Peripheral Nerve Injuries

(PNI)
Overview
 Definition
 Epidemiology
 Etiology
 Basic Medical Sciences
 Pathophysiology
 Classification of Nerve Injuries
 Clinical Manifestations
 Diagnosis
 Prognosis/Complications
 Medical/Pharmacological Management
 Rehabilitation
 Specific Nerve Injuries
Definition

 Peripheral
nerve injury may result in motor, sensory, and/or
sympathetic impairments.

 Inaddition, pain may be a symptom of nerve tension or

compression
Epidemiology

 PNI can occur in almost all ages

 UE > LE
 The median nerve is commonly entrapped at the wrist, more
common in women; occurs bilaterally in about 50% of cases,
associated with repetitive hand and wrist movements; great
majority of cases is idiopathic
 The ulnar nerve is 2nd most commonly entrapped
Etiology

 PNI may be caused by trauma (mc) due to blunt or

penetrating injury, constriction of facial bands, lacerations,
compression and crush injury, and stretching of nerves

 Fracture and fracture/dislocation carry a high risk associated

of nerve damage

 Nerve injury after shoulder dislocation occurs in 48% of cases

Etiology
 The incidence of radial nerve damage following humeral
fracture is 11%

 Ulnar neuropraxia is the most commonly identified nerve

lesion associated with fracture dislocation at the elbow

 PNImay also be injurious owing to violent pulling of arms,

blows or weight upon the neck, childbirth injuries, gunshot
and stab wounds, automobile accidents
Basic Medical Sciences
 Axolemma – surface membrane of an axon
 Endoneurium – connective tissues which surround each axon
 Perineurium – surrounds each fascicle
 Epineurium – surrounds the entire peripheral nerve fiber
 Schwann cell – forms the myelin sheath which insulates the
axon as well as speed the conduction along the nerve fibers
 Classification of Nerve Fibers By Speed of
Conduction and Size
 Peripheral
nerves contain a mixture of sensory, motor, and
sympathetic neurons

 Alpha motor neuron (somatic efferent fibers): cell bodies

located in the anterior column of spinal cord; innervates
skeletal muscles

 Gamma motor neurons (efferent fibers): cell bodies located in

lateral columns of spinal cord; innervates intrafusal muscle
fibers of the muscle spindle
 Classification of Nerve Fibers By Speed of
Conduction and Size
 Sensory neurons (somatic afferent fibers): cell bodies located
in the dorsal root ganglia; innervates sensory receptors

 Sympathetic neurons (visceral afferent fibers): cell bodies

located in the sympathetic ganglia; innervates sweat glands,
blood vessels, viscera & glands
Pathophysiology/MOI

 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
 Laceration
 Stretch
 Radiation
 Electricity
Pathophysiology/MOI
 Injury may be complete or partial and produces symptoms based on
the location of the insult

 Biomechanical injuries to the PNS 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
Pathophysiology/MOI

The insult can be acute from trauma or chronic from repetitive

trauma or entrapment. Sites where a peripheral nerve is more
vulnerable to compression, frictions, or tension include:
 Tunnels
 Branches of the NS (esp. if the nerve has an abrupt angle)
 Points at which a nerve is relatively fixed when passing close to
rigid structures (bony prominences)
 Specific tension points
Classification of Nerve Injuries

 Nerve injuries are classified based on structural and functional

changes that occur in the nerve with various degrees of
damage

 Determines effect on prognosis

 Seddon
 Sunderland
 Seddon’s Classification and
Characteristics of Nerve Injury
 NEUROPRAXIA
 Segmental demyelination
 Action potential slowed/blocked at point of demyelination; normal
above and below point of compression
 Muscle does not atrophy; temporary sensory symptom
 Cause: mild ischemia from nerve compression or traction
 Recovery is usually complete
 AXONOTMESIS
 Loss of axonal continuity but connective tissue coverings remain
intact
 Wallerian degeneration distal to lesion
 Muscle fiber atrophy and sensory loss
 Cause: prolonged compression or stretch causing infarction and
necrosis
 Recovery is complete – surgical intervention may be required
 NEUROTMESIS
 Complete severance of nerve fiber with disruption of connective
tissue coverings
 Wallerian degeneration distal to lesion
 Muscle fiber atrophy and sensory loss
 Cause: gunshot or stab wounds, avulsion, rupture
 No recovery without surgery – recovery depends on surgical
intervention and correct regrowth of individual nerve fibers into
endoneural tubes
Sunderland’s Classification
Sunderland Classification

