CLINICAL AND HISTOPATHOLOGICAL STUDIES ON THE LEPROSY OF THE LARYNX

Part I. CLINICAL STUDIES ON THE LEPROSY OF THE LARYNX

Abstract

The author examined the upper respiratory tract of the leprosy in-patients of the National Leprosarium Tama-Zenshoen during the period from 1938 to 1943 and also studied the histopathological changes of the autopsied cases of the leprosy of the larynx.
The monograph on the present author on "Leprosy of the Upper Re-piratory Tract" was destroyed while under printing by the bombing of Tokyo in 1943. Reported in the following is a part of the above monograph.
The author investigated the leprosy of the larynx of 973 leprosy patients (leprornatous type 711 cases, tuberculoid type 129 cases and neural type 133 cases) in respects of the rate and the time of the involvement, the part of predilection, symptoms and course of the disease.
Out of the 711 lepromatous patients including L1. L2 and L3, 460 cases (64.7% ) presented the lesions of some form in the larynx and the rate of the involvement was 96.6% for the highly advanced cases.
Tuberculoid changes in the epiglottis of the larynx were noticed in 7 tuberculoid cases (5.4%), one of which was confirmed to be free from tuberculosis on histopathological examination and animal experiment.
Paralysis of the laryngeal nerves was seen in 12 cases (9.0%) of the rteural leprosy. The larynx was involved, in the majority of the cases, during the 10 years period from the onset of leprosy and 55% of those occured within 6 years from the onset.
The initial lesion of the laryngeal involvement became manifest mostly in the epiglottis. Initial symptoms revealed as the congestion and the swelling of the epiglottis, arytenoids or vocal cords, but lasted generally only for several months being followed by recession to almost normal condition. After this apparently quiescent period of years, characteristic infiltration and nodulation developed in successive steps. Thus, it is the characteristic of the course of leprosy to present acute or subacute phase and spontaneous recession alternatively.
Nodules were frequently observed to occur around the entrance of the larynx and in the advanced stage they were observed in rosary shape.
Sometimes, plaques surrounded with red halo were noted to occur symmetrically on the arytenoid on both sides and to ulcerate superficially with relative Tepidity.
Diffuse infilti ations occur in the epiglottis, arytenoid as well as in the false and vocal cord. Infiltrated mucous membrane passes into dry and yellowing one and is covered with leukoplakia at the site of advanced hypertrophy.
Ulceration in the larynx was only observed in 9.4% of the total cases examined. Scar formation and constriction take place at the site of infiltration resulting in many kinds of distortions, e, g. backward inclination arid destruction of the epiglottis, stricture of the laryngeal tract.
Immobility of the cord rarely occurs in laryngeal leprosy, it develops the restrictiori of abduction of the cord as the result of the paralysis of m. posticus and, in more advanced cases, the fixation in the cadaver position of the cord owing to the paralysis of the recurrent laryngeal nerve which invites severe dispnoea.
The author confirmed, on a number of autopsy cases, the involvement of superior laryngeal nerve in all cases and that of the inferior nerve commonly in severe cases of the laryngeal leprosy.
In view of the above mentioned findings, the laryngeal dispnoea of the lepromatous leprosy is believed to occur as the result of the highly advanced infiltration and the paralysis of recurrent nerve owing to the lepromatous involvement.
As regard to the course of the laryngeal leprosy, lepromatous involvement frequently occurs during the period from 3 to 6 years after onset of leprosy, continual huskiness develops further 3 to 6 years after and the laryngeal stridor develops additional 3 to 6 years later.