Vertigo, Tinnitus, and Hearing Loss
in the Geriatric Patient

This section was compiled by Frank M. Painter, D.C.
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FROM:   J Manipulative Physiol Ther. 2000 (Jun); 23 (5): 352–362 ~ FULL TEXT

Kessinger RC, Boneva DV.

Kessinger Specific Chiropractic Clinic,
Cape Girardeau, MO 63701, USA.

OBJECTIVE:   To document clinical changes after a course of chiropractic care in a geriatric patient with vertigo, tinnitus, and hearing loss.

Clinical Features:   A 75–year-old woman with a longstanding history of vertigo, tinnitus, and hearing loss experienced an intensified progression of these symptoms 5 weeks before seeking chiropractic care. Radiographs revealed a C3 retrolisthesis with moderate degenerative changes C4–C7. Significant decreases in audiologic function were evident, and the RAND 36 Health Survey revealed subjective distress.

Intervention and Outcome:   The patient received upper cervical-specific chiropractic care. Paraspinal bilateral skin temperature differential analysis was used to determine when an upper cervical adjustment was to be administered. Radiographic analysis was used to determine the specific characteristics of the misalignment in the upper cervical spine. Through the course of care, the patient's symptoms were alleviated, structural and functional improvements were evident through radiographic examination, and audiologic function improved.

CONCLUSION:   The clinical progress documented in this report suggests that upper cervical manipulation may benefit patients who have tinnitus and hearing loss.

From the FULL TEXT Article


Vertigo, tinnitus, and hearing loss symptoms are usually attributed to the vestibular system. However, these symptoms may be the most obvious signs of a more complex presentation, especially in geriatric patients. Vertigo may be described as dizziness, faintness, lightheadedness, disorientation, or disequilibrium. Subjective vertigo is an illusion of movement of oneself, whereas objective vertigo is an illusion of movement of objects around oneself. Tinnitus is the perception of sound in the absence of an acoustic stimulus and may have a buzzing, roaring, whistling, or hissing quality or may involve more complex sounds that vary over time. Tinnitus is usually accompanied by hearing loss. [1]

The clinician can evaluate the cause of vertigo in 3 basic categories: peripheral, central, and systemic. [2–5] Vestibular functions belong to the peripheral category with the exception of the central nerve system and vascular supply, which compose the central category. Vestibular dysfunctions found in the systemic category may be important in the geriatric patient because they occur as a result of side effects from medications (eg, anticonvulsants, hypnotics, antihypertensives, alcohol, analgesics, tranquilizers) or an underlying systemic pathologic condition (diabetes, hypothyroidism).

A correlation between cervical spine disorders and vestibulocochlear symptoms have been reported. [6–12] The proprioceptive cervical afferent nerve fibers assist in the coordination of eye, head, body, and spatial orientation and the control of posture. [13] Dizziness and subjective balance disturbances are common symptoms in cervical pain syndromes. Hyperactivity of the spinovestibular afferents in the cervical spine brings on cervicogenic vertigo. [8] Cervical spondylosis with instability has been reported to produce Barré-Lieou syndrome, which may present as a triad of vertigo, tinnitus, and hearing loss. [14] Rzewnicki [9] reported that degenerative changes in the cervical spine often cause pain, vertigo, and pathologic results of otoneurologic test.

Bjorne et al [6] found a much higher occurrence of signs and symptoms of cervical spine disorders in patients diagnosed with Meniere's disease, a condition that includes acute attacks of vertigo with tinnitus and hearing loss, when comparing subjects in the general population. Most of these patients had problems in the upper cervical region. Hulse [15] reported that functional deficits in the upper cervical spine can lead to tinnitus, vertiginous episodes, a feeling of ear pressure, otalgia, and deafness and recommended chiropractic management of the upper cervical spine based on the results of his study involving 62 patients with vertebrogenic hearing loss.

Chiropractic care to the cervical spine has been reported to improve and ameliorate symptoms of vertigo, tinnitus, and hearing loss. [16–19] It is reasonable to conclude that successful chiropractic intervention in these cases occurred because of improved cervical spine function, with its neurologic and vascular components.



