With the aid of modern electromyography, numerous authors (Pabst and Esslen, I960; Sato, ig60; Orlowski and W6jtowicz, I962; Burger, I963; Blodi, van Allen, and Yar-brough, I964; Huber and Esslen, I969) have recently come to the (surprisingly) unanimous conclusion that a paradoxical innervation ofthe external rectus muscle ofthe affectedeye represents the pathogenetic principle of all the retraction syndromes (Stilling-Turk-Duane)(Duane, I905) and that the explanations given by the majority of earlier authors based on mechanical concepts (birth injury, congenital or acquired musculo-facialanomaly, etc.) are either insufficient or are at variance with the facts (Kriiger, I969). In this connection it must be emphasized that to accept a disorder of the antagonistic interaction of the extraocular muscles as the primary cause of the retraction syndromes does not exclude anatomical alterations of the muscular tissues, the more so as primary innervational disturbances are known to induce pathological changes in the muscles. An analysis of published cases (Lyle and Bridgman, I959; Malbran, 1953) and of our own series, has enabled us to distinguish threetypes of Duane's retraction syndrome:

Duane I (corresponding to Lyle's Type B or Malbramn's Type I) Marked limitation or complete absence of abduction, normal or only slightly defective adduction, narrowing of the palpebral fissure and retraction of the affected eyeball on adduction, widening of the palpebral fissure on attempted abduction (Fig. I).