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Neurology of the Upper

Cervical Subluxation
Subluxation
sub = Less Than
Luxatio = Dislocation
less than a dislocation
Medical use of the term traced back to 1688 by
Holme. a dislocation or putting out of
joint


Henderson, C. Subluxation Theory. Lyceum 2000
Subluxation
1934 Subluxation Specific, BJ Palmer
A vertebral subluxation is any vertebra out of
normal alignment, out of apposition to its co-
respondents above and below, wherein it does
occlude a foreman, either spinal or intervertebral,
which does produce pressure upon nerves, thereby
interfering and interrupting the normal quantity flow
of mental impulse supply between brain and body
and thus becomes THE CAUSE of all dis-ease.
Henderson, C. Subluxation Theory. Lyceum 2000
Subluxation
ACA and ICA adopted definition:
A motion segment in which alignment,
movement integrity, and/or physiologic
function are altered although contact between
the joint surfaces remains intact.
Henderson, C. Subluxation Theory. Lyceum 2000
Subluxation
A complex of function and/or structural and/or
pathological articular changes that
compromise neural integrity and may
influence organ system function and general
health.
Association of Chiropractic Colleges
Owens, E. J Can Chiropr Assoc 2002;46(4)
Neurology of the Upper Cervical
Subluxation
It has been shown that the average occipito-
atlantal misalignment in the frontal plane is
almost 3, which equates to about 1/8 of an
inch of linear movement.
This is significant because the upper cervical
spinal cord has a diameter of about half an
inch.
Neurology of the Upper Cervical
Subluxation
The upper cervical spinal cord is directly attached to:
the circumference of the foramen magnum,
the second and third cervical vertebrae,
posterior longitudinal ligament
The dentate ligaments are 21 paired lateral bands of
epipial tissue midway between the dorsal and ventral
attachments of the nerve roots.
The medial border of the dentate ligaments is
continuous with the pia mater of the spinal cord and
attaches to the dura mater laterally.

Neurology of the Upper Cervical
Subluxation
The rectus capitis posterior minor muscle
attaches to the dura mater of the upper
cervical spinal cord.
Attachment have also been found to the spinal
cord via:
the ligamentum nuchae
epidural ligaments

Neurology of the Upper Cervical
Subluxation
Neurological dysfunction may occur via two
mechanisms:
direct mechanical irritation of the nerves of the
spinal cord
The collapse of the small veins of the cord
producing venous congestion
The Spinocerebellar tracts
The spinocerebellar tracts lie
along the lateral edge of the
spinal cord (the most probable
site of maximal mechanical
irritation by the dentate
ligaments).
Proprioceptive tracts, which
regulates muscle tone and joint
position sense.
Irritation of these tracts could
lead to muscle tone imbalance of
the pelvic girdle resulting in a
functional short leg.
The Spinothalamic Tracts
Close to the attachment of the
dentate ligaments.
Responsible for conveying
pain and temperature into the
neuroaxis.
Mechanical irritation and/or
ischemic compromise to the
spinothalamic tracts possibly
explains particular cases of
severe low back and leg pain
being caused by an upper
cervical subluxation.
MECHANORECEPTIVE
DYSAFFERENTATION
Mechanoreceptors are so named because they
are activated by mechanical deformation.
The mechanoreceptors are primarily
responsible for the body's position sense
within the gravity environment.
Provide information orientating the head with
respect to the body to maintain equilibrium.
The vestibular apparatus (VA)
Informs the brain of the head's position and
works to keep it perpendicular with the
ground by altering the tone of the cervical
muscles.
The most important proprioceptive
information required for the maintenance of
equilibrium is derived from joint receptors of
the neck. Guyton
Mechanoreceptors
Type I: provide important information about joint position as
they signal the angle of the articulation throughout the range
of motion.
Type II: Have a low threshold and rapidly adapt to a stimulus.
Detect rate of movement at the articulation.
Type III: High threshold and slowly adapting receptors. They
are stimulated only at the extremes of joint movement.
Structurally similar to the Golgi tendon organ of the muscular
system
Type IV: Nociceptors; have a high threshold and do not
adapt. These pain receptors tend to be free nerve endings.
Mechanoreceptors
The cervical spine has more
mechanoreceptors, per surface area, than any
other region of the spinal column.

