Figure 43-1. Diagram showing the relationships of the peripheral nerve sheaths to the meningeal coverings of the spinal cord. The epineurium (EP) is in direct continuity with the dura mater (DM). The endoneurium (EN) remains unchanged from the peripheral nerve and spinal root to the junction with the spinal cord. At the subarachnoid angle (SA), the greater portion of the perineurium (P) passes outward between the dura mater and the arachnoid (A), but a few layers appear to continue over the nerve root as part of the root sheath (RS). At the subarachnoid angle, the arachnoid is reflected over the roots and becomes continuous with the outer layers of the root sheath. At the junction with the spinal cord, the outer layers of the root sheath become continuous with the pia mater (PM). (From Haller FR,
Low FM: The fine structure of the peripheral nerve root sheath in the subarachnoid space in the rat and other laboratory animals. Am J Anat 131:1, 1971, by permission.)
Figure 43-2. Diagram of the basic pathologic processes affecting peripheral nerves. In wallerian degeneration, there is degeneration of the axis cylinder and myelin distal to the site of axonal interruption (arrow) and central chromatolysis. In segmental demyelination, the axon is spared. In axonal degeneration, there is a distal degeneration of myelin and the axis cylinder as a result of neuronal disease. Both wallerian and axonal degeneration cause muscle atrophy. Further details are found in the text. (Courtesy of Dr. Arthur Asbury.)
Figure 43-3. Diagram of probable cellular events in acute inflammatory polyneuropathy (Guillain-Barré syndrome). A. Lymphocytes attach to the walls of endoneurial vessels and migrate through the vessel wall, enlarging and transforming as they do so. At this stage no nerve damage has occurred. B. More lymphocytes have migrated into the surrounding tissue. The first effect on the nerve is breakdown of myelin, the axon being spared (segmental demyelination). This change appears to be mediated by the mononuclear exudate, but the mechanism is uncertain.
C. The lesion is more intense, polymorphonuclear leukocytes being present as well as lymphocytes. There is interruption of the axon in addition to myelin sheath damage; as a result, the muscle undergoes denervation atrophy and the nerve cell body shows central chromatolysis. If the axonal damage is distal, the nerve cell body will survive, and regeneration and clinical recovery are likely. If, as in D, axonal interruption has occurred proximally because of a particularly intense root or proximal nerve lesion, the nerve cell body may die and undergo dissolution. In this situation, there is no regeneration, only the possibility of collateral reinnervation of muscle from surviving motor fibers. (From Asbury et al [1969], by permission.)
Figure 43-4 Patterns of sensory loss in leprosy. The localization of these areas to cooler portions of the body is unique to this disorder. There is almost universal analgesia but sparing of warmer regions such as the midline of the back, popliteal and antecubital spaces, lower abdomen and groin, and the head and neck. (From Sabin TD: Preservation of sensation in a cutaneous vascular malformation in lepromatous leprosy. N Engl J Med 282:1084, 1970, with permission.)