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Query: UMLS:C0028738 (nystagmus)
 7,431 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

This is a review of selected aspects of the history of the vestibular system (J. E. Purkyne, E. Mach, A. Crum-Brown) and of our current understanding of vestibular malfunction in clinical vertigo syndromes. Evidence is presented for a preliminary classification of central vestibular brainstem syndromes according to the three major planes of action of the vestibulo-ocular reflex (VOR): (1) disorders of the VOR in the horizontal (yaw) plane (horizontal nystagmus, pseudo 'vestibular neuritis'); (2) disorders of the VOR in the sagittal (pitch) plane (downbeat nystagmus; upbeat nystagmus); (3) disorders of the VOR in the frontal (roll) plane (ocular tilt reaction; lateropulsion). The pathophysiology of peripheral vestibular disorders is discussed: a specific gravity differential between the cupula fluid and the endolymph (buoyancy mechanism) causes vertigo in benign paroxysmal positioning vertigo and positional alcohol nystagmus. Vestibular neuritis is probably a partial unilateral vestibular paralysis due to viral infection of the superior division of the nerve trunk. The common post-traumatic vertigo is explained by otolith dysfunction secondary to dislodged otoconia resulting in unequal loads on the macula beds and a tonus imbalance between the two otoliths.
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PMID:Man in motion. Historical and clinical aspects of vestibular function. A review. 193 40

The study included 80 patients treated for sudden deafness over the last 5-7 years. Case history, laboratory findings, pure-tone audiogram and electronystagmography (ENG) findings were noted. If any abnormalities had been recorded in ENG studies, the studies were redone. ORL status was redefined and audiograms were obtained in all patients. When becoming ill, the 80 patients had not differed from the normal population in common cardiovascular risk factors. None of them had had signs of viral infection (paired serum samples had been taken at 2-week intervals; routine examinations had been done for common viral antigens). As many as 31 of the 80 patients with acute hearing loss had had abnormalities such as spontaneous nystagmus (PN), hypoexcitability (HE) and directional preponderance (DP) in the bithermal caloric tests (+44 degrees C, + 30 degrees C) of their ENG studies. Twenty of the 31 patients still had abnormal ENG studies after 5-7 years. Only 1 subject had positional nystagmus, and none had subjective vertigo. Patients with an abnormal ENG study showed a poor recovery of the speech reception threshold, whereas those with a normal ENG study showed slightly significant (p less than 0.05) recovery.
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PMID:Electronystagmographic findings and recovery of cochlear and vestibular function in patients suffering from sudden deafness with a special reference to the effect of anticoagulation. 280 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

Four cases of gaze paresis occurred in association with viral disease. In three cases the viral prodrome preceded the oculomotor disturbance. In one, gaze palsy was followed several days later by a viral syndrome. One had isolated bilateral horizontal ophthalmoplegia; another patient had motility disturbance with blepharoptosis and peripheral areflexia. Two patients had clinical evidence of brain-stem involvement: unilateral gaze paresis and gaze-evoked nystagmus in one and Parinaud's syndrome in the other. No accompanying long-tract signs or changes in mental status were present in any case. Recovery was complete in all four patients.
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PMID:Gaze palsy associated with viral syndrome. 403 36

The clinical and pathological findings after a natural intra-uterine infection with BVD-virus in a Friesian dairy herd are described. The virological and serological aspects will be discussed in a separate paper (30). In a period of 4 years, 11 calves were born with the following nervous symptoms: more or less serious incoordination, tremor, oscillating nystagmus, and a negative blinking reflex. The pupillary and sucking reflexes were normal. No ocular defects, such as lenticular opacity or retinal atrophy were observed. The first calf was born in 1979. Within 6 months the symptoms disappeared. After a normal conception and pregnancy this animal gave birth to 2 clinically normal calves in 1981 and 1982. The second calf died at the age of 2 months, due to an ulcerating enteritis. In 1980, again 8 calves with the same nervous symptoms were born within a period of 3 months. Two calves died at the age of 3 days and 5 weeks respectively; 2 calves were sold when 10 days and 3 weeks old; one calf did not improve and was necropsied at the age of 17 days. The remaining 3 calves showed only a slight hypermetria when examined after 6 months. At that time nystagmus was only visible with ophthalmoscopy. Two calves were slaughtered when 10 months old. The last one, a bull, proved to be sterile and was necropsied at the age of 1 1/2 year. A calf, born in 1981, recovered within a week and was necropsied at the age of 15 days. The last calf, born in 1982, did not improve at all and was necropsied at the age of 14 days. During these 4 years none of the other animals in the herd showed any symptoms due to an acute or chronic BVD-virus infection. At post mortem examination of 6 animals no macroscopically visible malformations were found. Hypomyelination and abnormal glial cells were evident in 5 cases, especially in the two youngest calves which did not show any improvement. One of them had had an obvious thymic hypoplasia. The calf which recovered within a week showed only very slight changes. In one of the calves slaughtered at 10 months, inflammatory lesions were found in the brain. The diagnosis was confirmed by virological investigations. Clinically as well as pathologically there was a close resemblance to Border disease in lambs and congenital tremor in piglets after prenatal exposure to Hog cholera virus.
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PMID:Neurological disorders, virus persistence and hypomyelination in calves due to intra-uterine infections with bovine virus diarrhoea virus. I. Clinical symptoms and morphological lesions. 664 98

