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from Section B2 - Vegetative and autonomic dysfunctions
Published online by Cambridge University Press: 04 August 2010
That “humans absolutely require a functionally intact sympathetic nervous system to tolerate the ‘nonemergency’ 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.
Anatomy and physiology
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).
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