The peripheral nerves are composed of axons which carry motor, sensory
&autonomic impulses. Many of these axons are surrounded by myelin sheath which is a lipoprotein membrane derived from Schwann cells. The axon is surrounded by connective tissue covering called endoneurium . The axons are arranged in bundles(fascicles) which are surrounded by perineurium , groups of these bundles are surrounded by epineurium to form the nerve trunk.
Transient ischaemia : acute nerve compression for 15 minutes causes numbness, for 30 minutes→ loss of sensation, for 45 minutes→ muscle weakness. these changes are due to transient anoxia &they leave no trace of nerve damage.
Neurapraxia: is transient physiological nerve conduction block result from segmental demyelination due to mechanical pressure(as in crutch palsy, tourniquet palsy &Saturday night palsy) leading to loss of some types of sensation & muscle power followed by spontaneous recovery after few days or weeks.
Axonotmesis: the axons are interrupted but their endoneurial tubes are intact, these injuries are seen in closed # and ≠. The distal parts of the axons will disintegrate &resorbed by phagocytes(Wallerian degeneration).
While the proximal parts, within hours, start regeneration inside their endoneurial tubes at a rate 1mm/day till they join their target organs(motor end-plate &sensory receptors) which must be in < 2years.
Neurotmesis: the nerve trunk is divided (axons, endo-, peri- &epineurium) as in open injury; or the endoneurial tubes are destroyed as in severe crush or stretching injury. The regenerating proximal axons will form neuroma.
Spontaneous recovery is unlikely.
First degree injury This includes transient ischaemia and neurapraxia, the effects of which are reversible.
Second degree injury This corresponds to axonotmesis. Axonal degeneration takes place but, because the endoneurium is preserved, regeneration can lead to complete, or near complete, recovery without the need for intervention.
Third degree injury This is worse than axonotmesis. The endoneurium is disrupted but the perineurial sheaths are intact and internal damage is

limited. The chances of the axons reaching their targets are good, but fibrosis and crossed connections will limit recovery.
Fourth degree injury Only the epineurium is intact. The nerve trunk is still in continuity but internal damage is severe. Recovery is unlikely; the injured segment should be excised and the nerve repaired or grafted.
Fifth degree injury The nerve is divided and will have to be repaired
Clinical features : Always look for nerve injury in any significant trauma because it is easily missed. Ask about numbness, parasthesia or muscle weakness in the related area. O/E: abnormal posture(e.g. foot or wrist drop), map of sensory disturbance(spinal or peripheral n.) &motor weakness (↓tone, power &reflexes). Anesthetic skin is dry(↓sweating).
Signs of chronic nerve injury
The anesthetic skin may become smooth & shiny with evidence of
↓sensibility like cigarette burn in median n. palsy or foot ulcer in sciatic n. palsy. Muscle groups will be wasted &deformity may become fixed.
Assessment of recovery: a low energy injury may cause neurapraxia while a high energy injury is likely to cause axonotmesis. An open injury or very high energy injury is likely to divide the nerve.
Tinel’s sign
: is the feeling of peripheral tingling on nerve percussion, it is –ve in neurapraxia & +ve in axonotmesis or neurotmesis.
If Tinel’s sign is not progressing 1mm/day→ neurotmesis.
EMG and NCS shows denervation potentials on the 3 rd week if the injury was axonotmesis or neurotmesis. Motor recovery is slower than sensory recovery; the more proximal muscle will function first.
Principles of treatment of nerve injury
1.
Nerve exploration: is indicated:
(a) if the nerve was seen to be divided;(b) if the type of the injury suggests that the nerve has been divided or severely damaged e.g. knife wound; (c) if recovery is delayed.
2.
Primary repair : at the time of wound toilet has a considerable advantage because nerve ends have not retracted or rotated &there is no fibrosis. It is contraindicated in (a) dirty wound; (b) traction injury; (c) presence of other more urgent injury.
3.
Delayed repair: after weeks or months, is indicated in (a) missed injury( < 2 years); (b) failure of primary repair (c) delayed recovery of closed injury.
4.
Care of the paralyzed part: while recovery is awaited
(a) the skin must be protected from injury &burn; (b) joints should be moved through their full range to prevent stiffness.

types of repair:
1- epineuroraphy:by suturing the epineurium.
2-perineuroraphy: by microscopic surgical repair of each bundle .
3- endoneuroraphy:suturing of each axon microscopically.
After any type of suturing ,we have to use splintage for 4-6 weeks followed by physiotherapy.
If we have a gap between the two ends of injuried nerve ,how we can close it:
1- proximal and distal release and mobilization.
2- nerve transposition.
3- joint flexion.
4-nerve graft(from where??)
5- bone shortening
Prognosis : of nerve injury depends on: 1- Type of injury: neurapraxia the best, neurotmesis the worst.
2-Level of injury, the higher the worst.
3-Type of the nerve, pure motor or pure sensory better than mixed. 4-Size of the gap. 5-Age, children better prognosis.
6-Delay of the repair. 7-Associated injuries(vascular, tendon). 8- Surgical technique(skill, facilities).
The diagnosis is obvious at birth, usually after a difficult delivery with excessive traction especially with the use of forceps; the baby has a floppy or flail arm. There are 3 types:
Erb's palsy: is caused by injury of the upper roots (C5,C6& sometimes C7) leading to paralysis of shoulder abductors & external rotators, elbow flexors, forearm supinators &if C7 is involved, there is paralysis of finger extensors. therefore the arm is held adducted, internally rotated, elbow extended &pronated.
Klumpke's palsy: is caused by injury of lower roots of the plexus (C8,
T1) leading to paralysis of all hand muscles, it is rare but more severe than Erb's palsy.There may be a unilateral Horner's syndrome.

Complete palsy: caused by injury of all roots of the brachial plexus
(C5---T1). It is a complete lesion result in paralysis of the entire limb.
Prognosis: after few weeks the paralysis may:
1 recover completely within 3 months especially for upper roots lesions(90%).
2 improve but residual weakness will persist.
3 remain unchanged as in lower or complete palsy.
Treatment:
1Conservative Ŗ by physiotherapy to keep joints mobile while waiting for recovery in early months.
2Operative Ŗ is indicated in early stages if there is no improvement after 6 months → exploration & nerve grafting .
Late: shoulder internal rotation may need subscapularis release
or rotation osteotomy of the humerus.
Adult lesions: are caused by severe traction injury as in fall
on the side of the neck or by stab wound at the root of the neck.
CF: is either (1) upper roots similar to Erb's palsy or
(2) lower roots lesion with paralysis of hand intrinsic muscles forming a claw hand deformity, weakness of wrist &finger flexors, sensory loss on ulnar side of arm &forearm &Horner syndrome.
The root lesion is either preganglionic in which roots are avulsed from spinal cord & this is irreparable with poor prognosis or
postganglionic which may recover or it is surgically reparable.
Features of preganglionic lesion: paralysis of scapular muscles or diaphragm, Horner's syndrome, cervical spine #, spinal cord dysfunction(↑reflexes in lower limb) &severe vascular injury.
Investigations: NCS, EMG, CT myelography &MRI.
Ŗ: Ŗ of associated injuries(vascular, chest wall,..). For preganglionic lesions → nerve transfer, tendon transfer or arthrodesis.
For postganglionic lesions→ nerve repair or graft.