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

Spontaneous, positional, and paroxysmal positional nystagmus were studied before and after sectioning the superior division of the vestibular nerve and the anterior vestibular artery in squirrel monkeys. Histopathologic study of the temporal bones confirmed the degeneration of the macula utriculi with release of statoconia, but failed to identify the released utricular statoconia within the vestibular endolymphatic space in any animal. Postoperatively the animals consistently demonstrated direction-fixed spontaneous nystagmus until the end of the experiment (five months). Positional tests and Dix-Hallpike maneuver occasionally changed the intensity of the spontaneous nystagmus, but never elicited paroxysmal positional nystagmus. Possible reasons for not demonstrating paroxysmal positional nystagmus in the squirrel monkey are as follows: a resorption of statoconia; slight morphological alteration of the sensory epithelia of the posterior cristae; interference of the posterior crista function due to partial collapse of the membranous ampulla; the existence of interspecies difference; or possibly a faulty hypothesis regarding the etiologic mechanism of benign paroxysmal positional vertigo.
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PMID:Superior vestibular nerve sectioning. Experimental studies in squirrel monkeys. 80 4

The inner ear pathology of experimental perilymphatic fistula (EPLF) is described. EPLF was produced by injecting artificial perilymph into the subarachnoid space, or by suctioning 4 microL of perilymph through one of the round window membranes of the guinea pig. The animals were either killed immediately, or were kept alive for 3 weeks to 3 months. The conventional celloidin embedding method was employed for morphologic study. Vestibular function of the animals was tested by observing spontaneous nystagmus and positional nystagmus after the experiment. The caloric test was also performed. Various pathologic changes of the membranous labyrinth were observed. In the cochlea these included rupture or collapse of Reissner's membrane, bulging of Reissner's membrane, loss of hair cells, and compression of the organ of Corti. Pathology of the otolithic organs and semicircular canals mainly consisted of collapse of the membranous labyrinth. Clinical symptoms in patients with perilymphatic fistula (PLF) are explained, based on our experimental findings. Electronystagmography (ENG) of EPLF animals showed either no caloric response or, with a longer duration, caloric irregularity. Prolonged unsteadiness in patients may be due to "floating" labyrinth.
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PMID:Inner ear morphology of experimental perilymphatic fistula. 159 82

An animal model of experimental perilymphatic fistula (EPLF) was developed in the guinea pig in order to study vestibular pathophysiology. In experimental animals, 4 microL of perilymph was suctioned from one cochlea via the round window membrane. Changes in vestibular function were as follows. 1) During the acute stage (5 hours postoperatively), spontaneous nystagmus directed toward the normal side was noted in 57.4% of the EPLF animals. This lasted less than 24 hours. 2) One week postoperatively, direction-fixed positional nystagmus toward the lesioned ear was present in 22.7% of the EPLF animals, especially when the lesioned ear was positioned inferiorly. 3) With the ice water caloric test, no response was present in 58.1% of the EPLF animals and an irregular response was found in 22.6% of them, 1 week postoperatively. These results tend to indicate that tests of vestibular function may differentiate between patients with Meniere's disease and those with perilymphatic fistula. Histologic findings indicate that a floating labyrinth is the cause of positional nystagmus and caloric irregularity. The absence of caloric responses was associated with collapse of the vestibular labyrinth.
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PMID:Vestibular pathophysiologic changes in experimental perilymphatic fistula. 162 10

The term "caloric irregularity" was coined to refer to a gross irregularity in the amplitude and/or frequency of a caloric-induced nystagmus, having a variable slow-phase velocity and prolonged duration. Twelve of 46 guinea pigs with experimentally induced perilymphatic fistula had irregular responses to the ice-water caloric test 1 week after creation of a fistula. The long-term vestibular consequences in animals with caloric irregularities were either resolution and return to normal function (i.e. caloric return) or continuing deterioration to canal paresis. Morphological examination of ears with caloric irregularity revealed that there had been partial collapse of the membranous labyrinth and the creation of a floating labyrinth.
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PMID:Caloric irregularity in experimentally induced perilymphatic fistula. 164 73

Analysis of the otoneurological symptomatology in 32 patients with hypophyseal tumors showed that they extended most frequently into the sphenoidal sinus, the cells of the ethmoidal sinus, the superoposterior parts of the nose, and the nasopharynx. The focal symptoms of compression of the adjoining parts of the brain (frontal, temporal) were manifested in 11 among 32 cases by olfactory disorders (loss of olfaction in 4 patients, diminished olfaction in 2, olfactory hallucinations in 4 patients, and impaired recognition of odors in 1 patient). Asymmetric action of the tumor on the subcortical structures in the fronto-parietal-temporal parts was manifested by side asymmetry of the experimental nystagmus, complete spatial disorientation of the patient after the rotation test with a false sensation of collapse to the side of the slow phase of nystagmus with vigorous motor compensatory disharmonic deviation of the trunk and limbs in the direction of the rapid nystagmus phase. The effect of the giant hypophyseal tumor on the brain stem was often manifested for a large distance (simultaneously on the diencephalic level, on the level of the midbrain, and in the posterior cranial fossa). Among a group of 32 patients 18 had the decompensated phase of affection of the vestibular apparatus. The effect of the tumor on the diencephalic parts of the brain was attended by sharply intensified vestibulovegetative reactions which should be considered as a stimulation symptom. In giant cell hypophyseal tumors, however, intensification of vestibulovegetative reactions after experimental vestibular tests does not occur in many cases, which is due to death and areactivity of the diencephalo-hypothalamic structures.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The otoneurological symptoms in giant adenomas of the hypophysis]. 166 32

