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At least 1,423 records · Page 79Linked to original sources
PubMed2003

Labyrinthine fistulae: pathobiology and management.

PURPOSE OF REVIEW: This article reviews literature on three manifestations of these pathologic mechanisms: leakage of perilymph from the inner ear into the middle ear, disruption of the bone of the labyrinth caused by cholesteatoma or other manifestations of chronic otitis media, and superior semicircular canal dehiscence syndrome. RECENT FINDINGS: Labyrinthine fistulae are caused by abnormal communications between the inner ear and surrounding structures. Under normal circumstances, the fluid-filled spaces of the membranous labyrinth are encased in the dense bone of the otic capsule with only two places of increased compliance: the oval window and the round window. Disruption of the labyrinthine bone can lead to areas of increased compliance, with symptoms and signs that can be understood based upon abnormal pressure transmission in the system. Communication between the endolymphatic and perilymphatic spaces of the labyrinth or passage of perilymph from the labyrinth into the middle ear or mastoid can lead to hearing loss and/or vestibular disturbances. SUMMARY: Findings on clinical examination as well as CT imaging of the temporal bone can be useful in making the diagnosis. Management is based upon the specific pathological factors and the impact of the symptoms and signs on the patient.

Cholesteatoma, Middle Ear↗
PubMed1999

Corticosteroid pharmacokinetics in the inner ear fluids: an animal study followed by clinical application.

OBJECTIVE: Autoimmune disease (e.g., Cogan syndrome) and other inflammatory inner ear diseases may ravage the labyrinth if not treated aggressively with antiinflammatory medication. Corticosteroids are the mainstay of treatment, yet, partly because of the existence of the blood-labyrinthine barrier, the ideal drug, dose, and route of administration are currently unknown. STUDY DESIGN: In the present study, we established cochlear fluid pharmacokinetic profiles of hydrocortisone, methylprednisolone, and dexamethasone in the guinea pig following oral, intravenous, and topical (intratympanic) administration. High-performance liquid chromatography was used to determine the drug concentrations, and comparisons were made with simultaneous pharmacokinetic profiles from blood and cerebrospinal fluid. RESULTS: Our findings demonstrated a much higher penetration of all three drugs into the cochlear fluids following topical application as compared with systemic administration, with methylprednisolone showing the best profile. DISCUSSION: The results suggested that intratympanic administration of corticosteroids might be more efficacious while avoiding high blood levels and therefore the deleterious side effects of systemic use. CLINICAL APPLICATION: Thirty-seven patients with various inner ear disorders causing sensorineural hearing loss were subsequently treated using intratympanic corticosteroids, 20 with dexamethasone, and 17 with methlyprednisolone. Patients with immune-mediated hearing losses showed the best results, with notable improvement also seen in several cases of a "sudden deafness." No benefit was seen in patients with cochlear hydrops or those with sudden deterioration of a preexisting hearing loss. Three patients developed a transient otitis media related to the treatments, easily controlled with antibiotics. There were no cases of treatment-induced hearing loss and no permanent tympanic membrane perforations. CONCLUSIONS: Overall injection of intratympanic corticosteroids for the treatment of hearing loss in inner ear disorders appears to be both safe and highly effective for certain disorders. The concept of this technique is supported by animal experimental data. The findings from the present study warrant further clinical application and experimental investigation.

Administration, Oral↗
PubMed1989

High-resolution MR imaging of the inner ear.

The magnetic resonance (MR) images of the temporal bones have been analyzed, these MR images taken with head coils utilizing a 1.5-Tesla magnet whole-body imaging system. The MR images were acquired by means of spin-echo pulse sequences, and the thickness of the sections was 2.5 mm. By this modality, the T2-weighted images could clearly delineate the details of the liquid-containing labyrinthine structures and facial nerve. MR imaging can provide information that is unobtainable from a CT scan in the diagnosis of inner ear disorders, particularly as to whether the membranous labyrinth is filled with the lymph fluid or is fibrosed. This point is one of the greatest advantages of MR imaging over a high-resolution CT scan.

