There are three components of the autonomic nervous system.

The sympathetic nervous system can function more generally with respect to its less precise influence on physiology as it mediates whole-body reactions involved in the ’fight or flight’ responses. Both the sympathetic and parasympathetic systems are tonically active to help maintain a stable internal environment in the face of changing external conditions which is best described as homeostasis.

Both the sympathetic and parasympathetic systems comprise preganglionic and postganglionic neurons. The cell bodies of preganglionic neurons in the sympathetic system are located in the intermediolateral cell column (IML) of the grey matter of the spinal cord between T1 and L2. The axons of these neurons exit the spinal cord via the ventral root with the motor neurons of the ventral horn. A branch known as the white rami communicans (myelinated) carries these fibres to the sympathetic chain ganglia where many of the preganglionic cells synapse with postganglionic cells. At cervical and lumbar levels, postganglionic sympathetic neurons form grey rami communicans (unmyelinated and slower conducting) that are distributed to vascular smooth muscle, piloerector muscle, and sweat glands via the spinal nerves and their branches. At cervical levels, some of the postganglionic neurons also project to the eye, blood vessels, and glands of the head and face via the carotid and vertebral arterial plexi. The cell bodies of parasympathetic preganglionic neurons are located in discrete nuclei at various levels of the brainstem and at the IML column of levels S2–4 in the spinal cord (vertebral level L1–2). In contrast to the sympathetic system, the preganglionic parasympathetic neurons are generally longer than the postganglionic neurons as they synapse in ganglia further from their origin and closer to the effector than the postganglionic neurons innervate.

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 the grey matter of the spinal cord. The postganglionic component neurons vary in location 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, 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 components: 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 periaqueductal 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 (PMRF).

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, and the vagus (CN X) and accessory (CN XI) nerves (Fig. 8.1). The vagus nerve and sacral nerve roots compose the major output route of parasympathetic enteric system control (Furness & Costa 1980). Axons of the preganglionic nerves of the parasympathetic system tend to be long, myelinated, type II fibres and the postganglionic axons tend to be somewhat shorter, unmyelinated, C fibres (see Chapter 7). The cell bodies of parasympathetic preganglionic neurons are located in discrete nuclei at various levels of the brainstem as described above and in the intermediolateral cell column of levels S2–4 in the spinal cord or vertebral level L1–2. In contrast to the sympathetic system, the preganglionic parasympathetic neurons are generally longer than the postganglionic neurons as they synapse in ganglia that are further from their origin and closer to the effector than the postganglionic neurons innervate.

Figure 8.1 This figure outlines the parasympathetic outflow to the body including the cranial nerves III, VII, and IX, the vagus nerve (CNX) and the pelvic division of spinal nerves.

The neurotransmitter released both pre- and postsynaptically is acetylcholine. Cholinergic transmission can occur through G-protein coupled mechanisms via muscarinic receptors or through inotropic nicotinic receptors. The activity of ACh is terminated by the enzyme acetylcholinesterase, which is located in the synaptic clefts of cholinergic neurons. To date, seventeen different subtypes of nicotinic receptors and five different subtypes of muscarinic receptors have been identified (Nadler et al. 1999; Picciotto et al. 2000).

Cholinergic, nicotinic receptors are present on the postsynaptic neurons in the autonomic ganglia of both sympathetic and parasympathetic systems. Cholinergic, muscarinic receptors are present on the end organs of postsynaptic parasympathetic neurons (Fig. 8.2).

Figure 8.2 This figure outlines the preganglionic and postganglionic neurotransmitters and receptors of the sympathetic and parasympathetic divisions of the autonomic nervous system. It also includes the transmitter (ACH⁻) of the ventral horn cell and the (nicotinic) receptors in muscle. Note that all preganglionic axons are myelinated and all postganglionic axons are unmyelinated.

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 reticular formation (MRF) and PMRF. 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 (Walberg 1960; Angaut & Brodal 1967; Brodal 1969; Brown 1974; Webster 1978). The relationship of the parasympathetic outflow to the immune system has received very little study to date and as a consequence very little is known about the influence of the parasympathetic or the enteric system on immune function.