 First degree injury:

 demyelinated nerve
 a physiological local conduction block
 neuropraxia in the Seddon scheme
 conservative management
 recovery expected over weeks to months
 Second-degree injury:
 some axons disrupted
 endoneurial sheaths and surrounding connective
tissue layers remain intact
 Wallerian degeneration distally
 equivalent to axonotmesis in Seddon scheme
 treatment is conservative
 regeneration of axons can be followed clinically by an
advancing Tinel's sign
 complete recovery can be expected over months
 Third-degree injury:
 axons and endoneurial sheaths disrupted
 scarring replaces existing structures
 perineurium and connective tissue layers outside of this remains
 most of these injuries will recover spontaneously but partially
 Fourth-degree injury:
 axon, endoneurium and perineurium disrupted
 scarring replaces existing structures
 epineurium remains
 scar blocks all neuronal regeneration
 no recovery likely without operative management
 Fifth-degree injury:
 nerve transection
 all structures including epineurium divided
 no recovery expected without operative management
(Comparison)
Clinical Manifestations

 Loss of motor function

 Muscle atrophy
 Alterations in cutaneous sensibility
 Alterations in reflex activity
 Diabetic neuropathy

Clinical Manifestations

 Disturbance in vasomotor activity; vasodilation in 2 weeks;

vasoconstriction to cold temperature, (-) sweating, pilomotor
erection; interruption of sympathetic fibers
 Trophic changes due to circulatory compromise; skin –
transparent, shiny, fibrosis of subcutaneous tissue, changes in
fingernails, increased hair
 Causalgia – triad of hyperpathia, trophic changes, autonomic
phenomena over the region of distribution of nerve
Diagnosis

 A complete diagnosis of a damaged nerve should include the

identification of the ff:
 Nerves injured
 Anatomical level of injury to the nerve
 Pathological type/class of injury
 Associated bone, vascular and tendon injuries
 Deformities and contractures
 Any evidence of recovery of the nerve palsy
Diagnostic Tests

 Electromyography (EMG). In an EMG, a thin-needle electrode

inserted into your muscle records your muscle's electrical activity at
rest and in motion. Reduced muscle activity can indicate nerve
injury.
 Nerve conduction study. Electrodes placed at two different points
in your body measure how well electrical signals pass through the
nerves.
 Magnetic resonance imaging (MRI). An MRI uses powerful
magnets and radio waves to produce detailed images of the nerves
that may be damaged and the affected area.
Prognosis/Complications

 Nerve conduction deficit is completely reversible in

neuropraxia. Large diameter fibers are affected more than the
smaller. Recovery begins on average 6 weeks post injury as a
result of remyelination
Prognosis/Complications

 There is good prognosis in axonotmesis although wallerian

degeneration occurs distal to the lesion. Nerve regeneration is
usually effective and proceeds at a rate of about 1 to 2 mm per
day, in serial order with more proximal muscles innervated
before distal muscles
Prognosis/Complications

 Neurotmesis has poor prognosis because of total fiber

disruption and this condition generally requires a repair
Prognosis/Complications

 Five possible outcomes of nerve regeneration:

 Exact innervation of its native target organ with return of function
 Exact innervation of its native target organ but no return of function
due to degeneration of the end organ
 Wrong receptor reinnervated in the proper territory, improper input
 Receptor reinnervation in wrong territory causing false localization of
input
 No connection with an end organ
Prognosis/Outcome

 Recovery depends on whether the nerve Is able to grow back

within the sheath

 Reestablishment of anatomic motor and sensory

reinnervation does not guarantee functional recovery

 Functional
recovery can take up to two yeas, and
improvement may be noted up to 4 years
Prognosis/Outcome