The patient's symptoms were consistent with Meniere's disease. Meniere's disease is characterized by recurrent prostrating vertigo, sensorineural hearing loss, and tinnitus. Many believe Meniere's disease results from abnormality in fluids of the inner ear, specifically the presence of endolymphatic hydrops in the vestibular apparatus. Although endolymphatic hydrops do exist, there has not been a significant correlation evident between Meniere's disease and endolymphatic hydrops. [44] Endolymphatic hydrops is a pathologic finding, whereas Meniere's disease is a clinical entity. [6] There is no single test to confirm the presence of Meniere's disease, [45] and many conditions may present with same or similar symptoms.

The patient's radiographs revealed signs of cervical instability at the C3/C4 motion segment with considerable cervical degeneration between C4–C7. Dechler [46] reported that degenerative changes in the cervical spine from C4–C7 are common with morbus Meniere's disease. This patient's audiometric studies revealed hearing deficits at higher frequencies, which is opposite of the expected symptom with Meniere's disease. The onset of Meniere's disease is usually seen in a younger patient; many geriatric patients may present with signs and symptoms that appear like Meniere's disease.

The clinical outcome in this case directs our attention to the cranio-vertebral junction as a possible source of pathophysiology.

Both the vestibular and cochlear nerves join at the internal auditory meatus to form the 8th cranial nerve, which enters the brain stem at the cerebellopontine angle (Figre 5). [47]

Figure 5.   Neurologic pathway of the vestibulocochlear nerve (Cranial Nerve VIII).
Copyright 1989. Novartis. Reprinted with permission from the Atlas of Human Anatomy,
illustrated by Frank H. Netter, M.D. All rights reserved.

Click to enlarge

The vestibular nerve projects to the vestibular nuclei in the medulla oblongata and into the inferior cerebellar peduncle. The cochlear nerve projects to the cochlear nuclei. Therefore the 8th cranial nerve consists of 2 functional divisions, equilibrium and hearing, which have a close relation to their respective nuclei in the medulla. [48]

The vestibular nuclei are located approximately at the junction of the medulla and pons and receive signals from the vestibular apparatus. The vestibular nuclei are richly interconnected with components of the brainstem reticular formation. [49] After receiving positional information, the vestibular nucleus sends motor responses to coordinate appropriate eye movement, neck movements, and body postural changes for maintaining balance. [26]

Auditory function begins in the cochlear portion of the vestibular apparatus. Auditory nerve signals are transmitted mainly by the inner hair cells in the organ of Corti. Nerve fibers from the spiral ganglion of Corti go to the dorsal and ventral cochlear nuclei, which are located in the upper portion of the medulla. All fibers synapse and many pass to the opposite side of the brain stem and terminate in the superior olivary nucleus. Some of these fibers also pass ipsilaterally to the superior olivary nucleus on the same side. From the superior olivary nucleus, the auditory pathway passes upward through the lateral lemniscus, with some of the fibers terminating in the lateral lemniscus nucleus. Many fibers bypass there and nearly all terminate in the inferior colliculus. The pathway then passes to the medial geniculate nucleus, where all fibers again synapse. The pathway then proceeds to the auditory cortex in the superior gyrus of the temporal lobe through the auditory radiation (Fig 6- not available). [26]

Interference in any portion of these neural pathways can bring about nerve-related hearing impairment.

Wilkins [51] reported that as part of the aging process, arteries elongate and the brain “sags.” As a consequence, redundant arterial loops and bridging of intrinsic hindbrain veins may cause cross-compression of cranial nerve root entry zones in the cerebello-pontine angle. This pulsatile compression can be seen to produce hyperactive dysfunction of the cranial nerve. The 8th cranial nerve may be affected, bringing on symptoms of tinnitus and vertigo.

