AAOS Comprehensive Orthopaedic Review

Section 1 - Basic Science

Chapter 8. Peripheral Nervous System

I. General Information

A. Peripheral nerves connect the central nervous system (CNS) to tissues such as bone, joints, muscles, tendons, and skin.


B. Nerves that supply the musculoskeletal system provide both motor and sensory function.

II. Histology

A. Cell body


1. Each neuron contains a cell body, which is the metabolic center that gives rise to two different processes: dendrites and axons (

Figure 1, A).


a. Dendrites are thin nerve processes that receive input from other nerves.


b. The axon is the primary distal offshoot of the cell body.


i. The axon is the primary route of conduction for the cell body to convey messages to tissues via action potentials.


ii. Axons typically measure 0.2 to 20 μm in diameter and arise from an axon hillock, which is responsible for the initiation of the action potential.


c. Myelin is a fatty insulating sheath formed by neighboring glial cells (specifically Schwann cells in the peripheral nervous system); it surrounds larger axons to speed the conduction of action potentials.


d. In unmyelinated nerves, a single Schwann cell envelops multiple axons, and conduction proceeds more slowly. In myelinated nerves, each axon is circumferentially laminated by a single Schwann cell.


e. Nodes of Ranvier are interruptions or gaps between Schwann cell segments of myelin sheath that allow for propagation of the action potential.


f. As an axon reaches its end organ, it divides into fine terminal branches with specialized endings called presynaptic terminals, which are responsible for transmitting a signal to postsynaptic receptors.


B. Nerve fibers


1. Nerve fibers are collections of axons with the Schwann cell sheaths surrounding them.


2. Afferent nerve fibers convey information from sensory receptors to the CNS.


3. Efferent nerve fibers transmit signals from the CNS to the periphery.


4. Nerve fibers have been classified based on their size and conduction velocity into three types—A, B, and C (

Table 1).


C. Nerve metabolism


1. Axoplasmic transport is made possible by the polarization of the neuron.


2. Proteins, which are created only in the cell body, travel via antegrade transport to support neural functions such as action potential propagation and neurotransmitter release.


3. Degradation products travel back to the cell body by retrograde transport.


4. The rate of axonal transport is slowed by decreasing temperature and by anoxia.


5. Several other factors also travel to the cell body in a retrograde fashion, including nerve growth factors, some viruses (eg, herpes simplex, rabies, and polio), tetanus toxin, and horseradish peroxidase (used in the laboratory to identify the location of a cell body in a dorsal root ganglion or in the spinal cord).

III. Nerve Physiology

A. Axon membrane—Made up of a selectively permeable lipid bilayer with sodium/potassium ATP-dependent pumps and gated ion channels. The sodium/potassium ATP-dependent pumps are responsible for an accumulation of sodium ions outside the membrane and the negative resting membrane potential within the axon membrane. When a


[Figure 1. A, The primary morphologic features of a peripheral nerve cell are the dendrites, cell body, axon, and presynaptic terminals. B, Communication between the terminal end of a nerve axon and an end organ occurs by synaptic vesicle release from the presynaptic terminal.]

   stimulus causes the gated ion channels to open, sodium flows rapidly into the axon, causing depolarization.


1. Conduction of signals along an axon begins with action potentials, which are generated when the membrane is depolarized beyond a critical threshold. The control of gated ion channels (Na+ and K+) is governed primarily by electrical, chemical, and mechanical stimuli.


2. The rate at which an action potential is conducted along an axon depends on the size of the axon (larger axon = faster) and the presence of myelin (myelin present = faster).


3. Within the nodes of Ranvier along the axon, dense collections of sodium channels propagate the action potential, allowing for saltatory conduction from node to node.


4. Most motor and sensory peripheral nerves are myelinated, with efferent motor axons being the most heavily myelinated. Autonomic fibers and slow pain fibers are examples of unmyelinated nerves.


