Introduction

Peripheral nerve is a term used synonymously to describe the peripheral nervous system. The
peripheral nervous system is a network of 43 pairs of motor and sensory nerves that connect the
brain and spinal cord (the central nervous system) to the entire human body. These nerves control
the functions of sensation, movement and motor coordination.
The peripheral nerves are a complicated, extensive network of nerves that are the tool for the
brain and spinal cord to communicate with the rest of the body. They are fragile and can be
damaged easily. When one of these nerves suffers injury or trauma, surgical treatment is
sometimes the only remedy.

Classification
The most widely accepted classification of nerve injuries are those described by Seddon (neuropraxia,
axonotmesis, and neurotmesis) and by Sunderland (Grade 15 nerve injuries).

Types of Nerve injuries

Nerve Injuries
1. Brachial Plexus Injury
Brachial plexus injury (BPI) is an umbrella term for a variety of conditions that may impair
function of the brachial plexus nerve network. The majority of pediatric and adult brachial
plexus injuries are caused by trauma.
2. Foot Drop Injury
A peroneal nerve injury (also called foot drop or drop foot), is a peripheral nerve injury that
affects a patients ability to lift the foot at the ankle. While foot drop injury is a
neuromuscular disorder, it can also be a symptom of a more serious injury, such as a nerve
compression or herniated disc.
3. Spinal Accessory Nerve Injury
A spinal accessory nerve injury can be caused by trauma or damage during surgery, such as a
lymph node biopsy or jugular vein cannulation.
4. Traumatic Nerve Injury
Injury to the peripheral nerve injury can occur through a variety of trauma. Common causes
of nerve injuries include:
a.

Laceration

b.

Focal contusion (gunshot wounds)

c.

Stretch/traction injury

d.

Compression

e.

Drug injection injury

f.

Electrical injury

Nerve compression and entrapment

1. Carpal Tunnel Syndrome
Carpal tunnel syndrome is a condition of nerve entrapment. It is caused when the tunnel
surrounding the tissues inside the bones of your wrist narrows, inflaming the tissues and your
median nerve. A mass may occupy the canal compressing the nerve.
The median nerve gives feeling to your thumb, and index, middle and ring fingers. When
tissues in the carpal tunnel, such as ligaments and tendons, get swollen or inflamed, they
press against the median nerve. That pressure results in the symptoms of carpal tunnel
syndrome.
2. Meralgia Paresthetica
Meralgia paresthetica is caused by nerve entrapment. The lateral femoral cutaneous nerve
running through your pelvis, groin and into the thighs becomes compressed. This can be
caused by swelling, trauma, or pressure narrowing these openings and squeezing the nerve.
3. Thoracic Outlet Syndrome
Thoracic outlet syndrome (TOS) is a condition caused by compression of nerves or blood
vessels in the thoracic outlet, the area between the base of the neck and the armpit, including
the front of the shoulders and chest.
There are three types of TOS:
a. Vascular. This can be a compression of the artery and vein.
b. Neurogenic. The nerves become compromised from an extra cervical rib, present
at birth.
c. Disputed or painful form. There is no neurological deficit but patients
experience neurological symptoms and pain. Typically these patients
electrodiagnostic studies (EMG / NCV) are normal, but they complain of pain.
4. Ulnar Nerve Entrapment
Ulnar nerve neuropathy due to ulnar nerve entrapment is often a painful disorder of the
outer side of the arm and hand near the little finger, caused by pressure on the ulnar nerve in
your arm.
Nerve Tumors
1. Malignant Nerve Sheath Tumors

These very aggressive tumors are cancerous nerve sheath tumors and should be managed by a
multi-disciplinary team. They can occur in association with neurofibromatosis Type 1.
2. Neurofibromas (neurofibromatosis)
Neurofibromas are benign (non-cancerous) tumors which grow on nerves in the body. A
common cause of neurofibromas is neurofibromatosis.
3. Schwannomas (schwannomatosis)
These are nerve sheath tumors and can occur in isolation. Less commonly these tumors can
occur in patients suffering from neurofibromatosis or schwannomatosis.