Model for the receptor activity in the normal,
nondysfunctional state (no abnormal vertebral position
or particular hypomobility or hypermobility).
Correct anatomical
position of vertebra(e)
Normal physiological pressure
and tension on fibrous joint capsule
Mechanoreceptors and
nociceptors are inactive
Resting muscle tone; equilibrium
between synergists and antagonists
No pain perception

Model for receptor activity as a result of vertebral segmental dysfunction
(abnormal vertebral position and/or somatic dysfunction with pain and
hypomobility, etc.).
Abnormal position
of vertebra(e)
Segmental dysfunction


Irritation of fibrous
joint capsule
Tonic-reflexogenic influence
on motor neurons of neck,
limb, jaw, eye muscles
(myotendinoses)
Pain perception

Correction of segmental
dysfunction
Less pain, normalization
of receptor activity Change
toward normal muscle tone
Stimulation of
mechanoreceptors
of type 1
Spinothalamic tract
Stimulation of mechanoreceptors
type II; inhibition of afferent
fibers; release of enkephalins

Stimulation of
Nociceptors
Additional impulses
(mechanical, chemical)
Spinal Adjustment
The Postural Spondylogenic Reflex Syndrome: Clinical
Correlation with Reflexes Linked to Nociceptors and
Mechanoreceptors
The clinical symptom of pain in muscles and other soft
tissues (spontaneous or elicited by palpatory pressure) has
been termed the Spondylogenic Reflex Syndrome by Sutter
(1974,1975).
Myotendinoses has been in observe the various systematic
response to an articular/somatic dysfunction involving the
individual apophyseal, occipito-atlanto-axial, and sacroiliac
joints.
Many systematic myotendinoses improve during the course
of therapeutic intervention in the individual patients.
It was therefore assumed that, in addition to other helpful
physical and therapeutic procedures, the mechanical and
functional correction of the spinal motion unit, according to
Schmorl and Junghanns (1968), can play a significant role, if
not the most crucial role in treatment.
The Postural Spondylogenic Reflex
Syndrome:
The absence of pain does not automatically mean lack of soft-tissue
findings.
It is well known that localized palpable muscle bands or systematic
myotendinoses can be elicited upon careful palpation in many
individuals who have no subjective pain complaints.
This situation is to be considered pathologic and correlates with the
latent state of intervertebral insufficiency according to Schmorl and
Junghanns (1968).
This could be explained on the basis of the tonic reflexogenic
influence of the type 1 mechanoreceptors upon the motor neurons
of the axial or peripheral musculature.
It has been shown that pain-inducing nociceptors have significantly
higher thresholds than pain-inhibiting mechanoreceptors. This may
explain the delay with which the individual may perceive his or her
pain.
The Postural Spondylogenic Reflex
Syndrome:
The nociceptive stimulation can be inhibited
presynaptically when there is sufficient stimulation
of the mechanoreceptors, mainly the type II
receptors.
This may occur by release of endorphins: cells in the
gelatinous substance of the dorsal horns.
Therefore, it would plausible to propose that these
and probably other related neurophysiologic
mechanisms may play at least as important a role in
manual therapeutic treatment as the pure mechanical
correction of one or several segmental dysfunctions.

