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At least 505 records · Page 28Linked to original sources

PubMed2000

Effects of vestibular cerebellum lesion on motion sickness in rats.

The importance of the vestibular apparatus in the development of motion sickness is widely accepted, although the role of the vestibular cerebellum remains controversial. We examined the effects of vestibular cerebellum lesion on the development of motion sickness in rats. Rats do not vomit, but the behaviour known as "pica", the eating of non-nutritive substances, such as kaolin, can be used as an index of motion sickness. A 2 h load of hypergravity induced pica in rats, indicating that they suffered from motion sickness. Pica was induced by hypergravity load even after surgical lesion to the bilateral cerebellar flocculus or to the cerebellar vermis. We concluded that the vestibular cerebellum was not essential in the development of motion sickness in rats.

Animals↗

PubMed1983

Vestibular-induced vomiting after vestibulocerebellar lesions.

Vestibular stimulation, by means of sinusoidal electrical polarization of the labyrinths of decerebrate cats, can produce vomiting and related activity resembling that seen in motion sickness. The symptoms include panting, salivation, swallowing, and retching as well as vomiting. These symptoms can be produced in cats with lesions of the posterior cerebellar vermis. In contrast to a previous proposal by Wang and Chinn in 1956, we suggest that a transcerebellar pathway from the vestibular apparatus through the nodulus and uvula to the 'vomiting center' is not essential for vestibular-induced vomiting and, by analogy, for the occurrence of many symptoms of motion sickness.

Animals↗

PubMed1989

Vestibular functions in conservatively treated chronic renal failure.

Chronic renal failure can produce malfunction of multiple organs, including auditory and vestibular apparatus. Twelve patients of chronic renal failure of varying etiologies treated conservatively were subjected to vestibular function tests. Only 33% of the patients had normal ENG data. Fifty-eight per cent of the patients had canal paresis and 8% showed hyperactive response. Ototoxic drugs like furosemide may be most important factor in aetiology of vestibular dysfunction in chronic renal failure.

Adult↗

PubMed1984

Responses to somatosensory input by afferent and efferent neurons in the vestibular nerve of the frog.

In the frog, we have recorded the activity of efferent and afferent fibers in the nerve of the horizontal semicircular canal in response to somatosensory stimulation. Recordings were made extracellularly by means of glass micropipettes filled with 2 M NaCl, and somatosensory stimulation was produced either by electrical stimulation of the sciatic nerve (ipsi- or contralateral to the recording side) or by vibratory stimulation of the gastrocnemius. The discharge frequency of 43% of the efferent fibers recorded was significantly increased by such stimulation, while the activity of the others was unaffected. The discharge rate of the afferent fibers was either significantly increased (in about 11% of the cases when the results were pooled together) or significantly decreased (in about 22% of the cases) by stimulation of the somatosensory system. The latencies of the responses ranged from 5 to 50 ms. These results show that: somatosensory input can influence the activity of the vestibular apparatus at the most peripheral level; modulation of the afferent discharge is mediated by the efferent vestibular system (EVS); the influence of the EVS on the vestibular afferent activity is both inhibitory and facilitatory, and the responses to somatosensory stimulation are mediated by both long-latency polysynaptic and short-latency oligosynaptic pathways. The functional significance of these two pathways is discussed.

Animals↗

PubMed1987

[Peripheral vestibular vertigo and functional disorders of the craniovertebral joint].

Some vertiginous lesions producing nystagmus (e.g. acute vestibulopathy, benign paroxysmal postural vertigo and Ménière's disease) are well-defined diseases of purely labyrinthine origin. The possible place of a functional disorder of the vertebral joints on their etiology and pathogenesis, has been discussed, but is purely hypothetical. Since the lesion almost always reaches with reduced function of the vestibular apparatus, the course of the disease depends crucially on central compensation of the peripheral disorder of vestibular function. Investigations of the effect of a functional disorder of the vertebral joints on the central compensation of vestibular functional disorders have not been described previously. Our own observations show that a functional disorder of the vertebral joints can crucially impair central compensation of peripheral vestibular vertigo. The pathological mechanism of the impaired compensation is discussed, and diagnostic and therapeutic consequences explained.