Ear, Inner↗
PubMedDate not supplied

Effects of hyperosmotic solutions on endolymphatic pressure.

Hydrostatic pressure changes in endolymph as well as perilymph and cerebrospinal fluid (CSF) following intravenous injection of glycerol, urea, and mannitol were studied in the guinea pig using a servo-controlled micropipet system. After the initial rise in pressure observed during and immediately after injection of each hyperosmotic agent, all pressures fell below baseline levels for about 20 minutes. The largest reductions in pressure with each of the hyperosmotics showed no significant difference between CSF and labyrinth. In the glycerol and urea studies, labyrinthine pressures stabilized at their minimum levels 20 to 40 minutes after injection, while CSF pressure recovered slowly. However, alteration of labyrinthine pressures induced by mannitol paralleled that of CSF. These results may suggest a possible osmotic dehydration effect in the labyrinth for glycerol and urea, but an ambiguous effect for mannitol.

Animals↗
PubMed1976

[Pathology of the endolymphatic duct and sac in inner-ear hydrops].

The morphological substrate of Menière's disease is the endolymphatic hydrops. That can be idiopathic or secondary as a sequence of a labyrinthine disease of another cause. It is possible to coordinate function loss of the sensory end-organs and pathohistological findings, but not all failures are light-microscopically explainable. The reason for the hydrops is certainly a disturbance in the endolymph physiology. For the pathogenesis are important, besides the biochemistry of the inner ear-fluids, problems of the membranes and pathological changes on ductus and saccus endolymphaticus and perimacular areals and plana semilunata. The perilymphatic space, documentated on the example of the secondary hydrops, is certainly not only passively enrolled in the procedure. All observations bring the initiation and periodicity of attacks to another point of view. A complete solution has not been possible so far, especially in the case of the etiology in idiopathic hydrops.

Ear, Inner↗
PubMed1976

Aspects on endolymphatic sac morphology and function.

Morphological evidence indicate that the main function of the endolymphatic sac is to act as a reabsorptive and defensive mechanism for the inner ear. This activity is markedly enhanced in labyrinthine trauma, such as injection of foreign particles into the labyrinth, blocking of the endolymphatic duct, and cryosurgical destruction of vestibular sensory epithelia. Light and dark epithelial cells of the intermediate portion of the sac are capable of reabsorbing endolymph and digesting cellular debris respectively. The extensive capillary network surrounding the endolymphatic sac exhibits endothelial characteristics suggestive of active fluid transport. The "dynamic-flow theory" of endolymph circulation suggests that a radial-flow should be considered for energy metabolism and ion exchange around the sensory cell regions whereas a longitudinal-flow should be considered for reabsorption of endolymph and disposal of high molecular waist products and debris by the endolymphatic sac. The earlier concepts of endolymph circulation thus need not any longer be considered conflicting.

Ear, Inner↗
PubMed1989

Sodium transfer from endolymph through a luminal amiloride-sensitive channel.

An in vitro preparation of frog semicircular canal was devised to study the mechanisms of Na transport across the labyrinthine epithelium. When the lumen of the semicircular canal was filled with perilymph-like solution, the structure was able to secrete K into and to absorb Na from the lumen and to generate a lumen-positive transepithelial potential. When the lumen of the semicircular canal was filled with endolymph-like solution, the electrochemical composition of the luminal fluid was partly maintained up to 2 h. In this last experimental condition net and unidirectional fluxes were calculated in absence or presence of transport inhibitors, separately for the ampulla and for the nonampullar part of the canal. Amiloride (10(-5) M) but not dimethyl amiloride (10(-5) M) inhibited 60% of the unidirectional Na efflux out of endolymph; this Na efflux decrease resulted in an increase of the inward net Na flux. The net Na flux was also increased after abluminal application of ouabain (10(-3) M), furosemide (10(-4) M), and bumetanide (10(-6) M). This study validates this isolated preparation as a suitable tool for the study of endolymph secretion, confirms that the secretion of endolymph is achieved in the ampulla, and provides evidence for an apical amiloride-sensitive Na channel through which Na is transferred out of endolymph along an electrochemical gradient provided by the activity of the abluminal Na+-K+-ATPase.