Monosynaptic connections between two structures suggest an important functional relationship between the two structures in question. Polysynaptic connections may be important as well but are not as well understood as monosynaptic connections. Monosynaptic connections have been demonstrated to exist between a variety of nuclei in the medulla, pons, diencephalon, and the preganglionic neurons of the IML (Smith & DeVito 1984; Natelson 1985). Nuclei with monosynaptic connections with the neurons of the IML include:

The hypothalamus is the only structure with direct monosynaptic connects to the nuclei of the brainstem and to the neurons of the IML. This suggests that the influence of the hypothalamus on autonomic function is substantial.

The projections from the cerebral cortex and their role in modulation of autonomic function are not well understood. However, existence of direct projections from the cortex to subcortical structures regulating autonomic function has been established (Cechetto & Saper 1990). Neurophysiological studies demonstrating autonomic changes with stimulation and inhibition of the areas of cortex also suggest a regulatory role. The following outlines the established areas of cortex and their projection areas:

The autonomic ganglion

The autonomic ganglion is the site at which the presynaptic neurons synapse on the postsynaptic neurons. The sympathetic ganglia are situated paraspinally in the sympathetic trunk or prespinally in the celiac and superior mesenteric ganglia. The parasympathetic ganglia are situated in close proximity to the target structures that they innervate. The autonomic ganglia consist of a collection of multipolar interneurons surrounded by a capsule of stellate cells and connective tissue.

Incoming and outgoing nerve bundles are attached to the ganglion (Fig. 8.3). The incoming bundles contain afferent fibres from the periphery returning to the spinal cord, preganglionic axons that synapse on the postganglionic neurons in the ganglion, preganglionic axons that pass through the ganglion giving off collateral axons to the interneurons as they do so, and descending axons from cholinergic neurons in the spinal cord that modulate the activity of the interneurons in the ganglion. The interneurons in the ganglion are referred to as small intensely fluorescent cells and they are thought to be dopaminergic in nature. The outgoing bundle contains postganglionic axons, and afferent fibres from the periphery entering the ganglion (Snell 2001). The presence of such a complex structure in the ganglion has led to the suspicion that the ganglion is not just a relay point but an integration station along the pathway of the autonomic projections.

Figure 8.3 This figure illustrates the synaptic connections of afferent and efferent axon fibres on the ganglion cells. Note that both afferent and efferent information modulates the activity of the ganglion cell, both directly and indirectly through interneurons.

The oculomotor parasympathetic fibres commence in the midbrain. These fibres are the axon projections of neurons located in the Edinger–Westphal nucleus (EWN) or accessory oculomotor nuclei. The parasympathetic projections travel with the ipsilateral oculomotor nerve and exit with the nerve branch to the inferior oblique muscle and enter the ciliary ganglion where they synapse with the postganglionic neurons. The axons of the postganglionic neurons then exit the ganglion via the short ciliary nerves and supply the ciliary muscle and the sphincter pupillae. Activation of the postganglionic neurons causes contraction of both the ciliary muscle, resulting in relaxation of the lens, and the sphincter pupillae muscle, resulting in constriction of the pupil. These actions can be stimulated separately or simultaneously as in the accommodation reflex (Fig. 8.4).

Figure 8.4 This figure outlines the anatomical relationships of the optic and oculomotor nerves, as well as the mesencephalic nuclei of the third nerve. Note the inset that shows the detailed anatomy of the oculomotor nerve.

Functionally, the Edinger–Westphal nucleus receives the majority of its input from the contralateral field of vision. This involves the stimulus of the ipsilateral temporal and contralateral nasal hemiretinas, which results in the constriction of the ipsilateral pupil. For example, a shining light from the right field of vision will stimulate the left nasal hemiretina and the right temporal hemiretina which project through the left optic tract to the left EWN. The left EWN stimulation results in constriction of the ipsilateral (left) pupil. Some fibres from the left optic tract also synapse on the right EWN, effectively resulting in constriction of both pupils. This constitutes the consensual pupil reflex. Comparison between the time to activation (TTA) and time to fatigue (TTF) in each pupil following stimulation from the contralateral field of vision can be used to estimate the central integrative state of the respective EWN. This, in addition to further evaluation of the oculomotor and trochlear function, can then be used to estimate the central integrative state (CIS) of the respective mesencephalon. In situations where the CIS of the EWN is healthy one would expect rapid TTA and normal TTF response times, relatively, equal in both pupils. In situations where the CIS of one EWN is undergoing transneural degeneration of relatively short duration, one would expect an extremely rapid TTA followed by a relatively short TTF in the ipsilateral eye when compared to the contralateral eye. In situations where the CIS of one EWN is such that transneural degeneration, long-standing in nature, is present then one would expect the pupil of the ipsilateral EWN to show an increased TTA and a decreased TTF in comparison with the contralateral eye. On prolonged stimulus a pupil in this condition will often fluctuate the pupil size between normal and partial constriction. This is referred to as hippus.