A 37-year-old woman with complaints of headache and nausea presented with temporary disturbance of consciousness, bulbar palsy and ataxic speech following flu-like symptoms. After the recovery of her consciousness, she developed orthostatic syncope and numbness all over the body. When she was admitted to our hospital two months later, she showed emaciation, diminished sweat production and butterfly-patch-like pigmentation. Neurologic examinations were remarkable for anisocoric pupils that sluggishly reacted to light, impaired left facial movements, bulbar palsy, numbness of the whole body, total loss of all tendon reflexes, incordination, ataxic gait and severe postural hypotension. Laboratory data included albuminocytogenic dissociation in cerebrospinal fluid, convergence nystagmus and dysmetria in electronystagmography, and right trigeminal paralysis in blink reflex. A sural nerve biopsy showed active axonal degeneration and severe loss of both myelinated and unmyelinated fibers. Examinations of autonomic nervous system disclosed diffuse impairment of sympathetic and parasympathetic postganglionic nerve. Based on these findings she was diagnosed as having acute pandysautonomia. High titer of serum EB virus antibody suggested that acute pandysautonomia and diffuse brainstem impairment may be related to EB virus infection.
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PMID:[A case of acute pandysautonomia and diffuse brain stem impairment associated with EB virus infection]. 772 95

Hydranencephaly without arthrogryposis was observed in three newborn Holstein-Friesian calves, born during one week in a 400-cow dairy herd in Zambia. The affected calves were blind and exhibited nystagmus and depressed behavior. Akabane virus infection was suspected based on the pathological findings and etiological data, however, we could not determine the exact causative agent.
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PMID:Hydranencephaly in newborn calves in Zambia. 835 35

A case of brainstem encephalitis of undetermined etiology is reported in 66-year-old woman who had a sudden onset of illness with left abducens palsy, nystagmus and ataxia. The symptoms progressed to complete paralysis of eye movements, dysphagia and left hemiparesis with generalized hyperreflexia. Examination of CSF, CT scan and MRI of the brain were normal. The patient died 4 months after onset of disease. Neuropathologic study disclosed in the brainstem numerous perivascular and nodular inflammatory cell infiltrations composed predominantly of lymphocytes T and B. Most intensive inflammation concerned midbrain and pontine tegmentum and to a lesser degree medulla oblongata, pontine nuclei and cerebellar nuclei. Basal ganglia, cerebral and cerebellar cortex were unaffected. Neuropathological finding was reminiscent of brainstem encephalitides related to viral infection or to paraneoplastic syndrome. However, HSV-1, EBV, and CMV antigens were not detected by immunohistochemistry, as well as evidences of malignancy were not present in this case.
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PMID:A case of the subacute brainstem encephalitis. 1007 3

Sudden, spontaneous, unilateral loss of vestibular function without simultaneous hearing loss or brain stem signs is generally attributed to a viral infection involving the vestibular nerve and is called acute vestibular neuritis. The clinical hallmarks of acute vestibular neuritis are vertigo, spontaneous nystagmus, and unilateral loss of lateral semicircular function as shown by impulsive and caloric testing. In some patients with vestibular neuritis the process appears to involve only anterior and lateral semicircular function, and these patients are considered to have selective superior vestibular neuritis. Here we report on two patients with acute vertigo, normal lateral semicircular canal function as shown by both impulsive and caloric testing, but selective loss of posterior semicircular canal function as shown by impulsive testing and of saccular function as shown by vestibular evoked myogenic potential testing. We suggest that these patients had selective inferior vestibular neuritis and that contrary to conventional teaching, in a patient with acute spontaneous vertigo, unilateral loss of lateral semicircular canal function is not essential for a diagnosis of acute vestibular neuritis.
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PMID:Inferior vestibular neuritis. 1196 Aug 14

Acute cerebellar ataxia is a relatively common neurologic disorder among children. Our aim was to characterize the clinical picture, etiology, and prognosis of acute cerebellar ataxia. The medical records of all children with a diagnosis of acute cerebellar ataxia hospitalized in our center and Hasharon Medical Center from 1990 to 2001 were reviewed. The diagnosis of acute cerebellar ataxia was based on the following criteria: acute onset of ataxia with or without nystagmus; absence of known genetic predisposing factors, such as familial degenerative disorders; and absence of drug intoxication, bacterial meningitis, and metabolic disorders. Thirty-nine children were identified; 54% were male; mean age at presentation was 4.8 +/- 3.8 years. All patients were observed for at least 1 year. A prodromal febrile illness was noted in 74.4%: varicella, 31%; mumps, 20%; nonspecific viral infection, 15.4%; mycoplasma, 5%; Epstein Barr virus, 3%. Latency from the prodromal illness to the onset of ataxia was 8.8 +/- 7.4 days. The most common associated neurologic findings were nystagmus and dysmetria. Full gait recovery took less than 2 weeks on average, and the longest duration of neurologic signs was 24 days (mumps-related). Acute cerebellar ataxia in childhood is a self-limited disease. The recovery was faster than that reported in previous publications and was complete in all children without any neurologic sequelae. Imaging studies are needed only in atypical presentation or if there is no spontaneous improvement after 1 to 2 weeks.
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PMID:Post-infectious acute cerebellar ataxia in children. 1455 15


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