Introduction

• Most common cause of neuropathies.
• Cause:
  • Accident - mechanical blow, road traffic accidents (RTAs), gunshot wounds, fractures, pressure and stretching.
  • Iatrogenic - crushing, cutting or spiking the nerve during surgery (especially orthopedic procedures) compression by casts, splints or other dressings, injection into or adjacent to nerve.
• Signs: depend on severity of injury: range from temporary loss of function to complete loss of function and muscle atrophy.
• Diagnosis: loss of nerve function.
• Treatment: surgical anastomosis, neurolysis, electromyography.
• Prognosis: depends on severity of lesion. Good to poor.

Pathogenesis

Etiology

• Accident: trauma, eg gunshot, RTA, mechanical blow, fracture, pressure, ischemia.
• Iatrogenic, eg cutting, crushing, spiking, compression by dressings, casts or splints, injections into or adjacent to nerve.
• Brachial plexus avulsion most common after automobile trauma.
• Peripheral limb nerves may be iatrogenically damaged during orthopedic surgery.

Predisposing factors

• Access to traffic.
• Use, eg gun dog, cattle dog.
• Orthopedic procedure.
• Intramuscular injections.

• Boisterous, clumsy, temperament.

Pathophysiology

• Trauma can occur to a single nerve (misplaced injection into the sciatic nerve) or multiple nerves (brachial plexus avulsion).
• The severity of involvement clinically will determine prognosis.
• Aneuropraxia(least severe injury) is an interruption in function and conduction in the nerve, usually associated with a lesion of the myelin without severe axonal involvement.
• Axonotmesissuggests separation and damage of axons, where neurotmesis (most severe injury) is complete severance of all structures of the nerve.
• The likelihood of regeneration is less with neurotmesis as compared to neuropraxia.

• Mild trauma → temporary conduction block → physiological disruption of axonal function → no structural damage to axon.
• More severe trauma → transection of axon (axotomy) → degeneration of distal axon divorced from cell body → impulses travelling down proximal stump no longer innervate muscle (motor) or receptor (sensory):
  • Motor disruption → loss of muscle function (paresis/paralysis), hypotonia, flaccidity.
  • Sensory disruption → anesthesia or dysthesia.
  
  First degree injury
• No structural damage, loss of function - neuropraxia.
  Second degree injury
• Axotomy, but basal lamina intact - axonotemesis.
• Loss of function to sensory dermatomes and muscle supplied by affected nerve.
  Third degree injury
• Axotomy with disruption of basal lamina; perimeurium, epineurium intact - neurotemesis I.
• Epineurial and perineurial scarring at site of injury may impede regeneration.
• Loss of function → endoneurial scarring reduces chances of reinnervation.
  Fourth degree injury
• Axotomy with basal lamina, perineurial and epineurial disruption, ie transection - neurotemesis II.
• Epineurial and perineurial scarring at site of injury most likely in this form of injury - may impede regeneration.
• Loss of function → endoneurial scarring reduces chances of successful reinnervation.
  Fifth degree injury
• Nerve completely severed.

Timecourse

• Neurological deficits immediately after injury.
• Onset of muscle atrophy after 7-10 days.

Diagnosis

Treatment

Prevention

Outcomes