situated in the dorsal portion of the lateral reticular formation of the medulla at the level of the dorsal nucleus of the vagus. There is also a chemoreceptor trigger zone in the floor of the fourth ventricle in the area postrema which influences the vomiting center. A 63 year old man with a three year history of metastatic malignant melanoma presented with nausea, projectile vomiting, gait ataxia and diplopia associated with horizontal and vertical nystagmus. CT scan showed a solitary brainstem metastasis without hydrocephalus and he was treated with radiotherapy with resolution of his vomiting after four weeks. At post mortem three months later a metastasis was found in the right middle cerebellar peduncle and lateral tegmentum of the pons; there was no pathological change in the area of the vomiting center or area postrema. It is postulated that this lesion caused projectile vomiting because of involvement of either afferent projections to the vomiting center. The neuroanatomy of vomiting is discussed.
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PMID:The neuroanatomy of vomiting in man: association of projectile vomiting with a solitary metastasis in the lateral tegmentum of the pons and the middle cerebellar peduncle. 407 83

A 72-year-old woman, previously in good health, suffered for 2 years from attacks of a complex neuropsychiatric syndrome lasting from 2 days to 4 weeks. These episodes, which were followed by intervals of nearly complete recovery, were usually marked by fever, headache, mental confusion, vomiting ataxia, anisocoria, epileptic seizures and stiffness of the neck. Neuroradiological investigation revealed only slight ventricular dilatation. In 13 CSF examinations, there was reduced glucose, increased protein, considerable rise of the IgG index and constant oligoclonal bands. There was also an increase of polymorphonuclear leucocytes, lymphocytes or epithelial-like cells. As all microbial, viral or mycotic tests were negative and the patient recovered, the case was considered to be benign recurrent meningitis of Mollaret. The nosological position of this rare disease, as well as its probable pathogenetic mechanisms, are discussed.
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PMID:A case of benign recurrent meningitis of Mollaret. 616 85

When a patient with a peripheral monocular paresis is forced to look with the paretic eye, head movements induce the sensation of an unstable visual world. The patient behaves as if he had acute bilateral labyrinthine lesions. These symptoms are due to the lack of compensatory ocular movement and the patients complain that the visual objects move in the direction opposite to the head. The patients develop ataxia, nausea, vomiting and past pointing. The symptoms, however, are transient and consistently disappear after approximately 48 hours. The central adaptation to looking and seeing with the paralysed eye is associated with a plastic change of the VOR. This plastic adaptation is probably induced by the large retinal slip produced by the lack of compensatory movement of the eye and can be studied in the normally mobile eye in the dark. The psychophysical adaptation is probably generated by an efferent copy or corollary discharge of the vestibular system to the visual system that cancels the retinal error.
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PMID:Looking with a paralysed eye: adaptive plasticity of the vestibulo-ocular reflex. 647 Jul 22


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