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I read with interest the article by Strausset al 1 on postoperative contralateral hearing loss which developed on the third day after microvascular decompression for trigeminal neuralgia. They attributed the symptoms to venous congestion at the ipsilateral inferior colliculus after dissection of the pontotrigeminal vein, which was documented by MRI. Symptoms resolved partially after intravenous rheologic medication for a total of 19 days. The authors' explanation for the delayed postoperative hypacusis, however, merits further discussion. Strauss et al 1provided preoperative and postoperative recordings of brain stem auditory evoked potentials: postoperatively, after stimulation on the operated side, ipsilateral waves I through V, and contralateral waves II through V are all clearly identifiable, contrasting with stimulation on the non-operated side, depicting only a small wave V bilaterally, but no other components. This pattern suggests a left sided lesion involving the generator of wave I—presumably the auditory nerve near the cochlea—and is also consistent with the patient's pancochlear hearing loss.2-4 By contrast, brain stem lesions—unless damaging the cochlear nucleus— are usually not associated with pure tone hearing loss, but rather with abnormal auditory localisation or interaural time discrimination,2 5 as auditory impulses are conveyed bilaterally in the brain stem.2-4 6Furthermore, a brain stem lesion causing profound hearing loss is likely to produce also contralateral wave IV/V abnormalities after stimulation on the non-affected side, but even the severest brain stem lesions, such as in evolving brain death, do not affect wave I.3 The vascular supply of the mesencephalic brain stem differs from that of the inner ear, the first being fed by mesencephalic arteries via the posterior cerebral or superior cerebellar artery, and drained through the superior petrosal vein; the second being supplied by the more caudally originating labyrinthine artery via anterior—or occasionally posterior—inferior cerebellar artery, and drained by the labyrinthine vein through the posterior part of the superior petrosal or transverse sinus, and the internal jugular vein.6 Although the patient's hearing may have been partially affected by the documented mesencephalic lesion, hearing loss may in fact be more likely caused by concomitant cochlear dysfunction. An ischaemic lesion seems probable, presumably postoperative vasospasm, or—less likely—unrelated embolism. In either situation, rheologic treatment may have been beneficial, as well as in venous congestion of the inferior colliculus. Concomitant cochlear dysfunction should have been considered as a cause of hearing loss in this patient, or ruled out by further examination.
We appreciate Kofler's comment on our paper and his interest in this unusual and still poorly understood clinical picture. We agree that the brain stem auditory potentials (BAEPs) after contralateral stimulation do not clearly point to a lesion of the ipsilateral colliculus; however, to our knowledge the neurophysiology of auditory pathways within the brain stem is not yet fully understood. For example, in our series of more than 300 cases of acoustic neurinoma monitoring we have made the observation that the contralateral wave V is much more pronounced compared with the ipsilateral wave V. The advantage of this case report is the preoperative and postoperative radiological and clinical documentation. The delayed onset of symptoms several days after the surgical procedure, the lack of effect of calcium blocker therapy—actually the patient's pure tone audiogram and speech discrimination deteriorated under nimodipine treatment—and the hearing improvement after heparinisation do not suggest vasospasm as the underlying pathophysiological mechanism. The literature on this rare yet important phenomenon of contralateral hearing loss after cerebellopontine angle surgery is purely speculative. By contrast this case report follows a straight course, which started at surgery with dissection of the pontotrigeminal vein, followed by a delayed contralateral hearing loss, and ended with a lesion of the ipsilateral colliculus. This lesion was not documented on preoperative MRI. Taking these findings into consideration, together with the neurophysiological findings of BAEPs in a still not fully understood auditory pathway within the brain stem, the “isolated vasospasm theory” seems unlikely.
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