Vestibular schwannoma tinnitus
Nearly two-thirds of patients with vestibular schwannoma (VS) are reporting a significantly impaired quality of life due to tinnitus. VS-associated tinnitus is attributed to anatomical and physiological damage of the hearing nerve by displacing the growth of the tumor. In contrast, the current pathophysiological concept of non-VS tinnitus hypothesizes maladaptive neuroplasticity of the central nervous system to a (hidden) hearing impairment resulting in a subjective misperception. However, it is unclear whether this concept fits VS-associated tinnitus.
An analysis of Baguley et al. does not identify any single one mechanisms for tinnitus as being the obvious culprit. In fact, even in a homogeneous group of patients such as this, there is evidence of multiple mechanisms that are not mutually exclusive. The association between increased tinnitus severity in older patients, patients with canal pareses on caloric testing, and tinnitus as a principal presenting symptom should be borne in mind by the clinician 1).
Tinnitus is attributed to partial sensory deafferentation resulting in central maladaptive neuroplasticity. Unfortunately, the agent of deafferentation is usually unknown or irreversible. In patients with unilateral vestibular schwannoma (VS), however, the auditory nerve is affected by a benign tumor. Hence, removal of the tumor can cease tinnitus. In turn, sustaining complaints after surgery indicate cortical neuroplasticity. A cross-sectional study aimed to track cortical structural changes by surface-based morphometry in 46 VS patients with sustained (i.e. centralized) or ceased (i.e. peripheral) tinnitus after surgery. A volumetric analysis of cortical and subcortical gray matter (GM) anatomy was performed on preoperative high-resolution MRI and related to the presence of hearing impairment, pre-and/or postoperative tinnitus. Patients with sustained (i.e. chronic) tinnitus showed an increased GM volume of the bilateral caudate nucleus, the contralateral superior colliculus, the middle frontal and middle temporal gyrus, the fusiform gyrus as well as the ipsilateral pars orbitalis when compared to those patients in whom tinnitus ceased postoperatively. Chronic tinnitus in VS patients is associated with characteristic structural changes in frontal, temporal, and subcortical areas. Notably, a significant GM change of the caudate nucleus was detected providing further support for the striatal gaiting model of tinnitus 2).
A study aimed to determine the clinical predictors of VS-associated tinnitus to ascertain the compatibility of both pathophysiological concepts.
This retrospective study includes a group of 478 neurosurgical patients with unilateral sporadic VS evaluated preoperatively regarding the occurrence of ipsilateral tinnitus depending on different clinical factors, i.e., age, gender, tumor side, tumor size (T1-T4 according to the Hannover classification), and hearing impairment (Gardner-Robertson classification, GR1-5), using a binary logistic regression.
61.8% of patients complain about preoperative tinnitus. The binary logistic regression analysis identified male gender [OR 1.90 (1.25-2.75); p = 0.002] and hearing impairment GR3 [OR 1.90 (1.08-3.35); p = 0.026] and GR4 [OR 8.21 (2.29-29.50); p = 0.001] as positive predictors. In contrast, patients with large T4 tumors [OR 0.33 (0.13-0.86); p = 0.024] and complete hearing loss GR5 [OR 0.36 (0.15-0.84); p = 0.017] were less likely to develop tinnitus. Yet, 60% of the patients with good clinical hearing (GR1) and 25% of patients with complete hearing loss (GR5) suffered from tinnitus.
These data are in good accordance with literature about non-VS tinnitus indicating hearing impairment as the main risk factor. In contrast, complete hearing loss appears a negative predictor for tinnitus. For the first time, these findings indicate a non-linear relationship between hearing impairment and tinnitus in unilateral sporadic VS. Our results suggest similar pathophysiology in VS-associated and non-VS tinnitus 3).