In 1950-51, Waardenburg (15,16,17) showed that some well-known developmental anomalies in the interocular region associated with deafness and certain pigmentary defects constitute a syndrome which is inherited as a dominant character. The syndrome consists of the following features: lateroverse dystopia of the medial canthi (estimated penetrance, 99 O/O), prominent nose root (78 O / o ) , hyperblasia of the medial part of the eyebrows with frequent overgrowth (synophrys) (45 O/O), heterochromia iridum (25 O/O), unilateral deafness or deafmutism (20 U/O), a white hair lock (17 O/O) and, in some cases, vitiligo-like pigmentary defects of the skin. Premature greying of the scalp hair is, according to Waardenburg, equivalent to the white hair lock.After having shown that the characteristic features of the syndrome are normal at the beginning of the third month of embryonic life, Waardenburg expressed the view that the syndrome owes its features to a fixation of the foetal characters through an arrest of normal development (14).A number of single cases have been published, including a sporadic one by the Danish investigator Brtendstrup (3) in 1941. An interesting divergent case with extensive vitiligo, cranial deformities and multiple dysplasia of the upper extremities was presented by Klein ( 8 ) in 1950. Keizer (7) and Wildervanck (13) added several Dutch families to the nine considered by Waardenburg. Other families have been described from Switzerland (2), France (lo), England (9, l l ) , Denmark (Arnvig (l)), Spain (6) and the U. S. A., where Di George et al. ( 4 ) presented the first cases among Negroes.These are of particular interest, since some of the patients had double-sided blue eyes, i. e. bilateral hypochromia of the irides.In histological studies of affected internal ears, Fisch ( 5 ) revealed the absence of the organ of Corti and of the greater part of the ganglion cells of the spiral ' $) Received October 12th 1962.

No abstract

In 1962, Wolff and Zimmerman (10) gave a detailed description of the histopathological picture of the deformation of the chamber angle which may occur after ocular contusion.The lesion consists of a tear in the ciliary body resulting in a split between the circular and longitudinal fibres of the ciliary muscle. The latter retain their attachment to the scleral spur, while the former fibres, together with the root of the iris, are displaced backwards, giving rise to a recession of the chamber angle: which is characteristic of the lesion. In many cases, atrophy of the circular muscle fibres and fibrosis and hyalinisation of the trabecular meshwork occur, accompanied by variable obliteration of the intertrabecular spaces and the canal of Schlemm. A new-formed hyaIine membrane often covers the trabecular meshwork and continues centrally into the membrane of Descemet, while it extends into the deepened chamber angle peripherally. These changes may lead to a type of secondary monocular glaucoma of insidious onset which develops a long time after the immediate effects of the contusion have disappeared when the trauma may have been forgotten.In 1944, Rcese (7) described this hyaline membrane and its significance in the pathogenesis of glaucoma. He assumed that the development of the membrane was due to either inflammation or trauma, or to a primary disease. In 1949, D'Ombrain (4) described the traumatic, monocular chronic glaucoma; like Reese, he assumed that its occurrence was referable to the aforementioned hyaline membrane.The first description of the pathological anatomy of the lesion was given in ") Recieved March 28th 1966. 51