Content uploaded by Michael Burcon
Author content
All content in this area was uploaded by Michael Burcon on Jun 03, 2016
Content may be subject to copyright.
Health Outcomes Following Cervical Specific Protocol in 300
Patients with Meniere’s Followed Over Six Years
Michael T. Burcon, B.Ph., D.C.1
ABSTRACT
Objective: Multiple factors and several common triggers contribute to Meniere’s disease (MD), but the hypothesis of this
study is related to one cause: an upper cervical subluxation complex (UCSC), the result of whiplash trauma, caused by
vehicular accident or blow to head.
Methods: UCSC pattern was established utilizing Tytron thermography, Thompson cervical syndrome and modified Prill
leg length inequality tests, determining when and where to adjust. Upper cervical adjustment listings were obtained by
Blair x-ray analysis. Ninety percent of patients had atlas listings of posterior and inferior on the opposite side of the
involved ear. When patients were in pattern, Palmer toggle recoil and/or Pierce Results knife-edge adjustments were
performed.
Results: Vertigo intensity rated by 300 patients on a scale of 0 to 10, with 10 being the worst imaginable. Prior to
treatment mean score was 8.5, six weeks post treatment average was down to 3.0, after one year 2.0, two years 1.4, three
years 0.9, four, five and six years 0.8, an improvement of over 90%. Ninety seven percent claimed a dramatic
improvement in vertigo. Three percent had side effect of headache.
Conclusion: Patients with a history of both vertigo and trauma should be referred to an upper cervical specific chiropractor for
examination.
Key Words: Meniere’s disease (syndrome), vertigo, Eustachian tube dysfunction, upper cervical subluxation complex, whiplash
Introduction
History
Prosper Meniere, Chief of Medicine at the Imperial Institute
for Deaf Mutes in Paris France, reported the gross
pathological findings in a young girl suffering from vertigo,
tinnitus, and deafness in a paper read in 1861. He pointed out
that episodic vertigo usually had a benign course and the
treatments typically used, including bleeding, leeching,
cupping and purging, could be more harmful than the disease
itself. Ironically, due to the fact that the central patient
Meniere described in his papers died from her disease, it is no
longer believed that she suffered from Meniere’s disease
(MD). Morbidity is not an outcome of MD.1 In 1938, Hallpike
and Cairns in London, and Yamakawa in Japan independently
described the pathological finding of endolymphatic hydrops
in the temporal bones of patients with MD at autopsy. In 1926
Georges Portmann carried out the first physiological operation
for MD. The operation, endolymphatic sac decompression
performed with hammer and gouge, was successful.2
ORIGINAL RESEARCH
1. Private Practice of Chiropractic, Grand Rapids, MI
1. Private Practice – Grand Rapids, MI USA
Meniere’s J. Upper Cervical Chiropractic Research – June 2, 2016 13
Parameters
In addition to the three hundred consecutive patients followed
from six to fourteen years at the Meniere’s Research Institute
(the MRI), over three thousand peer reviewed papers were
reviewed. Written verification of Meniere’s disease from an
otolaryngologist was required for inclusion in this study. The
first three patient questionnaires were filled out in the office;
the last five were mailed out. If a patient’s symptoms became
bilateral during the study, the originally involved ear was used
statistically. When a patient dropped out of the study, the next
consecutive patient was added.
Symptoms
The vertigo patient perceives either that the world is spinning
around them or that they themselves are spinning. With many
other disabilities, some portion of a normal life can be
continued. Vertigo disrupts virtually every aspect of life, since
the patient loses the ability to do anything normally, especially
when movement is involved. In addition to the obvious hazard
of falling, moving around is hampered by the fact that even
small head movements often make the spinning sensation
worse. The resulting nausea, sweating and vomiting combine
to make the patient subjectively very ill. Vertigo is to
dizziness what migraine is to headache.
Diagnosis
A differential diagnosis of Meniere's disease is a subjective
diagnosis of exclusion. When all other possible diseases with
the same symptoms are excluded, the condition is called
Meniere's disease. MD is sometimes referred to as Meniere's
syndrome. A syndrome is a collection of symptoms.
According to the Prosper Meniere Society a diagnosis of
Meniere's disease requires at least two spontaneous episodes
of vertigo, each lasting 20 minutes or longer, hearing loss
verified by a hearing test on at least one occasion, tinnitus or
aural fullness and exclusion of other known causes of these
sensory problems.3
The Merck Manual states that the cause of Meniere's disease is
unknown and the pathology is poorly understood. Based upon
the authors research, “…trauma to the head,” was added as a
risk factor.4 Although the underlying etiology of MD is
unknown, it appears that fluid build up in the endolymphatic
space, caused either by over production or reduced absorption,
exposes hair cells responsible for sensing movement and
balance to progressive damage and paralysis. However, recent
studies have demonstrated that not all Meniere’s patients have
endolymphatic hydrops, and that many patients with hydrops
do not suffer from Meniere’s disease.5 Previously, a diagnosis
of certain Meniere’s could only be proven upon autopsy,
which was rarely performed. Intratympanic delivery of
gadolinium selectively enhances perilymph, delineating it
from endolymph utilizing newer scanners with greater
magnetic strength and improved image sequencing have made
ultrastructural detail achievable.6 Interestingly, most patients
with unilateral MD were found to have bilateral idiopathic
lymphatic hydrops with this new imaging technique.
