Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report a case of primary position downbeating nystagmus due to an occult breast carcinoma in a 57-year-old woman with progressive oscillopsia and truncal ataxia. Acute nausea and vomiting precipitated hospitalization. Magnetic resonance imaging of the brain was normal, though a sterile mononuclear cerebrospinal fluid pleocytosis was present. Search for an occult malignancy disclosed an adenocarcinoma of the breast. Radical mastectomy and oral corticosteroid therapy did not alter the clinical course of the paraneoplastic syndrome in our patient. Primary position downbeating nystagmus is an uncommon manifestation of an occult malignancy. Our report and review of the literature suggests that investigations necessary for the diagnosis of occult malignancies of the lung, breast, uterus, and ovary be included in the search for cryptic causes of downbeating nystagmus.
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PMID:Paraneoplastic downbeating nystagmus. A sign of occult malignancy. 285 13

Eighty-one cases with vestibular neuronitis were examined. The diagnostic criteria were a sudden onset of vertigo without previous symptoms, spontaneous nystagmus towards the healthy side, totally extinguished caloric responses with 44 degrees C and 30 degrees C water irrigation and no involvement of hearing associated with the onset of the disease. The series was divided into a prospective and a retrospective group. The prospective group A was examined at the acute stage, about 1 month and 1 year afterwards. The retrospective group B fulfilled the same criteria as group A and was examined 1-8 years after the acute stage. The results of the acute stage in group B were analysed from the case history reports, electronystagmo- and audiograms. The preceding and predisposing factors and symptoms were inquired. The examination scheme included the clinical otoneurological examination, the nystagmographic, audiological and clinical neurophysiological measurements and the serological and hematological specimens were collected at the acute stage of group A to examine the role of virus infections in the etiology of vestibular neuronitis. The liquor specimens of 16 cases available in group A were analysed. A recent respiratory infection was reported by 9 cases (27.3 percent) in group A and by 18 cases (37.5 percent) in group B. The serological evidence (increase of IgM-antibodies) was observed in 1 case against influenza A and in 1 case against parainfluenza 3 and the hematological examinations revealed clues of virus infection in 6 cases (18.2 percent) of group A. Cell counts and protein analyses of the liquor specimens were within normal limits. Cases with arterial hypertension under medical control were observed in 15.2 percent of group A and 14.6 percent in group B. These figures do not exceed the age- and sex-correlated prevalence of arterial hypertension in Finnish population. The clinical symptoms included an acute chiefly rotatory vertigo associated with nausea and vomiting without subjective involvement of hearing. The prominent symptoms lessened gradually during the first week and most of the patients were able to their earlier work after one month. The prognosis of the disease was good. The clinical otoneurological findings of the acute stage included spontaneous nystagmus with Frenzel's glasses and disturbances of the vestibulospinal tests. These abnormalities improved markedly during the follow-up period. The results of electronystagmography were characteristic of a pure peripheral vestibular disorder. Nystagmic beats were observed almost regularly in the pendular eye-tracking test at the acute stage examination.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Vestibular neuronitis. An otoneurological evaluation. 306 52

A case of akinetic mutism was reported with reference to a marked improvement by levodopa, bromocriptine and trihexyphenidyl. A 39-year-old male, first seen on February 2, 1981, had an occipitalgia, accompanied by nausea and vomiting. For several months before this consultation, the patient had suffered from asthenopia. Brain CT scan and cerebral angiogram demonstrated internal hydrocephalus due to aqueduct stenosis of unknown etiology. After a ventriculoperitoneal shunt operation on February 20, 1981, he completely recovered. Two years and a half after the shunt insertion he had no difficulty in his daily life. He reentered the hospital on December 21, 1983, because of personality change, mental deterioration and bradykinesia. Brain CT scan showed recurrent hydrocephalus resulting from shunt blockage. Following the shunt revision, hydrocephalus was resolved. Nevertheless, the patient did not return to his previous state. And he became bed-ridden, incontinent of urine, and unable to take fluids or foods, following which he went into a state of akinetic mutism. Other neurological findings were as follows: upward gaze palsy, impaired convergence, convergence nystagmus, plastic rigidity of neck and all four limbs, and diffuse hyperreflexia with right Babinski's sign. Abnormal involuntary movement was not seen. On March 27, 1984, levodopa therapy was instituted and on April 2, trihexyphenidyl was combined with levodopa. Shortly after administration of levodopa and trihexyphenidyl, akinetic mutism began to improve, but upward gaze palsy was not affected. He began to speak and could walk unassisted by the end of July.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Akinetic mutism from recurrent hydrocephalus: successful treatment with levodopa, bromocriptine and trihexyphenidyl]. 343 88

