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(Stroke. 2003;34:837.)
© 2003 American Heart Association, Inc.
Letters to the Editor |
Service de Neurologie, Centre Hospitalier de Luxembourg, Luxembourg
To the Editor:
I very much appreciated the article by Lee et al1 on the important hearing loss in anterior inferior cerebellar artery (AICA) stroke as they address the neglected issue of hearing loss in neurologic disease. They confirm the notion that peripheral and central disorders of the VIIIth nerve are likely to be confounded.2 Despite the unusual work-up, there are several pitfalls in the terminology, and pathophysiology to be addressed.
The term auditory brain stem response (ABR) is strongly misleading and I advocate the use of auditory evoked potential (AEP). The former would imply a generation of the entire response in the brain stem. The latter describes the modality and the evoked response type. It has become increasingly clear that the wave I of the AEP is generated outside the brain stem, and probably represents the change of conductivity when the VIIIth nerve leaves the temporal bone. The same might apply to wave II, where the nerve enters the brain stem.3 So the interpeak latencies might reflect different pathophysiologies. The I-III interval may thus reflect a sensorineural lesion (delayed or abolished wave I/II) as well as a central lesion (wave III, probably generated at the level of the superior olivary complex.4,5 Interestingly, the AEP shown for the central-type shows complete loss of all waves, following standard criteria suggestive of peripheral loss.6 The lesions shown for the two cases do not differ significantly in my opinion, but demonstrate as well a spotty lesion pattern in the lateral pons as well as around the fourth ventricle, thus closely neighboring the auditory nuclei as well as their cranial projections.4 One has to keep in mind that the pure tone audiogram (PTA) can be pathological in peripheral as well as in central conditions, as well as the stapedius reflex might be unilaterally abolished in brain stem lesions, and the same can be true for speech discrimination tests.6 Unfortunately, the more challenging tests as gap detection or localization paradigms have not been applied, but could, together with the results of PTA and AEP give clues to the lesion localization. It might be of interest to perform MRI of the cochlea in the acute phase to see whether cochlear ischemia shows up or not. Furthermore, a thorough testing for additional central auditory disorders in the interval could separate peripheral and central hearing loss. The idea of testing the otoacoustic emissions might help, but anatomically, this depends on the integrity of the descending fibers from the auditory cortex to the superior olivary complex as well as Rasmussens bundle (olivocochlear tract). Thus, it remains open whether an AICA stroke constitutes a central or a peripheral hearing deficit.
References
1. Lee H, Sohn S, Jung DK, Cho YW, Lim JG, Yi SD, Lee SR, Sohn CH, Baloh RW. Sudden deafness and anterior cerebellar artery infarction. Stroke. 2002; 33: 28072812.
2. Thömke F, Hopf HC. Pontine lesions mimicking peripheral vestibulopathy. J Neurol Neurosurg Psychiatry. 1999; 66: 340349.
3. Scherg M, von Cramon DY. A new interpretation of the generators of BAEP waves I-V: results of a spatio-temporal dipole model. Electroencephalogr Clin Neurophysiol. 1985; 62: 290299.[CrossRef][Medline] [Order article via Infotrieve]
4. Webster WR, Garey LJ. Auditory system. In: Paxinos G, ed. The Human Nervous System. San Diego, Calif: Academic Press; 1990: 889944.
5. Levine RA, Gardner JC, Fullerton BC, Stufflebeam SM, Furst M, Rosen M. Multiple sclerosis lesions of the auditory pons are not silent. Brain. 1994; 117: 11271141.
6. Levine RA, Häusler R. Auditory disorders in stroke. In: Bogousslavsky J, Caplan LR, eds. Stroke Syndromes. 2nd ed. Cambridge: Cambridge University Press; 2001: 144161.
Department of Neurology, Keimyung University School of Medicine, Daegu, South Korea
Department of Neurology, UCLA School of Medicine, Los Angeles, California
Response
We appreciate the interest of Dr. Ulbricht in our article1 on the importance of hearing loss in anterior inferior cerebellar artery (AICA) stroke. We agree that the abbreviation AEP is probably better than ABR, but like many other areas of medicine, once an abbreviation such as ABR is well established, it is very difficult to change the usage. The two cases shown in our article do have similar brain stem lesions, but the audiometric testing suggests a different localization for the hearing loss in each case. Case 1 had a moderate hearing loss with good speech discrimination and normal auditory evoked responsetypical findings for a cochlear site. Case 2 had a mild hearing loss with severe impairment of speech discrimination and absent auditory evoked responsetypical findings for a lesion involving the 8th nerve or more central structures. We suspect that in the majority of our cases, both peripheral and central auditory structures were involved. That the inner ear can be infarcted in cases of AICA stroke is well documented in the literature.2,3 The inner ear is particularly vulnerable to ischemia since it has a complete absence of collateral circulation unlike the other structures supplied by AICA. We agree that it might be of interest to perform an MRI of the cochlea in the acute phase of AICA stroke, but one would need special equipment to improve the resolution of the inner ear images. Possibly a special coil for the ear along with high dose contrast would allow visualization of an ischemic cochlea.
References
1. Lee H, Sohn SI, Jung DK, Cho YW, Lim JG, Yi SD, Lee SY, Sohn CH, Baloh RW. Sudden deafness and anterior inferior cerebellar artery infarction. Stroke. 2002; 33: 28072812.
2. Hinojosa R, Kohut RI. Clinical diagnosis of anterior inferior cerebellar thrombosis: autopsy and temporal bone histopathology study. Ann Otol Rhinol Laryngol. 1990; 90: 261271.
3. Oas JG, Baloh RW. Vertigo and the anterior inferior cerebellar artery syndrome. Neurology. 1992; 42: 22742279.
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