In the first stage of MD the hearing loss affects only the low
tones (bass) when the levels of endolymph are high in the
cochlea. The hearing returns to normal after an attack of
dizziness. In the second stage the hearing continues to
fluctuate but it never returns to its normal levels. Over a
period of days or even several times in a single day, the
hearing may have different degrees of acuity. In the third stage
(burn out) the hearing is very impaired and distorted but more
stable. It may still fluctuate slightly but with a more linear
pattern, with the tinnitus and recruitment remaining very
troublesome.7 In patients who chose not to undergo surgical
treatments, it was found that over 71% of these patients
reported complete control of vertigo after 8 years. Thus, it is
true that for some patients the attacks of vertigo will subside
with time. The term burn-out is appropriate as this reduction in
vertigo is not due to a recovery of the balance system. Rather
it is because the balance portion of the inner ear becomes
irreversibly damaged, so that it no longer functions. This
natural time course of events makes the evaluation of clinical
treatments extremely difficult. The estimated benefit of any
given procedure or treatment must take into account the likely
decline of vertigo with time. The above data are average
figures and there is considerable variation from patient to
patient. Some patients may continue to have vertigo attacks
for 20 years or more.8
The percentage of cases that become bilateral varies greatly in
the literature, from less than ten to more than sixty percent,
averaging about thirty percent. The average time interval for
conversion from unilateral to bilateral Meniere's was 7.6
years. Patients should be counseled regarding this potential
when interventions are considered, especially with respect to
ablative treatments.9
Histopathology
New theories center on the fact that Meniere’s disease may not
have a single cause but may well be a common endpoint of a
variety of anatomic (structural) or physiologic (functional)
variables, including ischemic or even autoimmune injuries. A
theme in reports on etiology and pathology of Meniere's
disease is an increase in immunoglobulins both in the
endolymphatic fluid and in serum. This would suggest an
underlying infection, possibly viral, or autoimmune
component with this condition.10 Although the herpes virus is
often found in MD patients, it is no longer considered a
cause.11 Finally, a team of researchers at the University of
Virginia reported in 2002 that the vestibular nerve cells in
patients with unilateral Meniere’s disease are demyelinated.12
Cerebrospinal fluid
The fluid spaces of the inner ear are connected to the
cerebrospinal fluid (CSF) by a small duct called the cochlear
aqueduct. In most humans, this duct is believed to be patent,
so that pressure changes of the CSF are transmitted directly to
the ear. It has been reported that low CSF pressure is
associated with glaucoma and endolymphatic hydrops.13
Medical treatment
Physicians may initially suggest a reduced salt level diet, in
the range of 1400 mg/day, to see if symptoms can be
alleviated. Steroids, such as dexamethasone, also may help
control vertigo attacks in some people. This procedure can
14 J. Upper Cervical Chiropractic Research – June 2, 2016 Meniere’s
also be performed with local anesthesia applied by your
doctor. Although dexamethasone may be slightly less effective
than gentamicin, dexamethasone is not likely to cause further
hearing loss. The effectiveness of steroids can also be tried
orally. If vertigo attacks associated with Meniere's disease are
severe and debilitating and other treatments don't help, surgery
may be an option.
Surgical treatment
The endolymphatic sac plays a role in regulating inner ear
fluid levels. These surgical procedures may alleviate vertigo
by decreasing fluid production or increasing fluid absorption.
In endolymphatic sac decompression, a small portion of bone
is removed from over the endolymphatic sac. In some cases,
this procedure is coupled with the placement of a shunt, a tube
that drains excess fluid from your inner ear. In a previously
published double blind, placebo controlled study, the efficacy
of an endolymphatic sac-mastoid shunt was compared with a
purely placebo operation (mastoidectomy) in controlling the
symptoms in 30 patients with typical Meniere's disease.14 The
results were the same. Vestibular nerve section involves
cutting the nerve that connects balance and movement sensors
in your inner ear to the brain. With a Labyrinthectomy the
surgeon removes a portion the inner ear, thereby removing
both balance and hearing function from the affected ear. This
procedure is performed only if you already have near-total
hearing loss in your affected ear.
Chiropractic approach
The Meniere’s Research Institute has established a link
between whiplash (vehicular accident or fall to the head) and
Meniere’s disease. The mean average from the time of the
trauma to the onset of symptoms is fifteen years.15 (Fig. 1)
Insertion of a middle-ear ventilation tube can temporarily
alleviate Meniere’s symptoms, suggesting Eustachian tube
dysfunction (ETD) is a contributing feature. Clinical practice
also shows that treating disorders of the upper and lower
cervical spine and temporomandibular joints can lessen
Meniere’s disease symptoms. Similarly, stellate ganglion
blocks can be beneficial in controlling Meniere’s disease
symptoms, highlighting the influence of the autonomic
nervous system. In this reflex pathway, irritation of facet joints
can first lead to an activated anterior cervical sympathetic
system in the mediolateral cell column; simultaneously
leading to an axon reflex involving nociceptive neurons,
resulting in neurogenic inflammation and the prospect of
ETD.16
Methods
History
Harvey Lillard immediately became profoundly deaf while
exerting himself in a cramped, stooping position. Seventeen
years later, in 1895, magnetic healer D.D. Palmer racked the
second cervical vertebra, axis, into position by using the
spinous process as a lever, performing the first chiropractic
adjustment. Soon the man could hear as before.17 D.D.’s son,
B.J. Palmer, presented the hole-in-one (HIO) upper cervical
technique to the profession during Palmer School of
Chiropractic’s Lyceum in 1931.18 He believed that the
neurological component of the subluxation resulted from
pressure or tension applied to the spinal cord and its meninges,
creating an increased amount of heat. He started analyzing
spinal x-rays in 1908 and differences in bilateral paraspinal
temperatures in 1924. To locate the level of the subluxation he
developed the electroencephaloneuromentimpograph.19,20