Positional nystagmus of the central type and gaze paretic (gaze evoked) nystagmus have been reported in pathology of the posterior fossa. It has also been reported that positional nystagmus of the central type is only infrequently accompanied by vertigo and nausea. In this paper five cases are discussed which showed positional nystagmus of the central type and/or gaze paretic nystagmus. All cases showed severe vertigo, nausea and vomiting in the provocative head position. In four out of five cases the pathology was found to be in the area of the IVth ventricle. On the basis of recent neurophysiologic data an attempt is made to explain the manifestations of this pathology. It is concluded that positional nystagmus of the central type is presumably due to pathology of the IVth ventricle area. Also, that this type of nystagmus may be accompanied by severe vertigo, nausea and vomiting.
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PMID:Vestibular and oculomotor disturbances in pathology of the fourth ventricle. 696 35

In a random cross-over double-blind trial, the effects of intravenous physostigmine salicylate (2.0 mg) and placebo were observed in seven healthy volunteers 10 minutes after the intravenous administration of 1.5 mg/kg of ketamine. Recovery time was significantly shorter after physostigmine than after placebo. Nystagmus and blurred vision, which followed ketamine anesthesia, disappeared more rapidly when physostigmine was given. This study confirms previous observations that physostigmine counteracts some of the manifestation of ketamine aftereffects which resemble the so-called central anticholinergic syndrome. Nausea and vomiting were significantly more frequent after physostigmine administration.
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PMID:Physostigmine antagonizes ketamine. 699 46

Conditions associated with nausea and vomiting, such as motion sickness or side effects of medications, are commonly associated with a clinical picture consistent with parasympathetic activation and sympathetic withdrawal. It can be postulated, therefore, that vestibular stimulation contributes to sympathetic withdrawal. To test this hypothesis five normal volunteers, 24-33 years old, were studied during caloric vestibular stimulation while monitoring muscle sympathetic nerve activity directly through a needle electrode placed in a peroneal nerve. The ear was irrigated with water at a flow rate of 450 ml/min and 37 degrees C. The water temperature was sequentially lowered by 7 degree C intervals until intolerable side effects developed or a temperature of 16 degrees C was reached. Nystagmus was induced in all subjects, but heart rate, blood pressure, muscle sympathetic nerve activity and plasma norepinephrine levels did not change significantly during or after caloric stimulation, even when the subjects felt dizzy and nauseated. No evidence of sympathetic withdrawal was observed in any subject either by muscle sympathetic nerve activity or plasma norepinephrine measurements. In conclusion, we have found that selective vestibular stimulation is not accompanied by significant changes in the sympathetic nervous system function. In particular, no sympathetic withdrawal was observed. It could be argued that lack of sympathetic stimulation is an inadequate response to the symptoms associated with caloric stimulation.
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PMID:Effect of neurovestibular stimulation on autonomic regulation. 856 62

Experimental studies have shown that dextromethorphan, a noncompetitive N-methyl-D-aspartate antagonist is neuroprotective in experimental models of ischemic cerebral injury. The authors studied the safety and tolerability of oral dextromethorphan (DM) in humans, and correlated serum levels of this drug with cerebrospinal fluid (CSF) and brain levels. Neurosurgical patients undergoing intracranial surgery or endovascular procedures were given ascending doses of oral DM prior to and 24 hours after surgery. Serum, CSF, and brain levels of DM and its active metabolite, dextrorphan, were measured. One hundred eighty-one patients received a total of 212 courses of DM treatment in dose ranges of 0.8 to 9.64 mg/kg. Serum DM levels correlated highly with CSF and brain DM levels. Brain levels were 68-fold higher than serum levels, whereas CSF levels were fourfold lower than serum levels. The maximum DM levels attained were 1514 ng/ml (serum) 118 ng/ml (CSF), and 92,700 ng/g (brain). The maximum dextrorphan levels were 501 ng/ml (serum), 167 ng/ml (CSF), and 6840 ng/g (brain). In 11 patients, brain and plasma levels of DM were comparable to levels that have been shown to be neuroprotective in animal studies. Frequent side effects occurring at neuroprotective levels of DM included nystagmus (64%), nausea and vomiting (27%) distorted vision (27%), feeling "drunk" (27%), ataxia (27%), and dizziness (27%). All symptoms were reversible and no patient suffered severe adverse reactions. This study demonstrates that potentially neuroprotective doses of DM can be administered safely to neurosurgical patients. Brain and CSF levels of DM can be estimated from serum levels of the drug. Side effects, even at the highest levels, proved to be tolerable and reversible. Administration of DM to patients at risk for cerebral injury should be further explored.
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PMID:Dose escalation safety and tolerance study of the N-methyl-D-aspartate antagonist dextromethorphan in neurosurgery patients. 862 62

