PERIPHERAL NERVE INJURIES

Outlines

1. Anatomy of peripheral nerves

2. Mode of injury
3. Classification of peripheral nerve injuries
4. Treatment modalities of peripheral nerve injuries
5. Nerves injuries of upper limb
6. Nerves Injuries of lower limb
7. Nerve Entrapment Syndrome
Anatomy of peripheral nerve
Functions of the Nervous System
· Sensory input – gathering information
·To monitor changes occurring inside and outside the
body
· Integration - To process and interpret sensory input and
decide if action is needed
· Motor output
·A response to stimuli
·Activates muscles or glands
CLASSIFICATION OF NERVOUS SYSTEM
Peripheral 8 cervical

nervous
system 12 thoracic

5 lumbar
Spinal
nerves (31 5 sacral
pairs)
1 coccygeal
Cranial
nerves (12
pairs)
Peripheral Nerve
PN fare fairly strong because it
supported and protected by 3
connective tissue coverings:
1) Endoneurium
2) Perineurium Dorsal root -> sensory neuron &
3) Epineurium ganglion
Ventral root -> motor neurons
MODE OF INJURY
MODE OF INJURY
Mechanism of injury:
 Stretch-related injuries
 Ischemia
 Compression
 Laceration
Stretch-related injuries
When traction forces exceed the nerve's capacity to stretch, injury may occurs.
If the force applied is great enough, a complete loss of continuity may occur as
in a brachial plexus avulsion.
Injuries of this type can be seen:
 in isolation (eg: Erb palsy and similar brachial
 plexus birth-related injuries) or
 a/w extremity # at points where nerves and
bone are in close approximation (eg: radial
nerve injury following humeral #)
Laceration
Lacerations (eg: knife blade are another common PNI type)
These can be complete transections, but more often some nerve
element of continuity remains.
Compression
Radial nerve compression as well as entrapment neuropathies and do
not involve a tearing of the neural elements.
Total loss of both motor and sensory function may occur.
Transient ischemia
 Acute nerve compression causes:
numbness & tingling within 15 minutes
loss of pain sensibility after 30 minutes
muscle weakness after 45 minutes
 Relief of compression is followed by:
intense paraesthesia lasting up to 5 minutes
Feeling is restored within 30 seconds
Full muscle power after about 10 minutes
 These changes due to transient endoneurial anoxia & they leave no trace of nerve
damage
CLASSIFICATION OF PERIPHERAL NERVE
INJURY
CLASSIFICATION
 SEDDON’S
CLASSIFICATION
1. Neuropraxia:
• a reversible block to nerve conduction in which
there is loss of sensation & muscle power,
followed by spontaneous recovery after a few
days or weeks.
• The nerve is intact but there is demyelination of
axons in some segments
• seen in ‘Saturday night palsy’, torniquet palsy
2. Axonotmesis :

- seen typically after closed fractures and dislocations.

-axonal interruption.
- loss of conduction but the nerve is in continuity and the neural
tubes are intact.
- Wallerian degeneration. Distal to the lesion, and for a few
millimetres retrograde, axons disintegrate and are resorbed by
phagocytesproliferation of Schwann cells and fibroblasts lining
the endoneurial tubes.
-The denervated target organs (motor end-plates and sensory
receptors) gradually atrophy, and if they are not reinnervated
within 2 years they will never recover.
-Axonal regeneration starts within hours of nerve damage
- These axonal processes grow at a speed of 1–2 mm per day.
3. Neurotmesis :

