Fumio Satomi

Nocturnal Onset and Development of Bell's Palsy

Objective/Hypothesis: To examine the mechanism and pathophysiology of idiopathic peripheral facial palsy (Bells palsy), the mode of onset of facial palsy was investigated.

Change in gene expression in facial nerve nuclei and the effect of superoxide dismutase in a rat model of ischemic facial paralysis.

Peripheral nerve injury induces changes in gene expressions of a variety of neuroactive substances in cell somata, which may have roles in the adaptive response to the injury, neuronal survival, growth and regeneration. In this study, we designed a rat model of ischemic peripheral facial paralysis with a selective embolization technique, and observed mRNA expression of calcitonin gene-related peptide (CGRP), c-jun, and growth associated protein (GAP)-43 in facial nerve nuclei using in situ hybridization histochemistry. The rats were demonstrated to have a transient facial paralysis consistently, and thus this method was regarded as a model of minor peripheral nerve injury. The mRNA of CGRP, c-jun and GAP-43 showed a distinct pattern of induction and time course of increase after the ischemic nerve injury. The results suggest that the small injury to the peripheral nerve was able to induce changes in mRNA expression in the cell body of motoneurons. We also investigated the protective effect of superoxide dismutase (SOD), which is a free radical-scavenging enzyme involved in cellular antioxidant defenses. The SOD treatment clearly alleviated the behavioral impairment and decreased the CGRP mRNA expression at 3rd day after injury. These data suggest that a free radical generated by the ischemia may be partially responsible for ischemic nerve damage and the change in gene expression in motoneurons.

Subglottic plasma cell granuloma: report of a case.

A case of subglottic and tracheal plasma cell granuloma masquerading as tumor invasion by thyroid malignancy was successfully treated using CO2 laser. A 55-year-old woman with a history of inspiratory stridor of almost 10 months duration was admitted to our clinic, and examinations revealed a mass in the subglottic space and trachea obstructing the airway. CT scan findings was suggestive of tumor invasion from a thyroid gland malignancy, however, histopathological examination of a biopsy specimen showed it to be plasma cell granuloma. Cases of plasma cell granuloma of the larynx and trachea are reviewed and discussed.

Reconsideration on the hyoid syndrome.

In 1975, Christiansen et al.’ reported five cases of elongated styloid process encountered in a single 12-month period. After reviewing the literature on this subject, the authors urged that this conspicuous entity be generally accepted as the cause of the neuralgia.’ Eagle’ presented the first case in which clinical symptoms resulting from an elongated styloid process were noted. In 1962, Eagle3 also reiterated the importance of being aware of this syndrome when treating patients with pharyngeal pain and discomfort, many of whom are cancer-conscious and apprehensive that a malignancy may be present in the throat. Thus, the condition caused by an elongated styloid process came to be known as “Eagle’s syndrome.” However, it is generally less well appreciated that similar or identical symptoms can be produced by other parts of the hyoid apparatus (e.g., hyoid syndrome).‘ According to Kopstein; hyoid syndrome is characterized by symptoms related to any of the parts of the hyoid apparatus, which includes the styloid processes, stylohyoid ligaments, the hyoid bone, and the hyoid-thyroid cartilage junction.’ The human hyoid bone is actually suspended from the styloid process of the temporal bone by the stylohyoid ligaments, which attach to the lesser cornua. It is therefore reasonable to consider all the parts of the hyoid apparatus and the styloid process as a single unit. It is often difficult to clearly differentiate hyoid syndrome from styloid syndrome because of their similar symptoms and the anatomic proximity of these two structures. However, the greater cornu of the hyoid and the lower part of the hyoid bone arise embryologically from the third branchial arch,

Stellate ganglion block for facial palsy.

Although the cause of Bell’s palsy has still not been clarified, its main pathophysiology is thought to be due to ischemic conditions of the facial nerves in the temporal bone. Since there is an extremely strong relationship between the pathophysiology of Bell’s palsy and circulatory disorders of the nutrient blood vessels in the facial nerves, the main emphasis of the conservative treatment of this disorder by chemotherapy is aimed at circulatory improvement. On the other hand, at the pain clinic, improved blood flow to the facial nerve by stellate ganglion block (SGB) therapy is employed in treating patients with Bell’s palsy. Its efficacy has already been adequately confirmed. The improved blood circulation during treatment of Bell’s palsy by SGB is thought to be brought about by a vasculatory dilatation action due to the blocking effects on the sympathetic nerve. However, the detailed mechanism has not been adequately studied. Therefore, we report the effects of SGB on the common carotid artery blood flow volume and tissue blood flow volume in facial nerve tissue in patients at the acute stage of Bell’s palsy and in experimental animals.

Facial Nerve Paralysis Associated with Acute Otitis Media in Children; A Report of Four Cases.

In general, facial nerve paralysis after the onset of acute otitis media is related to the patients age. We have treated four children with of facial nerve paralysis associated with acute otitis media over a 10-year period. They were divided into two groups based on their outcome; excellent recovery of facial nerve function, and poor recovery of it. We reviewed difference in the treatment between these two groups as well as the incidence of facial nerve paralysis. It is concluded that facial nerve paralysis is related to the characteristics of the temporal bone in infants, the facial canal dehiscence. Further treatment for facial nerve paralysis is also discussed.

Morphological Changes in Ischemic Facial Nerve Paralysis

The etiology of idiopathic facial nerve paralysis is still obscure. Two major concepts are reported in the literature, ischemia of the nerve within the temporal bone, and viral infection of the facial nerve. In the present paper, the morphological changes of the paralyzed facial nerve, atraumatically induced by selective vascular embolization [2], are reported.

The Utility of Single-Fiber Electromyography in Facial Nerve Paralysis

Many studies on the etiology, diagnosis, treatment, and other aspects of facial nerve paralysis have been performed; however, the precise pathophysiology of facial nerve paralysis has not yet been resolved.

A case of congenital ossicular malformation with mild auricular deformity: embryological and surgical considerations.

A case of bilateral congenital conductive deafness with mild auricular deformity is presented, and the anomalous structure deformity of the ossicles was multi-focal in this case, and a previous report indicates that ossicular malformation in the ear with congenital conductive deafness is multi-focal when the external ear is only slightly deformed. Bilateral ossicular reconstruction with replacement of the stapes yielded satisfactory results.