5. Multiple sclerosis and Guillain-Barre syndrome are examples of nervous system diseases that lead to demyelination and slowed conduction velocities.


a. Multiple sclerosis is a chronic (and occasionally remitting) neurologic disorder characterized by perivascular infiltration of inflammatory cells followed by damage of the myelin sheath as well as nerve fibers. Patients develop problems with motor control (vision, strength, balance) and cognition.


b. Guillain-Barre syndrome is an acute inflammatory polyradiculoneuropathy. It is presumed to be an autoimmune disease (typically triggered by a viral or bacterial infection) that causes the production of antibodies that attack the myelin sheath. The loss of myelin leads to an acute impairment of sensory and motor nerve function ranging in severity from paresthesias and weakness to complete loss of sensation and paralysis.


B. Neuromuscular junction—This is the highly specialized region between the distal nerve terminal and a skeletal muscle fiber. It consists of the presynaptic terminal (the distalmost end of a nerve fiber), a synaptic cleft (the space into which neurotransmitters are released), and a postsynaptic membrane (the tissue responding to the nerve signal) (Figure, B1).


1. The arrival of an action potential at the presynaptic terminal triggers the vesicular release of acetylcholine.


2. Acetylcholine travels across the synaptic cleft and, once bound to receptors on the postsynaptic membrane, causes depolarization of the motor end plate and stimulation of the muscle fiber.


[Table 1. Classification of Peripheral Nerve Fibers]


Figure 2. The cell body of a sensory nerve resides in the dorsal root ganglion, far from its distal nerve ending. The dorsal root ganglion is located proximally, near the spinal cord where the spinal nerve enters the thecal sac. A, Projections of the central branch. B, Morphology of a dorsal root ganglion cell.]

IV. Embryology and Nerve Growth

A. Nervous system


1. The nervous system (and skin) is formed by the ectoderm (one of the three germ layers: ectoderm, mesoderm, and endoderm).


2. The ectoderm divides to form the neural tube (brain, spinal cord, and motor neurons), the neural crest (afferent neurons), and the epidermis.


3. The peripheral nervous system itself is divided into a purely motor visceral system (autonomic) and a mixed sensory and motor somatic system, which helps control voluntary motion.


B. Spinal nerves


1. Spinal nerves are collections of axons that exit the spinal cord at distinct levels. There are 8 cervical, 12 thoracic, 5 lumbar, 5 sacral, and 1 coccygeal spinal nerves.


2. The efferent ventral root transmits information from brain to muscle; the afferent dorsal root carries signals from the periphery back to the CNS (Figure 2).


a. The cell bodies for afferent sensory nerves are located in the dorsal root ganglion, which lies near the entry of the spinal nerve into the thecal sac.


b. The cell bodies for efferent motor nerves reside in the anterior horn of the spinal cord.


3. Spinal nerves frequently collect into plexuses (cervical, brachial, and lumbar) before branching.


C. Axonal growth and development—Initially guided by different nerve growth factors.


1. N-cadherin and neural cell adhesion molecule are adhesive membrane glycoproteins that are expressed on neural ectoderm and help guide growing axons.


2. Laminin and fibronectin are extracellular matrix glycoproteins that promote directional nerve fiber outgrowth.


3. Other factors believed to enhance nerve regeneration include nerve growth factor, fibroblastic growth factor, ciliary neuronotrophic factor, and insulin-like growth factor.



Figure 3. The anatomy of a peripheral nerve.]

V. Peripheral Nerve Anatomy and Biomechanics

A. Composition—Each nerve is composed of collections of nerve fibers called fascicles and neural connective tissue, which both surrounds and lies within each fascicle (Figure 3).


1. Axons within each fascicle are surrounded by a connective tissue layer referred to as endoneurium. Endoneurium is primarily composed of a collagenous matrix with fibroblasts, mast cells, and capillaries and forms a bilaminar sheath around the axon, Schwann cell, and myelin of each nerve fiber.


