Nerves of the PNS carry information to, or from, the CNS. The nerves that carry information to the CNS from the periphery are known as afferent nerves. Afferent nerves transmit a range of sensations, including touch, position, vibration, and pain. Sensory afferent nerves originate in the dorsal root ganglia just outside the spinal cord. The nerves that carry information from the CNS to the periphery are known as efferent nerves. Efferent nerves include both the somatic motor nerves that innervate skeletal muscles to make them contract voluntarily and the autonomic nerves that control involuntary muscles, such as smooth and cardiac muscle, and control glandular activity. Efferent somatic motor nerves originate in the anterior horn of the spinal cord.

Nerve cells, also known as neurons, are composed of a cell body, dendrites, an axon, and axon terminals (Fig. 15.1). The cell body contains the nucleus and various organelles (mitochondria, rough endoplasmic reticulum, ribosomes, and Golgi apparatus) needed to make proteins and process energy to maintain the nerve. The dendrites are branching and tapering extensions of the cell body that receive signals from other neurons. The axon is a projection that carries signals from the cell body toward the axon terminals where signals are then transmitted to other nerves or to end organs such as muscles. Where the axon terminal of one neuron (the presynaptic neuron) meets an end organ or a dendritic ending or cell body of another neuron (the postsynaptic neuron) is known as a synapse, with the gap between the presynaptic neuron and the end organ or postsynaptic neuron referred to as the synaptic cleft.

Neurotransmitters, proteins, and organelles are transported along axons using a system of microtubules and neurofibrils. Anterograde transport from the cell body of neurotransmitters and structures to replenish the plasmalemma is quick, whereas anterograde transport of proteins and organelles needed for axoplasm generation or replenishment (regenerating or mature neurons) is slow. Retrograde transport toward the cell body to return organelles to the cell body for disposal and to carry nerve growth factor toward the cell body also occurs slowly. Both anterograde and retrograde transport require an energy source that is compromised if the blood supply to the nerve is disrupted.

A nerve is made up of multiple nerve cell axons. Each axon is surrounded by a delicate layer of loose connective tissue known as the endoneurium. Groups of axons are then arranged in bundles called fascicles, and each fascicle is surrounded by perineurium, which is composed of flattened cells, basement membrane, and collagen fibers. Groups of fascicles, with arteries and veins between them, are then held together by a layer of dense connective tissue known as the epineurium to form a nerve (Fig 15.2). It is important to know this anatomy when performing regional anesthesia, as inadvertent intraneural injection of local anesthetic—into the nerve itself—can cause mechanical or ischemic nerve injuries, which are discussed later in this
chapter. Ultrasound is often used when performing regional anesthesia so that the anesthesia provider can visualize the location of the injection and thereby reduce the risk of intraneural or intrafascicular local anesthetic injection.

Some peripheral nerve cell axons are wrapped in concentric layers of myelin. If a nerve is myelinated, the myelin wraps around the outside of the epineurium. Myelin is a lipoprotein that acts as an insulator for the axon. The myelin around peripheral nerves is made by Schwann cells. Each Schwann cell forms a segment of myelin about 1 mm long. There are small gaps of uncovered axon between each of these segments known as nodes of Ranvier. The segments of axon between the nodes are called internodes (Fig. 15.3). Myelin accelerates the transmission of signals along the axon because impulses can jump from one node to the next rather than having to traverse the entire length of the axon. This jumping is known as saltatory conduction. Unmyelinated nerve cell axons conduct nerve impulses much more slowly than myelinated nerve cell axons.

Two positively charged ions, potassium (K⁺) and sodium (Na⁺), are primarily responsible for the transmission of signals along nerves. At rest, when no signal is being transmitted, there is more sodium outside the neuron and more potassium inside the neuron. These concentrations are maintained by sodium-potassium adenosinetriphosphatase (ATPase) pumps on the cell membrane. These pumps use ATP as their energy source to pump three sodium ions out of the cell for every two potassium ions they pump into the cell. This results in the inside of the cell being less positively charged than the outside, which is considered a relative negative charge. This negative charge, of about -65 mV, is known as the resting membrane potential.

When the nerve is sufficiently stimulated, sodium channels on the nerve membrane open allowing sodium ions to rapidly enter the neuron, causing the inside to become positively charged relative to the outside. More and more sodium channels open until all of the available channels are open. This causes a rapid rise in membrane potential, or depolarization, which is followed by sodium channel inactivation (closure). Once the sodium channels close, sodium ions no longer enter the neuron. Potassium channels then open, and potassium ions flow out of the nerve, causing the membrane potential to return to baseline. This sequential nerve depolarization and repolarization is known as an action potential (Fig. 15.4). To restore the membrane potential (repolarization), sodium is pumped
out of the cell and potassium is pumped into the cell. Action potentials can be initiated on the cell body or the axon, but they usually start at the axon hillock, the point where the axon leaves the cell body (see Fig 15.1) because this is the most readily excitable part of the nerve. Once an action potential occurs at any point on the axon, the resulting currents will trigger depolarization and an action potential on the neighboring stretch of membrane, with the signal then being propagated along the nerve in a domino-like fashion, until it reaches the end of the nerve. Since each action potential is generated anew along the next excitable stretch of axon, the signal does not decay in strength. Myelinated segments of axons are not excitable and do not produce action potentials. When an action potential reaches a myelinated segment, the current is quickly conducted, with some decay, to the next node of Ranvier where action potentials are generated to boost the signal. This saltatory conduction is much quicker than the sequential action potentials that occur along the entire length of unmyelinated nerves.

When the action potential reaches the axon terminal it generally triggers release of a neurotransmitter from vesicles in the axon terminal into the synaptic cleft. The neurotransmitter binds to postsynaptic receptors, causing activation of the end organ or excitation or inhibition
of a postsynaptic nerve. A postsynaptic neuron or end organ may receive excitatory and inhibitory inputs from many other neurons. With a sufficient predominance of excitatory inputs, the end organ will be activated or an action potential will start in the postsynaptic neuron and propagate along the length of this nerve.

Damage to nerves of the PNS is known as peripheral neuropathy. Neuropathy is usually classified according to its distribution and its cause. The typical distributions of neuropathy are mononeuropathy, mononeuritis multiplex, polyneuropathy, and autonomic neuropathy. A mononeuropathy is a neuropathy that only affects one nerve. Mononeuropathies are usually caused by compression, for example, carpal tunnel syndrome at the wrist or peroneal nerve compression at the knee after prolonged compression during surgery. Mononeuritis multiplex is simultaneous or sequential involvement of multiple nerves

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