Which part of the autonomic nervous system can be called a craniosacral system?

Sympathetic and Parasympathetic Innervation

Isolated fetal cardiac tissue has a lower threshold of response to the inotropic effects of norepinephrine than adult cardiac tissue and is more sensitive to norepinephrine throughout the dose-response curves.16 Because isoproterenol, a direct β-adrenergic agonist that is not taken up and stored in sympathetic nerves, has similar effects on fetal and adult myocardium, the supersensitivity of fetal myocardium to norepinephrine is probably the result of incomplete development of sympathetic innervation in fetal myocardium. Myocardial concentrations of norepinephrine in the fetus within several weeks of term are significantly lower than in newborn animals, and activity of tyrosine hydroxylase, the intraneuronal enzyme responsible for the first transformation in catecholamine biosynthesis, is also reduced.16 In contrast, adrenal gland tyrosine hydroxylase activity at the same gestational age is not suppressed, possibly because the decrease in myocardial activity is related to delayed sympathetic innervation rather than to a generalized immaturity.

Monoamine oxidase, the enzyme responsible for oxidative deamination of norepinephrine, is also present in lower concentrations in the fetal heart than in the adult. Histochemical evaluation of the development of sympathetic innervation using the monoamine fluorescence technique has further substantiated the delayed development of sympathetic innervation of the fetal myocardium. At term, sympathetic innervation is incomplete. Patterns of staining indicate a progression of innervation, starting at the area of the sinoatrial node and progressing toward the left ventricular apex.25,26

Although sympathetic nervous innervation appears to begin developing in the fetal heart by about 0.55 of term, β-adrenergic receptors seem to be present much earlier and can be stimulated by appropriate agonists before 0.4 of term.27 Before about 0.55 of term (80 days of gestation in the lamb), fetal myocardium may be affected by circulating catecholamines, but local reflex activity through the sympathetic nervous system is not likely to play a major role in circulatory regulation.

Vagal stimulation at about 0.85 of term produces bradycardia. Administration of atropine at 0.55 of term produces a modest increase in fetal heart rate,28 indicating that vagal innervation is present by this stage of development. Histochemical staining for acetylcholinesterase in close-to-term fetuses has shown that the concentrations of this enzyme, which is responsible for metabolism of acetylcholine, are similar to concentrations found in adults.

1.4 Parasympathetic system

Parasympathetic nervous system consists of the cranial and the sacral components (Purkayastha et al., 2013). The cell bodies of parasympathetic preganglionic fibers are located in the ganglia associated with oculomotor, facial, glossopharyngeal and vagus nerves and in the spinal cord segments S2–S4. The vagus nerve is the largest part of parasympathetic division that provides a wide parasympathetic outflow to the thoracal, abdominal and pelvic viscera. Preganglionic parasympathetic fibers associated with the oculomotor nerve originate from the Edinger-Westphal nucleus in the midbrain, synapse in the ciliary ganglion and innervate the ciliary muscle and the pupiloconstrictor fibers of iris. Preganglionic parasympathetic fibers from the superior salivatory nucleus located in the pons are associated with the facial nerve. Preganglionic fibers travel with the greater petrosal nerve, synapse in the pterygopalatine ganglion and extend within the maxillary nerve to regulate secretomotor function of the lacrimal, nasal and palatine glands. Other fibers from the superior salivatory nucleus leave with the chorda tympani, join the lingual nerve, synapse in the submandibular ganglion and provide inputs to the submandibular and the sublingual glands. Inferior salivatory nucleus in the upper medulla gives rise to the fibers associated with the lesser petrosal nerve, a branch of glossopharyngeal nerve, that synapse in the otic ganglion and provide postganglionic projections to the parotid gland. The vagus nerve originates from the dorsal motor nucleus of vagus in medulla. In contrast to the cranial parasympathetic ganglia, ganglia of the vagus nerve are located near or within the target organs; thus, postganglionic fibers are very short. Given its wide distribution, the vagus nerve is represented in various thoracal, abdominal and pelvic plexuses including myenteric plexus of the gastrointestinal tract. The vagus and the glossopharyngeal nerves contain a significant proportion of afferent fibers that carry impulses of the blood vessel wall tone to the NTS and contribute to the baroreflex.

Sacral parasympathetic outflow arises from the S2 to S4 segments of the spinal cord and via the pelvic splanchnic nerves innervates the smooth rectal muscles, the bladder detrusor, the internal urethral sphincter and the reproductive organs (Hamill et al., 2012).

