Anatomy and Physiology of the Autonomic Nervous System

One of the most important concepts in functional neurology is that we can utilize the motoric output of the nervous system end organs as a guide to the level of activation in the central nervous system. The first examination techniques we will explore will utilize this concept as it applies to the autonomic nervous system. First, a brief review of anatomy and physiology of the autonomic nervous system may be useful.

Organization of the Autonomic Nervous System

The autonomic nervous system comprises the major autonomous or non-volitional efferent outflow to all organs and tissues of the body, with the exception of skeletal muscle. Anatomically, the autonomic outflow from the spinal cord to the end organ occurs through a chain of two neurons consisting of a pre- and postganglionic component. The preganglionic component neurons live in a lateral area of grey matter of the spinal cord called the intermediolateral cell column or IML. The postganglionic component neurons vary in the locations with some living in the paraspinal or sympathetic ganglia, and others in ganglia distant from the cord, known as stellate ganglia. Although, historically, only the efferent connections were considered to be of functional importance, all of the projections of the autonomic nervous system are reciprocal in nature and involve both afferent and efferent components.

The autonomic system can be divided into three functionally and histologically distinct systems: the parasympathetic, sympathetic and enteric systems. All three systems are modulated by projections from the hypothalamus. Hypothalamic projections that originate mainly from the paraventricular and dorsal medial nuclei influence the parasympathetic and sympathetic divisions as well as the enteric division of the autonomic nervous system. These descending fibres initially travel in the medial forebrain bundle and then divide to travel in both the periaquaductal grey areas and the dorsal lateral areas of the brainstem and spinal cord. They finally terminate on the neurons of the parasympathetic preganglionic nuclei of the brainstem, the neurons in the intermediate grey areas of the sacral spinal cord and the neurons in the intermediolateral cell column of the thoracolumbar spinal cord. Descending autonomic modulatory pathways also arise from the nucleus solitarius, noradrenergic nuclei of the locus ceruleus, raphe nuclei, and the pontomedullary reticular formation.

The parasympathetic system communicates via both efferent and afferent projections within several cranial nerves, including the oculomotor (CN III) nerve, the trigeminal (CNV) nerve, the facial (CNVII) nerve, the glossopharyngeal nerve, the vagus (CNX) and accessory (CNXI) nerves. The vagus nerve and sacral nerve roots compose the major output route of parasympathetic enteric system control.1

Axons of the preganglionic nerves of the parasympathetic system tend to be long, myelinated type II fibres. The postganglionic axons tend to be somewhat shorter, unmyelinated C fibres, which means they conduct information at a much slower rate of speed. The cell bodies of parasympathetic preganglionic neurons are located in discrete nuclei at various levels of the brainstem and in the intermediolateral cell column of sacral 2-4 levels in the spinal cord or lumbar 1-2 vertebral level. In contrast to the sympathetic system, the preganglionic parasympathetic axons are generally longer than the postganglionic axons as they synapse in ganglia that are further from their origin and closer to the effector organ.

The neurotransmitter released both pre- and postsynaptically in the parasympathetic system is acetylcholine. Functionally, the neurological output from the parasympathetic system is the integrated end product of a complex interactive network of neurons spread throughout the mesencephalon, pons and medulla. The outputs of the cranial nerve nuclei, including the Edinger-Westphal nucleus, the nucleus tractus solitarius, the dorsal motor nucleus, and nucleus ambiguus are modulated via the mesencephalic and ponto-medullary reticular formation. This complex interactive network receives modulatory input from wide areas of the neuraxis including all areas of cortex, limbic system, hypothalamus, cerebellum, thalamus, vestibular nuclei, basal ganglia and spinal cord.2,3,4,5,6

The sympathetic system enjoys a wide-ranging distribution to virtually every tissue of the body. The presynaptic neurons live in a region of the grey matter of the spinal cord called the intermediomedial and intermediolateral cell columns located in laminae VII. Axons of these neurons exit the spinal cord via the ventral rami, where they further divide to form the white rami communicantes. The fibres then follow one of several pathways, including:

1) synapse in the paravertebral or prevertebral ganglia segmentally.

2) synapse in segmental regions of the paravertebral or prevertebral ganglion other than those at which they exited.

3) continue as presynaptic myelinated fibres into the periphery and do not synapse in the prevertebral or paravertebral ganglia.

