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PubMed2004

Acute migrainous vertigo: clinical and oculographic findings.

Migrainous vertigo (MV) is an increasingly recognized cause of episodic vertigo. However, the pathophysiology of MV is still a matter of speculation and it is not known to what extent the dysfunction is located in the central or peripheral vestibular system. The aim of this prospective study was to describe the clinical spectrum of acute MV and to clarify which structures of the vestibular system are involved. Testing of 20 patients with acute MV included neuro-otological examination, recording of spontaneous and positional nystagmus with 3D video-oculography, and audiometry. Pathological nystagmus was observed in 70% of patients during acute MV: six had isolated spontaneous nystagmus, five had isolated positional nystagmus and three had a combination of the two. Only a few patients showed additional ocular motor deficits. Imbalance was observed in all patients except one. Hearing was not affected in any patient during the attack. The findings during acute MV point to central-vestibular dysfunction in 10 patients (50%) and to peripheral vestibular dysfunction in three patients (15%). In the remaining seven patients (35%) the site of involvement could not be determined with certainty. MV should be considered in the differential diagnosis of vertigo with spontaneous and positional nystagmus and can present both as a central and a peripheral vestibular disorder.

Acute Disease↗
PubMed1991

[Physiologic and pathologic rebound nystagmus. Description and comparison].

Using a binocular, infrared charged coupled device (CCD), an eye tracker coupled with an Olivetti M24 PC (resolution up to 0.1 degrees, scanning with 80 frames/s), the eye movements of 20 normal individuals with normal visual acuity and binocular function were recorded to detect physiological endpoint (EPN) and rebound nystagmus (RN). Each subject was asked to fixate a target located in the primary position (PP) and after 5 s of recording time, to look at a target either 50 degrees to the right or left of the PP for approximately 20 s and then return for the last few seconds to the PP, EPN recordings were made with the room lights on and RN recordings were made both with the lights on and in total darkness. A forehead and chin rest with bite board were used. Twelve of the 20 subjects showed EPN and RN with the lights on. The 8 subjects that did not demonstrate EPN also showed no RN with the lights on. Recordings from all 20 subjects showed RN in darkness. No differences in amplitude were found between the abducted and adducted eyes. Although clear differences in the characteristics of gaze paretic or drug-related lateral gaze nystagmus and EPN have been found, no systematic differences in RN under lighted conditions had been observed between patients and normal subjects.

Adult↗
PubMed1999

Nystagmus induced by pharmacological inactivation of the brainstem ocular motor integrator in monkey.

A common cause of pathological nystagmus is malfunction of the mechanism by which the brain integrates eye velocity signals to produce eye position commands. For horizontal gaze, neurons in the nucleus prepositus hypoglossi-medial vestibular nucleus region (NPH-MVN) play a vital role in this neural integrator function. We studied the effects on gaze stability of pharmacological intervention in the NPH-MVN of monkeys by microinjections of eight drugs. Agents with agonist or antagonist actions at gamma-aminobutyric acid (GABA), glutamate, and kainate receptors all caused gaze-evoked nystagmus with centripetal eye drifts; glycine and strychnine had no effect. When the GABAA-agonist muscimol was injected near the center of MVN, the eyes drifted away from the central position with increasing-velocity waveforms, implying an unstable neural integrator. The observed effects of these drugs on gaze stability may be related to inactivation either of neurons within NPH-MVN or the cerebellar projections to them that control the fidelity of neural integration. Drugs that influence GABA or glutamine transmission may have a role in the treatment of nystagmus due to an abnormal neural integrator.

Animals↗
PubMed2003

[Multiple meningioma in 53 years old woman manifested only by unilateral hearing loss].

Meningioma is the most common intracranial tumour and comprises over half of extramedullar tumours of spinal canal. The causes of meningiomas occurrence are mostly unknown. Genetic factors, hormonal disorders, injuries, viral induction and ionizing radiation may play certain role in its developing. There are several histological types of meningiomas; endothelial or syncytial--the most common form (64%), fibrilplastic--12%, anaplastic--11%, transitory--7%, angioplastic--%, psammoma--3%, angiomatous--1%, warty--very rarely. Authors have presented the case of a 53-year-old farmer treated in the Department of Otolaryngology Medical Academy in Bialystok due to lipoma located behind the ear. The lipoma was removed surgically under local anaesthesia. Post-operative course was uncomplicated. During laryngologic examination sensorineural hearing loss of left ear was established. Broaden audiologic and otoneurologic diagnostics revealed sensorineural hearing loss of left ear ranged between 20 to 80 dB when impedance was normal. Constant latent polydirectional nystagmus, pathologic vibratory test and asymmetric optokinetic nystagmus were confirmed in ENG exam. Magnetic resonance was performed as the central nervous system pathology was suspected. During the exam, 4 tumours of similar morphology located paracerebrally were fond. The tumours were bounded by wide base with dura matter and corresponded to meningiomas. After neurosurgical consultation, the patient was classified to surgical treatment. Frontotemporal dextral craniotomy was performed and partial meningiomas were removed. Post-operative course was uncomplicated. Transiently, narrowed visual field was observed. Audiologic parameters did not undergo change for the worse.

