2.6 ANS

Sympathetic Division The anatomy of the sympathetic division is such that it can function better as a mass unit. Parasympathetic Division The parasympathetic division, in contrast, comprises relatively independent components

Pre-ganglionic myelinated efferents from the hypothalamus, medulla oblongata and spinal cord leave the cord with the ventral nerve roots of the first thoracic nerve down to the second, third and, in some subjects, the fourth lumbar spinal nerves (T1–L2–4). These efferents pass via the white rami communicantes to synapse in the sympathetic ganglia lying in the paravertebral sympathetic trunk, which is closely related throughout its length to the spinal column.

They synapse with post-ganglionic neurons, usually non-myelinated, some of which pass directly to viscera. Others pass back via the grey rami communicantes to rejoin the spinal nerves with which they travel to their effector sites. A number of preganglionic fibres (from T5 and below) synapse in collateral ganglia which are close to the viscera that they innervate. These collateral ganglia include the coeliac ganglion (receiving fibres from the greater and lesser splanchnic nerves) and the superior and inferior mesenteric ganglia. The adrenal medulla is innervated directly by pre-ganglionic fibres via the splanchnic nerves, which pass without relay through the coeliac ganglion.

The sympathetic supply to the head originates from three structures: the superior cervical ganglion, the middle cervical ganglion and the stellate ganglion. Distribution of the sympathetic supply to the viscera occurs via a series of sympathetic plexuses. The main three are the cardiac, the coeliac and the hypogastric plexuses The segmental sympathetic supply to the head and neck is from T1 to T5, to the upper limb from T2 to T5, to the lower limb from T10 to L2 and to the heart from T1 to T5.

The parasympathetic nervous system has a cranial and a sacral outflow. The cranial efferents originate in the brain stem and travel with the third (oculomotor), seventh (facial) and ninth (glossopharyngeal) cranial nerves. These pass via the ciliary, sphenopalatine, submaxillary and otic ganglia to subserve parasympathetic function in the head. The most important cranial efferent is the tenth (vagus) cranial nerve, which supplies the thoracic and abdominal viscera. Its fibres synapse with short post-ganglionic neurons that are on or near the effector organs.

The sacral outflow originates from the second, third and fourth sacral spinal nerves to supply the pelvic viscera. As with the vagus nerve, the fibres synapse with short post-ganglionic neurons that are close to the effector organs.

These mediate the afferent arc of autonomic reflexes and conduct visceral pain stimuli. The vagus has a substantial visceral afferent component, the importance of which is well recognized by anaesthetists who commonly have to deal with vagally mediated bradycardia or laryngeal spasm. Sympathetic afferent fibres are also involved in the transmission of visceral pain impulses, including those originating from the myocardium. This is the rationale for using stellate ganglion block to treat refractory angina pectoris. Sympathetic afferents are also involved in sympathetically maintained pain states such as the complex regional pain syndrome. There is usually no direct communication between afferent neurons and sympathetic post-ganglionic fibres, but following injury there is some form of sympathetic–afferent coupling

Sympathetic: acetylcholine is the neurotransmitter at sympathetic pre-ganglionic fibres (at nicotinic receptors). Noradrenaline is the neurotransmitter at most postganglionic fibres, apart from those to sweat glands and to some vasodilator fibres in skeletal muscle.
Parasympathetic: acetylcholine is the neurotransmitter throughout the parasympathetic division, acting at nicotinic receptors in autonomic ganglia, and at muscarinic post-ganglionic receptors thereafter.

conditions such as diabetes, chronic alcoholism, nutritional deficiency, Guillain–Barré syndrome, Parkinson’s disease and AIDS. . Rarely, it is seen as a primary condition in the Shy–Drager syndrome or familial dysautonomia Its clinical features include disordered cardiovascular responses and orthostatic hypotension, the absence of sinus arrhythmia and inability to compensate during the Valsalva manoeuvre.

Patients may complain of flushing, erratic temperature control with night sweats, episodic diarrhoea and nocturnal diuresis. The normal response to hypoglycaemia is lost, as are normal diurnal rhythms. A more recently identified form of autonomic dysfunction is the postural orthostatic tachycardia syndrome (POTS), treated by a high-salt diet and in more severe cases with mineralocorticoids.

Examples include lumbar sympathectomy, stellate ganglion block, and coeliac plexus block. Chemical or surgical sympathectomy has been used to improve the blood supply in vasospastic or atherosclerotic disorders of the peripheral circulation, to control hyperhidrosis and to treat pain associated with myocardial ischaemia. Sympathetic blocks also have a place in the management of sympathetically maintained pain (see under ‘Complex Regional Pain Syndrome’ in Chapter 3), although much of the evidence shows them to be no more effective than placebo.

the nerve distributes widely, hence its name; the word ‘vagus’ comes from the Latin, meaning ‘wandering’. (Had it been derived instead from Greek, then the nerve – improbably – would have been called the ‘plankton’). Sources of stimulation that can lead to bradycardia and sometimes to asystolic cardiac arrest include the dura, the zygoma, the extraocular muscles – particularly the medial rectus – the carotid sinus, the pharynx, the glottis, the bronchial tree, the heart, the mesentery and peritoneum, the bladder and urethra, the testis, and the rectum and anus. The Brewer–Luckhardt reflex describes laryngospasm that is provoked by a distant stimulus. Vagal reflexes can be attenuated by the use of an anticholinergic such as atropine, but in low doses this paradoxically can stimulate the vagus before it blocks it (the Bezold–Jarisch reflex).

In some pain syndromes, it appears that efferent noradrenergic sympathetic activity and circulating catecholamines have a role in maintaining chronic pain. There is usually no communication between sympathetic efferent and afferent fibres, but following nerve injury it is apparent that modulation of nociceptive impulses can occur not only at the site of injury but also in distal undamaged fibres and the dorsal root ganglion itself around which sympathetic axons may proliferate (see under ‘Chronic Regional Pain Syndrome’ in Chapter 3).