To the Editor:
We read with interest the paper by Michiels et al., who performed a study to characterize cervical spine issues in “Cervical Spine Tinnitus” (CST) (1). Our primary concern is the assumption that CST is a clinical entity. The theory behind CST is based on the supposition that aberrant cervical somatosensory information conveyed to the cochlear nucleus can cause tinnitus independent of cochlear hair cell loss or other auditory pathway pathology. Unfortunately, there is little scientific basis to this assumption in the literature. Additionally, causality or correlation between the tinnitus precept and cervical spine symptoms was not proven. This lack of causality is pervasive in the literature, as descriptions of neuronal connections between the cervical spine and auditory pathways have only been shown in cadaveric studies in a single animal species (2). Moreover, there is an absence of literature that demonstrates tinnitus directly caused by cervical spine abnormalities in animals or humans. Accordingly, the concept of cervical spine tinnitus is purely theoretical and currently an unproven and unestablished diagnosis, which should be acknowledged by the authors.
Furthermore, the authors use the Neck Bournemouth Questionnaire (NBQ) as an indicator of cervical neck pathology. The NBQ was originally designed to measure biopsychosocial aspects of neck pain as a symptom inventory tool for clinical trials and outcomes research (3). Consequently, there is a potential for confounding when using the NBQ to rate neck symptoms in the setting of tinnitus, as many of the risk factors for neck pain, including psychological health conditions (4), are also risk factors for tinnitus (5–7). In particular, perceived stress and anxiety have consistently shown to be related to neck symptoms (8) and tinnitus (5). Thus, it is conceivable that anxiety could be a common causative factor for neck pain and tinnitus exacerbation, leading to higher NBQ scores and the labeling of the patient with a CST diagnosis. However, the authors did not control for these confounding factors, which may have contributed to the differences found between the two groups.
Another limitation of the study is the creation of a single subjective criterion for the diagnosis of CST, which relies exclusively on patient recall to associate the onset or exacerbation of tinnitus and neck symptoms. Given that the annual prevalence of neck pain can be as high as 50% (4); this diagnostic criterion requires further validation before its use in clinical studies.
The finding that a statistically equal number of CST and non-CST patients reported modulation of tinnitus during one of their physiotherapeutic tests is counterintuitive. Indeed, if we were to assume CST to be an independent and distinct clinical entity with an established cervical somatosensory pathophysiology, we would expect to see a higher incidence of manipulation-related tinnitus modulation in the CST group when compared to the non-CST group.
Cervical spine tinnitus is a hypothetical clinical entity in need of validation in studies to establish the relationship between spinal pathology and tinnitus. Caution should be exercised when suggesting that “[the] presence of cervical spine complaints can be a first indicator for the CST diagnosis (1).”
Jay Bhatt M.D.
Yaser Ghavami M.D.
Harrison W. Lin M.D.
Hamid Djalilian M.D.
Division of Otology, Neurotology, and Skull Base
Surgery; Department of Otolaryngology–Head and Neck
Surgery, University of California, Irvine, California, U.S.A.
The authors report no conflicts of interest.
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