Epidemiology
Limited reported data are available to determine the incidence of peripheral nerve injuries. In North
America, data taken from a trauma population in Canada revealed that approximately 2-3% of patients
had a major nerve injury. In New South Wales, Australia, 2% of patients were reported to have a major
nerve injury.

Anatomy

Nerve Structure
Peripheral components of the neuromuscular
system include the alpha and gamma motor
neurons, their axons, and the skeletal muscles
they innervate; the sensory neurons and their
receptors located in the connective tissues,
joints, and blood vessels; and the neurons of
the autonomic nervous system. Connective
tissue surrounds each axon (endoneurium) as
well as fascicles (perineurium) and entire
nerve fibers (epineurium). The axolemma is
the surface membrane of axon. Schwann cells
lie between the axolemma and endoneurium;
they form myelin, which functions to insulate
the axon as well as speed the conduction of
action potentials along the nerve fiber. The
exceptions are very small fibers that are
unmyelinated. A peripheral nerve may consist
of a single fascicle or consist of several fascicles. The structure of a peripheral nerve with its connective
tissue and vascular layers.

Mobility Characteristics of the Nervous System

The peripheral and central nervous systems as a continuous tissue tract; simply stated, the tract is like an
H on its side. Structurally and functionally, there is continuity of the connective tissues, the impulse
transmission between the neurons, and the chemical flow of neurotransmitters. The system is designed to
be mobile and deform, while at the same time conducting impulses. When a joint moves and tension is
placed on a nerve bed, nerve gliding is toward the moving joint (convergence); and when tension is
relieved, nerve gliding is away from the moving joint (divergence). Initially, excursion of the nerve occurs
adjacent to the moving joint, but excursion of the nerve progresses more distant from the moving joint as
limb movement continues. Substantial mobility in the nervous system is needed for an individual to move
during functional activities. With movement of an extremity, before there is increased tension in the nerve
itself, the whole peripheral nerve moves, and there is movement between connective tissues and neural
tissues. The mobility is allowed without undue stress on the nerve tissue because:

The arrangement of the spinal cord, nerve roots, and plexes allows mobility. If any part of the H
is placed under tension, the force can be dissipated throughout the system.
The nerves themselves are wavy and can straighten when tension is applied.
The connective tissue around the individual nerves and bundles of nerves (epineurium,
perineurium, endoneurium) absorb tensile forces before the nerve itself stretches.

Cadaveric and in vivo ultrasound studies of median nerve mobility and strain have shown nerve
movement of 5 to 10 mm depending on the position and motion of each of the joints in the upper
extremity and neck, as well as a wavy appearance when on a slack (unloaded) and a straightening of the
nerve when under tension. Strain calculated in the stretch position (see upper limb tension test for the
median nerve described in the section on neural tension impairments) was 2.5% to 3.0%.21

Common Sites of Injury to Peripheral Nerves

Injury to the nerves of the peripheral nervous system can occur anywhere along the pathway from the
nerve roots to their termination in the tissues of the trunk and extremities.
As each nerve courses from the intervertebral foramina to its peripheral destination, there are sites that
increase its susceptibility to either tension or compression. Symptoms and signs of nerve impairments are
sensory changes or loss and motor weakness in the distribution of the involved nerve fibers. Because
nerves are composed of innervated connective tissue and blood vessels surround the axons, ischemic pain
or tension pain may also occur when these tissues are stressed. Also, because peripheral nerves include
sympathetic fibers, autonomic responses might occur. Whenever neurological symptoms and signs are
present, the entire nerve should be tested for mobility and signs of compression at key points along its
pathway. In this section, primary sites of compression, tension, or injury are identified for the peripheral
nerves in the upper and lower quarter regions including their origins at the nerve roots and pathways
through each of the plexuses.