Despite the widespread use of non-steroidal anti-inflammatory drugs (NSAIDs), the current number of reported cases of poisoning is small. However, with the introduction of 'over-the-counter' preparations of NSAIDs in some countries (e.g. ibuprofen in the UK and USA) an increased incidence of acute poisoning from this group of drugs can be expected. Conventionally, NSAIDs are divided into the following groups based on their chemical structure: arylpropionic acids, indole and indene acetic acids, heteroarylacetic acids, fenamates, phenylacetic acids, pyrazolones and oxicams. Unless NSAIDs are ingested in substantial overdose, acute poisoning with these agents does not usually result in significant morbidity or mortality. In most cases the clinical features are mild and confined to the gastrointestinal and central nervous systems, though acute renal failure, hepatic dysfunction, respiratory depression, coma, convulsions, cardiovascular collapse and cardiac arrest may complicate severe poisoning. Arylpropionic acid derivatives were thought initially to have a low order of toxicity in overdose but, in addition to anticipated gastrointestinal symptoms, headache, tinnitus, hyperventilation, sinus tachycardia, hypoprothrombinaemia, haematuria, proteinuria and acute renal failure have been described. In addition, drowsiness, coma, nystagmus, diplopia, hypothermia, hypotension, respiratory depression and cardiac arrest have been reported in severe cases of poisoning. Oxyphenbutazone and phenylbutazone are considerably more toxic in overdose. Complications of severe poisoning include coma, convulsions, hepatic dysfunction, acute renal failure, sodium and water retention, haematuria, cardiovascular collapse, respiratory alkalosis, metabolic acidosis, hypoprothrombinaemia and thrombocytopenia. In contrast, indomethacin appears to be much less toxic. In addition to gastrointestinal symptoms, indomethacin taken in overdose induces headache, tinnitus, dizziness, lethargy, drowsiness, confusion, disorientation and restlessness. Only 1 case of acute sulindac poisoning has been reported in the literature. A 16-year-old boy was admitted with hypokalaemia (2.2 mmol/L), transient granulocytosis and 'scanty' haematemesis after ingesting 12 g sulindac. No case of acute tolmetin poisoning have been reported. The fenamates (flufenamic acid, meclofenamic acid, mefenamic acid, tolfenamic acid) are, with the exception of mefenamic acid, not as widely prescribed as other groups of NSAIDs. In overdose, mefenamic acid may result in nausea, vomiting, diarrhoea, muscle twitching, convulsions and coma.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Acute poisoning due to non-steroidal anti-inflammatory drugs. Clinical features and management. 353 13

Morphological vestibular changes caused by barotrauma were studied in guinea pigs. Animals were exposed to rapid decompression from 2 absolute atmospheric pressures (ATA) to 1 ATA, which causes inner ear barotrauma in the guinea pig. During decompression, spontaneous nystagmus was recorded, which consisted of irritative symptoms initially, followed by paralytic nystagmus. After pressure loading and observation to confirm the absence of Preyer's reflex with vertigo, the animals were tested for caloric nystagmus using ice water and then sacrificed at varying intervals. Then, morphological changes in vestibular organs and the organ of Corti were studied. Half of the experimental animals showed canal paresis on caloric testing. Damage to the organ of Corti was severe while that to vestibular organs was very slight. Damage to the sensory cells of the vestibular organs was not clear on light microscopy, despite a partial collapse of labyrinthine membranes. Under scanning electron microscopy, local damage was observed in a portion of the crista ampullaris of the semicircular canals. In this area, incomplete or complete disappearance of kinocilia and stereocilia, similar to that seen after rotatostimulation, was observed. However, no damage to sensory hairs was seen in the utricles and saccules. The observed vestibular organ damage, resulting from inner ear barotrauma, suggested effects on endolymphatic flow.
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PMID:[Vestibular changes due to barotrauma]. 829 63

