UPPER CERVICAL NEUROLOGY
By Kirk Eriksen, D.C.
The neurological dysfunction related to the upper cervical subluxation can be explained by a few different mechanisms. However, it is likely that these mechanisms manifest concurrently in many patients. The two most plausible hypotheses have to do with spinal cord tension and mechanoreceptive dysafferentation. The upper cervical spinal cord is directly attached to the circumference of the foramen magnum, to the second and third cervical vertebrae and by fibrous slips to the posterior longitudinal ligament.[2] Hinson[3], Grostic[4] and others discuss dissection evidence showing a dural attachment at the atlas level. The uppermost denticulate ligaments are arranged almost horizontally, as compared to the inferiorly angled ligaments found around the rest of spinal cord. The most cephalad ligaments are also thicker and stronger to help anchor the spinal cord around the foramen magnum. These ligaments are so strong that they have been found to sever the upper cervical spinal cord in some cases of hydrocephalus.[5] Recent studies have also revealed a connective tissue bridge between the rectus capitis posterior minor muscle and the dura mater of the upper cervical spinal cord.[6] A similar attachment has also been found to the spinal cord via the ligamentum nuchae.[7] The spinal dura mater has been found to be innervated and a possible source of pain and neurological dysfunction.[8,9] These anatomical facts, as well as the biomechanical descriptions covered previously, reveal that the upper cervical spine is quite susceptible to injury and/or the entity called subluxation. The upper cervical spine has sacrificed stability for mobility as evidenced by ~50% of cervical rotation occurring between the atlanto-axial articulation. Grostic’s paper, The Dentate Ligament—Cord Distortion Hypothesis4, provides a compelling hypothesis for how these anatomical connections can lead to spinal cord distortion, in the presence of upper cervical misalignment. It is posited that the neurological dysfunction can occur via two mechanisms: 1) direct mechanical irritation of the nerves of the spinal cord, and/or 2) collapse of the small veins of the cord, producing venular congestion with a loss of nutrients necessary to carry on the high energy reactions necessary for nerve conduction. Spinal cord tension can affect the spinocerebellar tracts which can result in a functional short leg.
Afferent/efferent joint mechanoreceptive neurology also has interesting implications in this area of the spine. Mechanoreceptive innervation has been found in the cervical facet joints, ligaments, intervertebral discs.[10-13] The muscle spindle may be the most important proprioceptive receptor in the upper cervical spine. The spindles are intrafusal fibers that are imbedded within all muscles of the body; however, they are extremely dense in the suboccipital muscles.[14-20] The human experience is governed by receptors of all types. Cerebral cortical firing initiates efferent activity. However, the thalamus regulates the cerebral cortex through summation and integration. Another key point is that all sensory information goes through the thalamus (except aspects of olfaction).[21] It is apparent how these two functions are vitally important for neurological integrity and appropriate cortical representation. Mechanoreception is the primary input into the cerebellum due to life in a gravity environment. The primary load to the thalamus is via the cerebellum due to the vast amount of afferent input required to maintain upright posture. It is plausible to theorize that stimulating or regulating mechanoreceptors can have a significant impact on the neurological activity of the brain and many bodily functions.