Nerve Roots
Nerve roots emerge from the spinal canal and traverse the foramina of the spine, where they can become
impinged as a result of various
pathologies of the spine that reduce the
space in the foramina, such as
degenerative disc disease (DDD),
degenerative joint disease (DJD), disc
lesions, and spondylolisthesis. With
reduced spinal canal or foraminal space
(stenosis), extension, side bending, or
rotation to the side of the stenosis further
decreases the space where the nerve root
courses and may cause or perpetuate
symptoms. If adhesions place tension on a
nerve root, nerve mobility tests (described
later in this chapter) can reproduce
symptoms when the spine is side-bent
(laterally flexed) away from the side
causing the symptoms. When involved,
symptoms and signs include sensory
changes and/or loss of motor function in
the respective dermatome and myotome
patterns. Nerve roots of the upper quarter
include C5 through T1 and those of the
lower quarter L1 through S3.

Brachial Plexus
After emerging from the foramina, the nerve fibers divide into anterior and posterior primary rami.
Vasomotor fibers from the sympathetic trunk join the anterior primary rami to course within the brachial
plexus and peripheral nerves to the extremities. The brachial plexus is formed by the anterior primary
divisions of the C5T1 nerve roots. The plexus functions as the distribution center for organizing the
contents of each peripheral nerve. In addition, Butler11 suggested that the weave pattern in the brachial
plexus contributes to the mobility of the nerves such that when tension is placed on any one peripheral
nerve, the tension is transmitted to several cervical nerve roots rather than just one nerve root.
The brachial plexus courses through the region known as the thoracic outlet. There are three primary sites
for compression or entrapment of the neurovascular structures in this region.

Interscalene triangle, bordered by the scalenus anterior and medius muscles and first rib
Costoclavicular space between the clavicle superiorly and the first rib inferiorly
Axillary interval between the anterior deltopectoral fascia, the pectoralis minor, and the coracoid
process
Structural anomalies, such as a cervical rib or malunion of a clavicular fracture, may compress or
entrap a portion of the plexus

When vascular and/or neurological symptoms are caused by impairments in the thoracic outlet, it is
commonly referred to as thoracic outlet syndrome.

Upper plexus injuries (C5, 6): The most common injury to the plexus involves compression or
tearing of the upper trunk. The mechanism involves shoulder depression and lateral flexion of the
neck to the opposite side. There is loss of abduction and lateral rotation of the shoulder and
weakness in elbow flexion and forearm supination (waiters tip position). Erbs palsy occurs with
birth injuries when the shoulder is stretched downward, although Benjamin6 cautioned that there
are maternal and infant factors that could contribute to this injury in addition to the forces applied
during delivery. A stinger occurs with injuries that might be sustained when a football player
lands on the upper torso and shoulder with the head/neck laterally flexed in the opposite
direction.
Middle plexus injuries (C7): Rarely seen alone.
Lower plexus injuries (C8, T1): Usually due to compression by a cervical rib or stretching the
arm overhead. Klumpkes paralysis (paralysis of the intrinsics of the hand) occurs in birth injuries
when the baby presents with its arm overhead.
Complete or total injury of the plexus: Complete paralysis from a total brachial plexus injury
may occur as a complication of birth; it is known as Erb-Klumpkes paralysis and is associated
with Horners syndrome in one-third of those severely affected.

Peripheral Nerves in the Upper Quarter

The brachial plexus terminates in five primary peripheral nerves that are responsible for innervating the
tissues of the upper extremity: (1) musculocutaneous, (2) axillary, (3) median, (4) ulnar, and (5) radial
nerves. Patterns of impairments from muscle weaknesses for each of these nerves are summarized in.
Common sites for compression or tension injuries for each of the nerves are described in this section.

1. Axillary Nerve: C5, 6

The axillary nerve emerges from the posterior cord of the brachial plexus; it passes laterally
through the axilla, sends a branch to the teres minor muscle, courses behind the surgical neck
of the humerus, and innervates the deltoid muscle and overlying skin.

