A case of hypopharyngeal carcinoma associated with mycosis fungoides is reported. The patient, 71 year-old male, had suffered from mycosis fungoides for 12 years, and was treated with steroids, cyclophosphamides, and photochemotherapy (oral methoxsalen and longwave ultraviolet light). Since difficulty of swallowing began in March, 1978, and becoming worse, he visited our clinic in May, 1978. At that time, he was at infilurative stage (second stage) of mycosis fungoides. Fluoroscopy showed a space occupying lesion in the right piriform sinus, and biopsy confirmed a squamous cell carcinoma of hypopharynx. The hypopharyngeal lesion was irradiated (Linac 170 rads per day, total dose of 5950 rads), and pharyngectomy and right neck dissection were done in August, 1978. Reconstruction of the hypopharynx using laryngeal autograft was performed at the same time. Postoperative course was fairly well, and the patient was discharged one month after the operation. In January, 1979, mycosis fungoides exacerbated again, and refractory to ordinary medical treatments. This time, he was treated with electron beam irradiation, and consequently mycosis fungoides was well controlled. But in April, 1979, he complained of disphagia again, and recurrence of hypopharyngeal carcinoma in the laryngeal autograft was found. The recurrent lesion was treated with irradiation and bleomycin. He died of renal dysfunction and bronchopneumonia in July, 1979. Necropsy revealed metastases in the right parotid and right lung and no evidence of visceral involvement of mycosis fungoides. Renal failure was due to marked arteriosclerosis.
Department of Pathology, The Institute of Medical Science, Tokyo University, Tokyo Herpes simplex virus was inoculated through the round window membrane into the perilymphatic spaces of the guinea pig labyrinth. A new method for immunofluorescent antibody staining (formalin fixation, EDTA decalcification and trypsin treatment) was applied to detection of the viral antigens in the labyrinth with good preservation of the delicate structures. Immunofluorescent studies revealed that the viral antigens appeared in various areas of the labrinth. The viral antigens were seen in the perilymphatic, endolymphatic, sensory and ganglion structures of the injected side. Histopathological changes were correspondent with localization of the viral antigens, and characteristic morphological changes of the tectorial membrane were seen in some of the animals. Although there were slight or no pathological changes on the opposite side, the viral antigens were also detected with less fluorescent intensity in the endolymphatic, sensory and ganglion structures. The viral antigens were found in the labyrinth of the opposite side, but we have not yet been able to elucidate its routes and mechanism. Histopathological changes at the late stage of the viral infection were confirmed after longterm observations. The neutralizing antibody titer after intralabyrinthine inoculation was studied compared with that after intraperitoneal inoculation.
The posterior end of the vocal folds has been described differently by anatomists and clinicians. Anatomists seem to consider the posterior ends of the vocal ligament and vocal folds to be synonymous, thereby excluding the cartilaginous portion of the structure. In contrast, clinical narrations portray the vocal folds as consisting of both a cartilaginous and membranous portion. Unfortunately, neither clinicians nor anatomists have adequately defined and/or documented their descriptions of vocal fold length. Furthermore, both groups seem to be unaware that any descrepancy exists. The purpose of this paper is to discuss the definitions of the posterior end of the vocal fold and to offer one possible resolution to these divergent points of view. On the basis of a review of selected textbooks and our own careful observation of excised human larynges, we propose that the posterior end of the vocal fold is located at the posterior end of the laryngeal ventricle. The structure posterior to this presents a wall-like appearance and does not look like a fold. According to this definition, the posterior end of the vocal fold includes a cartilaginous structure, that is, the vocal process of the arytenoid cartilage. Since this cartilaginous portion is not included in anatomical definitions it has no anatomical name. Nevertheless, from both the anatomical appearance of the structure and a clinical point of view inclusion of this cartilaginous structure may be one way to resolve existing differences in viewing the vocal fold length.
