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(Aghan & Burke)
Multiple Sclerosis III
Parkinson's Disease IV
Visual Form Agnosia
Cerebral Palsy IV
(Labbadia & Taplin)
Multiple Sclerosis IV
Cerebellar Ataxia II
Huntington's Disease III
Smooth Pursuit II
Progressive Supranuclear Palsy
Postural Control II
Parkinson's Disease III
Huntington's Disease II
Phantom Limb III
Vestibular Rehabilitation and Concussion
Cerebral Palsy III
Multiple Sclerosis II
Myofascial Referred Pain
Seizure - Cortical Related
Visual Cortical Neurons
Learning to Dance - Observation vs Action
Restless Leg Syndrome
Grand Mal Seizure
Cerebral Palsy II
Duchenne Muscular Dystrophy
Basal Ganglia II
Saccadic Eye Movement
Shaken Baby Syndrome
Parkinson's Disease II
Alcohol & Cerebellum
(Leach & McManus)
Phantom Limbs II
Cerebellum & Motor Learning
Motor Unit Adaptation
Aging Nervous System
Dance & the Brain
Enteric Nervous System
Golgi Tendon Organs
Vestibular Occular Reflex
"For in Him we live and move and exist." Acts 17:28a
In his metaphysical philosophy of chiropractic, D.D. Palmer (founder of chiropractic) recognized an "Innate Intelligence" within the body. However, he also acknowledged that the body's ability to care for itself is being compromised by certain nerve interferences caused by spinal injury. In his own words, "Slightly displaced vertebrae which press against nerves causing impingements, the result being too much or not enough functionating." - this we know as vertebral subluxation.
How does vertebral subluxation interrupt the Creator's intended method of movement?
FUNCTIONAL ANATOMICAL REVIEW OF SPINAL CORD AND VERTEBRAL COLUMN
The spinal cord, the most caudal division of the central nervous system (CNS), originates at the base of the skull directly below the brain stem and extends to the first lumbar vertebra (L1). Beyond the terminal end of the spinal cord, the Conus Medullaris, spinal nerves dangle until the coccyx forming the cauda equina ( or "horse's tail") (Bridwell).
The cord is composed of gray matter coated with white matter. Nerve cell bodies reside in both the dorsal and central horns of gray matter. Specifically, peripheral sensory motor nuclei relay input to the dorsal horn while motor nuclei innervating muscles communicate via the ventral horn. Ascending pathways carrying sensory information to the brain and descending pathways conveying modulatory messages and motor commands from the brain run through the myelinated axons of white matter. (Kandel 319)
31 pairs of spinal nerves bundle fibers together. The dorsal root collects sensory information via axons from the body's internal organs, muscles, and receptors. Axons of motor neurons are also bundled together, passing through the ventral root to innervate corresponding muscles (Kandel 320). The cord is segmental; therefore, nerves exit through intervertebral foramen at multiple levels of the spinal canal, providing essential messages of functionality to all parts of the body (Bridwell). (Cervical = 8 pairs; thoracic = 12 pairs; lumbar = 5 pairs; sacral = 5 pairs; coccyx = 1 pair.)
