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

The electronystagmogram has its place in clinical neurological diagnosis as a recording method for the investigation of nystagmus with different conditions (spontaneous nystagmus, testing of eye-following movements, optokinetic nystagmus and rotational excitability). It must be used in all patients with complaints of dizziness, with clinically demonstrable nystagmus phenomena, in patients being examined for expert opinion after cranial traumata and in searching for vestibular involvement in certain diseases, e.g. vestibular disinhibition or dishabituation in multiple sclerosis.
 ...
PMID:[The electronystagmography in neurology (author's transl)]. 40 50

The present paper is based on an exact analysis of the neurootological findings in 30 cases of multiple sclerosis (MS). Ms-diagnosis was verified using Schumacher's criteria and cerebro-spinal fluid findings. Central vestibular disorders were found in most of the cases. From our observation it may be assumed that the brainstem is an early site of involvement causing imbalance which can only be verified by an accurate neuro-otological evaluation. The most important pathological findings are the following: central spontaneous nystagmus, gaze-deviation nystagmus, positional nystagmus, disinhibition of induced (caloric and galvanic) nystagmus, delay of the reversal phenomenon of galvanic nystagmus,dysrhythmia as well as distorted optokinetic nystagmus. An extensive neuro-otological investigation is of clinical importance with respect to detecting cases of MS at an early stage of this disease.
 ...
PMID:[The neuro-otological findings of the multiple sclerosis (author's transl)]. 57 5

Thirty-five patients with torsional nystagmus (TN) underwent vestibular and ocular motor assessment and magnetic resonance image (MRI) scanning of the head. Patients were divided into two groups according to whether TN was predominant and present in primary gaze (Group I, 23 patients) or elicited by head positioning or gaze deviation and less prominent than other concurrent nystagmus (Group II, 12 patients). The main aetiologies in both groups were demyelination, vascular disease and posterior fossa tumours. In Group I, a frequent pattern of findings, occurring in 30-50% of cases, was a caloric canal paresis contralateral to the direction of the fast phases ('beat') of the TN, whereas the duration of horizontal caloric/rotational nystagmus and the slow-phase eye velocity of pursuit and of optokinetic nystagmus were all reduced in the direction of beating. The TN was more frequently and consistently modulated by vertical canal stimuli (head oscillation in roll) than by otolith stimuli (static tilt). Statistical analysis of the MRI showed significant overlap of abnormal MRI signals in the area of the vestibular nuclei, on the side opposite to the beat direction of TN. These results suggest that TN originates in a central imbalance of vertical semicircular canal function, resulting from lesions involving the vestibular nuclei on the opposite side of the TN. Group II was heterogeneous with no consistent pattern of neuro-otological findings, although lesions ipsilateral to the TN were frequent occurrence; in these cases cerebellar system lesions may have produced ipsilateral vestibular nuclei disinhibition.
 ...
PMID:Torsional nystagmus. A neuro-otological and MRI study of thirty-five cases. 139 6

Two males suffering from Pelizaeus-Merzbacher disease were examined, one at the age of 1 year 4 months and at the age of 7 years, and the other at the age of 7 years 8 months. The former had spontaneous vertical pendular nystagmus. He also showed horizontal "micronystagmus", present only at the age of 1 year, which might be similar to "voluntary nystagmus". Both males had jerky bilateral gaze-evoked nystagmus, defective smooth pursuit and optokinetic responses and a hyporeactive vestibulo-ocular reflex (VOR). All three obligate carriers exhibited typical VOR disinhibition in the two horizontal nystagmus directions, which may be a distinctive feature. This feature was also found in one of the 7 possible carriers examined and was not observed in the 3 non-affected males, who had normal oculomotor responses.
 ...
PMID:Oculomotor and vestibular anomalies in Pelizaeus-Merzbacher disease: a study on a kindred with 2 affected and 3 normal males, 3 obligate and 8 possible carriers. 146 51

Positional and positioning vertigo and nystagmus syndromes can be attributed to either peripheral or central vestibular dysfunction. The most common form is benign paroxysmal positioning vertigo which is caused by cupulolithiasis into the posterior semicircular canal. Other labyrinthine manifestations such as positional alcohol nystagmus, positional nystagmus with macroglobulinaemia and "heavy water" or glycerol ingestion occur because of a specific gravity differential between the cupula and the endolymph (buoyancy mechanism). Neurovascular compression of the vestibular nerve may be a causative factor for "disabling positional vertigo" which is an insufficiently described entity. Hesitation is highly justifiable since retromastoid craniectomy for microvascular decompression is the recommended management. Central positional vertigo is either induced by head movements which result in a transient ischaemia of the ponto-medullary brainstem, or by a change in head position relative to the gravitational vector. The latter is comprised of at least three forms: positional downbeat nystagmus (nodulus), positional nystagmus without concurrent vertigo, and positional vertigo with nystagmus. The site of the lesion is always near the fourth ventricle and the vestibular nuclei. The most probable explanation for the positional response is a vestibular tone imbalance caused by disinhibition of the vestibular reflexes on perception, eye, head and body position.
 ...
PMID:Positional and positioning vertigo and nystagmus. 143 92