 Recovery of sensation varies but can be excellent or good

 In general, distal nerve injuries do better than proximal ones
 Younger persons tend to do better than older persons
 Pure sensory/motor > mixed nerve repair
 Cut/slice injuries tend to do better than crush injuries or
avulsion injuries
Medical/Pharmacological Management

 Treatment of underlying conditions

 Narcotic analgesics, local anaesthetics and corticosteroid
injection given for extreme pain and inflammation
 Surgical decompression or transposition of nerve
 Nerve grafts and transplants for severe traumatic injuries
 High caloric diet with Vit. B complex given for inflammatory
conditions
INJURIES OF INDIVIDUAL NERVES
Erb-Duchenne Palsy

 Upper-arm paralysis
 C5-C6 (upper plexus)
 Cause: traction injury, radiation
 Mechanism involves shoulder depression and lateral flexion of
the neck to opposite side.
 Loss of sensation down to the lateral side of arm
 Motor paralysis: there is loss of abduction and lateral rotation
of the shoulder and weakness on elbow flexion and FA
supination
 Waiter’s tip /
porter’s tip /
policeman’s tip:
Shoulder IR and
adduction; elbow
extended and FA
pronated
Klumpke’s Palsy

 Lower arm paralysis

 C8-T1 (lower plexus)
 Cause: obstetrical traction injury (when baby presents its
arm overhead; compression by a cervical rib or stretching
the arm overhead
 “clawhand” (paralysis of intrinsics)
 Horner’s syndrome (T1): ptosis, myosis, anhidrosis,
enopthalmia
Klumpke’s Palsy

 Lower Trunk involvement (C8-T1)

 Thoracic Outlet syndrome
 Pancoast syndrome
 Scalenus anticus sydrome
 Cervical rib syndrome
Cervical rib syndrome
Prognosis

 Upper arm paralysis- considerable return of power is to be

expected
 Lower arm paralysis- intrinsic muscles of the hands have
relative poor prognosis, and a claw hand deformity may
develop
 Palsy of the whole arm (Erb-Klumpke)- likely to show only
incomplete recovery
Nerve to Subclavius

 C5-C6
 Aka subclavian nerve
 Weakness or paralysis of the
subclavius muscle  slight forward
displacement of the lateral end of
clavicle
Suprascapular nerve

 C5-C6
 Motor: atrophy of the supraspinatus, infraspinatus, difficulty
initiating abduction and ER at the shoulder joint
Thoracodorsal nerve

 C6, C7, C8
 Associated with injury to the
posterior cord
 Paralysis of the latissimus dorsi
results in winging of the inferior
angle of the scapula and inability
to powerfully extend the arm
Subscapular Nerve

 C5-C6
 Damage to posterior cord; rare
 Paralysis of the subscapularis, weakness in IR
 Paralysis of the teres major
Subscapularis Teres Major
Axillary Nerve

 C5-C6
 Injury: Fracture at the surgical neck of the humerus, forceful
hyperextension of the shoulder
 Paralysis of the deltoids, flattening of the shoulders and loss
of its normal roundness
 Sensation: loss of sensation on the lateral aspects of the
upper arm
Deltoid muscle atrophy
Musculocutaneous Nerve

Loss of musculocutaneous nerve

leads to near-complete loss of
elbow flexion in almost all
patients. 

The rare patient maintains some

ability to flex the elbow using the
brachioradialis muscle innervated
by the radial nerve
Radial Nerve
 C5, C6, C7, C8, T1
Radial Nerve Injury
 1. Axillary (highest level)
 Crutch palsy – Fx of upper level of humerus
 All mm paralyzed
 (+) wrist drop

 2. Spiral Groove
 Most frequent site of injury of radial nerve
 Fx of midshaft of humerus
 Honeymooner’s palsy/Saturday night palsy
 (+) wrist drop
 Spared: triceps
 3. Elbow level

 Posterior interosseus nerve syndrome

 Supinator syndrome
 Radial tunnel syndrome
 Entrapment of the radial nerve
proximal to its bifurcation produces
both motor and sensory deficits
resulting in pain in the forearm,
weakness of finger and wrist extension,
and eventual muscle atrophy.
 Spared: triceps, anconeus, ECRL,
Brachioradialis
 (-) wrist drop
Radial Nerve Injury