Protection for such a powerhouse of nerves is vital, nevertheless, the vertebral column is up to the challenge. Its chain of 33 vertebrae is perfectly designed, allowing for functional movement, absorbing stressors, supporting the skeleton and musculature, and shielding the spinal cord. A typical vertebra features a body of spongy bone and red bone marrow coated with dense bone. A vertebral foramen is positioned dorsally within the body and, when linked with the other vertebral foramina, form a pathway for the spinal cord, known as the vertebral canal. Each foramen boast a spinous process and transverse process - projections to which muscles and ligaments attach. Vertebra are joined together by a pair of superior and inferior articular processes that restrict detrimental twisting of the vertebral column. Gelatinous pads surrounded by flexible fibrocartilage form intervertebral discs, adjoining neighboring vertebrae, supporting loads, and absorbing stress. Vertebrae are separated into groups: cervical, thoracic, lumbar, sacral, and coccygeal. Variations of the above generalized anatomy are seen from region to region, most prominently in the atlas and axis (C1 and C2, respectively), however the scope of these differences will not be covered in this space. (Saladin 261-62)
INPUT AND OUTPUT PATHWAYS
The Ascending Dorsal Column-Medial Lemniscal System
Proprioception and tactile sensation messages from the trunk and limbs ascend ipsilaterally in the sacral region of the spinal cord through the dorsal columns to the medulla. The dorsal columns separate at the upper spinal level into (1) the laterally located cuneate fasicle, containing fibers from the first cervical vertebra (C1) through the sixth thoracic vertebra (T6) and (2) the medially located gracile fasicle, containing fibers from ipsilateral the seventh thoracic vertebra (T7) through the twelfth thoracic vertebra (T12) . Axons of the fasicles terminate on their respective cuneate nuclei and gracel nuclei in the lower medulla and synapse with second order neuron . Axons decussate contralaterally and ascend to the ventral posterior lateral nucleus of the thalamus in the medial lemniscus. Fibers synapse in the thalamus with the third order neuron and project through internal capsule to the primary somatosensory cortex. (Kandel 446-48)
The Ascending Anterolateral System
Neurons transmitting pain and temperature from the trunk and limbs project in the spinal cord to the ipsilateral dorsal horn. The second order neuron decussates to the contralateral anterolateral column to one of two ascending pathways: (1) the spinothalamic tract projects to the ventral posterior lateral nucleus of the thalamus, synapses with its third order neuron, and projects to the somatosensory cortex, (2) the spinoreticular tract projects to the reticular formation of the medulla and pons, synapses with its third order neuron, and projects to the intralaminar and posterior nuclei of the thalamus. (Kandel 448-49).
The Ascending Spinocerebellar Pathway
Somatosensory information from muscle and joint proprioceptors regulating body a limb movements are conveyed through direct and indirect pathways. Muscle and lower limb axons enter the spinal cord, ascending the dorsal columns until the second lumbar vertebra (L2) where the synapse with the nucleus dorsalis in Clarke's column, forming the spinocerebellar pathway, and continue to ascend ipsilaterally into the cerebellum. Axons of the second thoracic vertebra and above ascend to the brain stem where they synapse with the accessory cuneate nucleus, forming the cuneocerebellar pathway, also projecting ipsilaterally to the cerebellum. (Kandel 841)
The Descending Medial and Lateral Brain Stem Pathways
Postural and proximal muscle control is mediated through three major medial pathways: reticulospinal (medial and lateral), tectospinal, and vestibulospinal (medial and lateral) tracts. These pathways project ipsilaterally down the ventral columns of the spinal cord to the interneurons and propriospinal neurons in the gray matter of the ventromedial spinal cord. Distal muscles are controlled via the lateral pathway, primarily, the rubrospinal tract. Fibers arise from the red nucleus in the midbrain, descending through the dorsal part of the lateral column in the spinal cord. The rubrospinal tract is organized somatotopically; fibers arising from the dorsalmedial red nucleus project to the cervical spine, fibers arising from the intermediate red nucleus project to the thoracic spine, and fibers arising from the ventrolateral red nucleus project to the lumbosacral spine. (Kandel 668).
The Descending Ventral and Lateral Corticospinal Tract
Spinal cord motor neurons are modulated by the cerebral cortex. The lateral corticospinal tract originates in Brodmann's area 1, 2, 3 (sensory areas), 4 and 6 (motor areas). 90 percent of corticospinal axons run the lateral tract through the internal capsule, decussate at the lower medullary level, and terminate in the gray matter of the spinal cord. The lateral tract, the remaining 10% of corticospinal axons, decussate at the segmental level. (Kandel 670)
There is little consensus on the nature of vertebral subluxation, resulting in several models attempting to explain its affects on neurological functioning. Nonetheless, this space will give focus to the afferent model of the vertebral subluxation complex and its supporting scientific research.
The vertebral subluxation complex states, injury to vertebrae prevent spinal joints from moving properly, creating "a movement deficiency" which results in dysafferentation and bone and soft tissue degeneration (Chestnut 92). More specifically, subluxation is responsible for altering afferent input, to which the body responds over time by making dysfunctional changes. If there is increased nociceptive input, the body retaliates with a decrease in proprioception (Chestnut 92).