• disruption on the continuity of axon &

supporting structures (nerve trunk)
• usually in open wound
• some recovery possible but much more
likely with surgical nerve repair
• Rapid wallerian degneration also occur, but
damage to endoneural tube is extensive and
multiple segments,so regenerated fibres
usually mingles with proliferated schwann
cells and fibroblast to form Neuroma.
Treatment Principles
Nerve Exploration
Closed injuries usually recover spontaneously and it is worth waiting until
the most proximally supplied muscle have regained function.
Exploration is indicated:
(1) if the nerve was seen to be divided and needs to be repaired
(2) if the type of injury (e.g. a knife wound or a high energy injury)
suggests that the nerve has been divided or severely damaged
(3) if recovery is inappropriately delayed and the diagnosis is in doubt.
Primary Repair
A divided nerve is best repaired as soon
as possible
Primary suture at the time of wound
toilet has considerable advantages:
the nerve ends have not retracted much
their relative rotation is usually
undisturbed
there is no fibrosis.
Delayed repair
Late repair, i.e. weeks or months after the injury, may be indicated
because: (1) a closed injury was left alone but shows no sign of recovery
at the expected time; (2) the diagnosis was missed and the patient presents
late; or (3) primary repair has failed.
The options must be carefully weighed: if the patient has adapted to the
functional loss, if it is a high lesion and re-innervation is unlikely within
the critical 2-year period, or if there is a pure motor loss which can be
treated by tendon transfers, it may be best to leave well alone.
 Nerve Grafting
Free autogenous nerve grafts can be
used to bridge gaps too large for direct
suture. The sural nerve is most
commonly used; up to 40 cm can be
obtained from each leg. Because the
nerve diameter is small, several strips
may be used (cable graft).
The graft should be long enough to lie
without any tension, and it should be
routed through a well-vascularized bed.
The graft is attach at each end either by
fine sutures or with fibrin glue.
Nerve transfer
In root avulsions of the upper brachial plexus, too
proximal for direct repair, nerve transfer can be
used. The spinal accessory nerve can be
transferred to the suprascapular nerve, and
intercostal nerves can be transferred to the
musculocutaneous nerve.
If biceps has failed because too much time has
passed since the injury, an entire muscle (gracilis
or latissimus dorsi) can be transferred as a free
flap, attached between elbow and shoulder and
then innervated by joining intercostal nerves or
the spinal accessory nerve to the stump of the
original nerve supplying that muscle.
Nerve Injuries Of The Upper Limb
LONG THORACIC NERVE,
C5, C6,C7
Nerve maybe damaged in shoulder or neck injuries or by carrying heavy
loads on the shoulder.
Classic sign of serratus anterior palsy: winging of the scapula.
Except in direct injury or division, the nerve usually recovers
spontaneously, though this may take a year or longer.
Spinal accessory nerve
Spinal nerve supplies sternocleidomastoid muscle and runs obliquely across the
posterior triangle of the neck to innervates upper half of the trapezius.
Easily injured in stab wounds and operations in the post. triangle of the neck.
Clinical features:
Pain in the shoulder
Weakness on abduction of the arm
Mild winging scapula on active abduction against resistant.
Wasting of the trapezius & drooping of the shoulder (in late cases)

Mx:
Explored immediately and repair the nerve-in stab injuries
If the exact cause is uncertain, wait for 6 weeks for signs of recovery. If no, nerve should
be repaired or grafted.
 Axillary nerve, C5,C6
Supply -motor: deltoid, teres minor
-sensory : skin over upper lateral part of arm
Injured during shoulder dislocation or # of the humeral neck.
Clinical features:
Patient cannot abduct the shoulder (even when pain subsides)
Deltoid weakness
Small patch of numbness over the deltoid
The nerve is spontaneously recover
If no signs of recovery by 8 weeks and electro-diagnostic tests
suggest denervation, the nerve should be explored and grafted.
Good prognosis is expected if surgery is performed within 12
weeks of injury.
If the surgery fails, consider arthrodesis or tendon transfer.
RADIAL NERVE INJURY
C5-T1
CAUSES and symptoms