The parasympathetic efferent projections of the facial nerve involve motor axons to the submandibular gland and the lacrimal gland. The motor fibres project in two different pathways and to two different ganglia. The motor projections to the submandibular gland arise from neurons in the superior salivatory nucleus in the medulla. The axons of these neurons emerge from the brainstem in the nervous intermedius and join the facial nerve until the stylomastoid foramen where they separate as the chorda tympani, which traverse the tympanic cavity until they reach and join with the lingual nerve. They travel with the lingual nerve until they reach and synapse on the postganglionic neurons of the submandibular ganglion. The axons from these neurons project to the submandibular glands via the lingual nerve supplying the secretomotor fibres to the gland. Activation of the postganglionic neurons results in dilatation of the arterioles of the gland and increased production of saliva (Fig. 8.5).

Figure 8.5 This figure outlines the motor and parasympathetic projections of the facial nerve (CN VII).

The motor projections to the lacrimal gland travel in the greater petrosal nerve through the pterygoid canal and synapse on the neurons of the pterygopalatine ganglion. The axons of the neurons in the pterygopalatine ganglion project their axons with the zygomatic nerve to the lacrimal gland and form direct branches from the ganglion to the nose and palate.

The efferent projections of the glossopharyngeal nerve contain axons that are secretory motor to the parotid gland. The projections start in the neurons of the inferior salivatory nucleus of the medulla and travel in the glossopharyngeal nerve through the tympanic plexus where they separate and travel with the lesser petrosal nerve to synapse on the neurons in the otic ganglion. The axons of these neurons then travel in the auriculotemporal nerve to the parotid gland. Activation of the neurons of the otic ganglion produces vasodilation of the arterioles and increased saliva production in the gland.

The motor projections of the vagus nerve arise from the neurons of the dorsal motor nucleus and the nucleus ambiguus of the medulla. The cardiac branches are inhibitory, and in the heart they act to slow the rate of the heartbeat. The pulmonary branch is excitatory and in the lungs they act as a bronchoconstrictor as they cause the contraction of the non-striate muscles of the bronchi. The gastric branch is excitatory to the glands and muscles of the stomach but inhibitory to the pyloric sphincter. The intestinal branches, which arise from the postsynaptic neurons of the mesenteric plexus or Auerbach’s plexus and the plexus of the submucosa or Meissner’s plexus, are excitatory to the glands and muscles of the intestine, caecum, vermiform appendix, ascending colon, right colic flexure, and most of the transverse colon but inhibitory to the ileocaecal sphincter (Fig. 8.6).

Figure 8.6 This figure outlines the projections of the vagus nerve.

The pelvic splanchnic nerves are composed of the anterior rami of the second, third, and fourth sacral spinal nerves. These nerves diverge, giving off several collateral branches to supply the pelvic viscera. Most of the projections merge with fibres of the sympathetic pelvic plexus and pass to ganglia located adjacent to their target structures, where they synapse with their postganglionic components.

Functionally, the CIS of the medulla can be estimated by examining the activities of the cranial nerves, which mediate the effector functions of end organs that can be measured. For example, a patient that presents with excessive watering of the eyes, increased salivation and nasal mucus production, difficulty in taking deep breaths, decreased heart rate, stomach pain, intestinal cramping, and frequent loose bowel movements may indicate an overactive medullary region. An underactivated medullary region may present with dry eyes, dry mouth, dry nasal cavities, increased heart rate, and constipation. This highlights the importance of conducting a thorough neurological examination of both the motor and visceral functions of the cranial nerves and relating the findings in a functional manner back to the neuraxial structures involved.

The sympathetic system enjoys a wide-ranging distribution to virtually every tissue of the body (Fig. 8.7). The presynaptic neurons live in a region of the grey matter of the spinal cord called the intermediomedial and intermediolateral cell columns located in lamina 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 (Fig. 8.8):

Figure 8.7 This figure outlines the wide range of projections of the sympathetic division of the autonomic nervous system.