Adult↗

PubMed1993

[Subablative gentamycin therapy in Menière's disease].

We have treated 20 patients suffering from unilateral Morbus Meniere (2 x 12 mg gentamicin for 7 days). These patients were controlled for 24 months. In 95% we regarded a complete or substantial control of definitive spells ("American Committee on Hearing and Equilibrium guidelines for reporting treatment results in Meniere's disease", Otolaryngol. Head and Neck Surg. 10/19-85). Only 1 patient with pretherapeutic equal caloric response showed a post-therapeutic destroyed vestibular apparatus on the treated ear. In the other 7 patients (35%), who had a loss of vestibular function after therapy, there was an already pretherapeutic more or less noticeable caloric hypoexcitability. It is possible to induce an only subablative damage with a clinical success in 95%.

Audiometry, Pure-Tone↗

PubMed1992

Acoustic neuroma: postoperative vertigo and the mechanisms of compensation.

Ninety-five percent of patients with acoustic neuroma experience some degree of vertigo preoperatively, postoperatively or both. Postoperative vertigo is often a debilitating condition that results when the eighth cranial nerve is severed during surgery to resect a tumor growing around the vestibular portion of this nerve. Thus, surgery for acoustic neuroma affects the membranous labyrinth, which is the functional part of the vestibular apparatus and is primarily concerned with equilibrium. Compensation for impaired equilibrium may be by biofeedback in the vestibular pathways, visual control, exercise or drug therapy. Nurses can significantly influence the recovery of acoustic neuroma patients by encouraging and reinforcing exercise and other mechanisms of vestibular compensation.

Adaptation, Physiological↗

PubMed1993

[Vestibular findings in divers].

The author investigated 21 professional divers who had worked in overpressure conditions for many years. Main abnormalities were found in the vestibular system, especially in the caloric and optokinetic tests; the changes appeared in 61.9% of the sample. Asymmetry and dysrhythmia of evoked nystagmic responses were ascertained in these cases. The results of the auditory and tympanometry tests were normal in most examined persons. The acoustic reflex threshold increased in 38.1%. The lower ventilatory function of the eustachian tube was found only in one case but the audiometrical test was normal. From the ethiopathogenetic point of view the frequent and intense changes of pressure, temperature and posture may cause vegetative dysregulation with the following vascular deviations in the peripheral and central vestibular apparatus and in the brain stem. The adaptive mechanisms also modify the nystagmic reactions: thus they participate in the vestibular abnormalities.

Adult↗

PubMed2004

Labyrinthectomy decreases bone mineral density in the femoral metaphysis in rats.

To determine whether the vestibular system could influence bone remodeling in rats, we measured bone mineral density with dual energy X-rays absorptiometry before and 30 days after bilateral labyrinthectomy. Comparatively to intact control rats, labyrinthectomized animals showed a reduced bone mineral density in distal femoral metaphysis (p = 0.007): the variations between D0 and D30 were +3.0% for controls and -13.9% for labyrinthectomized rats. No significant difference between the 2 groups was observed in the whole body mineral density. These results suggest that the peripheral vestibular apparatus is a modulator of bone mass and more specifically in weight bearing bone. We discuss possible mechanisms of this vestibular influence probably mediated by the sympathetic nervous system.

Absorptiometry, Photon↗

PubMed1989

Vestibular abnormalities in encephalopathia pugilistica.

Vestibulological examination of boxers revealed that 80% had vestibular abnormalities. These were obvious, but well compensated, so that they remained hidden in everyday life and appeared only on laboratory examination or under stress. Regarding the origin of vestibulo-ocular reflex, abnormalities in boxing contribute three etiopathogenetic factors: the first is the direct traumatization of the vestibular apparatus by a direct blow. The second is the diffuse damage of the brain-stem white matter and of vestibular nuclei. The third factor is the traumatization of the cervical spine via the traumatization of the proprioceptive systems, cervical sympathetic and the adjacent vascular mechanisms. One-third of the abnormalities are caused by direct labyrinthine traumatization. The findings of simultaneous EEG, OKN and ETT abnormalities in one-half of our subjects suggests that there are probably also supratentorial lesions caused by the above-mentioned mechanisms.