2. Perineurium is a thin, dense connective tissue layer that surrounds the fascicles.


a. It has a high tensile strength and maintains interfascicular pressure, providing a perineurial diffusion barrier. This barrier limits injury to nerve fibers by limiting the diffusion of epineurial edema, which occurs in stretch and compression type injuries. It also limits the diffusion of endoneurial edema that can occur when a nerve is compressed.


b. Spinal nerve roots have less perineurium than peripheral nerves and are more susceptible to stretch and compression injury.


3. Epineurium is the supportive sheath that contains the multiple groups of fascicles. It contains a well-developed network of extrinsic, interconnected blood vessels that run parallel with the nerve.


4. The structural organization of fascicles changes throughout the length of the nerve. Fascicles do not run as isolated, parallel strands from spinal cord to the presynaptic terminal or end organ. The number and size of fascicles changes as fascicular plexuses unite and divide within the nerve (

Figure 4).


a. At the joint level, fascicles are numerous and of smaller size to accommodate nerve deformation as the joint goes through a range of motion; eg, in the ulnar nerve at the elbow are many small fascicles, which minimize injury with elbow flexion and extension.


b. In contrast, at the level of the spiral groove, the radial nerve has a low number of large fascicles, which do not tolerate stretch very well. This level-specific internal anatomy places the radial nerve at higher risk for neurapraxia when it is mobilized and retracted from the spiral groove.


B. Blood supply—A peripheral nerve has both intrinsic and extrinsic vessels with multiple anastomoses throughout the length of the nerve.


1. At the epineurial level, there is no blood-nerve barrier.


2. At the capillary level within the endoneurium, however, there is a blood-nerve barrier, similar to the blood-brain barrier, which prevents diffusion of many macromolecules to maintain neural integrity. The blood-nerve diffusion barrier can be injured by infection, radiation, or metabolic disease.


C. Nerve endings—Afferent nerve fibers use specific primary receptors to collect sensory information from the periphery. There are three modalities and four attributes of sensory information that is conveyed.


1. Modalities


a. Mechanical stimulation (touch, proprioception, and pressure)


b. Painful stimulation (noxious, tissue-damaging stimulus)


c. Thermal stimulation (hot and cold)


2. Attributes: location, intensity, quality, and duration.


3. Nociceptors and thermoceptors consist of bare nerve endings (

Table 2).


4. Mechanoreceptors—Two types



Superficial skin mechanoreceptors: (small)


i. Meissner corpuscle, a rapidly adapting sensory receptor that is very sensitive to touch.


ii. Merkel disk receptors, which adapt slowly and sense sustained pressure, texture, and low-frequency vibrations.


Subcutaneous mechanoreceptors: (larger and fewer in number)

i. Pacini, or pacinian, corpuscles are ovoid in shape, measuring approximately 1 mm in


[Figure 4. The size, number, and arrangement of fascicles within a nerve vary along the course of the nerve. This figure depicts the percentage of cross-sectional area of the nerve devoted to fasciculi (given as a percentage of total cross-sectional area) in the radial nerve from the shoulder to elbow.]

[Table 2. Types of Receptors]


Table 3. Nerve Injury Classification]



length. They react to high-frequency vibration and rapid indentations of the skin.



Ruffini corpuscles are slowly adapting receptors that respond to stretching of the skin, such as occurs with finger motion.


D. Biomechanics


1. Nerves are viscoelastic structures demonstrating nonlinear responses to stretch.


2. When a nerve is stretched, it becomes ischemic before disrupting; for example, a nerve may undergo ischemia at 15% strain and rupture at 20% strain.


3. The ultimate strain of a nerve ranges from 20% to 60%.

VI. Peripheral Nerve Injury

A. Response to injury


1. Peripheral nerves respond to trauma with an initial inflammatory response.


a. This typically leads to increased epineurial permeability and edema, as the vessels within the epineurium lack a blood-nerve barrier.


b. If the injury involves disruption (crush or transection) that exposes the endoneurium, then the blood-nerve barrier is disrupted and the permeability of the endoneurial capillaries increases.