Low lesions
Fractures or dislocations at the elbow
Open wound
Surgical accident
Cannot extend metacarpophalangeal joints
High lesions
Fractures of the humerus
After prolonged tourniquet pressure
Fall asleep with the arm dangling over the back of a chair (Saturday night
palsy)
Obvious wrist drop due to weakness of the wrist extensors
Small patch of sensory loss on the back of the hand at the base of the thumb
Very high lesions
Pressure in the axilla (crutch palsy)
Triceps muscle is wasted and paralysed
Treatment
Injuries cause by pressure
Lesion is usually an axonotmesis
Spontaneous recovery is the rule
No sign of recovery by 8-12 weeks : nerve should be explored and
repaired or grafted
Open wounds
Should be explored and the nerve repaired or grafted as soon as
possible
Fracture humerus
If no nerve injury on admission and the signs appear only after
manipulation or operative treatment, chances of an iatrogenic
injury are high
Nerve should be explored and repaired
All cases
Wrist should be splinted in extesion and the
metacarpophalangeal and finger joint are kept moving while
waiting for recovery
Lesions that do not recover
Disability can be largely overcome by suitable tendon transfers
Ulnar nerve injury
C8-T1
 Causes and symptoms
Low lesions
Pressure (eg : deep ganglion)
Laceration at the wrist
Hypothenar wasting
Hand is clawed due to
paralysis of the intrinsic
muscle
Finger adduction is weak
Loss of thumb adduction
makes pinch difficult
(Froment’s test)
Sensation is lost over little and
a half of ring fingers
High lesions
Elbow fractures
Much later if malunion produces marked
cubitus valgus with tension on the nerve
where it skirts the medial epicondyle
Nerve entrapment in the cubital tunnel
(lying for long periods with the elbow
flexed and pressing on the bed)
Visible deformity is not marked (ulnar
half of flexor digitorum profundus is
paralysed and the fingers are therefore
less ‘clawed’)
Motor and sensory loss are the same with
low lesions
treatment
Exploration and suture the nerve
Transposing the nerve in front of the elbow
If No recovery occur:
Hand function is significantly impaired because of loss of power in
matacarpophalangeal flexion, finger adduction, pinch and grip
Tendon transfers – restore only a modest level of function
Median nerve injury
C5-T1
Causes and symptoms
High lesions
Forearm fractures
Elbow dislocations
Stabs and gunshot may
damage the nerve at any level
Signs same as in low lesions
plus long flexors to the
thumb, index and middle
fingers are paralysed
Low lesions
Cuts in front of the wrist
Carpal dislocations
Thenar eminence is wasted
Thumb opposition are weak
Sensation is lost over the radial
three and a half digits
Trophic changes may be seen
treatment
Nerve is divided and suture should always be atempted
If cannot be done without producing tension, nerve grafts
can be placed in the gap
If No recovery
Disability is severe (because of sensory loss)
Tendon transfer can restore thumb opposition
NERVE INJURIES OF THE LOWER LIMB
FEMORAL NERVE INJURY
L2-L4
 Causes
Direct injury (trauma)/ gunshot wound
Traction during an operation
Compression or entrapment of the nerve by nearby parts of the body or
disease-related structures (such as a tumor or abnormal blood vessel)
A broken pelvis bone
Internal bleeding in the pelvis or abdomen
Signs & Symptoms
Weakness of knee extension
Numbness of anterior thigh and medial aspect of the leg
Problem while ascending or descending stairs
especially down, with a feeling of the knee "giving way"
Depressed knee jerk
The quadriceps muscles may be smaller than normal
 Treatment
Thigh hematoma may need to be evacuated
Clean cut of the nerve may be treated successfully by careful suturing or
grafting
Removal of tumours
Corticosteroid injections for treating inflammation and swelling
Pain killers to control pain
SCIATIC NERVE
INJURY
L4-L5, S1-S3
Causes
Gunshot wounds
Operative (iatrogenic) accidents
Complication of hip replacement
Usually partial lesion
Misdiagnosed as a common peroneal compression injury