Parasympathetic Nervous System

Although the role of the parasympathetic nervous system in the control of ureteral peristalsis has not been well defined, muscarinic cholinergic receptors have been demonstrated in the ureter of a number of species including the human (Hernández et al., 1993;Latifpour et al., 1989, 1990;Sakamoto et al., 2006). There are five cloned muscarinic subtypes: M1 to M5. The excitatory muscarinic receptors, M1, M3, and M5, work through an excitatory G protein, Gq, and increase intracellular calcium by generating 1-, 4-, 5-trisphosphate (IP3) and 1-, 2-DG. The inhibitory muscarinic receptors, M2 and M4, work through an inhibitory G protein, Gi, with inhibition of adenylyl cyclase (van Koppen and Kaiser, 2003;Wu et al., 2000). Carbachol induced contractile responses are primarily mediated via the M3 receptor subtype (Tomiyama et al., 2003b). It has been suggested that M2 receptor activation may inhibit smooth muscle relaxation that results from activation of adenylyl cyclase (Hegde et al., 1997). There is a higher density of M2 than M3 muscarinic receptors in the human ureter (Sakamoto et al., 2006).

Acetylcholinesterase-positive nerve fibers have been demonstrated in the equine ureter (Prieto et al., 1994). The cholinergic innervation is especially rich in the distal and intravesical ureter (Hernández et al., 1993). Furthermore, ACh has been shown to be released from isolated guinea pig, rabbit, and human ureters in response to electric field stimulation (Del Tacca, 1978), and this release is inhibited by the neural poison tetrodotoxin. These data suggest, but do not prove, that the parasympathetic nervous system has at least a modulatory role in the control of ureteral activity.

The prototypic cholinergic agonist is ACh, which serves as the neurotransmitter at (1) neuromuscular junctions of somatic motor nerves (nicotinic sites); (2) preganglionic parasympathetic and sympathetic neuroeffector junctions (nicotinic sites); and (3) postganglionic parasympathetic neuroeffector sites (muscarinic sites). ACh synthesis involves

Acetyl CoA+Choline→acetyltransferasecholineACh

where CoA is coenzyme A. The ACh is stored in vesicles within the synaptic terminal; its release depends on the influx of Ca2+ into the terminal, which presumably causes vesicle fusion with the presynaptic terminal membrane, thereby expelling ACh into the synaptic cleft. ACh subsequently is hydrolyzed by acetylcholinesterase. The muscarinic effects of cholinergic agonists can be blocked by atropine. The effects of nicotinic agonists can be blocked by nondepolarizing ganglionic blocking agents or by high concentrations of the nicotinic agonist, which may cause ganglionic blockade by desensitization of receptor sites after an initial period of ganglionic stimulation.

Parasympathetic Nervous System and Immunity

The parasympathetic nervous system both sends immune signals to the CNS through the afferent fibers of the vagus nerve and modulates immune responses regionally through efferent fibers of the vagus nerve. Ganglia outside the spinal cord receive projections from the brainstem and further innervate visceral organs, such as the heart, lungs, gut, liver, and spleen. IL-1 receptors on paraganglia cells located adjacent to parasympathetic ganglia bind IL-1 and activate the vagus nerve, thus signaling the presence of peripheral inflammation to the brain.129-131 Inflammation in the gut or peritoneum leads to the inflammatory reflex, which results in the release of acetylcholine from efferent vagus nerve fibers and negative feedback control of inflammation.40 Cutting the vagus nerve prevents immune signaling to the brain and therefore prevents further activation of cholinergic brainstem regions.40,132,133 Acetylcholine is the primary parasympathetic neurotransmitter, which binds to two receptor subtypes, nicotinic and muscarinic cholinergic receptors, each of which consist of several different subunits that heterodimerize to provide cell and tissue specificity of cholinergic effects. Immune cells contain both receptors, but the α7 subunit of the nicotinic receptors specifically mediates cholinergic antiinflammatory effects in macrophages.