Pattern work as developed by B.J.’s clinic director, Lyle
Sherman, was used to help determine when and where to
adjust the cervical spine.21 In this study of three hundred
Meniere’s patients, thermographs of the cervical spine were
recorded using a Tytron C-300 instrument. (Fig. 2) In each
case a detailed case history was taken on the first visit,
followed by a spinal examination. A report of findings was
given, recommending a minimum set of three cervical x-rays
when evidence of an upper cervical subluxation was
discovered in each patient. X-ray analysis of the upper
cervical vertebrae based on the work of William Blair was
used to determine chiropractic listings of subluxation.22
Lateral cervical, A-P open mouth and nasium x-rays were
taken. Lateral films were analyzed to determine evidence of
whiplash injuries. Posterior atlas listings, along with the lack
of normal cervical curve, were considered evidence of a
history of neck trauma in this study. The A-P open mouth
view was used to study lateral deviations of the neural rings,
which may cause neurological irritation. With the nasium x-
rays the antero-lateral margins of each of the articulations
were classified as being either juxtaposed, overlapped, or
underlapped. Overlapping is synonymous with anterior and
superior atlas listings with laterality of the side of the overlap,
underlapping indicates posterior and inferior C1 listings on the
opposite side of the underlap. These appositional judgments of
each articulation may then be combined to deduce the actual
unilateral or ambilateral misalignment pathways of atlas in
relation to occiput, and an anatomically accurate misalignment
listing and adjustive formula may thus be derived.23 There are
only four atlas listings under this system; anterior and superior
on either the right or left, or posterior and inferior on either the
right or left. Using the anterior tubercle of atlas as the
reference point, considering the rocker configuration of the
atlanto-occipital articulation, if atlas moves posterior then it
must also move inferior.24
Leg length inequality checks were performed on each patient
visit, utilizing the work of Clay Thompson, DC, Ruth Jackson,
MD and Clarence Prill, DC.25-27 Thompson popularized the
cervical syndrome check for the upper cervical subluxation
complex in the 1940’s. Since then, no one has come up with a
reason relative leg length would change when a patient gently
turns their head from side to side, while either prone or supine,
thus not under the effects of gravity, except upper cervical
subluxation.28
Thompson cervical syndrome test: hold patient’s shoes with
thumbs under the heel, while applying very mild cephalic
pressure. Lift the legs one inch off from the table, keeping the
shoes one inch apart. Compare the welts to estimate the leg
length differential. Notate differential of short leg to closest
1/8 inch. Instruct patient to slowly turn their head to the right,
then to the left. If the legs change length only while turning to
the right, notate the amount of change as a right cervical
syndrome (RCS). If the legs change length only while turning
to the left, notate the amount of change as a left cervical
Meniere’s J. Upper Cervical Chiropractic Research – June 2, 2016 15
syndrome (LCS). If the leg length changes while turning the
head in both directions, notate the total amount of change as a
bilateral cervical syndrome (BLCS). If there is no change in
leg length when the head is turned, there is no cervical
syndrome. Positive cervical syndrome tests were considered
to be the strongest evidence of the presence of an upper
cervical subluxation complex in this study.
A conservative approach in determining evidence of
subluxation was used. That is, when in doubt, no adjustment
was given. The leg checks were the main criterion used to
decide when to adjust or not. To help determine whether the
major subluxation was at the level of atlas or axis, Prill
modified leg length tests were utilized.29 With patient prone,
patient was instructed to gently and steadily raise their feet
toward the ceiling, while the doctor resisted such movement
with his hands. The peripheral nerves were being tested, those
that innervate the postural muscles holding one upright in
gravity, so it was imperative that the patient only lift their legs
slightly and maintain this pressure for at least two seconds.
This test was for atlas, the top cervical vertebra. The occiput
“rocks” on atlas during flexion and extension. Instructing
patients to rotate their feet while the doctor provided
resistance and checking relative leg length was used to test
axis. This corresponds to the rotation of the head on the neck,
50% of which occurs at the level of C2.
When it was determined that the patient was in a pattern of
atlas subluxation, a toggle recoil adjustment was performed,
with the patient in a side-posture position, or a Pierce
technique30 adjustment was performed with the patient prone.
Side posture was used when laterality was the main
component of the subluxation. The term used for this type of
misalignment is translation, and most often occurs with a side
impact trauma, for instance, a “T-bone” type of automobile
accident. When posteriority was the major component of the
subluxation, the prone position was favored. This
misalignment usually is the result of the typical “rear ended”
type of vehicular accident. (Figs. 3,4)
A Thuli chiropractic table, using the cervical drop piece was
utilized. For side posture adjustments the headpiece was set to
drop straight down, and with prone adjustments, it was set to
drop down and forward. The patient was then rested for fifteen
minutes and rechecked, to make sure that the pattern had been
broken. Then all tests were repeated.
The need for a new technique came from observations made in
practice by Dr. Burcon. He found that x-rays forwarded from
full spine chiropractors rarely captured the atlanto-occipital
articulations; therefore, no atlas subluxation listing could be
derived. Medical films were usually taken with the patient
supine, outside of the effects of gravity. Furthermore, most
upper cervical specific chiropractors assumed that unbalanced
legs always indicated an upper cervical subluxation. Most
upper cervical techniques assume that a good upper cervical
adjustment will work its way down to the sacrum, correcting
misalignments along the way. Burcon believes that this is
possible, but often unrealistic when there is a significant kink
between two vertebrae in between the two ends of the spine.
For instance, many whiplash patients have a significant kink
in the area of C5. Burcon found that these patients failed to
hold their upper cervical adjustments until a lower cervical
adjustment was performed.
