No abstract

Twenty-two patients with unilateral acoustic neuromas and preoperative speech discrimination scores of 35% or more had intraoperative monitoring of the electrocochleogram (ECoG) using a transtympanic electrode, and of the brain-stem auditory evoked potentials (BAEP's) using scalp electrodes. Rapid feedback was provided about the status of the cochlear microphonics from the hair cells of the inner ear (CM of the ECoG), the compound action potential of the auditory nerve (N-1 of the ECoG or Wave I of the BAEP's) and the potentials from the lower brain stem (Wave V of the BAEP's). All patients had total removal of the tumor. In 21, the cochlear nerve was anatomically preserved, and 20 had good postoperative facial nerve function. Correlation of tumor size with postoperative hearing was as follows: discrimination scores of more than 35% in three of four patients with 1-cm tumors, two of eight with 1.5-cm tumors, two of six with 2- to 2.5-cm tumors, and one of four with tumors of 3 cm or more. Two other patients with 1.5-cm tumors had discrimination scores of less than 35%, and one patient with a 2-cm tumor had only sound perception. In two patients, the discrimination scores improved. At the end of the operation, all patients with hearing had a detectable N-1, and, when recorded, CM. All but one patient with no hearing had lost N-1, and CM was absent or reduced. Unless Wave V was unchanged, it was a poor predictor of postoperative hearing, and its absence did not preclude preservation of good hearing. The electrophysiological changes during each stage of the operation were analyzed and correlated with events during surgery. Areas in which there was an increased risk of loss of the potentials were determined. In some patients monitoring was unnecessary, because either there were no significant changes or the changes were abrupt and no recovery occurred. However, in other patients, monitoring alerted the surgeon to a possible problem and the method of dissection was altered. Possible mechanisms of hearing loss were suggested from the changes in the recordings.

This "new" high-incidence antigen has been named MAM and assigned high-incidence antigen number 901016 by the International Society of Blood Transfusion. The corresponding antibody, anti-MAM, has been shown to cause HDN and has the potential to shorten RBC survival after the transfusion of incompatible RBC units, as determined by monocyte monolayer assay. Immunoblotting and flow cytometry show that this new antibody reacts with various WBC lines in addition to RBCs. This antibody also appears to react with platelets in some assays.