Diagnosis, Differential↗
PubMed2001

Central positional nystagmus simulated by a mathematical ocular motor model of otolith-dependent modification of Listing's plane.

To find an explanation of the mechanisms of central positional nystagmus in neurological patients with posterior fossa lesions, we developed a three-dimensional (3-D) mathematical model to simulate head position-dependent changes in eye position control relative to gravity. This required a model implementation of saccadic burst generation, of the neural velocity to eye position integrator, which includes the experimentally demonstrated leakage in the torsional component, and of otolith-dependent neural control of Listing's plane. The validity of the model was first tested by simulating saccadic eye movements in different head positions. Then the model was used to simulate central positional nystagmus in off-vertical head positions. The model simulated lesions of assumed otolith inputs to the burst generator or the neural integrator, both of which resulted in different types of torsional-vertical nystagmus that only occurred during head tilt in roll plane. The model data qualitatively fit clinical observations of central positional nystagmus. Quantitative comparison with patient data were not possible, since no 3-D analyses of eye movements in various head positions have been reported in the literature on patients with positional nystagmus. The present model, prompted by an open clinical question, proposes a new hypothesis about the generation of pathological nystagmus and about neural control of Listing's plane.

Animals↗
PubMedDate not supplied

The effect of eye closure upon the pathological vestibular spontaneous nystagmus.

In the course of one year (September 1973 to September 1974) a total of 784 patients were examined with nystagmography. We were dealing with patients who consulted us for reasons of equilibrium disturbances, sensori-neural hearing loss and/or tinnitus. In 200 patients we observed a definite vestibular spontaneous nystagmus (SN) in supine position. Ocular pendular nystagmus was eliminated. On the basis of these 200 electronystagmographic recordings, the effect of eye closure upon the pathological spontaneous nystagmus was analysed. According to the statistical mean value, spontaneous nystagmus with open eyes in darkness was stimulated by eye closure. Further evaluation revealed, however, that 24% of our patients showed spontaneous nystagmus exclusively with open eyes in darkness, 30% only with closed eyes. Nevertheless, the occurrence of spontaneous nystagmus with either open or closed eyes in darkness, or in both conditions, does not permit topodiagnostic conclusions. The possibility of nystagmus inhibition by eye closure must be considered when the case history indicates a vestibular disturbance but a spontaneous nystagmus with closed eyes in absent in the electronystagmography. The clinical observations in one patient are described in detail for example. To exclude errors, one should search for a spontaneous nystagmus following the necessary examination behind Frenzel's glasses-in case of nystagmography-by closed as well as by opened eyes in darkness.

Adolescent↗
PubMed1985

[Importance of the general radiograph of the cervical spine in vertigo and pathologic proprioceptive cervical nystagmus].

The general roentgenogram of the cervical spine often shows manifold pathological alterations by patients without any clinical complaints. On the other hand, there are cervical vertigo and different symptoms caused by the cervical spine, its joints, muscles and ligaments without any X-ray manifestation. Nevertheless, some connections are assumed to exist between vertigo and alterations of the cervical spine an assumption supported especially by the frequently successful elimination of cervical troubles by chirotherapy. We compared the X-ray manifestations in patients complaining of vertigo with any and without any pathological proprioceptive cervical nystagmus provoked by examination according to Moser and revealed by electronystagmography. The extended posture of the cervical spine seems to point to a possible cause of vertigo. Likewise, some degenerative alterations seem to exercise a pathological effect, provoking cervical vertigo additionally if both effects are combined. Uncovertebral arthroses seem to have the same effect without occurring in combination with other effects. The general roentgenogram of the cervical spine in the sloping, lateral and anterior-posterior direction may consequently point to some possible causes of cervical vertigo.