Results
Vertigo averaged 8.5 before cervical specific chiropractic
adjustments. Most patients reported an inability to function,
i.e., drive, work or socialize, at a rating of 5 or above. After
six weeks it lowered to a mean of 3.0, after one year it was
down to a mean of 2.0, after two years it was down to 1.4,
three years 0.9 four years 0.8, holding at 0.8 after five and six
years. (Fig. 5) Many patients noticed an improvement before
they left the office after their first adjustment. The longest it
took for a patient to report a noticeable improvement was
fourteen weeks. The only negative side effect noted was an
increase in the frequency and magnitude of headaches in nine
patients. For them headaches increased an average of 2.3 to
5.7.
The improvements in these patients made a significant
difference for 291 out of 300 patients, affecting whether or not
they could work, drive and/or have a positive relationship with
their spouse. They might get dizzy, but would not have
vertigo. They might get nauseaous but would no longer vomit.
For those that still had attacks, they occurred less often, lasted
for a shorter duration and were not as intense. Recovery time
was also significantly shorter.
All 300 patients showed evidence of upper cervical
subluxation upon neurological examination, and all exhibited
both evidence of a history of whiplash and an existing atlas
subluxation in radiographs. Two hundred seventy out of 300
patients had posterior and inferior atlas listings, with atlas
laterality on the opposite side of the involved ear, causing a
subluxation on the involved side. (Fig. 6) It took an average of
fifteen years from the time of the head/neck trauma until the
onset of Meniere’s type symptoms.
Discussion
Meniere's disease not only includes the symptom complex
consisting of attacks of vertigo, low-frequency hearing loss,
aural fullness and tinnitus but comprises symptoms related to
the Eustachian tube, the upper cervical spine, the
temporomandibular joints and the autonomic nervous
system.31 The MRI whiplash as the cause of MD hypothesis
has been presented to over two thousand ear, nose and throat
surgeons and over one thousand chiropractors on four
continents.32-40 It provides a theory including the following six
neurological and structural irritations:
1. Inflammation of the subluxated Atlanto
Occipital articulation with edema putting
pressure on adjacent structures, i.e., the
Eustachian tube. (Fig. 7)
2. Traction of Cranial nerves VII through XII,
also Jacobson’s and Arnold’s nerves.
3. Torque of the Trigeminocervical nucleus and
tract causing Eustachian tube dysfunction.
4. Irritation of the sympathetic nerves can elicit
spasms within the vertebral artery, leading to
a decrease in blood flow to the brainstem.41
16 J. Upper Cervical Chiropractic Research – June 2, 2016 Meniere’s
5. Chronic CSF backjets into the fourth
ventricle due to obstruction of outflow
through the foramen magnum may affect the
flocculonodular lobe of the cerebellum
resulting in nystagmus, vertigo and balance
disorders.
6. The endolymphatic sac performs absorptive
and secretory, as well as phagocytic and
immunodefensive, functions. It is innervated
by the superior cervical ganglion, which is
located laterally adjacent to C2, axis. If
irritated by an upper cervical subluxation
complex it can send amplified sympathetic
signals to the sac.
Inflammation
Ninety percent of neck disorders are caused by trauma. Of
these 85% are caused by motor vehicle collisions. There is a
relationship between whiplash, the cervical syndrome, cervical
nerve root irritation, the sympathetic nervous system and
headaches, including migraines.42 MD patients are five times
more likely to have migraines than the general population. The
cervical nerve roots are more vulnerable to pressure of
irritation from ruptured discs, hemorrhage, inflammatory
process of the capsules, spurs, and abnormal motion of the
joints due to relaxation or tearing of the capsular and
ligamentous structures. Healing of sprained ligamentous
structures takes place by the formation of scar tissue, which is
less elastic and less functional than normal ligamentous tissue.
Therefore, sprains result in some degree of permanent injury.43
Following whiplash trauma, as time passes there is an
increased probability of abnormal motion or subluxations. The
resulting lesion can create chronic inflammation leading to
post traumatic fibrosis and adhesions. (Fig. 8) This irritation
will cause spasms of the associated cervical spinal muscles,
which in turn irritates the superior sympathetic ganglia and/or
postganglionic sympathetic fibers. Additionally, if not
properly treated, the lesion will cause ischemia leading to
chronicity of symptoms possibly including cervicalgia, hand
numbness, high blood pressure,44 vision problems, dizziness,
nausea, headache and deafness. Swelling, stiffness and
calcification lead to compression of the delicate nerve tissues
associated with the spinal cord and sympathetic nerve
pathways and ganglion. The Occipital-Atlanto-Axial Complex
is a diarthrodial-synovial joint, a freely movable joint. As the
head leaves vertical and moves horizontally, there is a
compensatory shifting of the vertebral spine to maintain a
center of gravity that is continued all the way through the
entire spine. Upper cervical specific chiropractors are always
trying to make the head vertical, the atlas horizontal and the
cervical spine vertical. Prolonged head tilt can make you
dizzy. The brainstem expects the eyes and ears to be level to
the horizon.
Traction
Although the dentate ligaments serve a protective role for the
central nervous system during normal spinal movement,
particularly the second pair, during abnormal movement of the
cervical vertebrae, i.e., cervical articular dysfunction causing
uncoupled subluxation, they are capable of transmitting
pathological forces to the spinal cord and brainstem. John D.
