Central tinnitus: A case report. (Original Article).
We report a case of acute-onset unilateral tinnitus in a 25-year-old woman. Analysis of imaging studies indicated that the tinnitus was likely caused by an acute hemorrhage of a small cavernous angioma that was located adjacent to the contralateral primary auditory cortex. This case provides substantial support for the concept that central tinnitus might indeed represent a pathologic activation of neural networks of nonspecific auditory perception.
Despite the efforts of various investigators, the precise neuronal mechanisms of tinnitus remain incompletely understood. (1-5) We report a case of acute-onset unilateral tinnitus related to an acute hemorrhage of a small cavernous angioma in the contralateral temporal lobe.
A 25-year-old right-handed woman suddenly developed intermittent tinnitus in her right ear. Her condition was characterized by episodes of loud and rhythmic noise of 5 to 10 minutes' duration. Neurologic examination revealed mild hemidysesthesia on the right. Computed tomography (CT) and magnetic resonance imaging (MRI) detected a small lesion that exhibited characteristics of a subacute hematoma (figure 1). The hemidysesthesia resolved within 24 hours, but the tinnitus continued intermittently for 10 days.
Follow-up MRI obtained on the 30th day after the onset of symptoms demonstrated a reduction in the volume of the lesion, as well as image characteristics typical of a cavernous angioma located immediately adjacent to Heschl's convolution in the left superior temporal gyrus (figure 2). The functionality of this cortical region was confirmed by activation studies with high-field MRI and statistical subtraction of a music-listening paradigm minus white-noise-listening (figure 3). (A detailed description of high-field MRI can be found elsewhere. (6,1)
The tinnitus subsided spontaneously, and the patient remains asymptomatic 5 years later.
It is generally believed that the primary structure responsible for the generation of tinnitus is the cochlea. Nevertheless, many investigators imply that cerebral cortices possess the potential to generate tinnitus (central tinnitus), as well. (1-5) The experience with our patient, we believe, demonstrates that such is the case. The right-sided unilateral tinnitus was likely caused by an acute hemorrhage of a small cavernous angioma that was located adjacent to the contralateral primary auditory cortex.
Since transient "positive" local signs are often encountered as a manifestation of neurologic events associated with a small acute hemorrhage, as illustrated by hemiballismus associated with hemorrhage in the subthalamic nucleus, this case provides substantial support for the concept that central tinnitus might indeed represent a pathologic activation of neural networks of nonspecific auditory perception.
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(2.) Kaltenbach JA. Neurophysiologic mechanisms of tinnitus. J Am Acad Audiol 2000;11:125-37.
(3.) Lenarz T, Schreiner C, Snyder RL, Ernst A. Neural mechanisms of tinnitus. Eur Arch Otorhinolaryngol 1993;249:441-6.
(4.) Zenner HP. A systemic classification of tinnitus generator mechanisms. Int Tinnitus J 1998;4:109-13.
(5.) Hazell JW, Jastreboff PJ. Tinnitus. I: Auditory mechanisms: A model for tinnitus and hearing impairment. J Otolaryngol 1990;19:1-5.
(6.) Kwee IL, Fujii Y, Matsuzawa H, Nakada T. Perceptual processing of stereopsis in humans: High-field (3.0-tesla) functional MRI study. Neurology 1999;53:1599-601.
(7.) Nakada T, Fujii Y, Suzuki K, Kwee IL. "Musical brain" revealed by high-field (3 Tesla) functional MRI. Neuroreport 1998;9:3853-6.
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|Comment:||Central tinnitus: A case report. (Original Article).|
|Publication:||Ear, Nose and Throat Journal|
|Article Type:||Brief Article|
|Date:||Dec 1, 2001|
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