The axons themselves contain a complex internal microtubular apparatus for maintaining the integrity of their membranes and for transporting substances such as neurotransmitters over long distances between the nerve cell body and the distant reaches of the nerve fiber. As discussed in Chap. 7 the long axons of sensory nerves can properly be considered to be dendrites but we use the term “axon” in this and other chapters to denote all the neuronal processes of peripheral enrves. Nerve fibers (axons) are coated with short segments of myelin of variable length (250 to 1,000 µm), each of which is enveloped by a Schwann cell and its membrane that constitute the myelin sheath. In fact, the PNS may be accurately defined as the part of the nervous system that is invested by the cytoplasm and membranes of Schwann cells. Each myelin segment and Schwann cell has a symbiotic relationship to the axon but is morphologically independent. The structure of the axonal membrane in the gaps between segments of the myelin sheaths (nodes of Ranvier) is specialized, containing a high concentration of sodium channels and permitting the saltatory electrical conduction of nerve impulses as described in Chap. 2. Unmyelinated fibers, more numerous in peripheral nerves than myelinated ones, also arise from cells in dorsal root and autonomic ganglia. Small bundles of these naked (unmyelinated) axons are enveloped by a single Schwann cell; delicate tongues of Schwann cell cytoplasm partition these bundles and separate individual axons. Each sensory nerve fiber terminates in a specialized ending which is designed to be especially sensitive to certain natural stimuli as discussed in Chaps. 7 and 8.
The features described previously enable one to conceptualize the possible avenues by which disease may affect the peripheral nerves. Pathologic processes may be directed at any one of the several groups of nerve cells whose axons constitute the nerves, that is, the cells of the anterior or lateral horns of the spinal cord, the dorsal root ganglia, or the sympathetic and parasympathetic ganglia. Each of these cell types exhibits specific vulnerabilities to disease, and if destroyed—as, for example, the motor nerve cells in poliomyelitis—there is secondary degeneration of the axons and myelin sheaths of the peripheral fibers of these cells. Neuropathic symptoms are also induced by alterations of function and structure of the ventral and dorsal columns of the spinal cord, which contain the fibers of exit and entry of anterior horn and dorsal root ganglion cells, respectively. The myelin of these centrally located fibers is constituted differently from that of the peripheral nerves, being enveloped by oligodendrocytes rather than Schwann cells and the nerve fibers are supported by astrocytes rather than fibroblasts.
Because of the intimate relation of the nerve roots to the CSF and to specialized arachnoidal cells (the arachnoidal villi), a pathologic process in the CSF or leptomeninges may damage the exposed spinal roots. Diseases of the connective tissues affect the peripheral nerves that lie within their sheaths. Diffuse or localized arterial diseases may injure nerves by occluding their nutrient arteries. In a large category of immune-mediated neuropathies, the damage is the result of a cellular or humoral attack on various components of myelin. A subset of these is characterized by the binding of circulating antibodies to the specialized regions at the nodes of Ranvier, causing a block of electrical conduction. A complement-dependent humoral immune reaction against the radicular or peripheral axon is also known. Toxic or immunologic agents that selectively damage the Schwann cells or their membranes cause demyelination of peripheral nerves, leaving axons relatively intact, or a toxin may specifically affect axons and dendrites by poisoning their cell bodies, the axolemma, or the lengthy and complex axonal transport apparatus.