Grostic’s “Dentate ligament-cord distortion hypothesis,”
provides a theory for how these tractional forces can lead to
spinal cord “embarrassment” in the presence of upper cervical
misalignment.45
Biomechanical ranges of motion in the OA (occipital-atlanto)
joint are primarily flexion and extension. There is minimal
lateral flexion and side bending in a coronal plane, with
relatively little or no rotation. Atlanto-axial (C1-2) joint range
of motion is generally considered to be rotatory motion. In the
absence of whiplash trauma, the upper cervicals tend to
subluxate anteriorly and superiorly, creating lesions by
impinging nerves. Non-specific chiropractors tend to adjust on
the symptomatic side, often exacerbating Meniere’s patients’
symptoms.
Trigeminal torqueing
The tensor veli palatini is a broad, thin muscle that is
innervated by the medial pterygoid nerve, a branch of
mandibular nerve, the third branch of the Trigeminal nerve
(CN V). Equalization of air pressure in the tympanic cavity is
essential for preventing damage to the tympanic membrane
and a resulting loss of hearing acuity. The auditory tube is
normally closed at its pharyngeal end. The major sensory
divisions of the trigeminal nerve carry primarily light touch,
pain, and temperature pathways to the thalamus by way of the
tract of trigeminal cervical nucleus. There is a significant
relationship between sensation and dysfunction in the face and
head region, and their relationship to craniovertebral region
dysfunction and hence referred pain in either direction.46
Reduced blood flow
Vertebral artery blood flow may also be altered, leading to
brain blood flow patterns and tissue compromise.47 Irritation
of sympathetic nerves can elicit spasms within the vertebral
artery, leading to decrease in blood flow to the brain stem.48
The vertebral arteries reach the interior of the skull by
ascending through the transverse foramina of the cervical
vertebrae, turning medially along the upper surface of the
posterior arch of atlas and then penetrating the posterior
atlanto-occipital membrane and the underlying dura to enter
the subarachnoid space. Subluxation of the atlas may diminish
blood flow through the vertebral arteries and their intracranial
branches that supply the spinal cord, CN VIII, medulla,
cerebellum and inner ear via the labyrinthine artery.
The dentate ligaments are strong enough to distort the spinal
cord and fold its peripheral blood vessels.49 These ligaments
may increase in strength and size after subjection to a long
period of abnormal stress. Collapse of the small veins of the
cord produces venous congestion resulting in nerves that are
more excitable, hence more susceptible to neurological
dysfunction.50 Guyton states that the most important
proprioceptive information for maintenance of equilibrium is
derived from joint receptors in the neck.
The role of the vertebral veins, also known as the vertebral
venous plexus (VVP), can cause chronic craniocervical
venous backpressure and subsequent neurodegenerative
conditions and diseases such as multiple sclerosis. It can lead
Meniere’s J. Upper Cervical Chiropractic Research – June 2, 2016 17
to chronic venous backups and edema in the brain, also
affecting cerebrospinal fluid pressure gradients and
subsequent flow and volume. Correct CSF volume is essential
to brain cushioning, protection and support. It may play a role
in normal pressure hydrocephalus, which has been associated
with Parkinson and Alzheimer’s disease.
The vertebral-basilar arterial supply to the brain and its likely
role in chronic ischemia which, like chronic edema from
backed up veins is one of the main suspects in demyelination
and other neurodegenerative conditions and subsequent
diseases. The tight neurovascular tunnels the VVP and
vertebral-basilar arteries must pass through in the upper
cervical spine and foramen magnum in the base of the skull on
its way to the motherboard of the brain, the brainstem.
“Insertion of a middle-ear ventilation tube can temporarily
alleviate Meniere's symptoms, suggesting Eustachian tube
dysfunction (ETD) is a contributing feature. Clinical practice
also shows that treating disorders of the upper and lower
cervical spine and temporomandibular joints51 can lessen
Meniere's disease symptoms. Similarly, stellate ganglion
blocks can be beneficial in controlling Ménière's disease
symptoms, highlighting the influence of the autonomic
nervous system. In this hypothetical reflex pathway, irritation
of facet joints can first lead to an activated anterior cervical
sympathetic system in the mediolateral cell column;
simultaneously leading to an axon reflex involving nociceptive
neurons, resulting in neurogenic inflammation and the
prospect of ETD.53
CSF flow dysfunction
The most likely place for obstruction to CSF flow to occur is
in the upper cervical spinal canal. The cause can be genetic
design problems and/or whiplash. Head tilt causes the brain,
blood and CSF inside the cranial vault to shift to the low side.
There is a principle in neurology when it comes to the brain
and the cranial vault, called the Monroe-Kellie principle.54
There are essentially three elements inside the cranial vault:
the brain, blood and CSF. Since the cranial vault is a closed
container for the most part, if the volume of one of the
elements increases, then one or both of the other two elements
must decrease in volume. A brain tumor for example can
compress blood and CSF vessels, as can Chiari malformations.
In a recent study, eight MS patient exhibited obstructions to
their CSF flow when examined by phase coded CSF
cinematography in the upright position. All MS patients
exhibited CSF flow abnormalities that were manifest on MR
cinematography as interruptions to flow or outright flow
obstructions somewhere in the cervical spinal canal,
depending on the location and extent of their cervical spine
pathology. Normal examinees did not display these flow
obstructions. Additionally it was found that peak CSF inflow
and peak CSF inflow velocity were sharply reduced in normal
examinees in the upright position when compared to inflow
and inflow velocity in the recumbent position.55
Edema formation frequently complicates head/neck trauma.
