Department of Rehabilitation Medicine, Columbia University College of Physicians & Surgeons, New York, USA
That "humans absolutely require a functionally intact sympathetic nervous system to tolerate the 'non-emergency' behavior of simply standing up" is testimony to the importance of the autonomic nervous system (ANS) and although orthostatic intolerance is the hallmark of sympathetic neurocirculatory failure it is but one manifestation among many of autonomic dysfunction (Goldstein et al., 2002). Clinical manifestations of ANS dysfunction can result from the disordered autonomic control of the cardiovascular, sudomotor, alimentary, urinary, and sexual systems. The etiology of autonomic dysfunction may be primary, such as pure autonomic failure (PAF), secondary, such as that due to cervical spinal cord injury (SCI) or due to drugs and chemical toxins (Mathias, 2003). An understanding of the components of the ANS, their function and their supraspinal, spinal and peripheral organization is essential to appreciate autonomic dysfunction. Additionally, the disturbance of ANS function such as that seen in persons with cervical SCI results not only from the loss of normal supraspinal control of the ANS, but also from changes caused by synaptic reorganization and neuronal plasticity in the damaged spinal cord.
The ANS has three peripheral components (the sympathetic, parasympathetic, and enteric nervous systems) and a supraspinal and spinal organization that is essential to its regulation of visceral function and maintenance of internal homeostasis. The control systems of the ANS involve: (1) supraspinal controlling and integrative neuronal centers;
(2) supraspinal, spinal, ganglionic, and peripheral interneurons; and (3) afferent neurons (Shields Jr., 1993). Afferent neurons have cell bodies in the dorsal root ganglia or cranial nerve somatic sensory ganglia. The sympathetic and parasympathetic nerves form an efferent pathway comprised of preganglionic and postganglionic neurons (Fig. 24.1). The second-order postganglionic neurons synapse upon smooth and cardiac muscle and also control glandular secretion. Norepinephrine (NE) is the main chemical messenger of the sympathetic nervous system and Acetylcholine (Ach) is the main messenger of the parasympathetic nervous system. Ach is also the neurotransmitter for all pregan-glionic axons, both parasympathetic and sympathetic. Thermoregulatory sweating is mediated by sympathetic postganglionic axons that release Ach (Shields Jr., 1993).
Ach receptors are of two types, muscarinic and nicotinic. Preganglionic axons synapse upon nicotinic receptors and postganglionic axons synapse upon muscarinic receptors. There are five identified subtypes of muscarinic receptors (M1-M5) involved in peripheral and central cholinergic responses (Table 24.1) (Gainetdinov and Caron, 1999). In mice, cholin-ergic contraction of smooth muscle is mediated primarily by the M3 subtype with a small contribution mediated by the M2 subtype (about 25% and 5% of the cholinergic contractility in the ileum longitudinal muscles and the detrusor muscles, respectively) (Takeuchi et al., 2004). M2/M3 knockout mice show virtually no cholinergic contraction of the ileal longitudinal smooth muscles in vitro yet maintain coordinated peristalsis suggesting that peristaltic movements can be maintained by local mediators
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