The axillary nerve is vulnerable to injury with dislocation of the shoulder and fractures of the
surgical neck of the humerus.
If the upper trunk of the brachial plexus is stretched or injured, it affects the function of the
axillary nerve. Shoulder abduction and lateral rotation are impaired when this nerve is
affected.

2. Musculocutaneous Nerve: C5, 6

The musculocutaneous nerve emerges from the lateral cord of the brachial plexus and crosses
the axilla with the median nerve; it pierces and innervates the coracobrachialis and then
travels distally to innervate the biceps and brachialis muscles. It continues between these
muscles to the flexor surface of the elbow; after emerging from the deep fascia at the elbow, it
becomes the lateral cutaneous nerve of the forearm.
Isolated impingement of this nerve is not common; injury to the lateral cord or the upper
trunk of the brachial plexus affects the musculocutaneous nerve. When affected, the patient is
unable to flex the elbow with the forearm supinated and may have some instability in the
shoulder.

3. Median Nerve: C6-8

Bundles from the medial and lateral cords of the brachial plexus unite in the uppermost part
of the arm to form the median nerve. The median nerve courses the medial aspect of the
humerus to the elbow, where it is deep in the cubital fossa under the bicipital aponeurosis,
medial to the tendon of the biceps and brachial artery; it then moves into the forearm between
the two heads of the pronator teres muscle.

Hypertrophy of this muscle can compress the median nerve, producing symptoms that mimic
carpal tunnel syndrome except that the forearm muscles (pronator teres, wrist flexors,
extrinsic finger flexors) are involved in addition to the intrinsic muscles.
To enter the hand, the median nerve passes through the carpal tunnel at the wrist with the
flexor tendons. The carpal tunnel is covered by the thick, relatively inelastic transverse carpal
ligament. Entrapment of the median nerve in the tunnel, called carpal tunnel syndrome,
causes sensory changes and progressive weakness in the muscles innervated distal to the
wrist resulting in ape hand deformity (thenar atrophy and thumb in the plane of the hand).
The branch innervating the opponens muscle hooks over the carpal ligament two-thirds of the
way up the thenar eminence and can be entrapped separately.

4. Ulnar Nerve: C8, T1

The ulnar nerve emerges from the medial cord of the brachial plexus at the lower border of
the pectoralis minor and descends the arm along the medial side of the humerus. It passes
posterior to the elbow joint in the groove between the medial epicondyle of the humerus and
the olecranon of the ulna.
The groove is covered by a fibrous sheath, which forms the cubital tunnel. The nerve
possesses considerable mobility to stretch around the elbow as it flexes, although the nerve
can be easily irritated or entrapped at the elbow owing to its superficial location and anatomic
arrangement. It then passes between the humeral and ulnar heads of the flexor carpi ulnaris
muscle, another site where impingement could occur.
The only extrinsic muscles innervated by the ulnar nerve are the flexor carpi ulnaris and ulnar
half of the flexor digitorum profundus. The ulnar nerve enters the hand through a trough

formed by the pisiform bone and hook of the hamate bone and is covered by the volar carpal
ligament and palmaris brevis muscle, forming the tunnel of Guyon.
Trauma or entrapment in this region causes sensory changes and progressive weakness of
muscles innervated distal to the site, resulting in partial claw-hand deformity. Injury to the
nerve after it bifurcates leads to partial involvement, depending on the site of injury.

5. Radial Nerve: C6-8, T1

The radial nerve emerges directly from the posterior cord of the brachial plexus at the lower
border of the pectoralis minor. As it descends the arm, it winds around the posterior aspect of
the humerus in the musculospiral groove and continues to the radial aspect of the elbow.
In the arm it innervates the triceps, anconeus, and upper portion of the extensor and supinator
group of the forearm. Injury to this nerve may occur with shoulder dislocations and
midhumeral fractures. Also known to all therapists is crutch palsy, a condition of nerve
compression caused by leaning on axillary crutches.