Two cases of bilateral Lermoyez's syndrome and one case of unilateral Lermoyez's syndrome are reported. The patients had recurrent episodes of vertigo with improvement of hearing or tinnitus, which is characteristic is Lermoyez's syndrome. In case 1, a 48-year-old female, dehydration with glycerol or furosemide induced nystagmus and improved bilateral hearing and the gain of the vestibulo-ocular reflex, while overhydration with drinking water impaired bilateral hearing with disappearance of nystagmus. These findings indicate that she had endolymphatic hydrops in both ears, suggesting that simultaneous changes in bilateral cochlear and vestibular function induce Lermoyez's syndrome. In case 3, a 52-year-old female, which we already reported, endolymphatic collapse in both ears may have changed bilateral inner ear function, resulting in Lermoyez's syndrome. On the other hand, patients 2, a 47-year-old male, experienced a vertigo attack with improvement of unilateral hearing after defibrinogenation therapy. In this case, slowly developing insufficiency of the inner ear blood supply may have caused the gradual hearing loss. It seemed that decreasing blood viscosity by defibrinogenation allowed blood to rush into the labyrinth, causing vertigo but at the same time improving hearing. We proposed that there are two types of Lermoyez's syndrome, bilateral (cases 1 and 3) and unilateral (case 2).
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PMID:[Three cases of Lermoyez's syndrome and its pathophysiology]. 885 32

1. In the guinea-pig, a unilateral labyrinthectomy induces postural disturbances and an ocular nystagmus which abate or disappear over time. These behavioural changes are accompanied by an initial collapse and a subsequent restoration of the spontaneous activity in the neurones of the ipsilateral vestibular nuclei. Recently, it has been shown that the vestibular neuronal activity remained collapsed over at least 10 h whereas its restoration was complete 1 week after the lesion. The aims of this study were to determine when restoration of spontaneous activity in the partially deafferented vestibular neurones started and to compare the time courses of the behavioural and neuronal recoveries in guinea-pigs that had undergone a unilateral labyrinthectomy. 2. Neuronal discharge measurements were made using chronic extracellular recording of single unit activity. After a left labyrinthectomy, electrodes, were placed on the site of the destroyed labyrinth to enable stimulation of the left vestibular nerve. Behavioural measurements included chronic recording of eye movements by the scleral search coli technique. After a left labyrinthectomy, lateral deviation of the head, twisting of the head, and eye velocity of the slow phases of the nystagmus were measured. 3. The neuronal activity of the rostral part of the vestibular nuclear complex on the lesioned side was recorded in alert guinea-pigs over 4 h recording sessions between 12 and 72 h after the lesion. 4. The criterion used to select vestibular neurones for analysis was their recruitment by an electric shock on the vestibular nerve. In addition, in order to explore a uniform population, we focused on neurones recruited at monosynaptic latencies (0.85-1.15 ms). 5. For each recording period, the mean resting rate was calculated animal by animal and the grand mean of these individual resting rate means was calculated. Previously, a decline in the grand mean resting rate from 35.8 +/- 6.0 spikes s-1 (control state) to 7.1 +/- 4.2 spikes s-1 during the first 4 h after labyrinthectomy has been shown. In the present study, the first sign of recovery was observed during the 12-16 h recording period when the resting rate grand mean increased to 16.3 +/- 3.9 spikes s-1. This grand mean activity did not change significantly during the following 12 h. Thereafter, restoration of neuronal activity improved and was complete 1 week after the lesion. 6. Although the abatement of the vestibular symptoms roughly paralleled the restoration of neuronal activity in the vestibular nuclei, some discrepancies between the time courses of both phenomena emerged. An important step in postural recovery (the animals managed to stand up) and a major part of the abatement of the nystagmus occurred before the recovery of vestibular neuronal activity. In addition, lateral deviation of the head disappeared while restoration of the neuronal activity was incomplete, but significant head twisting was still evident when vestibular resting rates had recovered completely. 7. We conclude that restoration of neuronal activity in the ipsilateral vestibular nuclei starts 12 h after the lesion and that restoration of neuronal activity in the ipsilateral vestibular nuclei is not the only mechanism underlying behavioural vestibular compensation.
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PMID:Dissociations between behavioural recovery and restoration of vestibular activity in the unilabyrinthectomized guinea-pig. 914 34

Albino guinea pigs (n = 28) were used to establish an animal model of the perilymph fistula (PLF) by suctioning 2-4 microliters of perilymph via the left round window membrane. At times varying from 1-3 weeks post-operatively, 9 animals had no caloric response, 5 had a weak caloric response and none had post-caloric nystagmus (PCN). The remaining 14 animals had caloric irregularity in lesioned ears; 12 of these (87%) also did not have PCN. Morphological study of the latter revealed an intact contour of the membranous labyrinth in the lateral semicircular duct and partial collapse of the utricular wall, a condition called the "floating labyrinth". We therefore believe that effective suppression of PCN in the experimental PLF is due to failure in short-term adaptation, caused by lesions in the peripheral vestibular organs, such as the floating labyrinth.
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PMID:Suppression of post-caloric nystagmus in experimental perilymph fistula. 1021 87


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