Cervical afferents have been postulated as the cause of cervicogenic vertigo [52, 53] and hearing loss. With abnormal function occurring in the joint receptors of the cervical spine, aberrant nerve signals are sent to the brain stem through ascending tracts; inappropriate adaptive responses follow because of incorrect environmental monitoring of positional change.

A 3-directional misalignment of the atlas may compromise the size of the neutral canal space [18, 54] and has been postulated to jeopardize some functions of the medulla. [55–57] Rosenberg et al [58] reported a case of cervical cord impingement without a demonstrable misalignment observed with magnetic resonance imaging, bringing on signs and symptoms of medulla compression. Hack et al [59] found a well-organized connective tissue bridge from the rectus capitus posterior minor muscle through the atlanto-occipital junction inserting onto the dura by way of the posterior atlanto-occipital membrane. The posterior atlanto-occipital membrane was securely fixed to the dura by several fine connective tissue fibers. These two structures appear to function as a single entity. Hinson and Zeng [60] have observed through dissection that fibrous connective tissue serves to bridge the posterior longitudinal ligament and the dura from the top of the odontoid process to the lower body of C2. The posterior longitudinal ligament was found to be firmly attached to the periosteum of the anterior canal at this level. In addition, posterior connective tissue bridging to the posterior arch of C1 and to the lamina of C2 was evident. These findings suggest that the cord at the cranio-vertebral junction may be influenced by biomechanic aberrations in the upper cervical spine, which are evident through protractor cervical radiograph views. [40, 41, 61, 62] Interruption of the neural pathways at this level could result in the symptoms reported in this case.

One theory has proposed that irritation of sympathetic nerves can elicit spasms within the vertebral artery, leading to a decrease in blood flow to the brain stem and brain. Terret63 reported that misaligned vertebrae that guide arteries to the brain, presumably in the upper cervical spine, could create sufficient stress on the arteries to constrict the lumen. A decrease in blood circulation to vital auditory and vestibular centers could result in the presenting signs and symptoms in this case.

Compromise of the first 4 cervical spinal nerves, first 5 thoracic spinal nerves, or the superior cervical sympathetic ganglion through atlas subluxation could have been a factor in the pathogenesis of this case. These structures may be affected by an aberrant C1 position directly and indirectly. The first 2 cervical spinal nerves and superior cervical ganglion can be directly affected by atlas misalignment, thus altering their function. The third and fourth cervical spinal nerves and upper 5 thoracic spinal nerves may be jeopardized because of biomechanic changes, with structural compressions occurring as a result of atlas subluxation. [17]

Any mechanisms proposed appear plausible for this case. One mechanism by itself is less likely than a combination of some or all of the suggestions.


The STDA performed on this patient was the sole criteria used to determine the presence or absence of aberrant neurophysiology in the cervical spine. Thus the timing of an adjustment in the upper cervical spine, as described, was determined by reading the STDA.

Thermoregulation is thought to be centered in the hypothalamus and refined through spinal neuronal function at each spinal cord segment. Logically, this occurs for the purpose of segmental adaptation from environmental stresses. The hypothalamic set point, the core temperature of the body as determined by the hypothalamus, is filtered at each spinal segment by way of thermoregulative C-sympathetic nerve cell bodies. Temperatures have been documented to vary 5° C at individual spinal segments. Wallace et al [34] illustrated

This set point, however, is refined at each spinal segment by thermoregulative “C” sympathetic nerve cell bodies. Local, segmental thermoregulation by spinal cell bodies was shown to function even in the absence of hypothalamic input in decerebrate rabbits. Spinal nerve-cell bodies respond to thermoceptive, nociceptive and mechanoceptive afferents within their respective (and sometimes adjacent) dermatomes.

At each dermatomal segment, efferent axons connect thermoregulatory spinal “C” cell bodies to the paraspinal ganglions. At the ganglion, these neurons synapse with postganglionic thermoregulative efferents, some of which terminate cutaneously. Cutaneous sympathetic thermoregulatory neuronal function regulates vasomotor activity within the dermal arterioles and capillaries. Vasodilation tends to increase skin temperature, resulting in a greater heat transfer rate to the surrounding environment. Conversely, vasoconstriction causes the skin to approach ambient temperature, tending to conserve core heat.