The output of the preganglionic neurons of the sympathetic system is the summation of a complex interactive process involving segmental afferent input from dorsal root ganglion and supra-segmental input from the hypothalamus, limbic system, and all areas of cortex via the mesencephalic and ponto-medullary reticular formations.6,7,8

Most post ganglionic fibres of the sympathetic nervous system release norepinephrine as their neurotransmitter. The chromaffin cells of the adrenal medulla, which are embryological homologues of the paravertebral ganglion cells, are also innervated by preganglionic sympathetic fibres which fail to synapse in the paravertebral ganglia as described above. When stimulated, these cells release a neurotransmitter/neurohormone that is a mixture of epinephrine and norepinephrine with a 4:1 predominance of epinephrine.9

Both epinephrine and norepinephrine are manufactured via the tyrosine- dihydroxyphenylalanine (DOPA)-dopamine pathway and are called catecholamines.When the body is in a neutral environment, catecholamines contribute to the maintenance of homeostasis by regulating a variety of functions such as cellular fuel metabolism, heart rate, blood vessel tone, blood pressure and flow dynamics, thermogenesis and, as explained below, certain aspects of immune function.

When a disturbance in the homeostatic state is detected, both the sympathetic nervous system and the hypothalamus-pituitary-adrenal axial system become activated in the attempt to restore homeostasis via the resulting increase in both systemic (adrenal) and peripheral (post ganglionic activation) levels of catecholamines and glucocorticoids. In the1930’s, Hans Selye described this series of events or reactions as the general adaptation syndrome or generalized stress response.10 Centrally, two principal mechanisms are involved in this general stress response; these are the production and release of corticotrophin releasing hormone produced in the paraventricular nucleus of the hypothalamus and increased norepinephrine release from the locus ceruleus norepinephrine releasing system in the brain stem. Functionally, these two systems cause mutual activation of each other through reciprocal innervation pathways.11 Activation of the locus ceruleus results in an increased release of catecholamines, of which the majority is norepinephrine, to wide areas of cerebral cortex, subthalamic and hypothalamic areas. The activation of these areas results in an increased release of catecholamines from the postganglionic sympathetic fibres as well as from the adrenal medulla.

Most Areas Modulating the Autonomic Systems Are Bilateral Structures

It is worth noting at this point that, with the exception of a few midline structures in the brainstem, the locus ceruleus and the raphe nuclei, all other structures that modulate the autonomic output are bilateral structures. This presents the possibility that asymmetric activation or inhibition lateralised to one side or the other may translate to the activity of the end organs and produce asymmetries of function from one side of the body to the other.12 Accurately assessing the asymmetric functional output of the autonomic nervous system is a valuable clinical tool in evaluating asymmetrical activity levels of cortical or supraspinal structures that project to the output neurons of the autonomic system.

Randy Beck, B.Sc., D.C., Ph.D., is a graduate of Canadian Memorial Chiropractic College. He has completed postgraduate studies in Psychology, Immunology and Neurology. He is presently involved in a number of international research projects and is co-authoring a textbook on Functional Neurology. He was formerly the Dean of Chiropractic and Basic Sciences and Director of Research at the New Zealand College of Chiropractic. Presently, he practices Chiropractic Functional Neurology at the Papakura Neurology Center and The Maungakiekie Clinic located in Auckland, New Zealand.

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6. Webster, K. E. The brainstem reticular formation. The biological basis of Schizophrenia. G. Hennings and W. A. Hemmings. Lancaster, M.T.P. Press.1978.

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8. Williams, P., L. and R. Warwick. Grey’s Ananatomy. Edinburgh, Churchill Livingston.1984.

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10.Selye, H. Thymus and the adrenals in the response of the organism to injuries and intoxications. Br. J. Experimental Pathology 17: 234-38, 1936.

11.Chrousos, G., P. and P. W. Gold. The concepts of stress and stress system disorders: Overview of physical and behavioral homeostasis. J. Amer. Med. Assoc. 267: 1244-52. 1992.

12.Lane, R.D. and Jennings J.R. Hemispheric asymmetry, autonomic asymmetry, and the problem of sudden cardiac death. In Brain Asymmetry. Davidson, R. J. and Hugdahl, K. eds. The MIT press, Cambridge, Massachusetts.1995.

 

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