2. Injury from ischemia and compression can cause increased endoneurial pressure, fluid edema, and capillary permeability while the perineurial vascular system remains unaffected.


a. In these cases, the positive fluid pressure inside the endoneurium affects blood flow (decreased nutrition and oxygen delivery) and the removal of waste products.


b. When persistent, intraneural edema can diminish nerve function as seen in chronic compressive neuropathies.


B. Seddon's classification of nerve injury (Table 3)


1. Neurapraxia


a. Neurapraxia is an immediate, localized conduction block with normal conduction above and below the injury site.


b. Neurapraxias are typically reversible. Axon continuity is maintained, but local demyelination and ischemia occur.


c. Mechanisms of injury include compression, traction, and contusion.


2. Axonotmesis


a. Axonotmesis involves axon disruption, but some degree of the surrounding neural connective tissue is preserved. The axon distal to the point of injury degenerates (Wallerian degeneration).


b. Some nerve function may be recovered as nerve fiber regeneration is guided by an intact neural connective tissue layer (eg, intact endoneurium).


c. Mechanisms of injury include crush and forceful stretch.


3. Neurotmesis


a. Neurotmesis is complete disruption of nerve.


b. No spontaneous recovery of the affected nerve can be expected.


c. Mechanisms of injury include open crush, violent stretch, and laceration.



Figure 5. Peripheral nerve injury, degeneration, and regeneration. A, Laceration of the nerve fiber. B, Degeneration of the proximal stump to the closest node of Ranvier and Wallerian degeneration of the distal stump. C, Axonal sprouting of the growth cone into a basal lamina tube. D, The Schwann cell forms a column (Bungner band) to assist directed axonal growth.]

4. Sunderland revised Seddon's classification by defining three subtypes of axonotmesis.


C. Pathoanatomy of injury


1. Laceration (Figure, A5 and B)


a. When the continuity of a nerve is disrupted, the two nerve ends retract, the cell body swells, the nucleus is displaced peripherally, and chromatolysis (dispersion of basophilic Nissl granules with relative eosinophilia of the cell body) occurs.


b. The nerve cell stops producing neurotransmitters and starts synthesizing proteins required for axonal regeneration.


c. Wallerian degeneration distal to the site of the injury begins within hours of injury and is characterized by axonal disorganization from proteolysis, followed by the breakdown of myelin.


d. Schwann cells become active in clearing myelin and axonal debris.


2. Compression


a. When a nerve is compressed, nerve fibers are deformed, local ischemia occurs, and vascular permeability is increased.


b. Edema then affects the endoneurial environment, leading to poor axonal transport and nerve dysfunction.


c. If compression continues, the edema and dysfunction persist and fibroblasts invade, producing scar tissue, which impairs fascicular gliding.


d. Tissue pressures up to 30 mm Hg can cause paresthesias and increased nerve conduction latencies. A tissue pressure of 60 mm Hg can cause a complete block of nerve conduction.


3. Ischemia


a. After 15 minutes of anoxia, axonal transport stops.


b. It can recover if reperfusion occurs within 12 to 24 hours.


D. Nerve regeneration after injury


1. With or without suture reapproximation of the disrupted nerve ends, nerve regeneration begins with axonal elongation across the zone of injury (Figure, C5 and D).


a. The zone of injury undergoes an ingrowth of capillaries as well as Schwann cells.


b. The Schwann cells migrate into the gap from both proximal and distal stumps and attempt to form columns (Bungner bands) to guide the tip or growth cone of the sprouting axons.


c. The growth cone is sensitive to neurotrophic growth factors, such as nerve growth factor, and neurite promoting factors such as laminin.



Figure 6. Illustration of electrode placement for three types of nerve conduction studies: antidromic sensory study (A), orthodromic sensory study (B), and motor nerve conduction study (C). G1 = active recording electrode; G2 = reference recording electrode; G0 = ground electrode; S = stimulating electrode; S1 = distal stimulation site; S2 = proximal stimulation site. The cathode is black and the anode is white.]