Figure 8.8 This figure illustrates the variety of pathways that sympathetic fibres may take in the paraspinal ganglion. Presynaptic fibres may pass directly through the ganglion and not synapse until they reach other ganglia usually deep in the tissues of the gut. Other presynaptic fibres may synapse with their postsynaptic cells at the same level as they exit the spinal cord. Other presynaptic fibres may travel up or down in the ganglionic chains to synapse many levels distant from the level they exited the spinal cord. The superior cervical ganglia are examples of this type of projection.

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 suprasegmental input from the hypothalamus, limbic system, and all areas of cortex via the MRF and PMRF (Donovan 1970; Webster 1978; Williams & Warwick 1984). Most postganglionic fibres of the sympathetic nervous system release norepinephrine as their neurotransmitter. The adrenergic receptors bind the catecholamines norepinephrine (noradrenalin) and epinephrine (adrenalin).

These receptors can be divided into two distinct classes, the alpha adrenergic and beta adrenergic receptors (see Fig. 8.2). 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 (Elenkov et al. 2000).

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 (postganglionic activation) levels of catecholamines and glucocorticoids. In the 1930s, Hans Selye described this series of events or reactions as the general adaptation syndrome or generalised stress response (Selye 1936). 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 (Chrousos & Gold 1992). 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.

Postganglionic sympathetic fibres that course to the periphery with peripheral motor nerves usually only supply the blood vessels of the muscle of the peripheral nerve. Activation of these fibres produces vasodilation. Sympathetic fibres that course to the periphery in peripheral sensory nerves usually supply the vasoconstrictor muscles of blood vessels, the secretomotor fibres of sweat glands, and the motor fibres of the piloerector muscles of hair follicles in areas supplied by the nerve. Stimulation of these fibres results in vasoconstriction of the blood vessels, usually an increase in sweat gland, and piloerector activity.

Sympathetic projections that innervate structures in the cranial region arise from preganglionic neurons in the spinal IML at the level of T1. Axons from these neurons exit the spinal column and pass uninterrupted through the cervicothoracic ganglion to reach the superior cervical ganglion where they terminate on the postganglionic neurons in the ganglion. Axons from these neurons then project via the internal carotid nerve, which courses with the carotid artery through the carotid canal into the cranium, where it enlarges to form the carotid plexus. Fibres emerging from the carotid plexus accompany all of the cranial nerves to innervate the blood vessels in the distribution of the cranial nerves. Visceromotor and vasomotor fibres course with the oculomotor nerve to the ciliary ganglion where they pass through uninterrupted to form the long ciliary nerves which course to the eyeball. The vasomotor fibres control the extent of vasoconstriction of the arterioles supplying the eyeball. The visceromotor fibres terminate on the dilatator pupillae muscle of the iris where activation results in pupillary dilation (Fig. 8.9). Some fibres course to the levator palpebrae superioris muscles of the upper eyelid, also known as Muller’s smooth muscle. Activation of these fibres results in the contraction of these muscles which retract the eyelid. The sympathetic supply to this muscle only composes a partial segment of the innervation, which is also contributed to by motor fibres in the oculomotor nerve. Other fibres emerge from the ciliary ganglia to innervate the ciliary muscles. Activation of these fibres results in contraction of the ciliary muscles, which causes the lens to relax for better focus of near objects.

Figure 8.9 This figure illustrates the sympathetic projection system from the hypothalamus to the pupil of the eye. Projections from the hypothalamus to the preganglionic cells located in the IML cell columns of the spinal cord between the levels of T1 and L2 modulate the activation of the these preganglionic cells, which then project axons to the postganglionic cells in the superior cervical ganglion. Postsynaptic cell axons then follow the carotid arteries into the head and branch to follow the oculomotor nerve to the eye.

Vestibulosympathetic reflexes are varied in nature due to the extensive interaction between the vestibular system, midline components of the cerebellum, and autonomic control centres. Major regions that mediate autonomic function and receive inputs from the vestibular system include the nucleus tractus solitarius (NTS), parabrachial nuclei (pons and midbrain), hypothalamic nuclei, rostral and caudal ventrolateral medulla (RVLM and CVLM), dorsal motor nucleus (DMN) of the vagus, nucleus ambiguus, and locus coeruleus. Other parasympathetic nuclei such as the superior salivatory nucleus (SSN) of the pons and the Edinger–Westphal nucleus of the midbrain also receive direct projections leading to salivation and tearing, and pupil constriction, respectively.