The pattern system is a system developed to analyze bilateral skin temperature differential data gathered through neurocalograph readings. Skin temperatures are constantly changing as a function of the adaptive process throughout the entire human system by methods previously described. [36] Differences in temperature found from one side of the spine to the other that are static and persistent over time (days, weeks, or months) indicate a lack of thermal adaptation and are thought to be the result of aberrant neurophysiology.

An STDA graph reading that is static and persistent over time is considered to be the patient's pattern. Palmer16 believed that a vertebral subluxation does not change in its general nature or fluctuate in vertebral positioning from day to day but becomes fixed, causing the same or similar neurologic insult over time. The upper cervical vertebrae are structurally unique and asymmetrical. [40, 41, 58, 59] The supporting soft tissues in the upper cervical spine have their inherent strengths and weaknesses. These 2 factors give upper cervical vertebrae a propensity toward returning to their original misaligned position in subluxation. Therefore we would expect that neuronal dysfunction as caused by a vertebral subluxation would consistently disturb neurologic function. Hence, bilateral skin temperature differentials are not balanced and do not change over time in the presence of vertebral subluxation.

Clinically, the STDA graph reading should be evaluated on each case, looking at its reproducibility and chronicity. There are characteristic deviations within each patient's pattern. When these deviations are constant, they compose the patient's individual subluxation pattern. The clinician arrives at identifying the patient's pattern by comparing the current STDA graph with previous readings to determine duplicating characteristic deviations. Each patient's pattern may have 2, 3, or even more of these specific break points, which are unique and must all be present to be considered a pattern.

It is thought that the spine, surrounding soft tissues, and injured neuronal tissue go through cycles of repair as part of the healing process. [30] Structural changes occurring as a result may present STDA graph readings with characteristics similar to the original pattern. However, these STDA graph readings are normal and transient. If the clinician will allow a short period of time, these readings will usually disappear. Therefore it is prudent to consider the administration of an upper cervical adjustment after seeing the original pattern on 1, 2, or even more office visits to distinguish between a true and false pattern. This is a clinical judgement made on each individual case. An adjustment in the upper cervical spine administered at the wrong time can be detrimental to the patient's outcome.

Duff [29] found after recording over 35,000 comparative full spine STDA scans that no constant, static deflection or bilateral asymmetry in skin temperature can be found below the C2 level of the spine when the upper cervical region is in its proper juxtaposition and not subluxated. His paraspinal readings were performed by thermocouple instrumentation with a constant glide neurotempometer to ensure accuracy in gliding speed. The readings were made on each patient in a copper-grounded and copper-shielded booth to eliminate variable external energies, such as radio waves, television waves, Hertzian waves, and electromagnetic waves, thus preventing their influence on the graph reading. Duff [29] concurred with Palmer's original thought [31]: that asymmetrical skin temperature differentials were the result of heat resistance build-up from a blockage of nerve energy or nerve interference. With the assumption that human electricity flowing through nerves operates on the same principle as electricity flowing through wires, interference to electrical force will cause a local elevation of temperature dispersing at 90–degree angles from the point of impediment. Some heat is lost from absorption before it reaches the skin as it travels through soft tissue. However, it is thought that a significant amount of this increased temperature is reflected in the skin and alters the symmetry of bilateral skin temperature paraspinally.


This case details changes before and after treatment with long-term follow-up care in a clinical setting. Daily notes, bilateral skin temperature readings, and clinical impressions were included to illustrate the day-to-day clinical thinking process in this case.

A case study is limited in its ability to provide conclusions; one single case should not be taken out of context. It is possible that the patient described here recovered through spontaneous remission or because she believed her problem had been discovered and improved, creating a placebo effect. The spinal structural changes recorded in this case along with neurophysiologic recuperation weigh against the placebo affect. The time span in which the patient had the original symptoms before the instigation of chiropractic care makes spontaneous remission less likely.

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