2. Distal reinnervation of muscle will be successful only if the muscle has viable motor end plates for the regenerating nerve to stimulate.


a. In the acute period after a nerve injury, the muscle increases the number of motor end plates, seeking nerve stimulus.


b. As fibrosis sets in over time, the number of motor end plates diminishes.


c. Typically, after 12 months, a muscle is no longer receptive to reinnervation.

VII. Diagnostic Studies

A. Overview


1. The primary tests used to evaluate the integrity of the peripheral nervous system are nerve conduction velocity studies and EMG.


2. These tests assess the function of sensory nerves, motor nerves, and muscles to confirm the diagnosis of neuropathies and myopathies.


3. They also can differentiate causes of weakness, identify the level and severity of nerve injury or conduction abnormality, and demonstrate the existence of denervated muscle and its reinnervation.


B. Nerve conduction velocity studies


1. Sensation


a. A stimulation recording from a mixed (motor and sensory) nerve is called a compound nerve action potential.


b. A sensory-specific recording is called a sensory nerve action potential (SNAP).


c. The nerve can be stimulated in an antidromic (from proximal to distal) or orthodromic (from distal to proximal) fashion (Figure 6). The speed of conduction is similar in either direction.


d. The distance (in millimeters) and time (in milliseconds) an action potential travels between electrodes must be known to quantify the speed of conduction.


e. Nerve conduction velocity (distance/time) or latency (time between the stimulus and the onset of the action potential) are typically recorded (

Figure 7). These values are negatively impacted by temperature, age, demyelination, and loss of axons.


f. The amplitude of the action potential can also be measured. Cold temperature increases SNAP amplitude, whereas age decreases it.


2. Motor nerve function


a. A motor nerve action potential is recorded from a muscle, where multiple muscle fibers are innervated by a single nerve. Thus, the information recorded is a compound muscle action potential (CMAP).


b. The CMAP measures not only the speed of a stimulus over the course of a nerve but also the transmission over the neuromuscular junction and muscle fiber conduction.


c. An F-wave is a late response recording from distal muscles during CMAP testing.


i. When a stimulus is applied, the signal travels in the typical proximal-to-distal fashion. However, a separate signal also may be sent distal-to-proximal along the nerve to the spinal cord anterior horn cells.


ii. With sufficient anterior horn cell stimulation, these cells may discharge another proximal-to-distal stimulus called an F-wave, which will be recorded after the initial CMAP.


C. Electromyography


1. EMG studies the entire motor unit (anterior horn cell, motor neuron, and muscle) and involves measuring insertional activity, spontaneous activity, motor unit action potentials (MUAPs), and recruitment (but not sensory information).


2. Insertional activity is measured as the needle is passed into the muscle belly.


a. Decreased insertional activity occurs from poor muscle viability, muscle fibrosis, or muscle atrophy.


b. Increased insertional activity may be a sign of denervation or a primary muscle disorder (eg, polymyositis or myopathy).


3. Spontaneous activity involves electrical discharges that occur without muscle contraction and without movement of the testing needle.


a. Fibrillations are an example of abnormal spontaneous activity; they occur in denervated muscle fibers and some myopathies. The density of fibrillations is graded from 1+ to 4+, but it is the amplitude that is helpful in understanding the timing of denervation. Large-amplitude fibrillations frequently occur acutely (within 3 to 12 months), and smaller amplitude fibrillations occur later in the process of denervation (after the muscle has atrophied).


b. Positive sharp waves are abnormal single muscle fiber discharges and can be seen in association with fibrillations. They can be seen without fibrillations when the muscle is traumatized but not denervated. Fibrillations and positive sharp waves typically appear 2 to 3 weeks after the onset of denervation.


c. Fasciculations are spontaneous discharges of a single motor unit and can be seen clinically on the skin. Fasciculations occur in various neuromuscular disorders (the syndrome of benign fasciculations, chronic radiculopathies, peripheral polyneuropathies, thyrotoxicosis, and overdose of anticholinesterase medications).


