Considerable skepticism still exists concerning the concept of neurovascular compression (NVC) syndromes of the eighth cranial nerve (8th N). If such syndromes exist, the sites of compression of the nerve must explain the symptoms encountered. We recorded compound action potentials of the cochlear nerve (CCAPs) during neurovascular decompression (NVD) to examine the topography of the three components of the 8th N. The sites of compression of the 8th N in cases of NVC syndrome confirmed at surgery were superimposed on the topography of the CN and vestibular nerve (VN) in order to determine the relationship between the sites of compression and the symptoms. CCAPs were clearly and consistently recorded on the caudal surface of the 8th N along the midline. In patients with vertigo and tinnitus there was vascular compression of the rostroventral (VN) and caudal surface (CN) of the nerve, respectively. In patients with both vertigo and tinnitus, there was compression of both VN and CN. Our findings clearly demonstrate that the symptoms of NVC of the 8th N depend on the part of the nerve that is compressed by blood vessels, and they support the concept of NVC syndrome of the 8th N.

Forty-three surgical cases were retrospectively analyzed to establish diagnostic criteria and operative indications for vertigo and tinnitus due to neurovascular compression (NVC) of the eighth cranial nerve (8th N). Many NVC syndromes were mistakenly diagnosed as Ménière's disease or benign paroxysmal positional vertigo. NVC was confirmed in 31 of the 43 patients. Neurovascular decompression (NVD) resulted in complete recovery or marked improvement of subjective symptoms in all 19 cases with vertigo (100%), and in 19 of 29 patients with tinnitus (65.5%). Multiple factor analysis revealed that abnormal caloric responses have high diagnostic value for vertigo due to NVC. Vertigo due to NVC is of short duration (a few sec to a few min.) in the early phase of the disease, which becomes longer and hearing becomes impaired as the history of NVC lengthens. Low pitch pulsatile and high pitch continuous tinnitus are probably due to NVC and are cured by NVD if hearing is still preserved. Tinnitus associated with hemifacial spasm is strongly indicative of NVD. Decompression of the 8th N should be performed in the early phase of disease, since cochlear and vestibular functions are irreversibly impaired if NVC continues for a long period of time.

It is the authors' opinion that sensorineural hearing loss and positive findings on magnetic resonance imaging are the most reliable evidence for the presence of tinnitus caused by NVC of the eighth cranial nerve.

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Thirty-four chronic myringitis cases were examined by otoscopy, pure tone audiometry, tympanometry, skull X-rays, and bacteriologic study of otorrhea. Five atypical cases are presented in detail. Three of these five cases had a perforation of the tympanic membrane preceding the appearance of typical chronic myringitis. The remaining two cases showed a transient small tympanic membrane perforation during the long course of chronic myringitis. These cases suggest that chronic myringitis could occur in some chronic suppurative otitis media and that myringitis could cause tympanic membrane perforation.