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Biomedical subjects

H Iritani

Publications and source records attributed to H Iritani.

7 recordsLinked to original sources
PubMed1996

Allograft stapes surgery for conductive hearing loss in patients with ossicular chain anomalies.

An allograft stapes was used during surgical intervention for conductive hearing loss due to ossicular malformations in 11 ears of seven patients. The external auditory canal and tympanic membrane were normal in all ears. The surgical findings for the ossicles were stapes fixation (7 ears), stapes fixation with discontinuity of the incudostapedial joint (in both ears of one patient), a deformed incus and stapes crura compressed by the facial nerve (one ear in which the stapes was not fixed) and an anomaly of the incus and stapes combined with a dermoid cyst (in one ear in which the stapes was also not fixed). In all ears, the following procedures were performed: stapedectomy followed by sealing the oval window with a vein graft and placing an allograft stapes between the oval window and the lenticular process of the incus or the handle of the malleus. The allograft stapes was placed with its capitulum on the oval window in all cases, and fibrin glue was used for stabilizing the seal and the allograft stapes. The indications for stapedectomy for conductive hearing loss due to ossicular chain anomalies and the utility of allograft stapes are discussed.

Adolescent↗
PubMed1992

Animal model for ischemic facial nerve paralysis with selective vascular embolization.

An experimental model that reliably and easily produces acute ischemic facial nerve paralysis would be useful for the controlled study of treatment and to improve our understanding of the pathophysiology and treatment of facial nerve palsy. Most documented models that simulate clinical facial nerve palsy cause direct damage to the nerve. We describe an experimental model for ischemic facial nerve paralysis in the cat that employs arterial block of the internal and external maxillary and posterior auricular arteries using embolizing material (Avitene). All animals develop stable acute ischemic facial nerve palsy lasting for approximately 2 months. Electromyographic study of this model revealed that the site of the lesion resulting from selective embolization may be within the temporal bone. This model has the advantages of simplicity of technique, cost-effective use of cats, and reproducibility of facial nerve palsy.

Animals↗
PubMed1991

Neurophysiology of ischemic facial nerve paralysis in an animal model.

The establishment of an animal model for facial nerve paralysis is assuming increasing importance in clinical medicine and also in basic facial nerve research. We previously reported an animal model for ischemic facial nerve paralysis using selective vascular embolization through the internal maxillary and posterior auricular arteries in cats using Avitene which contains bovine microfibril collagen. In this paper, we determined the exact site of the lesion in established facial paralysis. A descending signal produced by direct stimulation to the contralateral motor cortex was able to elicit firing of the motor nucleus of the facial nerve, the extra-temporal portion of the peripheral nerve, and the orbicularis oris muscle. After achieving complete facial nerve paralysis, this descending signal was completely abolished within the temporal bone area, whereas peripheral facial nerve stimulation elicited a normal evoked electromyogram of the orbicularis oris muscle. The present results suggest that the site of the lesion of ischemic facial nerve paralysis produced by embolization in an animal model is within the temporal portion of the seventh nerve, and this animal model may lead to the advancement of future facial nerve research which cannot be conducted in humans.

Angiography↗
PubMed1988

Vulnerable site of the facial nerve. From histopathology of seven temporal bones.

In the present work, a series of studies was made of seven temporal bones taken from 5 newborns within 6 h of death. In the 5 cases considered in this study, all of which had suffered from severe circulatory disease of congenital or unknown origin, destruction of the facial nerve as well as severe congestions were noted. The following findings were common to all seven temporal bones. (1) Bleeding together with destruction of the nerve had originated in the mid-section of the tympanic portion and increased distally up to the distal portion of the mastoid. (2) Bleeding was restricted mainly to the inner side of the perineurium or in the nerve trunk. (3) There was little bleeding in the epineurium, with the exception of both temporal bones in one of the cases. Although destruction of nerve fibres and the perineurium was prominent in all cases, in six of the temporal bones, traces of nerve trunk remained as a mould, with or without erythrocytes. In one temporal bone in case 5, which survived only 16 days, most of the nerve fibres had changed into fibrous tissue around which bleeding and small vessels containing erythrocytes were prominent. From these findings, it is postulated that the pathological change in the Fallopian canal of six of the temporal bones resulted from acute congestion after birth (due to acute reduction of oxygen density in the arterial blood resulting from severe congenital heart disease), while that of the remaining temporal bone resulted from chronic congestion which had already existed during gestation. It may be concluded that disturbance of blood flow is likely to occur from and distal to the tympanic portion of the Fallopian canal and that this may be due to the peculiar structure of the blood vessels in this area.

Bone Diseases↗