Amiloride↗
PubMed2004

Neuroradiological features of vertigo.

The diagnostic pathway in a patient with vertigo starts with the accurate evaluation of medical history followed by a general physical and neurological examination. This step can often lead to the identification of the correct cause of the disease or, at least, to a distinction between peripheral and central vertigo. Neuroradiological investigations have to be considered as elective diagnostic procedures and include: computed tomography (CT), magnetic resonance (MR), MR angiography (MRA), angiography. For the diagnosis of peripheral vertigo, benign paroxysmal positional vertigo, labyrinthitis, Meniere disease, perilymphatic fistula, local trauma, toxic labyrinthitis, acute otitis media and chronic middle ear effusion,the role of imaging techniques is controversial. CT and MR are performed to rule out other pathologies and to confirm the diagnosis. Increased resolution and application of special MR sequences enhancing the intralabyrinthine fluids have enabled more detailed analysis of labyrinthine structures and pathology. Both T2 and T1 contrast sequences are necessary. A high resolution CT study is required when otitis media is suspected and in the follow-up of post-traumatic vertigo. The causes of central vertigo are numerous and include: vertebro-basilar circulation vascular events, multiple sclerosis (MS), migraine-associated vertigo, cerebellar and brainstem tumors, CNS infections. Among them cerebrovascular ischemia and multiple sclerosis are the most frequent. In these situations imaging studies become mandatory. CT can diagnose most cerebellar hemorrhages and some cerebellar and brainstem acute ischemia, enhanced MR has proved to be the most sensitive tool to detect posterior fossa lesion. Diffusion-weighted MR can reveal acute ischemic changes before routine MR. There has been evidence that MR angiography, providing angiogram-like images of the intracranial vessels may sometimes avoid invasive angiography. MRA resolution is not as good as traditional angiography and may also be compromised by movements and other artifacts. Selective angiography of the posterior circulation is often indicated for therapeutic decisions.

Brain↗
PubMedDate not supplied

[Space motion sickness].

This review describes symptoms of space motion sickness (SMS) observed in many cosmonauts during the first day in orbit. It also discusses similar symptoms detected in them upon return to the Earth which constitute the readaptation syndrome. The paper gives a detailed discussion of different theories that explain the etiology and pathogenesis of SMS and the post-flight readaptation syndrome, viz, sensory conflict or sensory mismatch, disorders in the labyrinthine paired function, and blood and cerebrospinal fluid (CSF) circulation. It is emphasized that none of the theories used separately can clarify all aspects of the origin and development of SMS. The authors main tain that the mechanisms underlying the above changes are not contradictory but rather interrelated and complementary. Each of them having a larger or smaller specific weight may be involved in the development of SMS. In some people marked vestibular asymmetry may become the leading factor, in others inadequate adaptive capabilities to fluid redistribution may result in blood and CSF disorders, and in still others sensory conflict may play the crucial role. A correlation between SMS and vestibular adaptation is discussed. Results of studying the vestibular function during and after real space flights are presented.

Adaptation, Physiological↗
PubMed1995

Transcranial magnetic stimulation of the trigeminal nerve: intraoperative study on stimulation characteristics in man.

We studied responses from the masseter and nasalis muscles following magnetic stimulation (magStim) and compared these responses with those obtained by direct electrical stimulation of the trigeminal (NV) and facial (NVII) nerve near the root exit zone during microvascular decompression operations of NVII. We found that (1) magStim threshold to excite the nerve is high for NV and low for NVII; (2) excitation of all motor fibers is impossible for NV, and easy for NVII; (3) optimal coil placement is critical for NV, but not critical for NVII; and (4) between and within subjects, the excitation site is variable on NV, but stable on NVII. We estimated that the anatomical location of magStim to be either within or outside the cerebrospinal fluid for NV, and to be in the labyrinthine segment of the facial canal for NVII. Physical models explain and clinical lesion models support these differences found between NV and NVII.