The Postural Spondylogenic Reflex Syndrome:
Irritation Zone Spondylogenic Myotendinosis
Changes Skin, subcutaneous tissues, tendons,
muscles, joint capsule
Muscles, ligaments
localization In area of the disturbed spinal segment,
topographically defined in region
around spinous or articular processes
Muscles, ligaments (referred pain?)
Time course (latency)

Immediate reaction to a segmental
dysfunction
Apparent after a certain latent period
Qualitative palpatory
findings
Decreased ease of skin displacement,
increased tissue tension, localized pain
Increased resistance, less resiliency,
tender upon pressure with radiation
(trigger points?)
Quantitative palpatory
findings
Related to the degree of abnormal
segmental function

Dependent on the duration of
segmental dysfunction
Changes observed with
successful treatment

Immediate decrease in quality and
quantity
May disappear after a certain latency
period (possibly reflexively)

Force of the UC Adjustment
Depending upon the type of cervical manipulative
technique used, preload forces range from 0 to
approximately 50 N, and peak impulse forces range
from approximately 40 N to approximately 120 N.
The forces delivered during cervical manipulations
develop faster than during manipulation of the thoracic
spine and sacroiliac joint.
Impulse duration lasts from approximately 30 ms to
approximately 120 ms.
J.G. Pickar / The Spine Journal 2 (2002) 357371
Mechanical Forces from the Adjustment
The mechanical force introduced into the
vertebral column during a spinal manipulation
may directly alter segmental biomechanics by
releasing trapped meniscoids,
releasing adhesions
or by reducing distortion
the mechanical input may ultimately reduce
nociceptive input from receptive nerve endings
in innervated paraspinal tissues.
J.G. Pickar / The Spine Journal 2 (2002) 357371
Neurology of the Chiropractic
Adjustment
The mechanical thrust could either stimulate or silence non-
nociceptive, mechano-sensitive receptive nerve endings in
paraspinal tissues, including skin, muscle, tendons, ligaments,
facet joints and intervertebral disc.
These neural inputs may influence pain producing
mechanisms as well as other physiological systems controlled
or influenced by the nervous system.
These changes in sensory input are thought to modify neural
integration either by directly affecting reflex activity and/or
by affecting central neural integration within motor,
nociceptive and possibly autonomic neuronal pools.
Either of these changes in sensory input may elicit changes in
efferent somatomotor and visceromotor activity.
J.G. Pickar / The Spine Journal 2 (2002) 357371
UC Subluxation and Neurologic
Compromise
Dentate Ligament Cord Distortion
Medullary Lock Kessinger
Sensory Neurologic Feedback
Central Sensitization

Dentate Ligament Cord Distortion
Medullary Lock
The upper cervical spinal cord is directly
attached to:
the circumference of the foramen magnum,
the second and third cervical vertebrae,
posterior longitudinal ligament

Dentate Ligament Cord Distortion
The dura mater is a strong, fibrous membrane which forms a wide,
tubular sheath; this sheath extends below the termination of the medulla
spinalis and ends in a pointed cul-de-sac at the level of the lower border of
the second sacral vertebra.
The dura mater is separated from the wall of the vertebral canal by the
epidural cavity, which contains a quantity of loose areolar tissue and a
plexus of veins; between the dura mater and the subjacent arachnoid is a
capillary interval, the subdural cavity, which contains a small quantity of
fluid, probably of the nature of lymph.
The arachnoid is a thin, transparent sheath, separated from the pia mater
by a comparatively wide interval, the subarachnoid cavity, which is
filled with cerebrospinal fluid.
The pia mater closely invests the medulla spinalis and sends delicate
septa into its substance; a narrow band, the ligamentum denticulatum,
extends along each of its lateral surfaces and is attached by a series of
pointed processes to the inner surface of the dura mater.
Dentate Ligament Cord Distortion
the strongest ligaments
are in the upper
cervical region
short, thick, and pass
almost perpendicularly
from the pia mater to
their attachments on
the dura mater.
Dentate Ligament Cord Distortion
The upper cervical area is the only area where
in the dentate ligaments are perpendicular to
the cord.
From full extension and full flexion of the
cervical spine the cervical canal length
changes about 30 mm.
during extension there is some compression of
the cord, during flexion there is stretching of
the cord
Dentate Ligament Cord Distortion
Based on these observations, it may be a
primary role of the upper cervical Dentate
ligaments to restrict the downward-pulling
axial forces created by the lengthening of the
canal when the neck is flexed from being
transmitted unattenuated to the brainstem.
JD Grostic
Dentate Ligament Cord Distortion
In normal flexion the dentate ligaments are
strong enough to slightly deform the cord.
Chronic tension on a ligament may produce
thickening and strengthening of the ligament,
decreasing the ligament's ability to damp the
distortive forces before they can deform the
cord. Kahn