Recent studies have revealed the existence of a brain-wide
paravascular pathway for cerebrospinal (CSF) and interstitial
fluid (ISF) exchange, the glymphatic system. In cytotoxic
edema, energy depletion enhances glymphatic CSF influx,
while suppressing ISF efflux. Paravascular inflammation plays
a critical role in vasogenic edema.56
One-Sided Neurological Disorders
Twenty-four of the patients in this study are currently or have
previously suffered from Trigeminal neuralgia57-58, sixty from
migraine59 and one hundred and twenty with TMJ
dysfunction.60 Since half of these patients that have
derangement in the craniovertebral region also have
complaints of headache, we would also assume that treatment
of these regions should reduce the afferent/sensory input to the
trigeminal cervical nucleus and reduce the headaches. Bell’s
palsy is a common condition that results in weakness or total
paralysis of one half of the face.61-62 Early symptoms may
include pain in or behind the ear. This is followed by a rapidly
worsening weakness of one half of the face. Bell’s palsy was a
precursor to Meniere’s disease in fifty-nine of these cases.
Symptoms included unilateral facial paralysis, extreme
sensitivity to sound, pain in the TMJ joint and neck pain.
Patients suffering from Bell’s palsy may benefit from a
holistic chiropractic approach that not only includes a focus on
face and TMJ, but from significant vertebral subluxation.
Two patients in the study also have Glossopharyngeal
neuralgia. Simultaneous TN and GPN suggest a structural
lesion in an area that could capture both trigeminal and
glossopharyngeal nerve pathways. From an anatomic
perspective, the spinotrigeminal nucleus and tract (CN V), the
solitary nucleus (CN VII, IX, and X) and the nucleus
ambiguus (CN IX and X) are in close proximity in the
medulla.63
The adult head weight averages twelve pounds. It rests on two
articulations approximately one inch long by one half inch
wide, resulting in twelve pounds per square inch of pressure
when the head is balanced. When atlas is subluxated forward
and to the side, pressures can build to forty pounds per square
inch on the opposite side. Because every misalignment is
different, different combinations of neurological insults occur
near the brainstem, resulting in the varying degree of severity
of the symptoms MD patients suffer. It was determined that
whiplash subluxations tend to be found in pairs, with atlas and
C5 being the most common. These patients’ chief complaints
were vertigo with vomiting. The second most common was
axis and C6 found with hearing problems, ear fullness and
tinnitus. The third most common pair of subluxations was both
C1 and C5, and C2 and C6, with one pair being the major and
one pair being the minor.
Conclusion
One hundred percent of three hundred consecutive patients
medically diagnosed with Meniere’s disease also having
suffered a whiplash trauma is unlikely coincidental.
Furthermore, ninety percent having a listing of posterior and
inferior towards the opposite side of the effected ear is
significant, as is ninety seven percent getting their vertigo
under control within six weeks. All patients with a history of
vertigo should be questioned about a history of trauma,
especially whiplash from an automobile accident, contact
sports injury, or serious falls. Patients often forget these
18 J. Upper Cervical Chiropractic Research – June 2, 2016 Meniere’s
accidents, thinking that they were not hurt because they did
not break any bones and were not bleeding. All films; MRIs,
CT Scans and x-rays, should be taken with the patient in a
weight bearing position, seated or standing, not lying down.
Patients with a history of both vertigo and trauma should be
referred to an upper cervical specific chiropractor for
examination.
Acknowledgement
Research engineer Johan Hedbrant served as scientific
advisor.
References
1. Baloh R. Prosper Meniere and His Disease, Arch Neurol.
2001; 58(7):1151-1156.
2. Sterkers O. Meniere’s disease update, Kugler
Publications, The Hague, Netherlands, 1999.
3. Dornhoffer J. Prosper Meniere Society, Dept. of
Otolaryngology, Head and Neck Surgery, University of
Arkansas for Medical Science, Little Rock, AR.
4. The Merck Manual, Eighteenth Edition. Berkow MD,
Robert Rahway, NJ: Merck Research Laboratories, Merck
& Co., Inc., 794-795, 2006.
5. Berlinger NT. Meniere's disease: new concepts, new
treatments, Paparella Ear, Head and Neck Institute,
Minneapolis, USA. Minn Med. 2011 Nov; 94(11):33-6.
6. Hornibrook J, Coates M, Goh T. MRI imaging of the
inner ear for Meniere’s disease, Journal of the New
Zealand Medical Association, 27-August-2010, Vol 123
No 1321
7. Arevalo JD. Meniere’s Disease: A Diagnosis of Exclusion
with Controversial Therapies, ENT Today, January 2008.
8. Salt A, Cochlear Fluids Research Laboratory, Washington
University, St. Louis, 2012.
9. House JW. Meniere's disease: prevalence of contralateral
ear involvement, Otol Neurotol. 2006 Apr; 27(3):355-
6118.
10. El Refaie A. Pathogenesis and new trends in management,
Meniere’s disease: Pathogenesis and new trends in
management, University of Bristol, 2009. Kotimaki, J.
Meniere's disease in Finland, an epidemiological and
clinical study on occurrence, clinical picture and policy,
Department of Otorhinolaryngology, University of Oulu.
11. Gartner M, Bossart W, Linder T. Herpes virus and
Ménière's disease, ORL J Otorhinolaryngol Relat Spec.
2008;70(1):28-31; discussion 31. doi:
10.1159/000111045. Epub 2008 Feb 1.
12. Spencer, R. F., A. Sismanis, J. K. Kilpatrick, and W. T.
Shaia. "Demyelination of Vestibular Nerve Axons in
Unilateral Meniere’s Disease." Ear, Nose and Throat
Journal 81 (November 2002): 785-789.
13. Nakashima T, Sone M, Teranishi M. A perspective from
magnetic resonance imaging findings of the inner ear:
Relationships among cerebrospinal, ocular and inner ear
fluids, Auris Nasus Larynx.