Adolescent↗

PubMed1997

Evidence that perihypoglossal neurons involved in vestibular-auditory and gaze control functions respond to nerve growth factor.

Nerve growth factor (NGF), which has long been considered to be a trophic factor for peripheral sensory and sympathetic neurons, has been found recently to influence cholinergic neurons in the basal forebrain and neostriatum. In the present study, we provide evidence that brainstem neurons in the perihypoglossal area that relay information from the inner ear and vestibular apparatus to the cerebellum and tectum are responsive to NGF. These neurons, which are located in the nucleus prepositus hypoglossi (NPH), spinal vestibular nucleus, cochlear complex, and gigantocellular and paragigantocellular nuclei of the reticular formation, express functional receptors for NGF and up-regulate the expression of trkA receptors after injection of NGF into targets. In addition, the developmental up-regulation of NGF in the cerebellum coincides with the differentiation of the perihypoglossal nuclei. These results suggest that neurons representing the principal brain relays for auditory and vestibular pathways and perihypoglossal neurons involved in gaze coordination are a novel group of central neurons (besides cholinergic neurons in the basal forebrain and neostriatum) that respond to NGF.

Animals↗

PubMed2003

Bedside diagnosis of vertigo: value of the history and neurological examination.

Vertigo is caused by disturbance of the input or central processing of sensory signals from the vestibular apparatus that provide information regarding the position of the body in space. It is caused either by asymmetric disruption of sensory input from the vestibular organs or asymmetric integration of vestibular input into the central nervous system. Vertigo is readily differentiated from other causes of dizziness by a sensation of motion. A crucial aspect of the management of the emergency department patient with vertigo is the differentiation of vertigo associated with acute stroke syndromes from vertigo due to peripheral causes. Routine computerized axial tomography imaging is insensitive for posterior circulation strokes, so for emergency physicians, the history and neurological examination remain the most useful diagnostic tools. This article emphasizes the history and physical examination in the localization of the lesion in patients with vertigo and offers a rational basis for decisions regarding the need for special neurological imaging and consultation. It also emphasizes subtle findings that may prevent the erroneous diagnosis of peripheral vertigo in the presence of an acute stroke syndrome.

Dizziness↗

PubMed2004

Vestibular-evoked myogenic potentials in three patients with large vestibular aqueduct.

An enlarged vestibular aqueduct (LVA) is a common congenital inner ear anomaly responsible for some unusual vestibular and audiological symptoms. Most of the cases show bilateral early onset and progressive hearing loss in children. The gross appearance on CT scan of the inner ear is generally normal. However, precise measurements of the inner ear components reveal abnormal dimensions, which may account for the accompanying auditory and vestibular dysfunction. Despite extensive studies on hearing and the vestibular apparatus, saccular function is not studied. To our knowledge this is the first report of saccular malfunction in three patients with LVA by means of vestibular evoked myogenic potentials. Conventional audiograms revealed bilateral severe sensorineural hearing loss in two patients and mixed type hearing loss in one patient. Two of the patients complained about vertigo and dizziness but vestibular assessments of the patients showed normal results. The diagnosis had been made by high-resolution CT scans and MR images of the skull that showed LVA in the absence of other anomalies. The VEMP threshold measured from the ear with LVA in two patients with unilateral enlargement of the vestibular aqueduct was 75-80 dB nHL whereas the threshold from normal ears was 95 dB nHL. The third patient with mixed type hearing loss and bilateral LVA had VEMP responses despite a big air-bone gap in the low frequency range. The VEMP in this patient was greater in amplitude and lower in threshold in the operated ear (the patient had a tympanoplasty which did not improve her hearing). These findings and results of other patients with Tullio phenomenon and superior semicircular canal dehiscence, who also showed lower VEMP threshold, confirmed the theory of a 'third window' that allows volume and pressure displacements, and thus larger deflection of the vestibular sensors, which would cause the vestibular organ to be more responsive to sound and pressure changes.

Adult↗

PubMed1997

Pre- and postnatal expression of glycoconjugates (3-fucosyl-N-acetyllactosamine and HNK-1 epitopes) in the mouse inner ear.