Both modalities, nociception and proprioception, utilize the dorsal root ganglion neurons to convey their somatosensory information. Nonetheless, peripheral terminals of these neurons determine their selective responses to certain forms of energy. The dorsal root ganglion neuron functions to 1) convert a stimulus to an electrical impulse and 2) to transport the information to the central nervous system. The cell body, within the ganglion, has two branches projecting from its axon. The peripheral branch leads to nerve terminals of sensory receptors such as nociceptors and mechanoreceptors. The central branch, in conjunction with the remainder of the peripheral branch, makes up the primary afferent fiber of the dorsal root ganglion neuron which carries the message to the spinal cord and brain via ascending pathways (explained above).
Nociceptors, strategically placed sensory receptors in the peripheral and subcutaneous tissue, are sensitive to noxious stimuli. When harm is done to the skin, joints, or muscles, nociceptive afferent fibers transmit signals to the cell bodies of the sensory peripheral neurons found in the trigeminal ganglia and dorsal root ganglia (Kandel 472-73). Afferent information that arrives to the spinal cord via A-delta or C fibers is typically nociceptive. Important to the neurology of subluxation is understanding that spinal joints are primarily innervated by C fibers - sensitive to slow, persisting pain. Spinal joints are densely populated with nociceptors, indicating that the body is designed to sense tissue damage and chemical inflammation. Toxicity of nociceptors is thus encouraged by injury to the spine, causing an increased firing rate of these receptors. (Subluxation)
While nociceptors specialize in detecting noxious stimuli, mechanoreceptors are given over to deciphering proprioceptive information. By responding to physical deformation of touch, tension, pressure, stretch, and vibration, mechanoreceptors afford the body with a sense of limb-position and kinesthesia. (Kandel 443)
As a result of subluxation, there is an increase in nociception, inflammation, and pain and consequentally less movement within the joint. Thus, with a deficiency in movement there is a functional decrease in mechanoreceptor activity. (Subluxation)
The vertebral subluxation complex relies on the functional relationship of the spinal joint and dorsal root ganglia. The origin of subluxation arises from location of the dorsal root ganglia between adjoining vertebrae. Lantz gives a detailed review on these structures, emphasizing pain and discomfort caused by compression of the dorsal root ganglia. The ganglia are immensely vascularized and its capillaries highly permeable, leading to a range of potential problems including viral and bacterial infection and hypersensitivity to mechanical stimulation when inflamed. Thus afferent information, arising primarily from the dorsal root ganglia, is interrupted with subluxation of the vertebrae. (Lantz 2)
Taylor and her colleagues saw the afferent model as plausible based on two well-established principles of the CNS: (1) the CNS is plastic, readily adapting to its continuously changing environment, and (2) modifications in CNS functionality can be produced by an increase (hyperafferentation) or decrease (deafferentation) in afferent input.
"Vertebral subluxation > Altered afferent input > Altered somatosensory processing > Altered sensorimotor integration > Altered motor control > Altered funtion" (Taylor et al)
Proprioceptive afferent input was evaluated in subjects with subclinical recurrent neck pain. Rather than assuming injury damages peripheral sensory signals, researchers suspect that changes to the CNS effect the interpretation and transformation of proprioceptive signals. Accurate kinaesthetic sensations is formed by the CNS interpreting these signals within an internal reference frame. Thus, altered afferent input will effect the choice of reference frame and kinaesthetic sensations, resulting in a modification of head/limb position. This study measured shoulder, head, trunk, and whole-body position in response to active and passive shoulder elevation and depression and vibration of the trapezius muscle. Subjects with neck pain significantly over-estimated shoulder position during passive elevation. Thus, results show that altered proprioceptive input may modify the reference frame used by subjects with neck pain. (Paulus et al)
Seaman's research emphasizes the cerebellum's influence on the CNS. The ratio of afferent input to efferent input to the cerebellum is overwhelming, 40:1, signifying the importance of mechanoreceptive and nociceptive input. Information courses through the cerebellar peduncles to the cerebrocerebellum, spinocerebellum, and vestibulocerebellum divisions. Specifically, the vermis receives afferents from spinal structures while the paravermal region (intermediate cortex) responds to input from the extremities. Spinal movement in particular stimulates the vermis, relaying mechanoreceptive input to the brain to control equilibrium, posture, locomotion, and muscle tone. When spinal subluxation is adjusted, movement is normalized, followed by accurate proprioception. (Seaman)
The vertebral subluxation complex incorporates five components: (1) kinesiopathology, (2) neuropathology, (3) myopathology, (4) histopathology, and (5) biochemical abnormalities (Lantz 1). While this space is primarily concerned with the neural aspects of subluxation, the effects of deviation from normal movement (kinesiopathology) are prominent in today's society. Toxic activity patterns (low fitness levels, poor posture, etc...) lead to a decay of spinal and neuromuscular health (Chestnut 91-92). Such decay translates to joint immobilization and degeneration, the central concept in the kinesiopathological model of the vertebral subluxation complex (Lantz 1). Consequently, the major clinical focus of chiropractic care is to restore healthy joint motion and function to the patient.