Adult↗
PubMed1991

Transcranial magnetic stimulation of the facial nerve: where is the actual excitation site?

The site where excitation on the facial nerve to transcranial magnetic stimulation occurs was studied by recording the muscle responses of 13 patients who had facial nerve lesions at different locations, and by comparing the latencies of muscle responses to transcranial magnetic and direct electrical stimulation of the facial nerve recorded in another 5 patients undergoing posterior fossa surgery. The results of both approaches of this study led independently to the conclusion that magnetic stimulation acts within the proximal part of the facial canal. It is suggested that the cerebrospinal fluid (CSF) conducts the magnetically induced stimulation currents into the labyrinthine segment of the facial canal, where the facial nerve is still surrounded by CSF for about 10 mm.

Action Potentials↗
PubMed2005

Mechanism of acute fetal cardiovascular depression after maternal inflammatory challenge in mouse.

Intra-amniotic lipopolysaccharide (LPS) causes an acute inflammatory response and cardiac dysfunction in fetal mice. We hypothesized that the placenta protects the fetus against maternally administered bacterial toxins, delaying the onset of a fetal inflammatory response and vascular compromise. At 14 to 15 days of gestation, DBA mice were randomized to receive LPS (2.4 mg/kg) or vehicle intraperitoneally. Doppler ultrasonography of fetal cardiovascular hemodynamics was performed before and 6 hours after maternal LPS. Six hours after the LPS, maternal serum concentrations of tumor necrosis factor-alpha and interleukin (IL)-6 (P < 0.05) were increased. Placenta showed severe maternal vascular dilatation and congestion. The expressions of tumor necrosis factor-alpha, IL-1alpha, and IL-6 (P < 0.05) were increased, and the expression of Toll-like receptor 4 was constitutive in placenta. The expression of Toll-like receptor 2 increased (P < 0.05) and was detected in labyrinthine macrophages. No inflammatory activation was found in fetal tissues, and amniotic fluid revealed no significant increase in cytokines. The ultrasonographic examination demonstrated increased fetal cardiac afterload after LPS, with 65% of the fetuses exhibiting atrioventricular valve regurgitation. In conclusion, maternal inflammatory insult activates placental labyrinthine macrophages leading to an acute increase in placental vascular resistance and fetal cardiac dysfunction without an inflammatory response in fetus.

Amniotic Fluid↗
PubMedDate not supplied

Vein of the vestibular aqueduct.

The vein of the vestibular aqueduct (VVA) was investigated in a series of 40 human temporal bones. The processing included vascular injection with a colored medium, decalcification and cutting in serial, thick sections, which were put in a clear fluid and studied with a stereo-microscope. The labyrinthine roots of the VVA are the single veins of the ampulla and simple limbs of the semicircular canals and of the posterior wall of the utricle. They drain the rich capillary bed of the simple endolymphatic walls of the canals and the utricle, as well as a small peripheral area of the cristae and the utricular macula. The VVA leaves the vestibule through an individual bone canal running parallel to the vestibular aqueduct up to the dura of the posterior side of the petrosa in the area of the endolymphatic sac. It then opens in the inferior petrosal sinus or the jugular bulb. The vein receives other branches from the bone, dura and sac. Correct information on the course of this vein appears to be lacking in contemporary textbooks and articles, although it has been correctly described since the last century.

Acoustic Maculae↗
PubMed1994

[Analysis of the blood-labyrinthine barrier in a model of progressive osmotic change].

The AA. working with Gerbils (Meriones unguiculatus) experimentally deprived of their kidneys attempt to find out the behaviour of the BLB. The study was accomplished through the dynamic examination of the osmolality and ureic concentrations of the perilymph, the blood and in spinal fluid as well. Furthermore the role of the BLB in the origin of labyrinthine osmotic variations, as provocative cause of the inner ear pathology, is contemplated.

Animals↗