MYELINATION OF CNS AND PNS AXONS
Central myelination of axons is provided by oligodendroglia. Each oligodendroglial cell can myelinate a single segment of several separate central axons. In the PNS, sensory, motor, and preganglionic autonomic axons are myelinated by Schwann cells. A Schwann cell myelinates only a single segment of one axon. Unmyelinated sensory and autonomic postganglionic autonomic axons are ensheathed by a Schwann cell, which provides a single enwrapping arm of cytoplasm around each of several such axons. The space between adjacent myelin segments of an axon is called a node of Ranvier; this site of axon membrane contains sodium channels and allows the reinitiation of action potentials in the course of propagation down the axon, a process called saltatory conduction.
The integrity of the myelin sheath is essential for proper neuronal function in both the CNS and the PNS. Disruption of the myelin sheath around axons in either system results in the inability of the formerly myelinated axons to carry out their functional activities. In the CNS, the myelin sheath of central axons can be attacked in an autoimmune disease such as multiple sclerosis, resulting in a variety of symptoms, such as blindness, diplopia caused by discoordinated eye movements, loss of sensation, loss of coordination, paresis, and others. This condition may occur episodically, with intermittent remyelination occurring as the result of oligodendroglia proliferation and remyelination. In the PNS, a wide variety of insults, including exposure to toxins and the presence of diabetes or autoimmune Guillain-Barré syndrome, result in peripheral axonal demyelination, which is manifested mainly as sensory loss and paralysis or weakness. Remyelination also can occur around peripheral axons, initiated by the Schwann cells. Clinically, the status of axonal conduction is assessed by examining sensory evoked potentials in the CNS and by conduction velocity studies in the PNS.