The act of micturition is both reflex and voluntary. When the normal person desires to void, there is first a voluntary relaxation of the perineum, followed sequentially by an increased tension of the abdominal wall, a slow contraction of the detrusor, and an associated opening of the internal sphincter; finally, there is a relaxation of the external sphincter (Denny-Brown and Robertson). It is useful to think of the detrusor contraction as a spinal stretch reflex, subject to facilitation and inhibition from higher centers. Voluntary closure of the external sphincter and contraction of the perineal muscles cause the detrusor contraction to subside. The abdominal muscles have little role in initiating micturition except when the detrusor muscle is not functioning normally. The voluntary restraint of micturition is a cerebral affair and is mediated by fibers that arise in the frontal lobes (paracentral motor region), descend in the spinal cord just anterior and medial to the corticospinal tracts, and terminate on the cells of the anterior horns and intermediolateral cell columns of the sacral segments, as described earlier. The coordination of detrusor and external sphincteric function depends mainly on the descending pathway from the posited centers in the dorsolateral pontine tegmentum.
Regulation of Bowel Function
The colon and anal sphincters are obedient to the same principles that govern bladder function. Unique to the bowel, however, is an intrinsic enteric nervous system that originates in the myenteric (or Auerbach) plexus and the submucosal plexus (of Meissner), located in the gut wall. The first stimulates smooth muscle and the latter also regulates mucosal secretion and blood flow. This embedded system controls peristalsis largely independent of other autonomic influences but is highly responsive to local chemical and mechanical stimuli. As outlined in the thorough review by Benarroch that should be consulted by interested readers, acetylcholine is the dominant neurotransmitter in the enteric nerves but nitric oxide and numerous peptide transmitters are found in profusion.
The autonomic nervous system and the adrenal glands were accepted for many years as the neural and humoral basis of all instinctive and emotional behavior. In states of chronic anxiety and acute panic reactions, depressive psychosis, mania, and schizophrenia, all of which are characterized by an altered emotionality, no consistent autonomic or endocrine dysfunction has been demonstrated except perhaps for diminished responses of growth hormone in panic disorders. The lack of cortisol suppressibilty by injection of adrenocorticotropic hormone (ACTH) had for some time also been considered to be a consistent aspect of depressive illnesses but that too, has not been entirely specific. This has been disappointing, as the emergency theory of sympathoadrenal action provided by
Cannon was such a promising concept of the neurophysiology of acute emotion, and Selye had extended this theory so plausibly to explain all the reactions to stress in animals and humans.
According to these theories, strong emotion, such as anger or fear, excites the sympathetic nervous system and the adrenal cortex (via corticotropin-releasing factor [CRF] and ACTH), which are under direct neural and endocrine control. These sympathoadrenal reactions are brief and sustain the animal in “flight or fight” as discussed in Chap. 24. Animals deprived of adrenal cortex or human beings with Addison disease cannot tolerate stress because they are incapable of mobilizing both the adrenal medulla and adrenal cortex. Prolonged stress and production of ACTH activates all the adrenal hormones (glucocorticoids, mineralocorticoids, and adrenocorticoids) and has been studied extensively in relation to immune reactions and other systemic functions but with no consistent findings that are yet clinically applicable.
Tests for Abnormalities of the Autonomic Nervous System