Neural Control

The parasympathetic nervous system is the most important determinant of bronchomotor tone and when activated can completely obliterate the lumen of small airways. Both afferent and efferent nerve fibers travel via the vagus nerve (X) with efferent ganglia in the bronchial walls. Afferent nerves arise from receptors under the tight junctions of the bronchial epithelium and respond either to noxious stimuli acting directly on the receptors or to cytokines released by cellular mechanisms such as mast cell degranulation. Efferent nerves release acetylcholine, which acts at M3 muscarinic receptors to cause contraction of airway smooth muscle, while also stimulating M2 prejunctional muscarinic receptors to exert negative feedback on acetylcholine release. Stimulation of any part of the reflex arc results in bronchoconstriction. Some degree of resting tone is normally present and therefore permits a small degree of bronchodilation when vagal tone is reduced in a similar fashion to vagal control of heart rate.2

In contrast to the parasympathetic system, the sympathetic system is poorly represented in the lung and not yet proven to be of major importance in humans. Indeed, it appears unlikely that there is any direct sympathetic innervation of airway smooth muscle.

The airways are provided with a third autonomic control system, the nerves of which are neither adrenergic nor cholinergic, and are referred to as noncholinergic parasympathetic nerves (Fig. 29.1).2 This is the only potential bronchodilator nervous pathway in humans, though the exact role of these nerves remains uncertain. The efferent fibers run in the vagus nerve and pass to the smooth muscle of the airways where they cause slow (minutes) and prolonged relaxation of bronchi. The major neurotransmitter is vasoactive intestinal peptide, which produces airway smooth muscle relaxation by promoting production of nitric oxide (NO). How NO relaxes airway smooth muscle is not as fully understood as its effect on vascular smooth muscle, but resting airway tone does seem to involve NO mediated bronchodilation.

The parasympathetic nervous system

The PNS is comprised of cranial and sacral components that cause constriction of the pupils, decreases in heart rate and volume, bronchoconstriction, increase in peristalsis, sphincter relaxation, and glandular secretion, whilst the pelvic component inhibits the detrusor muscle of the bladder (Craven 2008).

The cranial outflow is conveyed to the oculomotor nerve (III), facial nerve (VII), glossopharyngeal nerve (1X), and vagal nerves (X). Knowledge of the neural innervation and response of the PNS and SNS is essential for any proposed manual intervention. The insidious nature of thoracic pain and the associated postural dysfunction and stress (DeFranca & Levine 1995) may predispose the ganglion to mechanical pressure (Bogduk 1986), ischaemia (Conroy & Schneiders 2005), and somatic dysfunction via the CNS (Shaclock 1999).

Central pain mechanisms are deeply embodied in the psychophysical problem of pain, and are becoming increasingly recognized as playing a major role in the generation and maintenance of pain and disability associated with neuromusculoskeletal problems. Central mechanisms participate in all pain states, both acute and chronic. They are universally influenced by psychological and physical factors, whether or not a specific pathology can be identified. Common misconceptions that arise are that manual therapy operates on peripheral mechanisms without influencing the central ones and that, when a central problem exists, psychological management is preferable. In reality, as key players in the healing process, central mechanisms are profoundly affected by manual therapy even when it is directed at a peripheral problem. Treatment of peripheral mechanisms can be performed through central techniques because both peripheral and central mechanisms are always part of the same clinical problem. Consequently, manual therapy must integrate central mechanisms into clinical practice as a means of improving therapeutic efficacy and to prevent the descent of acute pain into chronic pain. Hendler (2002) suggested that 25–75% of cases of misdiagnosed complex regional pain syndrome type I (CRPS1) are actually upper extremity nerve entrapment affected more often by the scalenes and pectoralis minor muscles. Given the mounting evidence that chronic muscle pain syndromes may be sympathetically driven or maintained, it may be pertinent that chronic thoracic pain should be approached from the hypothetical perspective of muscle spindles under constant sympathetic excitation, meaning that the term ‘sympathetic intrafusal tension syndrome’ should replace myofascial pain syndrome as the appropriate description (Berkoff 2005) (Table 6.2).

Uncovering stressful condition-stimuli and evaluating their potential clinical relevance is vital. Relaxation, breathing, biofeedback, and cognitive behaviour therapy techniques are all useful in the management of increased sympathetic sensitivity. Here, the management of physical measures to alleviate pain and discomfort must be integrated in a multidisciplinary manual and biopsychosocial approach; a purely biomedical approach to physical therapy is too reductionist. Therapy needs to shift from symptomatic treatment to an emphasis on education, rehabilitation, facilitation of ownership, personal responsibility, and continuing management (CSAG 1994), in order to achieve longer lasting results and restoration of function.

