Cervical Spondylosis (CS) is a common, age-related condition characterized by the gradual wear and tear of the spinal disks and vertebrae in the neck. This degenerative process often leads to the formation of bone spurs (osteophytes) and affects the spinal joints. Tinnitus is the perception of sound, such as ringing or buzzing, when no external sound is present. While tinnitus is often associated with hearing loss, evidence suggests a recognized link between neck pathology and auditory symptoms. This article investigates the connection between changes in the cervical spine and the onset of tinnitus.
The Connection Between Neck Issues and Tinnitus
There is a recognized relationship between issues in the neck and the perception of sound in the ears. This specific manifestation is often termed Cervicogenic Somatic Tinnitus (CST), or “cervical tinnitus.” Unlike primary tinnitus, which originates from the auditory system, CST arises from sensory input originating outside the ear. This type of tinnitus is frequently associated with conditions that affect the cervical spine, including the degenerative changes seen in cervical spondylosis.
A distinguishing feature of CST is that the perceived sound is often modulated by changes in neck posture or movement. Turning the head, flexing the neck, or applying manual pressure to certain neck muscles may temporarily alter the pitch or volume of the tinnitus. This modulation suggests the auditory disturbance is linked to the musculoskeletal structures of the neck, rather than solely to the inner ear. The connection involves an influence from the somatosensory system on the auditory pathways.
Neurological and Vascular Pathways of Cervicogenic Tinnitus
The mechanism by which neck pathology influences auditory function involves two primary, interconnected pathways: neurological cross-talk and a vascular component. Both explain how the degenerative changes of cervical spondylosis can lead to the perception of sound.
One major mechanism involves the dorsal cochlear nucleus (DCN), which is the brainstem’s initial relay center for auditory information. The DCN receives somatosensory input from the upper cervical spinal nerves, specifically C2 and C3, as well as the trigeminal nerve. Degeneration in the upper cervical spine, common with CS, can cause irritation or chronic stimulation of these nerve roots and surrounding muscles. This aberrant sensory input from the neck is then transmitted to the DCN, where it can be misinterpreted as sound, leading to the perception of somatic tinnitus.
This neurological cross-talk causes a “mis-wiring” where non-auditory signals from the neck are processed as sound by the central auditory system. Increased muscle tension or nerve root compression from cervical osteophytes can enhance the excitability of neurons in the DCN. This enhanced excitability and synaptic reorganization create the persistent sound perception, even without external noise.
The second mechanism relates to vascular compression, particularly of the vertebral arteries. These arteries run through bony canals in the cervical vertebrae to supply blood to the brainstem and the inner ear. Bone spurs or misalignment resulting from cervical spondylosis can intermittently compress a vertebral artery, especially during certain head movements. This compression can temporarily reduce blood flow, causing a state of temporary ischemia, or oxygen deprivation, in the auditory centers of the brain or the inner ear.
Reduced blood flow to the inner ear structures can cause ischemic changes that manifest as tinnitus or dizziness. In some cases, CS-related compression can lead to pulsatile tinnitus, where the sound is perceived as a rhythmic throbbing synchronized with the heartbeat. This vascular component shows how the mechanical changes of CS directly affect the blood supply required for normal auditory function.
Clinical Assessment and Differential Diagnosis
Determining if cervical spondylosis is the cause of tinnitus requires clinical assessment and differential diagnosis. The goal is to confirm neck pathology and establish a clear link to the auditory symptom while excluding other common causes. Evaluation begins with a detailed patient history, focusing on the temporal relationship between neck symptoms and the onset or exacerbation of tinnitus.
A thorough physical examination is performed to assess the neck’s musculoskeletal function, including range of motion, muscle palpation for trigger points, and segmental mobility testing. Specific clinical cervical spine tests, such as the manual rotation test or the adapted Spurling test, can be used to provoke or modulate the patient’s tinnitus, which strongly suggests a cervicogenic origin. The presence of sensitive myofascial trigger points in the upper neck and shoulder muscles is often correlated with a diagnosis of CST.
Imaging studies, such as X-rays or Magnetic Resonance Imaging (MRI) of the cervical spine, confirm the extent of degenerative changes, including bone spurs and disc disease. Radiological findings alone are insufficient to confirm CST, as many people have CS without tinnitus. The diagnosis of CST relies on excluding other causes and correlating clinical neck signs with tinnitus modulation. Before attributing tinnitus to the neck, conditions like Meniere’s disease, noise-induced hearing loss, ototoxicity, and acoustic neuromas must be ruled out through audiological assessments.
Treatment Strategies for Neck-Related Tinnitus
Management for cervicogenic tinnitus focuses on addressing the underlying cervical spondylosis and associated musculoskeletal dysfunction. Treatment is conservative and multidisciplinary, targeting the sources of nerve irritation and muscle tension. The primary intervention involves physical therapy, which aims to restore normal neck function and posture.
Physical therapy protocols include specific exercises designed to improve the strength and endurance of the deep neck flexors, correct posture, and increase cervical range of motion. Manual therapy techniques, such as joint mobilization and soft tissue manipulation, reduce muscle tension and restore proper joint mechanics. This reduction in mechanical stress on the cervical nerve roots (C2/C3) helps decrease the aberrant somatosensory input contributing to DCN over-excitability.
Pharmacological interventions manage acute symptoms, including muscle relaxants for neck tension and non-steroidal anti-inflammatory drugs (NSAIDs) to reduce inflammation. For chronic cases, interventional procedures, such as nerve blocks or radiofrequency ablation of specific cervical nerve branches, may interrupt the sensory signaling pathway. Lifestyle and ergonomic adjustments are also important, including optimizing workstation setup to maintain a neutral neck position. Stress management techniques should be incorporated, as tension often exacerbates neck muscle tightness and tinnitus.