A procedure of vestibular decompensation for clinical diagnosis. I. Animal experiments

Vestibular lesions are often so effectively compensated that their diagnosis may be difficult. Certain chemicals can decompensate the central vestibular system and thus uncover symptoms present before compensation. This study attempts to devise a procedure which can utilize such decompensation for the benefit of clinical diagnosis. Unilateral labyrinthectomies were performed in rats. Pathological movements and body positions due to the vestibular loss were compensated within about one week. Systemic application of cholinomimetic drugs (physostigmine and nicotine) led to consistent decompensation which lasted, however, too long and was accompanied by too severe side effects to be considered for clinical diagnostic purposes. Local application of these drugs into the middle ear of the healthy side were without effect. Brief inhalation of nitrous oxide (up to 79 vol.%) caused decompensation during the first four postoperative weeks but not consistently at longer survival times. Inhalation of halothane in N2O and O2 for 90 seconds caused a reliable decompensation at all times during the six month postoperative observation period. It is concluded that a brief halothane-N2O anesthesia may prove to be useful in a diagnostic search for compensated vestibular deficits.