Chiropractic Neurology



Joseph Angleitner, DC, DACNB

What is Chiropractic Neurology?

As in medicine and dentistry, the chiropractic profession has individual specialists. Through education, training and board certification, these doctors choose to limit their practice to a certain specialty to assist members of their profession and allopathic physicians in the diagnosis and treatment of a variety of conditions. Within the chiropractic profession, there are specialists in radiology, orthopedics, neurology, and rehabilitation.

Typically, a chiropractic neurologist serves in the same consulting manner as a medical neurologist. The difference is that the therapies or applications of a chiropractic neurologist do not include drugs or surgery. As a result, certain conditions are more customarily seen by a chiropractic neurologist as opposed to a medical neurologist, and vice versa.

Chiropractic Neurologists see patients with a variety of movement disorders, dystonias, post-stroke rehabilitation, and radiculopathy or nerve entrapment syndromes that are consequences of peripheral or central types of lesions.

Chiropractic neurologists can provide therapies and treatments as well as counsel when there is a diagnostic dilemma or a question of appropriateness of care regarding an individual lesion or scenario.

The training to become a board certified neurologist in the chiropractic profession is an additional three years after the doctor’s degree, which is conducted under the auspices of an accredited university or college that is recognized by the U.S. Office of Education. During that training there is didactic and residency – based / clinical based training. After completing those requirements, the chiropractor will sit for a board examination in neurology, which is held once per year by our independent examining board. The areas that are examined are specific to the field of neurology and include clinical and diagnostic techniques and knowledge of neurophysiology. The certification examination includes oral and practical portions as well as a battery of psychometric testing.


The central nervous system consists of the brain and spinal cord. The peripheral nervous system consists of nerves found peripherally; i.e. in the head and body. The brain is designed to receive information from, and send information to, the head and body.

The brain is receptor driven via afferent projections to cerebellar and thalamic nuclei.  Receptor activation through primary afferent nerves is modality specific (retinal receptors transmit light, cochlear receptors transmit sound, etc) and requires an adequate stimulus to propagate synaptic transmission to the brain for interpretation, modulation and execution.  The greatest input into the brain and nervous system is from environmental stressors that are constant; i. e., those related to the earth’s gravitational pull on muscle spindle cells, Golgi tendon organs, the gamma motor apparatus, and joint mechanoreceptors.  An additional population of mechanoreceptors is found in the labyrinthine mechanism of the inner ear to provide constant appraisal of our orientation in the earth’s gravitational field.  Plasticity (learned behavior) in this pathway provides the foundation for reflexogenic midline shunt stability in the newborn, conjugate movement of the eyes and vertebral motion segments, and establishment of cervical and lumbar lordoses.

Activation of gravitational receptors initiates the central transmission through primary afferent nerves to synapse on their second order projections to summate in the cerebellum and thalamus.  Cortical activation in human kind is largely due to thalamic integration resulting from cerebellar output and second order dorsal column projections.  The thalamus is the “terminal” of all sensory input to the brain, without which adequate human perception cannot exist.  Integrity of thalamic neurons is vital to our well-being and can only be guaranteed through constant activation.

Non-gravitational receptors (light, sound, taste, touch,etc) are referred to as “trivial”, in that they are not constant and are not critical for survivabiltiy.

The function of all neurons is to promote survivability through the receipt and tramsmission of information as a consequence of their frequency of firing.  All neurons require fuel and activation.  Activation may be either excitatory or inhibitory, but it must be constant.  Such activation may be direct, via gated Na+ or K+ channels, or indirect, via G protein coupled mechanisms, such as a Na+ activated channel coupled to a G protein, which activates K+ efflux, to cause inhibition.  Oxygen and glucose provide fuel required for all metabolic processes.

Primary afferent nerves relaying proprioception are the largest diameer fibers, classified as groups I and II.  Their impulses travel from 60 to 120 meters per second.  One of their functions is to segmentally inhibit the transmission of fibers that relay the sensaton of pain, or C type fibers, which are the smallest and slowest in the nervous system, travelling at only .5 to 2 meters per second.  Another function is to promote fuel delivery through the functional embryological homologue of the dorsal root ganglion, the autonomic visceral ganglion, via excitation of the intermedial lateral cell column in the spinal cord, the IML, or type B fibers.

The smallest diameter nerves are the most resistant to compression.  The largest are the first to be affected, resulting in decreased post-synaptic metabolic rate; decreased activation and fuel, an eccentric nucleus, decreased protein replication, and a shift toward the Na+ equillibrium potential, decreased mitochondrial oxidative metabolism, decreased ionic pumps, and swelling.  Spontaneous firing, fatigue and aberrant perception of non-constants may be seen as a consequence of decreased intracellular anionic substrate.

All neurons are located in homologous columns, maintaining a rostral / caudal relationship in their firing sequence, further guaranteeing survivabilty.  A decreased frequency of firing of a presynaptic pool will result in the PROBABILTY of a decreased post-synaptic neuropil, decreased cIEG, decreased frequency of firing of postsynaptic pools, and decreased cellular integrity.

Activation of the musculoskeletal system is largely the result of sensorimotor activity via the contralateral rostral (mesencephalic) reticular formation, via the rubrospinal sysem.   Mesencephalic reticular neurons are excitatory to brain via thalamic projections.  They are excited by Sensory Motor Cortex which is gated via basal ganglionic activation, primarily from frontal cortex.

The majority of output of the brain is monosynaptic to ipsilateral vital centers in the caudal (pontomedullary) reticular formation, which facilitates fuel delivery (gastric activity, absorption of material and metabolic conversion) and activation.  It is from this area that a variety of activity of an inhibitory nature occurs at the cord level.  Although the pontomeducllary reticular formation’s output is excitatory, its effect is primarily on inhibitory neurons.

Output of the pontomedullary centers (1) affects the gain of spindle receptors via polysynaptic activation of ventral horn cells, (2) inhibits the IML ipsilaterally, (3) inhibits inhibition of ventral horn cells ipsilaterally, and (4) promotes inhibition of anterior ventral horn cells above T6, and posterior ventral horn cells below T6, ipsilaterally.

The ipsilateral effect of IML excitation facilitated by the mesencephalic reticulospinal output is largely inhibited by the ipsilateral inhibitory output of the pontomedullary reticulospinal system, resulting in contralateral excitation of the IML via mesencephalic reticulsopinal projections.

Although 60% of our pathways are canalized, 40% are unique to our individuality and function.  Most pathways in humankind are inhibited to promote survivability via gene activaton and replication of protein.  Most disorders of humankind seem to be related to a loss of inhibition of inhibitory pathways, or a loss of inhibitory activation directly, as seen in compartmental syndromes; i.e., peripheral nerve entrapments.

Unilateral deafferentation via cerebellipetal and second order dorsal column projections may result in contralateral decreased activation and survivability, or hemisphericity, resulting in decreased ipsilateral descending suprasegmental modulation and loss of inhibition.

Hemisphericity results in altered angulation of peripheral joints, predisposing to peripheral nerve entrapment neuropathies and conditions such as peripheral nerve impingement syndrome (sciatica), tennis elbow, frozen shoulder, IT – band syndrome, plantar fascitis, etc. Hemisphericity frequently has autonomic consequences, such as increased blood pressure, tachycardia, cardiac arrhythmia, and other symptoms associated with increased activity to the sympathetic nervous system. Increased sympathetic activity is associated with increased sensitization to pain and chronic pain states.

Non-pharmaceutical applications appropriate to one’s hemisphericity and metabolic rate have been effective at defeating hemisphericity.