[Figure 7. Conduction velocity (CV) is the distance from the stimulating electrode to the receiving electrode divided by the time from the stimulus to either the onset of the action potential (onset latency) or the peak of the action potential (peak latency).]

4. MUAPs can measure voluntary muscle activity and are characterized by the duration, amplitude, and shape of the action potential.


a. The amplitude characterizes the density of the muscle fibers within the motor unit.


b. The duration and shape of the wave produced by the MUAP are affected by the quality of conduction. For example, as a partially denervated motor unit is reinnervated with axonal sprouting, the MUAP will be prolonged in duration and polyphasic in shape. If no reinnervation occurs, no MUAP will be generated.


5. Recruitment is also measured by MUAPs and can be used to understand whether muscle weakness is the result of a decrease in the peripheral motor neurons and motor units or a central recruitment problem from a CNS lesion, pain, or poor voluntary effort.


D. Magnetic resonance imaging


1. MRI can be a useful adjunct to electrodiagnostic studies for assessing various disorders of the peripheral nervous system.


2. MRI can show changes in muscle from denervation. For example, chronic denervation will show evidence of fatty atrophy.


3. High-resolution images with sufficient contrast are required to emphasize the underlying peripheral nerve anatomy and nerve morphology.


4. These scans take advantage of signal differences between distinct intraneural tissues, specifically differences in the water content and physical structure of fascicles, perineurium, and epineurium.

VIII. Peripheral Nerve Pharmacology

A. Local anesthetics


1. Create a sensorimotor nerve block, causing transient numbness and paralysis by temporarily disrupting the transmission of action potentials along the course of axons.


2. Lidocaine, mepivacaine, and bupivacaine (all amide-type) have different durations of action based on their specific biochemistry, with lidocaine the shortest duration of action and bupivacaine the longest.


3. C-type nerve fibers (cutaneous pain fibers) are most susceptible to local anesthetics, and A-type fibers (motor axons and deep pressure sense) are the least susceptible.


4. Local anesthetics (amide type) are processed by the liver (P450 enzyme) into more water-soluble metabolites, which are then excreted in the urine.


5. Epinephrine may be combined with these anesthetics for vasoconstriction.


a. This reduces systemic absorption of local anesthetics from the injection site by decreasing blood flow in these areas.


b. Systemic blood levels are lowered up to 30%.


c. Local neuronal uptake is increased in the region of drug administration as local vasoconstriction causes less of the drug to be absorbed systemically.


B. Botulinum toxin


1. Botulinum toxin can be injected into muscle to treat muscular spasticity.


2. The bacterium Clostridium botulinum produces botulinum toxin.


3. The toxin works at the level of the neuromuscular junction, blocking vesicular release of acetylcholine at the presynaptic clefts and leading to chemical denervation (paralysis) when injected into muscle.


4. The beneficial effect begins at approximately 7 to 14 days and typically lasts 3 months.

IX. Treatment of Peripheral Nerve Injuries

A. Nonsurgical treatment


1. Nonsurgical treatment is appropriate for all neurapraxias and most axonotmeses.


2. While awaiting nerve recovery, great care should be taken to maintain limb functionality and viability. Specifically, distal joints should be mobilized and distal muscle groups stretched or protectively splinted to avoid contractures.


3. Osteopenia, joint stiffness, and muscle atrophy can occur if the affected limb is ignored.


B. Recovery of an injured sensory nerve occurs in the following sequence:


1. Pressure sense


2. Protective pain


3. Moving touch


4. Moving 2-point discrimination


5. Static 2-point discrimination


6. Threshold sensation (Semmes-Weinstein monofilament and vibration).


C. Surgical repair


1. Prerequisites to nerve repair (neurorrhaphy) include a clean wound, a well-vascularized repair bed, skeletal stability, and viable soft-tissue coverage.


