The risk of SNHL increased with DBS viral load. Further studies should investigate whether DBS CMV testing has a role in identifying asymptomatic congenitally infected neonates at risk of SNHL, and whether antiviral treatment can reduce this risk.

Objective-Tinnitus may be caused by a lesion or dysfunction at any level of the auditory system. This study explores cochlear mechanics using otoacoustic emissions in patients with tinnitus after head injury, in whom there seems to be evidence to support dysfunction within the CNS. Methods-The study included 20 patients with tinnitus and other auditory symptoms, such as hyperacusis and diYculty in listening in background noise, after head injury, in the presence of an "intact" auditory periphery (normal or near normal audiometric thresholds). They were compared with 20 normal subjects and 12 subjects with head injury, but without tinnitus, who had similar audiometric thresholds. In all subjects otoacoustic emissions, including transient clickevoked (TEOAEs) and spontaneous otoacoustic emissions (SOAEs), were recorded, and a test of eVerent medial olivocochlear suppression, consisting of recording of TEOAEs under contralateral stimulation, was performed. Results-A significantly higher prevalence of SOAEs (100%), higher TEOAE response amplitudes, and reduced medial olivocochlear suppression in patients with tinnitus in comparison with subjects without tinnitus have been found. Conclusion-These findings have been interpreted to be an extracochlear phenomenon, in which the reduction in central eVerent suppression of cochlear mechanics, leading to an increase in cochlear amplifier gain, was subsequent to head injury. Auditory symptoms in these patients seemed to constitute the "disinhibition syndrome". (J Neurol Neurosurg Psychiatry 1998;65:523-529)

Self-reported vestibular symptoms, measured by the PVSQ, discriminated between children presenting with vestibular symptoms and healthy controls and should be used to identify and quantify vestibular symptoms that require additional assessment and management.

Fourteen patients with hereditary motor and sensory neuropathy (HMSN), 12 of Type I and 2 of Type II, were assessed for auditory dysfunction. Five patients complained of hearing loss and all had pure-tone audiograms outside the normal range, while one patient who did not complain of hearing impairment also had an abnormal pure-tone audiogram. Assessment of loudness function, speech audiometry and brainstem auditory evoked potentials (BAEP) suggested that the hearing loss was the result of VIII nerve dysfunction, a conclusion supported by the abnormality of the electrocochleogram (ECochG) in one patient.