14. Bretlau P, Thomsen J, Tos M, et al. Placebo effect in
surgery for Meniere’s disease: a three-year follow-up
study of patients in a double blind placebo controlled
study on endolymphatic sac shunt surgery. Am J Otol
1984 Oct; 5(6):558-61.
15. Burcon M. Upper Cervical Protocol for Ten Meniere’s
Patients, Upper Cervical Subluxation Complex, A Review
of the Chiropractic and Medical Literature, Kirk Eriksen,
Lippincott, Williams & Wilkens, Baltimore, MD, 2004,
pp 284-286.
16. Franz B, Anderson C. The potential role of joint injury
and Eustachian tube dysfunction in the genesis of
secondary Meniere’s disease. Int Tinnitus J. 2007;
13(2):132-7.
17. Palmer, BJ. History in the Making. Volume XXXV.
Davenport, Iowa: Palmer School of Chiropractic, 1957.
18. Eriksen K, Rochester R, Orthospinology Procedures, an
Evidence-Based Approach to Spinal Care, Lippincott,
Williams & Wilkens, Baltimore, MD, 2007, p 5.
19. Burcon M. “BJ’s $50,000 ‘Timpograph still captures our
imagination after more than fifty years,” Chiropractic
Economics, Nov/Dec 1995.
20. Hart J, Boone R. Pattern Analysis of Paraspinal
Temperatures: A Descriptive Report. J Vert Sublux Res
1999-2000:3(4).
21. Sherman L. Neurocalometer-
neurocalographneurotempometer Research. Eight BJ
Palmer Chiropractic Clinic Cases. Davenport, IA: Palmer
School of Chiropractic; 1951.
22. Addington E. Blair Cervical Spinographic Analysis.
Conference of Research and Education, Monterey, CA
June 21-23, 1991.
23. Blair W. Blair upper Cervical Spinographic Research;
primary and adaptive malformations; procedures for
solving malformation problems; Blair principle of
occipito-atlanto misalignment. Davenport, IA: Palmer
College of Chiropractic; 1968.
24. Blair, Wm. G. A synopsis of the Blair upper cervical
Spinographic research. Science Review of Chiropractic
(International Review of Chiropractic: Scientific Edition)
I (1) : I- 19 (Nov. 1964)
25. Shambaugh P, Sclafani L, Fanselow D. Reliability of the
Derifield-Thompson test for leg length inequality, and use
of the test to demonstrate cervical adjusting efficacy, J
Manipulative Physiol Ther. 1988 Oct; 11(5):396-9.
26. Jackson R. The Cervical Syndrome, Springfield, IL 1956.
27. Prill, C. The Prill Chiropractic Spinal Analysis
Technique. 2001.
28. Knutson G. Tonic Neck Reflexes, Leg Length Inequality
and Atlanto-occipital Fat Pad Impingement. Chiropr Res J
1997; 4(2:64-67.
29. Burcon M, Olsen E. Modified Prill Leg Check Protocol.
11th Annual Vertebral Subluxation Research Conference,
Sherman College of Straight Chiropractic, Spartanburg,
SC 2003.
30. Painter, F. Pierce Results System, The Chiropractic
Resource Organization.
31. Franz B, Anderson C. The potential role of joint injury
and Eustachian tube dysfunction in the genesis of
secondary Meniere’s disease. Int Tinnitus J. 2007;
13(2):132-7.
32. Burcon M. Upper Cervical Protocol and Results for 300
Meniere’s patients Followed for a Minimum of Five
Years, 7th International Symposium on Meniere’s Disease,
Rome, Italy, Oct 2015.
33. Burcon M. Research Results of Upper Cervical Specific
Care with One-Sided Neurological Disorders, Blair
Annual Conference, St Louis, MO, Nov, 2012.
Meniere’s J. Upper Cervical Chiropractic Research – June 2, 2016 19
34. Burcon M. Cervical Specific Protocol and Results for 300
Meniere’s Patients, Upper Cervical Symposium, New
Zealand Chiropractic College, Auckland, NZ, July 2012.
35. Burcon M. Upper Cervical Protocol and Results for 300
Meniere’s Patients, 6th International Symposium on
Meniere’s Disease, Kyoto, Japan, Nov 2010.
36. Burcon M. Upper Cervical Protocol and Results for 139
Meniere’s Patients, Fifth International Research and
Philosophy Symposium, Sherman College of
Chiropractic, Spartanburg, SC, Oct 2008.
37. Burcon M. Upper Cervical Protocol and Results for 139
Meniere’s Patients, 13th International Symposium and
Workshops on Inner Ear Medicine and Surgery, Prosper
Meniere Society, Austria, Mar 2008.
38. Burcon M. Cervical Specific Protocol and Results for 139
Meniere’s Patients, 26th Politzer Society Meeting,
Cleveland Clinic, Cleveland, OH, Oct 2007.
39. Burcon M. Upper Cervical Specific Protocol for One
Hundred Meniere’s Patients, 12th International
Symposium and Workshops on Inner Ear Medicine and
Surgery, Twenty Fifth Anniversary of the Prosper
Meniere Society, Austria, Mar 2006.
40. Burcon M. Upper Cervical Protocol for Thirty Meniere’s
Patients, Poster Presentation, 5th International
Symposium on Meniere’s Disease & Inner Ear
Homeostasis Disorders, House Ear Institute, Beverly
Hills, CA, Apr 2005.
41. Filipo R, Ciciarello F, Mancini P. Cerebrospinal Venous
Insufficiency in Patients with Meniere’s Disease, Eur
Arch Otorhinolaryngol, Jan 7, 2015; 272(1):77-82.