 4. Wrist level
 (+) cheralgia paresthetica or
Wartenberg disease
 Compression or trauma to the
superficial branch
 Cause: tight watches & wrist band,
handcuffs
 Numbness, tingling, burning or
pain
 No motor impairment
Ulnar Nerve (C8-T1)

1. Elbow Level (highest)

 Cubital tunnel syndrome
 “tardy ulnar palsy”
 Entrapment of the ulnar nerve at the elbow
 Weakness, numbness, paresthesia or pain
in the 4th and 5th fingers
 Provoked during prolonged elbow flexion
Normal carrying angle: 5 degrees for males; 10-15 degrees for females
If >15 degrees = cubitus valgus
If <5 degrees = cubitus varus
 Ulnar Nerve

2. FCU
 Under the arcuate ligament,
between 2 heads of the FCU
 *same as cubital tunnel syndrome
Ulnar Nerve
3. Wrist
 At the Tunnel of Guyon
 Spared: FCU & ½ of FDP
 Muscular atrophy - Primarily the hypothenar muscles and
interossei with muscle sparing of the thenar group:
▪ weakened finger abduction and adduction (interossei)
▪ weakened thumb adductor (adductor pollicis)
 Sensory loss and pain -
▪ May involve the palmar surface of the fifth digit and
medial aspect of the fourth digit.
▪ Dorsum of medial aspect of the fourth finger and the
dorsum of the fifth finger don’t have sensory loss.
 Ulnar Claw may present (sign of Benediction)
 Unopposed action of the EDC in
the 4th and 5th digits
 MCP hyperextended and DIP
and PIP are flexed
 Inability to abduct and adduct
fingers
 Inability to flex DIP weak thumb
opposition
 Total loss of opposition and
abduction of little finger
Median Nerve (C5-T1)

 Injury Levels:
 Above the elbow
 At the elbow
 Within the proximal FA
 At the wrist
 Within the wrist
Biker’s Palsy
Median Nerve Injury
1) Above the elbow
• Common mechanism of injury: A supracondylar humerus fracture
• Motor deficit: Loss of pronation of forearm, weakness in flexion of
the hand at the wrist, loss of flexion of radial half of digits and
thumb, loss of abduction and opposition of thumb.
• Presence of an ape hand deformity when the hand is at rest, due to
hyperextension of index finger and thumb, and an adducted thumb.
• Presence of benediction sign when attempting to form a fist, due to
loss of flexion of radial half of digits.
• Sensory deficit: Loss of sensation in lateral 3 1⁄2 digits including their
nail beds, and the thenar area
 Median Nerve Injury

2) At the elbow
 Entrapment at the level of
the elbow or the proximal
forearm could be due to the
pronator teres syndrome.
Median Nerve Injury

3) Within the proximal forearm: Anterior interosseous syndrome

 Common mechanisms: Tight cast, forearm bone fracture

 Motor deficit: Loss of pronation of forearm, loss of flexion of radial half of digits
and thumb.
 Sensory deficit: None
Normal Abnormal

(-) OK sign / Kiloh-Nevin syndrome

Median Nerve Injury

4) At the wrist
 Common mechanism: Wrist laceration
 Motor deficit: Weakness in flexion of radial half of digits and thumb,
loss of abduction and opposition of thumb.
 Presence of an ape hand deformity when the hand is at rest, due to and
hyperextension of index finger and thumb, and an adducted thumb.
 Presence of benediction sign when attempting to form a fist, due to
weakness in flexion of radial half of digits.
 Sensory deficit: Loss of sensation in lateral 3 1⁄2 digits including their
nail beds, and the thenar area.
Median Nerve Injury
 Median Nerve Injury

5) Within the wrist: Carpal tunnel

syndrome

 Common mechanism: Carpal tunnel

syndrome, an injury by compression in the
carpal tunnel, without transection of the
median nerve, due to overuse by activities
such as keyboard typing and cooking.

 Motor deficit: Weakness in flexion of radial

half of digits and thumb, weakness in
abduction and opposition of thumb.
Median Nerve Injury
 Sensory deficit: Numbness and tingling in lateral 3 1⁄2 digits
including their nail beds