Cervical Vertebrae↗
PubMed1977

Transitory impairment of vision after light head trauma in childhood.

From a group of 101 children, eleven (10.9 p.c. ranging in age from 4--12) reported transient visual disturbances such as blurred vision, grey vision or photopsias immediately after a light head trauma. As to the origin of these impediments all evidence points to the occipital areas. Oculopupillary defects or pathological nystagmus phenomena were in no case associated. The frequency of pathological EEG recording over the occipital area was statistically significant (chi-quadrat = 4.27; p less than or equal to 0.05). The pathogenetic mechanism may be explained by means of a local oedematous reaction.

Adolescent↗
PubMed1976

Multiple sclerosis. The value of clinical vestibular examination.

A clinical vestibular examination was carried out on 82 patients with multiple sclerosis (MS) selected on McAlpine's criteria. Spontaneous nystagmus, positional nystagmus or pathological caloric test were found in 49 (60%) patients. Pathological horizontal optokinetic nystagmus occurred in 47 (57%) patients. In 36 cases horizontal optokinetic nystagmus was pathological to both sides, in 28 cases combined with a pathological vertical optokinetic nystagmus, indicative of diffuse intracerebral lesions. Lesions in the central vestibular system and in the optokinetic pathways were frequently discovered in early or atypical cases of MS.

Adult↗
PubMed2000

Prospects for treating acquired pendular nystagmus with servo-controlled optics.

PURPOSE: To determine whether a device featuring electronically controlled motor-driven prisms can reduce oscillopsia and improve acuity in patients with acquired pendular nystagmus (APN). METHODS: A device was developed that senses eye movements and, by the use of motor-driven prisms, oscillates the image of the world in lockstep with the pathologic nystagmus, to negate its deleterious visual effects. Unlike existing optical and surgical treatments for nystagmus, the device negates only the pathologic movements. Voluntary and normal reflex eye movements required for normal vision are unaffected. The benefits of the device were assessed by its impact on acuity in five patients with medication-refractory APN. RESULTS: All patients reported decreases in oscillopsia when the device was in operation. Averaged across patients, the device increased the percentage of time in which retinal image velocity was within +/-4 degrees/sec from 12.8% to 33.3%. Acuities improved in four of five patients, by an average of 0.21 logMAR units. CONCLUSIONS: The symptoms of pendular nystagmus can be treated with a servomechanical device. Further refinements in the device should result in greater improvements in acuity, and a portable, wearable version is feasible using existing technologies.

Adult↗
PubMed1998

Oculomotor testing in the differential diagnosis of degenerative ataxic disorders.

BACKGROUND: Oculomotor abnormalities have been reported in patients with degenerative ataxic disorders. OBJECTIVE: To assess the diagnostic sensitivity and specificity of oculomotor deficits in patients with Friedreich ataxia (FA), cerebellar atrophy (CA), and olivopontocerebellar atrophy (OPCA). SETTING: Neurology clinic at a university hospital in Lübeck, Germany. PATIENTS: Seven patients with FA, 9 with CA, and 10 with OPCA were studied. These patients were selected from an ongoing follow-up study. MAIN OUTCOME MEASURES: Eye movements were recorded by electro-oculography; an extensive battery of quantitative tests was used. RESULTS: A proven CAG repeat expansion on chromosome 6 or 14 was significantly associated with reduced saccadic eye velocity and vertical gaze palsy (P<.001, Mann-Whitney U test). All 6 patients with OPCA and slow saccades had an autosomal-dominant inheritance; 4 of them were proved to have spinocerebellar atrophy type 1. In 9 of these patients (4 with FA, 1 with CA, and 4 with OPCA), the genetic defect could not be identified. Saccadic dysmetria, impairment of smooth pursuit and optokinetic nystagmus, deficient suppression of the vestibulo-ocular reflex by either visual or otolith input, and pathological nystagmus were attributed to degenerative lesions in different parts of the cerebellum. However, these symptoms failed to clearly distinguish between the different groups of patients, whereas decreased vestibulo-ocular reflex gain, slow saccades, and vertical gaze palsy pointed to an extracerebellar manifestation of the degenerative disease, occurring only in patients with OPCA and FA. CONCLUSIONS: In this prospective study, oculomotor disturbances were mainly related to cerebellar dysfunction. Only a few of them were caused by extracerebellar manifestations of the disease, such as slowing of saccades, which was characteristic for patients with OPCA of autosomal-dominant inheritance.

Adult↗