Lumbosacral Plexus
The lumbar plexus is formed by the anterior primary divisions of the nerve roots L1, L2, L3, and part of
L4; the sacral plexus is formed from L4, L5, S1, and parts of S2 and S3. As with the brachial plexus, the
branches and divisions of the LS plexus organize the content of each of the peripheral nerves coursing
into the lower extremity. In addition, the anterior primary rami of the plexus receive postganglionic
sympathetic fibers from the sympathetic chain that innervate blood vessels, sweat glands, and piloerector
muscles in the lower extremity. Isolated injuries to the lumbar plexus or sacral plexus are not common;
symptoms more commonly arise from disc lesions or spondylitic deformities that affect one or more
nerve roots or from tension or compression of specific peripheral nerves.

Peripheral Nerves in the Lower Quarter

The lumbosacral plexus terminates in three primary peripheral nerves, which are responsible for
innervating the tissues of the lower extremity. They are the femoral and obturator nerves from the lumbar
plexus and the sciatic nerve from the sacral plexus. Common sites for compression or tension injuries are
described in this section.

1. Femoral Nerve: L2-4

The femoral nerve arises from the three posterior divisions of the lumbar plexus. It emerges
from the lateral border of the psoas muscle superior to the inguinal ligament and descends
underneath the ligament to the femoral triangle, lateral to the femoral artery, to innervate the
sartorius and quadriceps muscle group.
The iliopsoas is supplied superior to the ligament. Injuries to the nerve may occur with
trauma, such as fractures of the upper femur or pelvis, during reduction of congenital
dislocation of the hip, or from pressure during a forceps labor and deliveryresulting in
weakness of hip flexion and loss of knee extension. Symptoms may occur from neuritis in
diabetes mellitus.

2. Obturator Nerve: L2-4

The obturator nerve arises from the three anterior divisions of the lumbar plexus. It descends
through the obturator canal in the medial obturator foramen to the medial side of the thigh to
innervate the adductor muscle group and obturator externus.
Isolated injury to this nerve is rare, although uterine pressure and damage during labor may
cause the injury. If damaged, adduction and external rotation of the thigh are impaired, with
the individual having difficulty crossing his or her legs.

3. Sciatic Nerve: L4, 5; S1-3

The sciatic nerve emerges from the sacral plexus as the largest nerve in the body; its
component partsthe tibial and common peroneal nervescan be differentiated in the
common sheath. Muscles in the buttock region (external rotators and gluteal muscles) are
innervated by small nerves from the sacral plexus, which emerge proximal to formation of the
sciatic nerve. The sciatic nerve exits the pelvis through the greater sciatic foramen and
typically courses below, although sometimes through, the piriformis muscle.
Piriformis syndrome may occur from a shortened muscle, causing compression and irritation
of the nerve at this site. The nerve is protected under the gluteus maximus as it courses
between the ischial tuberosity and greater trochanter, although injury may occur in this region
with hip dislocation or reduction.
The tibial portion of the sciatic nerve innervates the biarticular hamstring muscles and a
portion of the adductor magnus; the common peroneal portion innervates the short head of
the biceps femoris. Proximal to the popliteal fossa, the sciatic nerve terminates when the
tibial and common peroneal nerves emerge as separate structures.

4. Tibial/Posterior Tibial Nerve: L4, 5; S1-3

The tibial nerve forms from the anterior primary rami of the sacral plexus, courses with the
common peroneal nerve as the sciatic nerve, and then emerges as a separate nerve proximal
to the popliteal fossa.
After coursing through the popliteal fossa, it sends a branch that joins a branch from the
common peroneal nerve to form the sural nerve and continues on as the posterior tibial nerve.
In the leg, it innervates the muscles of the posterior compartment, including the plantar
flexors, popliteus, tibialis posterior, and extrinsic toe flexors.

5. Commoin Peroneal Nerve: L4, 5; S1, 2

After it bifurcates from the sciatic nerve in the knee region, the common peroneal nerve
passes between the biceps femoris tendon and lateral head of the gastrocnemius muscle,
sends a branch to join the tibial nerve and form the sural nerve, and then comes laterally
around the fibular neck and passes through an opening in the peroneus longus muscle .

