To investigate the pathophysiology of tinnitus accompanied by HFS, we used magnetoencephalography (MEG) to study patients and analyzed the relationship between the presence of tinnitus and the MEG results. However, the pathophysiology of tinnitus is still controversial, especially if tinnitus is accompanied by HFS. The pathophysiology of HFS has been relatively well studied. It has been suggested that some forms of tinnitus may be caused by neurovascular compression in the cerebellopontine angle. If tinnitus is accompanied by HFS, the surgical outcome following microvascular decompression has a relatively high success rate, especially in cases in which the cochlear nerve is affected. This type of tinnitus was encountered in 10 of 142 patients with HFS in a study by Ryu et al. Interestingly, some patients experience ipsilateral tinnitus accompanied by HFS. And this type of Tinnitus is similar to other neurovascular compression syndromes, such as hemifacial spasm (HFS) and trigeminal neuralgia. Microvascular decompression surgery has been used to treat tinnitus because neurovascular compression of the cochlear nerve is assumed to be one of the causes of tinnitus. However, some types of tinnitus such as pulsatile tinnitus, which can be caused by vascular compression of the auditory nerve, may require different therapeutic approaches. Because tinnitus usually coincides with various ear disorders, surgical treatment of chronic tinnitus mainly focuses on ontological surgery. A wide range of therapies including pharmacological and surgical intervention have been proposed for the treatment of tinnitus symptom.
Approximately 5-15% of the population in western societies experience chronic tinnitus for more than 6 and up to 12 months. Tinnitus may be the result of spontaneous and aberrant neural activity of the auditory system. Tinnitus is defined as the subjective perception of a sound in the absence of any physical sound source. The neurovascular compression that causes sensory input from the pathologic facial nerve activity may contribute to this hyperactivity of the central auditory nervous system. The MEG results from normal-hearing patients who had tinnitus accompanied by hemifacial spasm suggest that the hyperactivity of the auditory central nervous system may be a crucial pathophysiological factor in the generation of tinnitus in these patients. ResultsĬochlear nerve activity in patients with tinnitus was increased with a shorter latency (p = 0.016) and stronger ECD strength (p = 0.028) compared with patients without tinnitus. We compared the difference in the latency and the ratio of the equivalent current dipole (ECD) strength between the ipsilateral and contralateral sides of the spasm and tinnitus. We used magnetoencephalography (MEG) to estimate the activity of the cochlear nerve in patients with and without tinnitus on the ipsilateral side. Participants were 29 subjects who presented with hemifacial spasm and neuroradiological evidence of vascular compression of the cranial (facial/cochlear) nerve. Traditionally, tinnitus accompanied by hemifacial spasm has been considered a type of hyperactive neurovascular compression syndrome that is similar to hemifacial spasm alone because of the anatomically close relationship between the facial nerve and cochlear nerve as well as the hyperactive clinical nature.
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