The onset of acute chest pain, which may be very distressing for patient and family, is a major health problem in the Western world, and the most common reason for hospital admissions (McCaig & Nawar 2004). In over 50% of cases, the aetiology appears to be non-cardiac (Chambers et al 1999; Eslick et al 2001) and often no definitive diagnosis can be made (Panju et al 1996). Many thoracic dysfunctions have a mechanical cause originating from the T-spine, and referring to the upper extremities, chest, and cervical and lumbar spine, together with reverse referral patterns (Lee 2003; Proctor et al 1985; Wickes 1980).

The heart, pleura, and oesophagus are all potential generators of visceral pain in the T-spine. Sensory fibres from cardiac and pulmonary structures are routed through T1 to T4 and T5. Irritable bowel syndrome (IBS) is accompanied by altered visceral perception and back pain (Accarino et al 1995; Zighelboim et al 1995), and patients often demonstrate visceral and cutaneous hyperalgesia via viscerosomatic neurons (Tattersal et al 2008). The overlap between fibromyalgia syndrome (FMS) and IBS is considerable, with 70% of patients with FMS reporting chronic visceral pain and 65% of those with IBS having primary FMS (Veale et al 1991).

Chronic visceral pain syndromes are more common in women than men and manifest such conditions as abdominal pain, migraine, and FMS (Table 6.3), reflecting the influence of hormonal factors on the algesic response both peripherally and centrally. The direct effect of oestrogen, progesterone, and testosterone on organ function, and psychological and social factors cannot be underestimated within the assessment process (Giamberardino 2000; Heitkemper & Jarrett 2001).

Recent findings have indicated that spinal manual therapy produces concurrent hypoalgesia and sympathoexcitatory effects (Sterling et al 2001). Therefore it is pertinent that, with regard to patients exhibiting sympathetically maintained pain or increased hypersensitivity of the SNS, manual mobilization may indeed add to both hypersensitivity and pain pattern. Thus great care should be taken in both the examination of and intervention in any hypersensitive thoracic states.

Heart Rate

Sympathetic and parasympathetic nervous system influences underlie the cardiovascular system's first response to exercise—an increase in heart rate. Sympathetic outflow to the heart and systemic blood vessels increases while vagal outflow decreases. Vagal withdrawal is responsible for the initial change of 10 to 30 beats per minute, and the remainder is thought to be largely sympathetically mediated. Of the two major components of cardiac output, heart rate and stroke volume, heart rate is responsible for most of the increase in cardiac output during exercise, particularly at higher levels. Heart rate increases linearly with workload and oxygen uptake. Increases in heart rate occur primarily at the expense of diastolic, not systolic, time. Thus, at very high heart rates, diastolic time may be so short as to preclude adequate ventricular filling.

The heart rate response to exercise is influenced by several factors, including age, type of activity, body position, fitness, the presence of heart disease, medications, blood volume, and environment. Of these, the most important factor is age; a decline in maximal heart rate occurs with increasing age. This decline appears to be due to intrinsic cardiac changes rather than to neural influences. It should be noted that there is a great deal of variability around the regression line between maximal heart rate and age; thus age-related maximal heart rate is a relatively poor index of maximal effort (see Chapter 5). Maximal heart rate is unchanged or may be slightly reduced after a program of training. Resting heart rate is frequently reduced after training as a result of enhanced parasympathetic tone.

The parasympathetic nervous system

The neurones of the parasympathetic nervous system leave the central nervous system with the third, seventh, ninth and tenth cranial nerves, and the second and third sacral nerves. This branch is also called the craniosacral outflow. In this case the postganglionic fibres are close to the organ being supplied, and not the vertebral column.

The parasympathetic becomes active when the individual is in the relaxed state, and tends to work in the opposite manner to the sympathetic. Each branch which leaves with a cranial nerve has a specific effect. The oculomotor (III) constricts the pupil and controls accomodation for near vision. The facial (VII) stimulates the production of tears by the lacrimal duct, and with the glossopharyngeal (IX), saliva from the salivary glands. The vagus (X) supplies a large number of organs. It slows the heart, constricts the coronary blood vessels and bronchial muscles and stimulates the secretion of the gastric glands and the peristaltic contraction of the gut and the gall bladder. Those branches leaving with the sacral nerves contract the urinary bladder, relax the anal and urethral sphincters and cause vasodilatation in the genitalia. The parasympathetic is therefore active in the digestive processes, micturition and defaecation, and sexual activities, all of which are best suited to a state of relaxation.

Is the sympathetic nervous system considered craniosacral?

What is the name of the ganglia associated with the craniosacral division of the autonomic nervous system?

Is cranial sympathetic or parasympathetic?

Which nervous system is also called the craniosacral nervous system quizlet?