Pathophysiology
Peripheral nerve injury may result in demyelination, axonal degeneration, or both. Clinically, both
demyelination and axonal degeneration result in disruption of sensory function, motor function, or both in
the injured nerve. Depending on the severity and degree of nerve injury, recovery of function occurs with
remyelination and with axonal regeneration and reinnervation of the sensory receptors, motor end plates,
or both.

Etiology
Nerves are mobile and capable of considerable torsion and lengthening owing to their arrangement. Yet,
they are susceptible to various types of injury including:

Compression (sustained pressure applied externally, such as tourniquet, or internally, such as

from bone, tumor, or soft tissue impingement resulting in mechanical or ischemic injury).
Laceration (knife, gunshot, surgical complication, injection injury).
Stretch (excessive tension, tearing from traction forces).
Radiation.
Electricity (lightning strike, electrical malfunction).

Injury may be complete or partial and produces symptoms based on the location of the insult.

Biomechanical injuries to the peripheral nervous system are most commonly the result of friction,
compression, and stretch. Secondary injury can be from blood or edema.
Compressive forces can affect the microcirculation of the nerve, causing venous congestion and
reduction of axoplasmic transport, thus blocking nerve impulses; if sustained, the compression
can cause nerve damage. The endoneurium helps maintain fluid pressure and may provide
cushioning for nerves, especially when the nerves are close to the surface and subject to greater
pressure.
The insult can be acute from trauma or chronic from repetitive trauma or entrapment. Sites where
a peripheral nerve is more vulnerable to compression, friction, or tension include tunnels (soft
tissue, boney, fibro-osseus), branches of the nervous system (especially if the nerve has an abrupt

angle), points at which a nerve is relatively fixed when passing close to rigid structures (across a
boney prominence), and at specific tension points.
Response to injury can be pathophysiological or pathomechanical, leading to symptoms derived from
adverse tension on the nervous system. Results may be intraneural and/or extraneural.

Intraneural. Pathology that affects the conducting tissues (e.g., hypoxia or demyelination) or
connective tissues of the nerve (e.g., scarring of epineurium or irritation of dura mater) may
restrict the elasticity of the nervous system itself.
Extraneural. Pathology that affects the nerve bed (e.g., blood), adhesions of epineurium to
another tissue (e.g., a ligament), and swelling of tissue adjacent to a nerve (e.g., foraminal
stenosis) may restrict the gross movement of the nervous system in relation to surrounding
tissues.

Recovery from Nerve Injuries

Nerve tissue that has become irritated from tension, compression, or hypoxia may not have permanent
damage and shows signs of recovery when the irritating factors are eliminated. When the nerve has been
injured, recovery is dependent on several factors including the extent of injury to the axon and its
surrounding connective tissue sheath, the nature and level of the injury, the timing and technique of the
repair (if necessary), and the age and motivation of the person.

Nature and level of injury. The more damage to the nerve and tissues, the more tissue reaction
and scarring occur. Also, the proximal aspect of a nerve has greater combinations of motor,
sensory, and sympathetic fibers, so disruption there results in a greater chance of mismatching the
fibers, thus affecting regeneration. Regeneration is often said to occur at a rate of 1 inch per day,
but rates from 0.5 to 9.0 mm per day have been reported based on the nature and severity of the
injury, duration of denervation, condition of the tissues, and whether surgery is required.
Timing and technique of repair. Laceration or crush injuries that disrupt the integrity of the
entire nerve require surgical repair. For optimal nerve regeneration, timing of the repair is critical,
as are the skill of the surgeon and the technique used to align the segments accurately and avoid
tension at the suture line. Different regenerative potential outcomes following nerve repair have
also been reported based on groupings of specific nerves.
o Excellent regenerative potential: radial, musculocutaneous, and femoral nerves
o Moderate regenerative potential: median, ulnar, and
o tibial nerves
o Poor regenerative potential: peroneal nerve
Age and motivation of the patient. The nervous system must adapt and relearn use of the
pathways once regeneration occurs. Motivation and age play a role in this, especially in the very
young and the elderly.