The effect of vestibular activation on the sympathetic system is mediated largely through the CVLM and RVLM. The RVLM is a region of the medullary reticular formation that contains tonic vasomotor neurons, i.e. neurons that exert tonic excitation of the IML. The CVLM can be activated by the vestibular system and higher nervous system centres directly, or indirectly via the NTS. It contains neurons that inhibit the RVLM.

Therefore, there are two phases to vestibulosympathetic reflexes: excitatory and inhibitory phases. In some instances, vestibulosympathetic reflexes will consist of an early excitatory phase and a late inhibitory phase. This type of reflex helps to protect the individual from the effects of orthostatic stress, which occurs when one stands up quickly. Therefore, orthostatic hypotension is not only dependent on baroreceptor activity, but also on vestibulosympathetic reflexes.

These reflexes are very complex and it appears that certain neurons within the vestibular system may have a greater effect on the excitatory phase and others have a greater effect on the inhibitory phase. Whatever the case, it should be clear that increased output from the vestibular nucleus or vestibular receptors can increase both sympathetic and parasympathetic activity at the same time. For example, this may result in a rise in blood pressure and sweating due to activation of the RVLM and hypothalamus and increased tearing and bowel activity due to activation of the SSN and the DMN of the vagus. A loss of vestibular activity may lead to orthostatic hypotension due to poor maintenance of vasomotor tone when changing posture. Significant overactivity of the vestibular system could also create the symptoms of light-headedness due to excessive vasomotor tone throughout the carotid tree.

Disruption of the sympathetic chain at any point from the hypothalamic or supraspinal projections to the oculomotor nerve can result in a spectrum of symptoms referred to as Horner’s syndrome. The classic findings in this syndrome include ptosis, miosis, and anhidrosis but a number of other abnormalities may also be present. Ptosis or drooping of the upper eyelid is caused by the interruption of the sympathetic nerve supply to the muscles of the upper eyelid. Miosis or decreased pupil size is a result of the decreased action of the dilator muscles of the iris due to decreased sympathetic input. This results in the constrictor muscles acting in a relatively unopposed fashion, resulting in pupil constriction. A Horner’s pupil will still constrict when light is shined on the pupil although careful observation is sometimes required to detect the reduced amount of constriction that occurs. Another test that can be used in these cases utilises the ciliospinal reflex, which results in pupil dilation in response to pain. A pinch applied to the neck region will result in bilateral pupil dilation under normal conditions. However, in the case of unilateral disruption of the sympathetic innervation as in Horner’s syndrome, the pupil on the effected side will show decreased or absent dilation response. Occasionally, the appearance of enophthalmos or retraction of the eyeball into the eye socket occurs because of the relaxation of the eyelid muscles. Anhidrosis or reduced sweating capability sometimes also occurs on the ipsilateral face and neck in Horner’s syndrome. The affected skin will usually appear shiny and will feel smooth to the touch compared with the non-involved areas. Anhidrosis is usually not associated with postganglionic lesions or lesions above the superior cervical ganglion because sympathetic projections to the face and neck emerge from the sympathetic chain prior to the superior cervical ganglion. However, if the disruption occurs in the hypothalamic projections to the IML, anhidrosis may actually be present on the entire upper quarter on the ipsilateral side. The causes of Horner’s syndrome can be multiple and varied and include (Fig. 8.10):

Figure 8.10 This figure outlines the anatomy and location of a variety of causes of Horner’s syndrome. The inset shows the detailed anatomy of the fibres innervating the pupil.

The distribution of the sympathetic projections is widespread and in fact includes all tissues of the body. Distribution from the major ganglia is discussed below.

The superior cervical ganglion arises from the axons of preganglionic neurons located in the spinal cord levels T1–2 and is physically located at the second and third cervical vertebral levels. Postganglionic axons project to the structures of the head and neck including:

The middle cervical ganglion arises from the axons of the preganglionic neurons in the IML of spinal cord levels T2–4 and is physically located at the sixth cervical vertebral level. Postganglionic axons project to structures of the neck including:

The cervicothoracic or stellate ganglion arises from the axons of preganglionic neurons in the IML at the spinal cord levels T5–6 and is physically located at the vertebral levels C7–T1. Postganglionic axons project to structures of the neck and upper chest including:

Sympathetic distribution in the thoracic area is consistent with the projections of the paraspinal ganglia at each vertebral segmental level. However, the formation of the splanchnic nerves deserves mention. The splanchnic nerves are formed by preganglionic myelinated fibres that pass through the paraspinal ganglia without synapsing, although some evidence suggests that collateral branching of these fibres which do synapse in the ganglia may occur (see Fig. 8.3).

