Peripheral nerve damage affecting the upper extremities can vary widely in cause and extent. Many disorders, ranging from mild carpal tunnel syndrome to severe brachial plexopathy, need to be considered in a patient presenting with pain, sensory loss, or weakness involving the shoulder, arm, or hand.

1. Prepared by:
Dr. Abdullah K. Ghafour
3rd year IBFMS trainee
Supervised by:
Dr. Hamid Ahmed Jaff

2.  Peripheral nerve damage affecting the upper
extremities can vary widely in cause and extent.
 Many disorders, ranging from mild carpal tunnel
syndrome to severe brachial plexopathy, need to
be considered in a patient presenting with pain,
sensory loss, or weakness involving the
shoulder, arm, or hand.

3.  Nerve roots emerge from the spinal cord formed
by ventral (anterior rami) of cervical spinal
nerves C5-C8 and thoracic spinal nerves T1
form brachial plexus.
 Brachial plexus is responsible for cutaneous
(sensory) and muscular (motor) innervation of
the entire upper limb.

4.  5 main nerves arise from brachial plexus:
1. Axillary nerve (C5,C6)
2. Musculocutaneous nerve (C5,C6,C7)
3. Radial nerve (C5,C6,,C7,C8 &T1)
4. Median nerve (C5,C6,,C7,C8 &T1)
5. Ulnar nerve (C8 &T1)

5. Brachial Plexus

6.  Nerves can be injured by ischaemia, compression,
traction, laceration or burning.
 Damage varies in severity from transient and quickly
recoverable loss of function to complete interruption and
degeneration.
 There may be a mixture of types of damage in the
various fascicles of a single nerve trunk.

7. I. Seddon’s classification (1942) :
i. Neurapraxia; mechanical pressure causing segmental
demyelination
ii. Axonotmesis; axonal interruption with loss of conduction but
the nerve is in continuity and the neural tubes are intact.
iii. Neurotmesis; division of the nerve trunk with loss of continuity.
II. Brain’s classification (1943) :
i. Localised degeneration of the myelin sheaths
ii. Complete interruption of axons with Preservation of supporting
structures (Schwann tubes, endoneurium, perineurium)
iii. All essential parts destroyed, Interruption can occur without
apparent loss of continuity

8. III. Sunderland classification (1978):
i. First degree injury; This embraces transient ischaemia
and neurapraxia
ii. Second degree injury; axonal distruption (Axonotmesis)
iii. Third degree injury; The endoneurium is disrupted but the
perineurial sheaths are intact and internal damage is
limited.
iv. Fourth degree injury Only the epineurium is intact.
v. Fifth degree injury The nerve is
divided.

9.  History
• Which nerve ?
• What level ?
• What is the cause ?
• What degree of injury ?
• Old or fresh injury ?

10.  Motor:
• All muscles distal to the injury – paralyzed & atonic
• Atrophy : 50 -70 % in 1st two months
• Striations & motor end plate configurations retained for 12 –
18 months (critical limit of delay)
 Sensory loss
• usually follows a definite anatomical pattern, although factor
of overlap from adjacent nerves may be present
• Autonomous zone
• Weber 2 point discrimination test
• Tinel’s sign

11.  Reflex ;
• Abolishes all reflexes transmitted by that nerve, either afferent or
efferent arc.
• Complete & incomplete lesion. So , not a reliable guide to injury
severity.
 Autonomic :
• Loss of sweating
• Loss of pilomotor response
• Vasomotor paralysis in autonomous zone
 Others:
• Trophic Changes Esp. hand and feet
• Skin – thin, glistening, breaks easily to form ulcers
• Fingernails – Ridged, distorted and brittle
• Osteoporosis (Reflex sympathetic dystrophy)

13.  In upper plexus injuries (C5 and 6) the shoulder
abductors and external rotators and the forearm
supinators are paralyzed. Sensory loss involves the outer
aspect of the arm and forearm.
 Erb-Duchenne palsy: (Waiter’s tip position)The limb
hangs by the side adducted and medially
rotated by unopposed pectoralis major.
The forearm extended and pronated
because the action of biceps is lost.

14.  Pure lower plexus injuries;
(klumpke pulsy) are rare. Affects T1 nerve root. Wrist and
finger flexors are weak and the intrinsic hand muscles are
paralysed. Sensation is lost in the ulnar forearm and hand.
 If the entire plexus is damaged, the whole limb is
paralysed and numb.