Diagnostic Imaging

Imaging studies are appropriate in cases of suspected nerve tumors, though false-negative and
false-positive findings are possible in MRI evaluation of nerve tumors.
Imaging studies are appropriate in cases of suspected brachial plexus avulsion injury to evaluate
for avulsion of the nerve roots from the spinal cord. Computed tomography (CT) myelography
can be used to investigate for suspected brachial plexus avulsion injury, though it has largely been
replaced with magnetic resonance imaging (MRI) in this setting.

Electrodiagnostic studies are useful in detecting nerve injury, nerve compression, or both,
as well as in identifying early stages of recovery.
Electromyography (EMG) is performed at least 4 weeks after nerve injury. EMG testing
done earlier than this may yield false-negative findings because it takes 4-6 weeks for
muscle fibrillations to become apparent. Evidence of denervation is indicated by the
presence of fibrillations in the muscle. Reinnervation is signaled by the presence of motor
unit potentials (MUPs).
Nerve conduction studies are particularly useful in identifying secondary compression
sites that may be present. If the nerve is compressed at an entrapment site, such as the
carpal tunnel or the cubital tunnel, axonal regeneration may be impeded and thus limit
reinnervation. In cases of brachial plexus injury, nerve conduction studies can help
determine the presence of an avulsion injury. Intact normal distal sensory nerve
conduction and motor denervation are diagnostic of an avulsion injury.

Pharmacological Treatment
Narcotic analgesics
Pain control is essential to quality patient care. Analgesics ensure patient comfort, promote pulmonary
toilet, and have sedating properties, which are beneficial for patients who have sustained trauma or
injuries.
1. Fentanyl transdermal patch

Potent narcotic analgesic with much shorter half-life than morphine sulfate. DOC for
conscious sedation analgesia. Ideal for analgesic action of short duration during anesthesia
and immediate postoperative period.

Excellent choice for pain management and sedation with short duration (30-60 min) and easy
to titrate.

Easily and quickly reversed by naloxone.

After initial dose, subsequent doses should not be titrated more frequently than q3h or q6h
thereafter.

When using transdermal dosage form, pain in majority of patients controlled with 72-h
dosing intervals; however, some patients require dosing intervals of 48 hr.

2. Oxycodone

Relieves moderately severe to severe pain.

3. Morphine sulfate

DOC for analgesia because of reliable and predictable effects, safety profile, and ease of
reversibility with naloxone.

Various IV doses used; commonly titrated until desired effect attained.

4. Methadone

Used in management of severe pain; inhibits ascending pain pathways, diminishing

perception of and response to pain.

Tricyclic antidepressants
These agents are a complex group of drugs that have central and peripheral anticholinergic
effects as well as sedative effects. They have central effects on pain transmission and block the
active re-uptake of norepinephrine and serotonin.
1. Amitriptyline

By inhibiting re-uptake of serotonin and/or norepinephrine by presynaptic neuronal

membrane, may increase synaptic concentration in CNS.

Useful as analgesic for certain chronic and neuropathic pain.

2. Nortriptyline

Has demonstrated effectiveness in treatment of chronic pain.

By inhibiting reuptake of serotonin and/or norepinephrine by presynaptic neuronal

membrane, may increase synaptic concentration in CNS.

Pharmacodynamic effects, such as desensitization of adenyl cyclase and down-regulation of

beta-adrenergic receptors and serotonin receptors, also appear to play role in its mechanisms
of action.

Anticonvulsants
These agents are used to manage severe muscle spasms and provide sedation in neuralgia. They
have central effects on pain modulation.
1. Gabapentin

Has properties common to other anticonvulsants and has antineuralgic effects. Exact
mechanism of action not known. Structurally related to GABA but does not interact with
GABA receptors.

2. Lamotrigine

Triazine derivative used in neuralgia. Inhibits release of glutamate and inhibits voltagesensitive sodium channels, leading to stabilization of neuronal membrane.

