Recent data have focused on the peripheral nerve myelin glycoprotein PO as
a putative autoantigen involved in the autoimmune etiology of some cases of
Meniere's disease, idiopathic sensorineural hearing loss and sudden deafne
ss. To determine whether antibodies to myelin PO can alter cochlear functio
n, 13 healthy guinea pigs were immunized with purified porcine myelin PO wh
ile 10 controls were injected with saline water. The animals were then eval
uated for evidence of evolving inner ear disease using immunological, elect
rophysiological and morphological methods. Twenty-six experimental ears wer
e rested weekly with a brainstem auditory evoked potential technique for a
period of 4 months and were compared to 20 control ears. Uniformly, all PO-
sensitized guinea pigs showed antibodies to myelin protein PO as evidenced
by ELISA. Clinical signs of inflammatory demyelination were not discernible
in PO-sensitized guinea pigs and all the animals were qualitatively normal
. No significant increase of evoked potential thresholds was found in the P
O-sensitized animals when compared to controls (P > 0.05). Peak latencies o
f waves I, II, III, IV and V and inter-peak latencies in PO-sensitized guin
ea pigs did not significantly differ from those of controls (P > 0.05). His
tological sections of inner ear and peripheral nerves were free of disease
in both groups. These findings indicate that the sole presence of antibodie
s to myelin PO in the sera of guinea pigs or patients suspected of having a
utoimmune inner ear diseases is unlikely to elicit auditory abnormalities a
nd that additional factors are necessary for the pathogenic development of
these disorders. (C) 2001 Elsevier Science B.V. All rights reserved.