15.  SENSORY SUPPLY
• skin of lateral forearm
 MOTOR SUPPLY
• anterior compartment of arm (BBC)
 biceps – flexes elbow, supinates forearm
 brachialis – flexes elbow
 coracobrachialis – flexes and adducts the
arm at the glenohumeral joint
 COMMON INJURIES
• musculocutaneous nerve injuries are rare, as the nerve is
protected beneath the bulk of the biceps muscle
• it may be damaged by stab wounds to the upper arm

16.  SENSORY LOSS
• numbness over lateral forearm
 MOTOR DEFICIT
• paralysis of anterior compartment of arm – very weak elbow
flexion and weak forearm supination
• absent biceps reflex
 DEFORMITY
• wasting of anterior compartment of arm
• elbow usually held in extension with forearm pronated

17.  Sensory function: sensation of an
oval shaped area over the lateral
shoulder “ sergeant's patch “
 Motor function: it innervates the
deltoid (shoulder abduction) and
teres minor (shoulder external
rotation) muscles.
 Common causes of injury:
Trauma, usually with shoulder
dislocation or humeral fracture,
iatrogenic

18.  Sensory loss: sharply-defined region of
sensory loss over the lateral shoulder
“sergeant's patch “
 Motor loss: The patient complains of
shoulder ‘weakness’. Although
abduction can be initiated (by
supraspinatus), it cannot be maintained.
 Deformity: wasting of the deltoid

19.  Sensory function: posterior arm and
forearm , lateral ⅔ of dorsum of hand
and proximal dorsal aspect of lateral 3½
fingers
 Motor function: posterior compartment
of the arm and forearm
 Common causes of injury: fractures of
proximal humerus, shaft of humerus
or radius, stab wounds to antecubital
fossa, forearm or wrist

20.  Low lesions; The patient complains of
clumsiness and, on testing, cannot extend
the MCP joints of the hand. In the thumb
there is also weakness of extension. Wrist
extension is preserved.
 High lesions; There is an obvious wrist
drop, due to weakness of the radial
extensors of the wrist, as well as inability to
extend the MCP joints or elevate the
thumb. Sensory loss is limited to a small
patch on the dorsum around the
anatomical snuffbox.
 Very high lesions; In addition to weakness
of the wrist and hand, the triceps is
paralysed and the triceps reflex is absent.

21.  Sensory function: Skin over thenar eminence, lateral ⅔
palm of hand and palmar aspect of lateral 3½ fingers
 Motor function: all muscles of anterior compartment of
forearm except flexor carpi ulnaris and the medial two parts
of flexor digitorum profundus
 Common causes of injury:
supracondylar fractures of
humerus , compression by carpal
tunnel syndrome

22.  Low lesions; The patient is unable to
abduct the thumb, and sensation is lost
over the radial three and a half digits. In
longstanding cases the thenar
eminence is wasted and trophic
changes may be seen.
 High lesions; in addition, the long
flexors to the thumb, index and middle
fingers, the radial wrist flexors and the
forearm pronator muscles are all
paralysed ‘pointing sign’.

23.  Sensory function: skin over
hypothenar eminence, medial ⅓
palm of hand ,palmar aspect of
lateral 1½ fingers
 Motor function: two muscles of
anterior compartment of forearm ,
and most of the intrinsic muscles of
the hand
 Common causes of injury:
supracondylar fractures of humerus ,
compression cubital tunnel in the
elbow.

24.  Low lesions; There is numbness of the ulnar
one and a half fingers. The hand assumes
claw hand deformity with hyperextension of
the MCP joints of the ring and little fingers, due
to weakness of the intrinsic muscles. Finger
abduction is weak and this, together with the
loss of thumb adduction, makes pinch difficult.
 High lesions; The hand is not markedly
deformed because the ulnar half of flexor
digitorum profundus is paralysed and the
fingers are therefore less ‘clawed’ (the ‘high
ulnar paradox’). Otherwise, motor and sensory
loss are the same as in low lesions.

25.  Nonoperative
• observation with sequential EMG
 indications
 neuropraxia (1st degree)
 axonotmesis (2nd degree)
 Operative
• surgical repair
 indications
 neurotomesis (3rd degree)
• nerve grafting
 indications
 defects > 2.5 cm
 type of autograft (sural, saphenous, lateral antebrachial, etc)
 no effect on functional recovery

26.  Indications for surgery:
1. When a sharp injury has obviously divided a nerve.
2. When abrading, avulsing or blast wounds have rendered
the condition of nerve unknown.
3. When a nerve deficit follows a blunt or closed trauma &
no clinical or electrical evidence of regeneration has
occurred after an appropriate time.
4. When a nerve deficit follows a penetrating wound as stab
or low velocity gunshot wound, part observed for
evidence of nerve regeneration for appropriate time.

27.  Types of Nerve Repair :
1. Endoneurolysis
2. Partial Neurorrhaphy
3. Neurorrhaphy
a) Epineural
b) Epi-perineural
c) Perineural
4. Nerve grafting

28.  Time of Surgery:
• Primary repair : First 6 – 8 hours
• Delayed primary repair : First 7 – 18 days
• Secondary repair : > 3 weeks

29.  Factors that influence regeneration after neurorrhaphy:
1. Age of patient
2. Gap between nerve ends
3. Delay between time of injury and repair
4. Level of injury
5. Condition of nerve ends
6. Experience & technique of surgeon

30. TIME FOR QUESTIONS