Dentate Ligament Cord Distortion
Tension on the dentate ligaments may cause
distortion to the spinal dura causing:
Mechanical irritation to the spinal tracts
Spinal Cord Ischemia
Tethering the Spinal cord
Dentate Ligament Cord Distortion
Mechanical irritation to the spinal tracts
The spinocerebellar tracts (proprioception) are
located at the site of maximal mechanical
irritation.
Spinal cord irritation by dentate ligament
traction may cause hypertonicity and
spasticity in the muscles of the pelvic girdle
and lower extremities.
Dentate Ligament Cord Distortion
Mechanical irritation to the spinal tracts
Pain in the low back and legs may be caused
by mechanical irritation of the spinothalamic
tract (pain, temperature, itch and crude touch)
in the upper cervical cord due to traction of
the dentate ligaments.
The trigeminal nerve spinal nucleus may be
tractioned by a lateral deviation and rotation
of the atlas.
Dentate Ligament Cord Distortion
Spinal Cord Ischemia
Dentate ligament may cause mechanical stresses to the cord.
Mechanical obstruction of the veins of the upper cervical cord
could cause stasis of blood and ischemia in the portion of the
spinal cord drained by these veins.
Venous stasis would tend to first cause ischemia in the lateral
columns of the cord
These veins operate at such low pressures and are easily occluded
by compressive forces.
Ischemia may first increases the irritability of nerves and
increased sensitivity to the effects of mechanical irritation
Jarzem et al. (1992) experimental cord distraction produced a
decrease in spinal cord blood flow and concurrent interruption of
somatosensory evoked potentials.