Follow manufacturer's recommendation for dose adjustments.

3. Pregabalin

Structural derivative of GABA. Mechanism of action unknown. Binds with high affinity to
alpha2-delta site (a calcium channel subunit). In vitro, reduces calcium-dependent release of
several neurotransmitters, possibly by modulating calcium channel function. FDA approved
for neuropathic pain associated with diabetic peripheral neuropathy or postherpetic neuralgia
and as adjunctive therapy in partial-onset seizures.

Anesthetics
These agents stabilize the neuronal membrane so the neuron is less permeable to ions. This prevents the
initiation and transmission of nerve impulses, thereby producing the local anesthetic action.
1. Lidocaine anesthetic

Several recent studies have advocated topical administration of lidocaine as treatment of

PHN.

Lidocaine gel (5%) in a placebo-controlled study showed significant relief in 23 patients

studied. Lidocaine tape also decreased severity of pain.

PT Management
In general, recovery from nerve injury can be viewed as occurring in three phases.
Acute phase. This is early after injury or surgery when the emphasis is on healing and prevention
of complications.
Recovery phase. This is when reinnervation occurs. Emphasis is on retraining and re-education.
Chronic phase. This occurs when the potential for reinnervation has peaked, and there are
significant residual deficits. The emphasis is training compensatory function.

Acute Phase
Following injury or immediately after surgery (e.g., following decompression and release or following
repair of a lacerated nerve), there may be a brief period of immobilization to protect the nerve, minimize
inflammation, and minimize tension at the injured/repaired site. As soon as allowed, begin:

Movement. Begin range of motion (ROM) to minimize joint and connective contractures and
adhesions. This is dictated by the surgeon and type of surgery.

Splinting or bracing. Splinting or bracing may be necessary to prevent deformities due to

strength imbalances (e.g., use of a radial nerve splint to prevent wrist drop; a median nerve splint
to position the thumb in opposition; a plantarflexion splint to prevent foot drop) and to prevent
undue stress on the healing nerve tissue.
Patient education. Teach the patient safe movements and ways to protect the extremity to avoid
injury due to loss of sensation.

Recovery Phase
The recovery phase begins with signs of
reinnervation (volitional muscle contraction
and hypersensitivity). With nerve regeneration
and recovery, begin:
Motor retraining.When signs of
volutional muscle contraction occur,
position the muscle in its shortened
position; then ask the patient to hold.
Provide assistance as needed to
prevent the part from falling out of
the shortened position.
o Use electrical stimulation to
reinforce this active effort.
o When the muscles demonstrate
control of some range, begin
gravity-eliminated, activeassistive ROM. Continue to
protect the weak muscles with a
splint or brace.
Desensitization.As nerves regenerate,
the person experiences increased
sensitivity (hypersensitivity) in the
area that had previously been without
sensation. Use a graded series of
modalities and procedures to decrease
the irritability and increase sensory
awareness.
Discriminative sensory re-education.
This is the process of retraining the
brain to recognize a stimulus once the
hypersensitivity diminishes.
Techniques are summarized in
Patient education. Instruct the patient
to resume use of the extremity
gradually while monitoring pain,
swelling, or any discoloration; if
necessary, modify or temporarily avoid any aggravating activities. While the nerve is recovering
or if nerve recovery is incomplete, teach the patient preventive care to avoid injury

Chronic Phase
When the potential for reinnervation has peaked and there are minimal or no signs of reinnervation,
emphasize training for compensatory function. The person will probably have to continue to wear the
supportive splint or brace, and preventive care must continue indefinitely.

Reference:
Therapeutic Exercise Foundations and Techniques, Sixth Edition - Kisner, Carolyn
http://www.hopkinsmedicine.org/neurology_neurosurgery/centers_clinics/peripheral_nerve_surgery/condi
tions/peripheral_nerve_system.html
http://emedicine.medscape.com/article/1270360-overview#a9
http://www.medscape.com/viewarticle/758724_5