The distribution of two glycoconjugates 3-fucosyl-N-acetyllactosamine (CD15) and HNK-1 epitope (CD57) in the inner ear of the NMRI mouse was analysed from the eighth day of gestation to the 16th day after birth. CD15 epitope distribution is developmentally regulated. The up- and down-regulation of expression, the change in the number of cells which are positive, the ingrowth of CD15-positive cells and their distribution, intracellular and/or cell-surface-associated expression, all assume a characteristic appearance at each developmental stage. Distribution of CD57 documented the nerve outgrowth and formation of the innervation of the vestibular apparatus and cochlear duct. Correlation between CD15 and CD57 expression patterns revealed differences in the interaction of the ingrowing fibres and epithelial tissue between the vestibular organ and the cochlea and differences in the development of the cristae and maculae.

Animals↗

PubMed1990

[Ototoxicity].

Ototoxic drugs, the best known of which are aminoglucoside antibiotics, can cause irreversible lesions in the ciliate cells of the organ of Corti and the maculae and crests of the vestibular apparatus. The cellular lesion is linked to the formation of complex substances between the ototoxic drug and the polyphospho-inositides of the cellular membrane. Auditory and vestibular monitoring must be ensured permanently throughout the use of such drugs, especially in the presence of risk factors. The lesions induced experimentally in animals having studied by electrophysiological methods, with recordings of the cochlear and brainstem potentials, and by histological methods with the technique of surface preparation of the organ of Corti, and by electron microscopy.

Adult↗

PubMed1999

Normal and altered cytoarchitecture of the inner ear.

Scanning electron microscope gave new insights into real morphology of the inner ear and has enhanced basic research. In fact, during the last twenty years, the cellular system that composes the organ of Corti and the vestibular apparatus has been clearly described by many authors. We now have a better understanding of each cell type and that they have a physiological functioning as ear and vestibular system. In addition, new insights into the damage caused by many drugs, such as aminoglucosides, can be investigated by studying the morphological changes and the reparative process following the injury. Animals such as guinea pigs can be used as ideal models to investigate the alterations in the sensory epithelium of the cochlear and vestibular receptors following ototoxic poisoning.

Aminoglycosides↗

PubMedDate not supplied

Posturally-evoked vomiting; Association with posterior fossa lesions.

Posturally-evoked vomiting (PEV) dissociated from vertigo was present in two patients with proven posterior fossa mass lesions. In both instances PEV was a major aspect of the patients' symptomatology before other findings clearly indicated the presence of an infratentorial mass lesion. A distinction is drawn between benign postural vertigo, which almost always indicates a benign disorder of the peripheral vestibular apparatus, and PEV which indicates a central lesion within the posterior fossa. A possible anatomic-physiologic basis is offered for PEV, based on the dissociation of the "vestibular syndrome," in which PEV increases while vertigo and nystagmus diminish.

Adenocarcinoma↗

PubMed2000

Effects of nitric oxide on the vestibular functional recovery after unilateral labyrinthectomy.

The effects of nitric oxide on the vestibular function recovery following unilateral labyrinthectomy were studied. Male Sprague-Dawley rats treated with N-omega-nitro-L-arginine methyl ester (L-NAME), a nitric oxide synthase (NOS) inhibitor, were subjected to destruction of the unilateral vestibular apparatus and spontaneous nystagmus was observed. To explore the role of nitric oxide on the potassium current, the whole cell patch clamp technique was applied on isolated medial vestibular nuclear neurons. The frequency of spontaneous nystagmus that appeared in L-NAME-treated rats was higher and maintained longer than in control animals. Potassium currents in the isolated medial vestibular nucleus were inhibited by nitric oxide liberating agents, sodium nitroprusside and S-nitroso-N-acetylpenicillamine. After blockade of calcium dependent potassium currents by high EGTA (11 mM)-containing pipette solution, sodium nitroprusside did not inhibit the outward potassium currents. 8-Bromoguanosine 3,5-cyclic monophosphate, a membrane-permeable cGMP analogue, produced similar effects to inhibit the outward potassium currents as sodium nitroprusside. These results suggest that nitric oxide production after unilateral labyrinthectomy would help to facilitate vestibular compensation by inhibiting calcium-dependent potassium currents through increasing intracellular cyclic GMP, thereby increasing excitability in ipsilateral vestibular nuclear neurons.

Animals↗