Traction and compression are more common and occur with

local trauma
 Signs & Symptoms
Foot drop
Numbness and parasthesia in the leg and foot
Painful limb (direct injury to nerve)
Muscles below the knee are paralysed and sensation is absent in most of
the leg
If only the deep peroneal component of the nerve is affected, paralysis is
incomplete and the signs are easily mistaken for common peroneal nerve
injury
Late features : wasting of calf muscles and trophic ulcers
Treatment
Iatrogenic lesions
Direct injury : the nerve should be explored
Otherwise : wait for spontaneous recovery
In all cases : foot should be splinted to prevent a permanent
equinus deformity
PERONEAL NERVE INJURY
L4-S3
Causes
Lateral ligament injuries
Knee forced into varus
Pressure from a splint or a plaster cast
Lying with the leg externally rotated
Signs & Symptoms

Foot drop
Both dorsiflexion and eversion are weak. Causing a tendency to trip and fall while
walking
Loss of sensation over the front and outer half of the leg and dorsum of
the foot
Superficial branch
Peroneal muscles are paralysed, eversion are lost, loss of sensation over the outer
side of leg and foot
Deep branch
Threatened in anterior compartment syndrome
Pain, abnormal sensation and weakness of dorsiflexion, sensory loss around the
first web space on the dorsum of foot
 Treatment
Threatened compartment syndrome
Treat as emergency and may need immediate decompression
Open wound : explore nerve and suture
Apply splint to control foot drop while recovery is awaited
Protect skin against ulceration
No recovery :
Improve disability by transferring the tibialis posterior tendon to the
dorsum of the foot ( acts as dorsiflexor)
alternative : operative stabilization of hindfoot
Permanent splintage
Nerve Entrapment Syndromes
Carpal Tunnel Syndrome
Median nerve
Most common entrapment neuropathy sensory distribution
Median nerve compression by the Median nerve

transverse carpal ligament

More women than men
Often bilateral but almost without exception
more prominent in the dominant hand
Paresthesia usually in median nerve
distribution
(thenar eminance spared as supplied by
palmar cutaneous sensory branch which
comes off proximal to the carpal tunnel
Advanced cases may have thenar muscle Flexor tendons
Transverse
weakness/wasting effecting thumb
carpal ligament
opposition and abduction
Causes of CTS

Often idiopathic
Repeated stress to connective tissue
Repetitive hand use
Individuals with small carpal tunnel
Thenar eminence wasting
Systemic disorders (RA,
hypothyroidism, DM, sarcoid,
amyloidosis
Mass in wrist (ganglion cyst,
neurofibroma, arteriovenous
malformation)
Persistent wrist flex ie during sleep
 Phalen’s good specific (75-93%) and
moderate sensitive (64-75%) for CTS
 Tinel’s similar spec & sens (tetro et al,
PHALEN’S TEST
1995 Bolland et al, 2008) Holding the wrist fully flexed for a minute
 Carpal compression test more spec less Tingling/ pain
sensitive
 Nerve Conduction Study (NCS) and
Electromypography (EMG) can help
confirm diagnosis and discount others
(however can be normal in 25% of
cases)
Treatments for CTS
Remove causative factors Wrist stretches
Splints (night) Wrist mobs
NSAIDs Median nerve mobs
Surgical decompression (open safer
than closed but longer recovery)
Ulnar Neuropathy at the Elbow
Second most common PNE in upper
limb
Caused by compression of ulnar nerve in
the ulnar groove or cubital tunnel
Results from repeated trauma,OA
following #, ganglion/tumours/fibrous
tissue
Manifests as progressive loss of grip and
pinch strength and interosseus muscle
function
Clumsiness
Wasting hypothenar eminence
Thenar and hypothenar eminence wasting in the left hand
Interosseous muscle wasting
Ulnar neuropathy cont

