Nerve Injury and Mechanism


Peripheral nerve injury may result in motor, sensory, and/or sympathetic impairments. In addition, pain may be a symptom of nerve tension or compression because the connective tissue and vascular structures surrounding and in the peripheral nerves are innervated and the peripheral nerve function is sensitive to hypoxic states. Knowing the mechanism of injury and the clinical signs and symptoms help the clinician determine the potential outcome for the patient and develop a plan of care.

Nerve Injury

Mechanisms of Nerve Injury

Nerves are mobile and capable of considerable torsion and lengthening owing to their arrangement. Yet they are susceptible to various types of injury including6 :

Ø  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)

Ø  Laceration (knife, gunshot, surgical complication, injection injury)

Ø  Stretch (excessive tension, tearing from traction forces)

Ø  Radiation

Ø  Electricity (lightening 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 result most commonly from 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, it can cause nerve damage. The endoneurium helps

maintain fluid pressure and may provide cushioning for nerves, especially when 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, bony, fibro-osseus), branches of the nervous system (especially if the nerve has an abrupt angle), points where a nerve is relatively fixed when passing close to rigid structures (across a bony 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.


 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.


 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.

Classification of Nerve Injuries

Nerve injuries are classified using either the Seddon or Sunderland classification systems; both are based on structural and functional changes that occur in the nerve with various degrees of damage. These systems describe the degree of injury to nerve substructures and the effect on prognosis. Seddon’s system describes three levels of pathology:

neuropraxia, axonotmesis, and neurotmesis.

Nerve Injury

Seddon’s Classification and Characteristics of Nerve Injury


Segmental demyelination

Action potential slowed or blocked at point of demyelination;

normal above and below point of compression

Muscle does not atrophy; temporary sensory symptoms

Cause: mild ischemia from nerve compression or traction

Recovery is usually complete


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 incomplete—surgical intervention may be



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 in endoneural tubes


Recovery of 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. Timing of the repair is critical, as is the skill of the surgeon and technique used to align the segments accurately and avoid tension at the suture line for optimal nerve regeneration. Different regenerative potential outcomes following nerve repair have also been reported based on groupings of specific nerves.

Ø  Excellent regenerative potential: radial, musculocutaneous, and femoral nerves

Ø  Moderate regenerative potential: median, ulnar, and tibial nerves

Ø  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.
Smith described five possible outcomes of nerve regeneration.
Exact reinnervation of its native target organ with return of function 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.



Acute phase:

immediately after injury or surgery

Immobilization: time dictated by surgeon

Movement: amount and intensity dictated by type of

injury and surgical repair

Splinting or bracing: may be necessary to prevent deformities

 Patient education: protection of the part 

Recovery phase:

 signs of reinnervation (muscle contraction,

increased sensitivity)

 Motor retraining: muscle “hold” in the shortened position

 Desensitization: multiple textures for sensory stimulation;


 Discriminative sensory reeducation: identification of

objects with, then without, visual cues

Chronic phase:

 reinnervation potential peaked with minimal

or no signs of neurological recovery

Compensatory function: compensatory function is minimized

during the recovery phase but is emphasized when

full neurological recovery does not occur

Preventive care: emphasis on lifelong care to involved


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