There are several components of the peripheral nervous system. These include sensory and motor nerve fibers (axons) which pass through nerve roots, plexi and the peripheral nerves, themselves. Sensory nerve fibers (axons) have their origin in receptive elements that may be in the skin, muscles, joints, bones or even the internal organs. They typically have cell bodies located in the dorsal root ganglia located close to the spinal cord. Somatic motor nerve fibers (axons)
arise from motor neurons in the ventral horn of the spinal cord. These nerve fibers terminate on muscle fibers at the neuromuscular junction or on muscle spindles (setting the sensitivity to muscle stretch).
Autonomic motor nerve fibers terminate on glands, organs or smooth muscle fibers. These are unique since there are typically 2 neurons in a sequence (with the postganglionic neuron located in a ganglion).
The peripheral nerves not only include the nerve fibers but also several layers of connective tissue (endoneurium, perineurium and epineurium) and blood vessels.
Nerve fibers have a high metabolic demand and little reserve of energy stores. Therefore, circulation is
critical for moment-to-moment supply of oxygen and metabolic substrates. Peripheral nerves receive collateral arterial branches from adjacent arteries which anastamose with other arteries entering the nerve, above and below. There is usually sufficient collateral circulation to survive damage to one of the feeding arteries.
Individual nerve fibers consist of axons that may be myelinated or unmyelinated. Myelin in the peripheral nervous system derives from Schwann cells, which adhere to nerve cell membranes and create multiple layers or wrapping of the membrane. These are fused layers of Schwann cell membrane, comprising an electrically insulating lipid-rich layer around the nerve fibers. In between these Schwann cells are the nodes of Ranvier, a short segment of the nerve fiber devoid of myelin. At these nodes there is a high density of voltage-gated Na ion channels that facilitate membrane depolarization. The role of myelin is to increase the velocity of nerve conduction with speed being proportional to the distances between adjacent nodes of Ranvier. The use speed of large myelinated fibers is 40-70 meters/ second.
The function of nerve fibers can, to some extent, be deduced from the velocity of conduction (see Table 12-2). Most somatic motor axons are large, heavily myelinated fibers. This is also true of the sensory nerve fibers innervating muscle spindle (stretch) and Golgi tendon organ (tension) receptors.
Intermediate size fibers convey touch and proprioception , joint position sense. Lightly myelinated fibers convey sharp pain sensation and autonomic preganglionic motor function. Pathologic processes that primarily affect myelin tend to effect functions mediated by the most heavily myelinated nerve fibers and would also profoundly affect the speed of nerve conduction.
Unmyelinated nerve fibers conduct very slowly by a continuous mode of propagation of electrical signal (non-saltatory). These fibers convey aching, burning pain and temperature sensation and also include the sympathetic, postganglionic motor nerves. Their speed is approximately 1 meter/second.
Nerves are protected from pressure by connective tissue padding and they are also protected from traction by the connective tissue. Nerve roots are less protected because there is less connective tissue.
In order to accurately diagnose disorders affecting peripheral nerves it is important to recall the
anatomical distribution of sensory fibers in the nerve roots (Fig. 9-2) and peripheral nerves (Fig. 9-3).
Nerve roots have nearly complete overlap, so there is limited sensory loss (usually distally, where there is less overlap) with damage to a single nerve root. Peripheral nerve injuries usually produce more sensory loss. It is important to note that there is significant variability in the precise borders of the peripheral nerve distribution of although the general pattern is quite consistent. It is also important to understand the motor innervation of certain major nerve roots and peripheral nerves (Table 10-5).
There may be weakness of shoulder abductors and external rotators with C5 nerve root lesions,
weakness of elbow flexors with C6 nerve root lesions, possible weakness of wrist and finger extension with C7 nerve root lesions and some weakness of intrinsic hand muscles with C8 and T1 lesions. In the lower extremity, there may be some weakness of knee extension with L3 or L4 lesions, some difficulty with great toe (and, to a lesser extent, ankle) extension with L5 lesions and weakness of great toe plantar flexion with S1 nerve root damage.
It is critical for the survival of nerve fibers that they be able to maintain a stable resting membrane potential by sustaining ion gradients across the axonal membrane. This requires normal integrity of the membrane constituents (lipid layers, membrane proteins and ion channels). It also requires energy, which the neuron uses to create the ion gradients and for transport, moving constituents from the cell body down the axon, and back to the cell body. All of this requires high blood flow to the nerve.
Diminished blood flow (ischemia) is poorly tolerated by nerves.
Axonal transport is critical to the function of the peripheral nerve. All protein constituents of the nerve
are synthesized in the neuronal cell body. Microtubules within the axon perform the transport function and may extend over distances that can exceed a meter in the longest nerve fibers. Therefore, all
structural proteins as well as enzymes that function in the nerve terminal come from the cell body. Even structural components, such as the mitochondria in the nerve terminal, are transported down the axon.
There is a class of protein compounds (trophic factors) that travel orthodromically to the periphery or antidromically to the cell body. These factors are critical to the health of the innerved tissues.
Additionally, there are trophic factors released by the peripheral tissues, taken up by nerve terminals and transported in a retrograde manner back to the nerve cell bodies. Loss of these trophic factors can result in either the death of neurons or atrophy of peripheral tissues. This is the reason why a muscle whose innervating axon is sectioned undergoes atrophy much more quickly and severely than one where the axon is intact, as in demyelination with conduction block... In both cases, there is complete weakness of the muscle, although only in the former case are trophic factors lost.
It is important to note that nerves receive innervation by way of the nervi nervorum. Most of these nerve fibers are either sensory or motor (from the sympathetic nervous system). The density of this innervation is not uniform and varies with the particular nerve in question as well as with the location along the nerve. These fibers may be responsible for some pain with nerve injury.