2. Nerve ends are sharply debrided of injured or devitalized nerve, scar, and fibrosis to expose healthy nerve fascicles.

3. A repair should occur urgently, within the first few days after injury, because disrupted nerves retract and scar tissue and neuromas form quickly.


4. Postoperatively, limited immobilization for 2 to 3 weeks prevents stress at the repair site.


5. Currently the most effective repair technique is an epineurial repair (suturing repair of the epineurium only) performed with a fine monofilament nylon suture (eg, No. 9-0) using microsurgical instrumentation and technique.


a. In reapproximating the nerve ends with an epineurial repair, care should be taken to orient the nerve ends to match fascicles as accurately as possible. This technique typically minimizes scar formation.


b. It can be performed with suture or with fibrin glue.


c. The repair should be done under minimal tension.


6. A group fascicular repair involves reapproximating fascicular groups by perineurial repair. This technique is more precise than epineurial repair, but it typically requires intraneural dissection, which leads to more scar tissue formation and intraneural fibrosis.


7. Muscular neurotization involves implanting the nerve end directly into the muscle belly.


8. Nerve grafting is used when segmental defects in a nerve exist that cannot be overcome with joint flexion or nerve transposition.


a. Autografts are inset in the same manner as a primary repair, although it is recommended to reverse the graft to decrease axonal dispersion through the nerve graft.


b. The sural nerve is a common autograft that can be cut into parallel sections to create a cable graft of greater diameter.


c. Fresh allografts require immunosuppression and are infrequently used.


d. In lieu of an autograft, nerve gaps can be bridged with either biologic (vein graft) or bioabsorbable nerve conduits (polyglycolic acid or collagen).


9. Results of peripheral nerve repair vary.


a. Young patients with early repairs of distal single-function nerves using short nerve grafts or direct repair do better than older patients with late repairs of proximal, mixed nerves using long nerve grafts.


b. The rate of nerve regeneration after repair also varies and has been historically estimated to be 1 to 2 mm per day in humans, which is approximately equal to the rate of axonal transport of neurofilament proteins essential to nerve growth.

Top Testing Facts

1. Schwann cell myelination speeds transmission of action potentials by saltatory conduction occurring at nodes of Ranvier.


2. Most motor and sensory nerves are myelinated except for autonomic and slow pain fibers.


3. Nerve fibers (axons) are surrounded by endoneurium, collections of nerve fibers (fascicles) by perineurium, and collections of fascicles by epineurium.


4. Nerve injury causes loss of distal function in the following sequence: motor, proprioception, touch, temperature, pain, and sympathetics. Nerves recover in the inverse order.


5. Neurapraxia is a reversible conduction block (traction or compression); axonotmesis involves axon disruption with preserved neural connective tissue (stretch or crush); neurotmesis is complete disruption of a nerve (open crush or laceration).


6. Tissue pressures up to 30 mm Hg can cause paresthesias and increased nerve conduction latencies.


7. Temperature, age, demyelination, and loss of axons decrease rate of transmission.


8. Fibrillations are an EMG finding of abnormal spontaneous activity that occur in muscle fibers 2 to 3 weeks after denervation (transient or complete).


9. Nerve repair (neurorrhaphy) involves reapproximation of the nerve ends with fascicles appropriately oriented under minimal tension using a fine monofilament epineurial suture. Group fascicular repair increases scarring at the repair site.


10. Nerve grafts may be cabled to increase diameter; they should also be reversed to minimize early arborization of regenerating nerve fibers.


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Lundborg G: A 25-year perspective of peripheral nerve surgery: Evolving neuroscientific concepts and clinical significance. J Hand Surg Am 2000;25:391-414.

Robinson LR: Role of neurophysiologic evaluation in diagnosis. J Am Acad Orthop Surg 2000;8:190-199.