A fresh cadaveric study of the paratubal muscles: implications for eustachian tube function in cleft palate.

The aims of this anatomic investigation were to examine the levator veli palatini, tensor veli palatini, and salpingopharyngeus muscles in relation to normal eustachian tube function and to analyze the clinical implications of these data for tubal physiology in cleft palate individuals. Detailed dissections under 3.2x loupe magnification were conducted on the paratubal muscles of 15 fresh human adult cadaveric head specimens, paying particular attention to their cranial base anatomy. Each half of the cadaveric heads was examined separately, giving a sample size of 30. The cranial base origin of the levator veli palatini was the junction of the cartilaginous and bony parts of the eustachian tube. Contrary to statements in the existing literature, it had no origin from the quadrate area of the petrous temporal bone. In its path toward the velum, it was related inferiorly and lay almost parallel to the tube. The tensor veli palatini originated from the scaphoid fossa of the sphenoid bone and the tube. In contrast to previous descriptions, it was found to consist of a single sheet of muscle with no bilaminar structure. Its axis was oblique to that of the tube. The salpingopharyngeus was a slender muscle attached to the posteroinferior aspect of the pharyngeal end of the tube. It inserted into the palatopharyngeus inferiorly. These morphologic characteristics and anatomic relationships suggest that (1) the levator veli palatini opens the eustachian tube by isotonic contraction that results in displacement of the medial tubal cartilage and the tubal membrane, (2) the tensor veli palatini opens the tube directly by traction on the lateral tubal membrane and indirectly by rotation of the medial tubal cartilage by means of traction on the lateral tubal cartilage, (3) because of its consistently small size, the salpingopharyngeus is probably functionally the least important of the paratubal muscles, (4) the levator veli palatini is unable to cause tubal dilatation in cleft palate because it can only contract isometrically, and (5) tensor veli palatini function is probably unaffected by clefting. However, its mechanism of action may be disrupted iatrogenically by complete hamular fracture or division of its tendon.