42. Murphy D. The Cervical Syndrome as a Cause of
Migraine: Research Review, The American Chiropractor,
Sept 2009.
43. Schafer R. Chapter 6: General Causes and Potential
Effects of the Subluxation Complex, Basic Principles of
Chiropractic Neuroscience, ACA Press, LaGrange, IL,
2009.
44. Dickholtz M, Atlas vertebra realignment and achievement
of arterial pressure goal in hypertensive patients: a pilot
study. J Hum Hypertens. 2007 May;21(5):347-52. Epub
2007 Mar 2.
45. Grostic JD. Dentate ligament-cord distortion hypothesis,
Chiro Res J 1988; 1(1):47-55.
46. Roubal. P. The Neurobiomechanical Basis of
Cervicogenic Headaches, Novi Headache Symposium,
Novi, MI, 1994.
47. Schafer R. General Causes and Potential Effects of the
Subluxation Complex, Basic Principles of Chiropractic
Neuroscience, ACA Press, LaGrange, IL, 2009.
48. Biesinger E. Vertigo caused by Disorders of the Cervical
Vertebral Column; Diagnosis and Treatment. Adv
Otorhinolaryngol. 1998; 39:44-51
49. Kahn EA. The Role of the Dentate Ligaments in spinal
cord Compression, J Neurosurg. 1947; 4:191-199.
50. Kobrine A, Evans D, Rizzoli H. The effects of ischemia
on long-tract neural conduction in spinal cord, J
Neurosurg 1979; 50(5):639-44.
51. Bjorne A, Agerberg G. Symptom relief after treatment of
temporomandibular and cervical spine disorders in
patients with Meniere's disease: a three-year follow-up;
Vertigo Tinnitus, and Pain Unit, Ystad Hospital, Public
Dental Service, County of Skane, Sweden. Cranio. 2003
Jan;21(1):50-60.
52. Luttgens K, Wells K. Kinesiology: Scientific Basis of
Human Motion, McGraw-Hill College, Jun 1, 1982.
53. Burkhard F, Colin A. The Potential Role of Joint Injury
and Eustachian Tube Dysfunction in the Genesis of
Secondary Ménière's Disease, Intern. Tinnitus Journal,
Vol.13, No 2; Jul/ Dec 2007.
54. Mokri B. The Monro-Kellie hypothesis: applications in
CSF volume depletion, Neurology. 2001 Jun 26;
56(12):1746-8.
55. Damadian R, Chu D, The Possible Role of Cranio-
Cervical Trauma and Abnormal CSF Hydrodynamics in
the Genesis of Multiple Sclerosis, Journal Physiological
Chemistry and Physics and Medical NMR , Sept. 20,
2011, 41: 1-17
56. Thrane V, Nedergaard M. Drowning stars: reassessing the
role of astrocytes in brain edema. Trends Neurosci. 2014
Sep 15. pii: S0166-2236(14)00153-2.
57. Burcon M. Resolution of Trigeminal Neuralgia Following
Chiropractic Care to Reduce Cervical Spine Vertebral
Subluxations: A Case Study, Journal of Vertebral
Subluxation Research, Oct 2009, pp 1-7.
58. Hinson R, Brown S. Chiropractic management of
trigeminal neuralgia, 130th Annual Meeting of the Public
Health Association; Nov 11, 2002; Philadelphia, PA
59. Jackson R. The Cervical Syndrome as a Cause of
Migraine, Journal of the American Medical Women’s
Association, Dec 1947, Vol 2, No 2, pp529-534.
60. Magnusson T, Carlsson GE. Recurrent headaches in
relation to temporomandibular joint pain-dysfunction,
Acta Odontol Scand. 1978; 36(6):333-8.
61. Alcantara J, Plaugher, Van Wyngarden D. Clinical Case
Study: Chiropractic Care of a Patient with Vertebral
Subluxation and Bell’s Palsy, Journal of Manipulative and
Physiological Therapeutics, May, 2003.
62. Cotton B. Care of a 47-year-old woman with chronic
Bell's palsy: a case study, J Chiropr Med. 2011
December; 10(4): 288–293.
63. Burcon M. Resolution of Glossopharyngeal Neuralgia
with Spastic Dystonia following Chiropractic Care to
Reduce Vertebral Subluxations, International Research
and Philosophy Symposium, Sherman College of
Chiropractic, Spartanburg, SC, October 2012.
20 J. Upper Cervical Chiropractic Research – June 2, 2016 Meniere’s
Figure 1 - Notice the cropping of MD cases that were diagnosed about fifteen years after whiplash.
Figure 2 - Line analysis pattern work of a typical whiplash patient pre-treatment and six weeks post
(red). The middle lines, the Delta-T, create the informational color graph seen on the right.
Figure 3 - Whiplash results in head translation, forward head position and/or head tilt.
Meniere’s J. Upper Cervical Chiropractic Research – June 2, 2016 21
Figure 4 - Examples of side posture toggle recoil (Atlas) and Pierce technique (C5) adjustments.
Figure 5 - Vertigo cut by more than 60% at six weeks, more than 90% after four years.
Figure 6 - Atlas is underlapped on the right articulation with Occiput, creating right head tilt. Atlas is in
juxtaposition and the patient is medication and symptom free after six weeks.
22 J. Upper Cervical Chiropractic Research – June 2, 2016 Meniere’s
Figure 7 - Close proximity of Eustachian Tube and the upper cervicals
Figure 8 - Typical degenerative changes 15 years post whiplash.
Meniere’s J. Upper Cervical Chiropractic Research – June 2, 2016 23