Reciprocal connection between the olfactory bulb and the pyriform cortex in the rat was studied with the degeneration (Nauta-Gygax, Fink-Heimer techniques) and the retrograde (Horseradish peroxidase, HRP) tracing methods. Moreover, the feedback system from the pyriform cortex to the olfactory bulb was investigated. The following conclusions were drawn from the present study. 1. Whole areas of the pyriform cortex receive fibers from the olfactory bulb via two separated pathways. (1) Passing through the lateral olfactory tract, mitral cells in the main olfactory bulb send their fibers to the superficial half of the plexiform (I A) layer of the pyriform cortex. (2) Projection fibers from the anterior olfactory nucleus, running through the deep layers of the pyriform cortex and the anterior limb of the anterior commissure, terminate in the deep half of the plexiform (I B), II and III layers of the pyriform cortex. 2. Descending fibers from the pyriform cortex pass through the deeper layer of the cortex, the anterior limb of the anterior commissure, the medial forebrain bundle and the lateral olfactory tract. The rostral and middle parts of the pyriform cortex send fibers to the anterior olfactory nucleus. And it was clearly demonstrated that the main olfactory bulb receives cortical fibers exclusively from the rostral pyriform cortex. Whole cortical regions issue fibers to the nucleus of the horizontal limb of the diagonal band (HLDB) and the lateral hypothalamic area (LHA), many neurons in these two nuclei are always labelled after HRP injection into the main olfactory bulb, and to the mediodorsal nucleus of the thalamus (MD) and the lateral habenular nucleus (LH). 3. The present study exhibited that direct feedback impulse may come from the rostral pyriform cortex to the main olfactory bulb. Activity of the bulb will be indirectly influenced by descending fibers originated in the middle and caudal cortical areas via the anterior olfactory nucleus, and the HLDB and the LHA, respectively. Moreover, the fact that the MD and the LH receive fibers from whole cortical regions suggests strongly a possible existence of other feedback mechanisms to the bulb from heigher cortical centers via the two nuclei.
The ototoxicity and nephrotoxicity of netilmicin were compared with those of dibekacin, kanamycin and amikacin. Groups of five rabbits each were given doses of 50 or 100mg/kg of either one of the four drugs for 30 days. Ten days after the last injection, all animals were prepared for histopathological studies of inner ears and kidneys. Histological results of inner ears obtained by the rabbit show the least ototoxicity of netilmicin in comparison to the other three aminoglycoside antibiotics. No significant differences were observed among the nephrotoxicity of netilmicin and dibekacin or amikacin.
Localization of laryngeal motoneurons of cats were identified utilizing the horseradish peroxidase (HRP) technique. The results were partically confirmed by direct faradic stimulation of the nuclei selected muscles with a bipolar glass electrode. All laryngeal motoneurons were found ipsilaterally in the nucleus ambiguus except the cricothyroid (CT) motoneurons. Only CT motoneurons were recognized in the retrofacial and ambiguus nuclei and its cell column was extended from the level which is just rostral to the rostral end of the inferior olivary nucleus to the level where the principal nucleus of the inferior olivary nucleus is best developed. The cell column of the posterior cricoarytenoid (PCA), the thyroarytenoid (TA), the lateral cricoarytenoid (LCA) and the interarytenoid (IA) motoneurons were located between the caudal end of CT motoneurons and the caudal end of the inferior olivary nucleus. Their cell columns were situated more caudal than that of CT in the order of PCA, TA, LCA and IA. In the nucleus ambiguus, CT motoneurons were found in the ventral part, PCA motoneurons in the middle part, TA motoneurons in the dorsal part, LCA and IA motoneurons in the whole part. Laryngeal activities caused by the electrical stimulation (30-50 Hz, 0. 1 msec duration, 0.2 mA) at the following two different locations of the nucleus ambiguus were recorded electromyographically: (1) 4mm lateral from the medial line at the level of the first branch of the hypoglossal nerve and (2) 1.5 mm caudal to the first point. Electrical stimulations of the former location caused electric potentials of CT and the cricopharyngeus muscle and those of the latter produced excitation of PCA and/or TA.