The greater splanchnic nerve is formed from preganglionic fibres of IML neurons located at the spinal cord levels T5–9. These axons project to the celiac and aorticorenal ganglia and the suprarenal glands where they synapse with their respective postganglionic counterparts. The lesser splanchnic nerve arises from the preganglionic neurons in the IML at the spinal cord levels T9–10. These axons project to the aorticorenal ganglion. The sympathetic projections of the lumbar area are formed from axons of the IML neurons at the levels T8–12 and project to the intermesenteric and superior hypogastric plexuses. The postganglionic fibres from this level, arising from the paraspinal ganglia, form the projections that course with the obturator and femoral nerves to the thigh.

The pelvic sympathetic projections are formed from the axons of the preganglionic neurons of the IML at the spinal cord levels T10–L2. These axons project to a series of four ganglia that lie adjacent to the sacrum. Postganglionic fibres of these ganglia course with the tibial, pudendal, inferior, and superior gluteal nerves to their respective distributions.

The autonomic innervation of several clinically important areas will be considered in detail.

Innervation of the heart

Preganglionic parasympathetic neurons that modulate the heart rate reside in the medulla and synapse with postganglionic neurons adjacent to the heart. Parasympathetic fibres project from the nucleus tractus solitarius, dorsal vagal nucleus, and the nucleus ambiguus and course to the periphery in the glossopharyngeal (CN IX) and vagus (CN X) cranial nerves. Direct connections exist between the sensorimotor cortex and the NTS, DMV, and RVLM. These direct cortical projections to the NTS/DMV provide the anatomical basis for cortical influences on both the baroreceptor reflex and cardiac parasympathetic control (Zamrini et al. 1990). These connections also display an ipsilateral predominance.

The neurons of the NTS, DMN, and nucleus ambiguus also send projection fibres to the preganglionic sympathetic neurons in the IML and to other brainstem nuclei that modulate sympathetic outflow (Lane & Jennings 1995). The right and left vagal projections demonstrate an asymmetric distribution with the right vagal projections innervating some aspects of the anterior right and left ventricles and the left vagal projections innervating the posterior lateral aspects of the ventricles. However, the predominant innervation of the vagal projections terminates on the atrial aspects of the heart and include the sinus (SA) node, which usually determines the rate of the heartbeat. The influence of the vagal projections on the ventricles appears to be limited to counteracting the sympathetic innervation (Rardon & Bailey 1983).

Sympathetic innervation of the heart can be separated into left and right sympathetic limbs, based on physiological studies. The right postganglionic sympathetic projections arising from the paravertebral sympathetic ganglia including the stellate ganglia course to the heart and innervate the atria and the anterior surfaces of the right and left ventricles. The left sympathetic projections have a more posterior lateral distribution and innervate the atrioventricular (AV) node and the left ventricle (Levy et al. 1966; Randall & Ardell 1990). Stimulation of the sympathetic projections results in different physiological effects on the heart. Stimulation of the right stellate ganglia produces mainly chronotropic effects such as increases in heart rate, and stimulation of the left stellate ganglia mainly results in inotropic effects such as altered contractility, changes in rhythm, and increase in systemic blood pressure (Levy et al. 1966; Rogers et al. 1978) (Fig. 8.11). Increased stimulation to either or both ganglia results in a decreased fibrillation threshold (Schwartz 1984; Swartz et al. 1994). With respect to cortical control of cardiovascular function, the research suggests that asymmetries in brain function can influence the heart through ipsilateral pathways. It is quite clear that stimulation or inhibition at various levels on the right side of the neuraxis results in greater changes in heart rate, while increased sympathetic tone on the left side of the neuraxis results in a lowered ventricular fibrillation threshold. This occurs because parasympathetic mechanisms are dominant in the atria, while sympathetic mechanisms are dominant in the ventricles (Lane et al. 1992).

Figure 8.11 This figure outlines the autonomic innervation to the heart. The different projection patterns of the left and right nerve supplies may explain the different clinical findings of right and left autonomic dystonia.