Dentate Ligament Cord Distortion
Tethering the Spinal cord
The UC subluxation causing abnormal motion may
cause a disruption of the normal function of the
dentate ligaments which would not allow for full
motion of the spinal cord during flexion and
extension.
Traction of the spinal cord will cause a decrease in
the action potentials of spinal neurons.
Mechanical deformation has shown to cause
neurologic dysfunction.
Sensory Neurologic Feedback
After the intertransverse ligament at T3-T4 in 4-week-old chickens was
stretched mechanically and repeatedly for 60 minutes. Various areas of the
nervous system then were sectioned and processed immunohistochemically
to identify areas of Fos production in nerve cell bodies. The presence of Fos
indicated neurons that had been stimulated by the stretching the ligament,
including interneurons along the feedback pathway.
The Fos protein was identified in: nerve cell bodies in the dorsal root
ganglia and intermediate gray matter of the spinal cord at the level of
stimulation as well as at several spinal cord levels above and below the site
of stimulation (on the ipsilateral and the contralateral sides), in sympathetic
ganglia at these sites, nerve cell bodies in the combined nucleus cuneatus
and gracilis in the medulla oblongata, the vestibular nuclei, and the
thalamus.
Stretching a single lateral ligament of the spine produces a barrage of
sensory feedback from several spinal cord levels on both sides of the spinal
cord.
Information from this study allowed Jaing to trace the relay system of
neurological afferent synapse through the CNS.
Jiang H. Spine. 22(1):17-25, January 1, 1997
Sensory Neurologic Feedback
The cervico-sympathetic reflex [that can alter heart rate and blood
pressure] appears to originate from muscle spindles in the dorsal neck
musculature, it is very likely that the suboccipital muscle group is
involved in the reflex because these muscles have an extremely high
muscle spindle content."
"Additional evidence for the involvement of the suboccipital muscle
group in the cervico-sympathetic reflex comes from changes in blood
pressure associated with chiropractic manipulations of the C1 vertebrae,
which would result in altering the length of fibers in the suboccipital
muscle group."
"The projection from the INTERMEDIATE NUCLEUS to the
NUCLEUS TRACTUS SOLITARIUS identified in this study therefore
places it in an ideal position to mediate cardiorespiratory changes to
neck muscle afferent stimulation, because the NUCLEUS TRACTUS
SOLITARIUS is a major integratory area for autonomic control
circuits."
Ian J. The Journal of Neuroscience August 1, 2007; 27(31); pp. 8324-8333
Sensory Neurologic Feedback
A theoretical model
showing components that
describe the relationships
between spinal
manipulation, segmental
biomechanics, the nervous
system and physiology.
The neurophysiological
effects of spinal
manipulation could be
mediated at any of the
numbered boxes.
J.G. Pickar / The Spine Journal 2 (2002) 357371
Central sensitization
debilitating fatigue, the majority of patients with
chronic fatigue syndrome (CFS)
Prolonged or strong activity of dorsal horn neurons
caused by repeated or sustained noxious stimulation
may subsequently lead to increased neuronal
responsiveness or central sensitization
These changes cause exaggerated perception of
painful stimuli (hyperalgesia), a perception of
innocuous stimuli as painful (allodynia) and may be
involved in the generation of referred pain and
hyperalgesia across multiple spinal segments
Mira Meeus & Jo Nijs. Clin Rheumatol (2007) 26:465473
Central Sensitization
Diseases Associated with Central Sensitization
Syndrome:
Fibromyalgia
Chronic fatigue syndrome
Irritable bowel syndrome
Depression
Insomnia
Abnormal Heart rate variability
Central Sensitization
AKA: Central facilitation
The increased excitability or enhanced
responsiveness of dorsal horn neurons to an afferent
input.
Central facilitation can be manifested by
increased spontaneous central neural activity,
by enhanced discharge of central neurons to an afferent
input
by a change in the receptive field properties of central
neurons.
J.G. Pickar / The Spine Journal 2 (2002) 357371
Central Sensitization
Motoneurons could be held in a facilitated
state because of sensory bombardment from
segmentally related paraspinal structures.
The motor reflex thresholds also correlated
with pain thresholds, further suggesting that
some sensory pathways were also sensitized
or facilitated in the abnormal segment.
J.G. Pickar / The Spine Journal 2 (2002) 357371
Central Sensitization
We currently know that the phenomenon of central
facilitation increases the receptive field of central neurons and
allows innocuous mechanical stimuli access to central pain
pathways.
In other words, subthreshold mechanical stimuli may initiate
pain, because central neurons have become sensitized.
Removal of these subthreshold stimuli should be clinically
beneficial.
One mechanism underlying the clinical effects of spinal
manipulation may be the removal of subthreshold stimuli
induced by changes in joint movement or joint play.
J.G. Pickar / The Spine Journal 2 (2002) 357371
Central Sensitization
The dorsal horn is not simply a passive relay
station for sensory messages but can modulate
the messages as well.
Natural activation of A-a and A-b fibers (like
the spinal adjustment) has been shown to
reduce chronic pain and increase pain
threshold levels.
J.G. Pickar / The Spine Journal 2 (2002) 357371
Central Sensitization
Spinal manipulation increased the average
pressure/pain threshold of six tender spots in
the neck region by approximately 50% (from
2 kg/cm
2
to 2.9 kg/cm
2
)
The effect of spinal manipulation on pain
could also be mediated by the neuroendocrine
system. The endogenous opiate system is
known to modify pain processes.
J.G. Pickar / The Spine Journal 2 (2002) 357371
ALTERED SENSORIMOTOR INTEGRATION WITH
CERVICALSPINE MANIPULATION
Spinal manipulation of dysfunctional cervical joints
may alter specific central corticomotor facilitatory
and inhibitory neural processing and cortical motor
control.
This suggests that spinal manipulation may alter
sensorimotor integration.
These findings may help elucidate the mechanisms
responsible for the effective relief of pain and
restoration of functional ability documented after
spinal manipulation.
Haavik Taylor, Murphy. J Manipulative Physiol Ther 2008;31:115-126

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