Vestibular symptoms frequently occur in patients with migraine headache. The common migraine is defined in neurology as a unilateral, pulsating headache, which may be associated with nausea and vomiting, and lasts one or several days. In the classic form patients have visual prodromal symptoms. Focal neurological signs in the migraine complique include, for example, oculomotor palsy and vestibular abnormalities. This so-called vestibular migraine is different from basilar migraine, which involves the irritation of the cervical sympathetic system, and can cause symptoms that resemble transient brainstem ischemia. In order to evaluate vestibular dysfunction electronystagmography (ENG) was used. Patients frequently had abnormal caloric test responses, especially with a directional preponderance, and most had a spontaneous nystagmus. In the migraine attack the patients are presumed to have hypersensitivity of the labyrinth with nausea and vomiting, while in the headache-free period the ENG was almost normal. At present, we have had a high success rate in treating patients with pyracetam. Diazepam was used to treat basilar migraine and flunarizine to prevent vestibular migraine.
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PMID:Vestibular disorders in patients with migraine. 906 28

We present a case of persistent hiccups (singultus) after a lateral medullary cerebrovascular accident. The patient presented with a two-day history of nausea and vomiting. Clinically, the patient had a loss of pain and temperature on the left side of the face, a loss of pain and temperature on the right side of the trunk, a mild left hemiparesis, and a left-sided ataxia. Nystagmus, diplopia, and hiccups were also evident. A left lateral medullary syndrome in the vascular distribution of the posterior inferior cerebellar artery was diagnosed. Work-up included a magnetic resonance imaging angiogram, which revealed an occlusion v high-grade stenosis of the basilar artery. The patient reported that the most distressing symptom was the chronic hiccups (25/min), which interfered with nutrition, sleep, and activity. While in the acute care hospital, the patient was treated with prochlorperazine, promethazine, and chlorpromazine. Each of these medications was unsuccessful in stopping the hiccups. After a search of the European literature revealed that baclofen was recommended as the drug of choice for stopping persistent hiccups, the patient was given 5 mg of baclofen by mouth three times per day, and the hiccups abated within 48 hours. The baclofen was discontinued after one week of therapy, and the hiccups did not return. We recommend consideration of baclofen for the treatment of persistent hiccups after lateral medullary syndrome because of its desirable side effects and reported success rate compared with other drugs used to treat chronic hiccups.
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PMID:Hiccups associated with lateral medullary syndrome. A case report. 912 21

Adult onset Leigh syndrome with a nucleotide (nt) 8993 mutation in mitochondrial (mt) DNA is reported. A 43-year-old woman with a 6-year-history of insulin-resistant diabetes mellitus developed muscular weakness, intractable nausea and vomiting, and anemia. These were followed vertigo, blindness, and deafness with nystagmus. Magnetic resonance imaging (MRI) revealed abnormal high intensities in the bilateral medial regions of the thalamus and periaqueductal gray matters. Autopsy disclosed well-demarcated necrotizing lesions with prominent capillaries in the areas detected by MRI, which were sufficiently diagnostic for Leigh syndrome. MtDNA analysis performed on DNAs extracted from formalin-fixed tissues including liver, heart, brain, muscle, kidney and pancreas showed a T-->G mutation at nt 8993. This is the first case of adult Leigh syndrome demonstrating on mtDNA mutations.
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PMID:Adult Leigh syndrome with mitochondrial DNA mutation at 8993. 1020 83


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