Innervation of the urinary bladder

The innervation of the bladder is complex. Afferent sympathetic fibres emerge from the muscle tissue of the bladder, the detrusor muscle, and course through the hypogastric nerve to the upper lumbar sympathetic ganglia. They then course with the posterior nerve roots to the IML neurons at the levels T9–L2 in the spinal cord. These fibres probably transmit proprioceptive and nociceptive information from the bladder. Efferent sympathetic fibres project from the IML neurons at the levels T11–12 and course with the white rami to the hypogastric plexus where they synapse and join the hypogastric nerve to reach the detrusor muscle and internal sphincter of the bladder. Excitation of these fibres results in contraction of the internal sphincter muscle and inhibition of the detrusor muscle. Parasympathetic innervation involves both afferent and efferent projections. The afferent projections arise from the bodies of the detrusor and internal sphincter muscles and course with the pudendal nerve to the S2–4 posterior nerve roots, terminating in the anterolateral grey areas of the spinal cord at these levels. These fibres probably carry proprioceptive, nociceptive, touch, temperature, and muscle stretch information from the bladder tissues. The efferent parasympathetic fibres pass from the S2–4 segments of the spinal cord to the hypogastric plexus where they synapse and project to the detrusor and internal sphincter muscles. Excitation of these fibres results in excitation of the detrusor and inhibition of the internal sphincter muscles.

The external sphincter is innervated by the pudendal nerve, which arises from the anterior horns of the S2–4 spinal roots. These fibres are under voluntary control and excitation results in contraction of the external sphincter muscle. Afferent fibres carried by the pudendal nerve relay proprioceptive and nociceptive information from the external sphincter muscle and posterior urethra.

Cortical control over micturition also exists. Areas in the paracentral lobule of the cortex evoke excitation of bladder contractions; this may play a role in the voluntary control over micturition (Chusid 1982) (Fig. 8.12).

Figure 8.12 This diagram outlines the anatomy and nerve pathways involved with penile and clitoral erection.

The sympathetic nerves to the detrusor muscle have little or no action on the smooth muscle of the bladder wall and are mainly distributed to the blood vessels. In the male, sympathetic activation results in contraction of the sphincter and bladder neck during ejaculation in order to prevent seminal fluid from entering the bladder. Urination is brought about by activation of the parasympathetic system that results in contraction of the detrusor muscle and relaxation of the internal sphincter along with voluntary relaxation of the external sphincter through cortical stimulus.

Referred visceral pain

Since most of the viscera is only innervated by autonomic projections, afferent autonomic nerve pathways must relay nociceptive, temperature, and proprioceptive information back to the central nervous system. Usually, visceral pain is poorly localised and difficult to qualitatively describe. Frequently, information transferred by afferent autonomic fibres is perceived in other areas of the body also innervated by the same segmental levels. This phenomenon is called referred pain. Certain areas of the body have been consistently identified with referred pain from specific organs. These are referred to as referred pain patterns (Fig. 8.13).

Figure 8.13 This figure outlines the referred pain patterns from a variety of organs.

What components of the neurological, physical, or orthopaedic examinations allow one to gain information about autonomic function? Complete examination techniques are covered in Chapter 4. However, due to the importance of the autonomic examination in determining the functional state of the neuraxis the autonomic examination is reviewed again here.

Ophthalmoscopy – vein to artery (V:A) Ratio and vessel integrity

Ophthalmoscopy is useful for assessing the vascularity of the optic disc and retina. This should accompany measurement of the blind spot size, as changes in the morphology of the optic disc and peripapillary region of the retina could explain the shape or size of the blind spot. Changes that occur before and after an adjustment or other activity are functional in nature.

The V:A ratio refers to the difference in size of the veins and arteries that branch from the central retinal artery. A large difference may be due to increased sympathetic output, which causes greater peripheral resistance and constriction of arteries. The condition of blood vessels can also be helpful as an indicator of cerebrovascular integrity (Figs 8.14 and 8.15).

Figure 8.14 This figure illustrates the concept of the vein to artery ratio (V:A ratio) in the arteries of the retina. A normal ratio is 1.5:1 which indicates that the vein is slightly larger than the artery. If the V:A ratio increases it may mean the vein has expanded or the artery has contracted. A common cause of an increased V:A ratio is sympathetic overactivation.

Figure 8.15 This figure demonstrates the normal anatomy of the retina.

Nystagmus can also be detected very easily.