An equilibriometric study has been performed on 20 healthy young women before and after the intake of 7 times 100 mg minocycline during 3 days. A systematic neurootological equilibriometry was performed analyzing the vestibular ocular, the vestibular spinal, the retino-ocular and the spontaneous nystagmus pathways. The results demonstrate that the tetracycline minocycline provokes a ponto-medullary liberation of the central vestibular regulating mechanisms. The central vestibular disinhibition could be exhibited by the monaurally elicited vestibular ocular nystagmus as well as by the radar image like cranio-corpography recordings of the head and body movements during a vestibular spinal stepping test. In parallel with these findings the participants of the study increasingly complained about vertigo of the rocking type, instability, malaise and wretching. Thus, the untoward side effects of a tetracycline like minocycline which is a frequent complaint of the patients, appears to be due to a central disinhibition of the vestibular equilibrium regulating mechanisms.
 ...
PMID:[Equilibriometric measurements of central vestibular dysregulation following administration of minocycline]. 349 10

Oculographic recordings of refixation saccades and pursuit movements during nystagmus-free intervals in a patient with periodic alternating nystagmus revealed cerebellar ocular motor disturbances that support the hypothesis that cerebellar disinhibition plays a role in the pathogenesis of periodic alternating nystagmus.
 ...
PMID:Ocular motor control disorder during the neutral phase of periodic alternating nystagmus. 615 93

A patient had periodic alternating Ping-Pong gaze and massive bilateral ischemic cerebral infarction proved at autopsy. In previous cases, bilateral hemisphere involvement appears to have been common in most cases. Eye movements in Ping-Pong gaze are similar to the slow-eye movements seen in sleep, anesthesia, and other obtunded states, a result of disinhibition of inherent rhythms in the oculovestibular system. They are like release phenomena and appear whenever fixational ability is lost or suspended, and during full consciousness they are inhibited by supranuclear cortical mechanisms. Ping-Pong gaze represents a distinct third variety of periodic alternating gaze disturbance, and the differential diagnostic features between it and periodic alternating gaze deviation and periodic alternating nystagmus are discussed.
 ...
PMID:Periodic alternating ping-pong gaze. 731 36

We videotaped the eye movements of syncope in 25 healthy volunteers who induced fainting by hyperventilation and Valsalva maneuver on a tilt table. In an additional three subjects, syncope was similarly induced during horizontal sinusoidal oscillation on a rotating chair while eye movements were recorded by electro-oculogram. Fourteen of 25 subjects experienced syncope on the tilt table. Six had downbeat nystagmus (DBN) at the onset that evolved into upward eye deviation, whereas seven showed isolated tonic upward deviation. In one subject the eyes remained in primary position. The gain of the vestibulo-ocular reflex (VOR) increased by 65% on average during syncope with concurrent vestibular stimulation. DBN, upward eye deviation, and increased VOR gain may all be caused by vestibular disinhibition caused by cerebellar hypoperfusion.
 ...
PMID:The eye movements of syncope. 878 96

In 1914, Von Monakow described diaschisis, the recovery of lost cortical function in regions positionally distant from, but linked by neuronal tracts to, the primary site of cortical damage. Cerebellar diaschisis after cortical insult is detailed in the literature; however, cortical diaschisis after cerebellar insult remains a rarely reported occurrence. We describe a 36-year-old woman with rupture of a right-sided cerebellar arteriovenous malformation who developed such expected cerebellar signs as ataxia, dysmetria, and nystagmus. Days later, the patient developed profound impulsivity, disinhibition, and psychomotor agitation. Single photon emission computed tomography (SPECT) showed decreased perfusion of the bilateral frontal and temporal lobes, consistent with regional loss of neural activity. Eventual clinical improvement corresponded with reperfusion of those regions, identified on follow-up SPECT. This case documents cortical diaschisis following cerebellar insult and shows that diaschisis must be considered in patients with cerebral injury manifesting cortical deficits remote from the site of primary pathology.
 ...
PMID:Cerebral diaschisis following cerebellar hemorrhage. 916 80


1 2 3 Next >>