Subluxation, defined by the Association of Chiropractic Colleagues as "a complex of functional and/or structural and/or pathological articular changes that compromise neural integrity and may influence organ system function and general health”, interferes with the Creator's intended design of His creation. While the chiropractic world does not fully agree on the nature of subluxation, there is significant evidence supporting the vertebral subluxation complex and afferent model. When the spine is injured, subluxation occurs. Afferent input provided by nociceptors is increased, while mechanoreceptor activity is decreased, resulting in a functional loss of movement.
Dysafferentation - an imbalance of afferent input
Nociception - a physiological, not psychological, sensation of pain supplied by noxious stimuli
Proprioception - an unconscious perception of kinesthesia (sense of movement in space) and spacial orientation of the body
Subluxation - a complex of functional and/or structural and/or pathological articular changes that compromise neural integrity and may influence organ system function and general health
Interactive Nerve Chart
A chart illustrating the many relationships between the spine and the nervous system. Interference to the spine by subluxation negatively affects the function of the systems tied to each vertebrae. Provided by Hall Family Chiropractic.
Chiropractic Subluxation and Neurology Articles
A compilation of articles provided by Frank M. Painter, D.C.
1. Define subluxation.
2. True or false? There is relative agreement on the nature of vertebral subluxation.
3. Name two potential problems the highly vascularized, highly permeable dorsal root ganglia present.
4. According to Seaman, input flows through cerebellar peduncles to which division(s) of the cerebellum?
a. the cerebrocerebellum
b. the spinocerebellum
c. the vestibulocerebellum
d. both a. and b.
e. all of the above
5. True or false? Decreased nociception leads to decreased proprioception.
6. Considering the above information, what neuropathological effect does poor posture create?
Bridwell, K. (2010). Nerve Structures of the Spine. Vertical Health, LLC. Retrieved from
Chestnut, J. L. (2005). Innate Physical Fitness & Spinal Hygiene. Victoria, BC: Global Self Health Corp.
Kandel, E. R., Schwartz, J. H., & Jessell, T. M. (2000). Principles of Neural Science, 4th ed. New York, NY: McGraw-Hill.
Lantz, C. A. (1989). The Vertebral Subluxation Complext PART 1: An Introduction to the Model and Kinesiological Component. Chiropractic Research Journal, 1(3), 23-36.
Lantz, C. A. (1990). The Vertebral Subluxation Complex PART 2: The Neuropathological and Myopathological Components. Chiropractic Research Journal, 1(4), 19-38.
Paulus I., & Brumagne S. (2008). Altered Interpretation of Neck Proprioceptive Signals in Persons with Subclinical Recurrent Neck Pain.
J Rehabil Med., 40, 426-32.
Saladin, K.S. (2007). Anatomy and Physiology: the Unity of Form and Function, 4th ed. New York, NY: McGraw-Hill.
Seaman, D. R., & Winterstein, J. F. (1998). Dysafferentation: a novel term to describe the neuropathophysiological effects of joint complex dysfunction. A look at likely mechanisms of symptom generation. J Manipulative Physiol Ther, 21(4), 267-280.
Subluxation and the Nervous System. Retrieved from
Taylor, H. H., Holt, K., & Murphy, B. (2010). Exploring the Neuromodulatory Effects of the Vertebral Subluxation and Chiropractic Care. Chiropractic Journal of Australia, 40(1), 37-44.
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