 May be minimal sensory loss reported

but may be evident 4th and 5th finger on
assesment
 Elbow pain common spreading to wrist
 Ulnar nerve may be palpable and tender
 Paresthesia provoked by tinel’s, ulnar
nerve compression or elbow flexion
 Making a fist may result in 4th and 5th
finger not flexing (FDP innervated by
UN)
Ulnar neuropathy cont
Several classic hand postures may be
present
Benediction posture
Wartenberg’s sign
Froment’s sign
Treatment for UNE
Conservative treatment ie avoid
aggrevating factors
Elbow splint
Surgical options
Transportation
Decompression cubital tunnel
Medial epicondylectomy
Many will recover spontaneously but
surgery very effective (Padua et al 2002) Ulnar nerve transportation
90% of pt’s with mild symptoms will
recover with conservative Rx (Robertson
& Saratsiotis 2005)
Thoracic Outlet Syndrome
Thoracic outlet syndrome is a
group of disorders that occur
when the blood vessels or nerves
in the space between the
collarbone and the first rib
(thoracic outlet) become
compressed. This can cause pain
in the shoulders and neck and
numbness in the fingers.
 Causes
 Anatomical defects. Inherited defects
Repetitive
 activity. Doing the same thing
that are present at birth (congenital) may
repeatedly can, over time, wear on the body's
include an extra rib located above the tissue.
first rib (cervical rib) or an abnormally
tight fibrous band connecting the spine to Px may notice symptoms of thoracic outlet
the rib. syndrome if their job requires to repeat a
movement continuously, such as typing on a
computer, working on an assembly line or
 Poor posture. Drooping the shoulders or
lifting things above the head, ie stocking
holding the head in a forward position shelves.
can cause compression in the thoracic Athletes, such as baseball pitchers and
outlet area. swimmers, also can develop thoracic outlet
syndrome from years of repetitive movements.
 Trauma. A traumatic event, such as a car
accident, can cause internal changes that
then compress the nerves in the thoracic
outlet. The onset of symptoms related to
 Types
 Neurogenic (neurological) thoracic
outlet syndrome. This form of
thoracic outlet syndrome is
characterized by compression of the
brachial plexus. The brachial plexus
is a network of nerves that come
from the spinal cord and control
muscle movements and sensation in
the shoulder, arm and hand.
 In the majority of thoracic outlet
syndrome cases, the symptoms are
neurogenic.
 Vascular thoracic outlet
syndrome. This type of thoracic outlet
syndrome occurs when one or more of
the veins (venous thoracic outlet
syndrome) or arteries (arterial thoracic
outlet syndrome) under the collarbone
(clavicle) are compressed.
 Nonspecific-type thoracic outlet
syndrome. This type is also called
disputed thoracic outlet syndrome.
-People with nonspecific-type thoracic
outlet syndrome have chronic pain in the
area of the thoracic outlet that worsens
with activity, but the specific cause of the
pain can't be determined
 Symptoms
When nerves are compressed
Wasting in the fleshy base of thumb
(Gilliatt-Sumner hand)
Numbness or tingling in the arm or fingers
Pain or aches in the neck, shoulder or hand
Weakening grip
When vessels are compressed
Discoloration of the hand (bluish color)
Arm pain and swelling, possibly due to blood
clots
Blood clot in veins or arteries in the upper
area of the body
Lack of color (pallor) in one or more of the
fingers or entire hand
Weak or no pulse in the affected arm
Cold fingers, hands or arms
Arm fatigue after activity
Numbness or tingling in fingers
Weakness of arm or neck
Throbbing lump near collarbone
Diagnosis and treatment
X-ray.  Conservative (physical therapy,
Ultrasound.  medications)
Computerized tomography Surgical
(CT) scan. 
Magnetic resonance imaging
(MRI). 
Arteriography and venography.
 Electromyography
(EMG). Nerve conduction
study. 
REFERENCES:
1. APLEY 9th edition
2.ORTHOBULLET