Nerve injury

Neurons don’t multiply during lifetime but cutting or crushing of nerve fibers can lead to damage, undergo repair and become functional.

Fig- Structure of Neuron

Damage to neurons is variable depending upon extent of injury (According to Sunderland’s classification)-

  1. I degree injury (Neuropraxia)
  2. II degree injury (Axonotmesis)
  3. III, IV, V degree injury (Neurotmesis)
  1. Neuropraxia- There is only pressure on the nerve causing occlusion of blood flow and hypoxia. Only mild demyelination but not a true degeneration. Axon loses function temporarily and recovery is possible within a few hours to a few days, which is called the “conduction block”.
  2. Axonotmesis- Prolonged severe pressure on a part of the neuron due to crushing injury that causes wallerian degeneration. This type of injury divides axon but endoneural sheath remains continuous. Complete recovery in about 18 months.
Fig- Cross section of a nerve
  1. Neurotmesis- Both axon and endoneural tube are divided in this type of injury. Only endoneurium; endoneurium with epineurium and perineurium; complete transaction is seen in III, IV and V degree injury respectively. Regeneration is incomplete and complex and depends upon alignment of endoneural tube.

Degenerative changes in the neuron-

When a peripheral nerve fiber is damaged, the degenerative changes occur in the nerve cell body and fiber of the neuron. These changes are classified as-

  1. Wallerian or orthograde degeneration
  2. Retrograde degeneration
  3. Transneuronal degeneration
  1. Wallerian degeneration-

Pathological changes that start within 24 hours of injury, in distal cut end of axon is called wallerian degeneration, named after its discoverer Waller.

Changes in nerve-

  1. Retrograde degeneration-

Pathological changes in nerve cell body and axon proximal to the cut end.

Changes in Nerve cell body-

 Commence within 48 hours. Chromatolysis is seen-

  • Nissl granules disintegrate into fragments with a swelled, round cell body due to accumulation of fluid.
  •  Neurofibrils disappear associated with reduction in the number of golgi apparatus followed by displacement of nucleus towards the periphery.

Changes in axon proximal to injury-

Changes similar to distal cut end are seen in the proximal stump up to the nearest node of Ranvier.

  1. Transneuronal degeneration-

Degenerative changes occur in the neuron with which afferent nerve fibre synapses, is called transneuronal degeneration.

Regeneration of nerve fiber-

It starts as early as the 4th day after injury with the growth of the axis cylinder into the neurilemmal tube, but becomes effective after 30 days  and is completed in about 80 days. 

Criteria for regeneration-

  • Less than 3mm gap between cut ends
  • Two cut ends should be aligned
  • Neurilemma should be present
  • Nucleus must be intact

Stages of regeneration-

  • 100 pseudopodia-like extensions called regenerative sprouts or fibrils grow from the proximal cut end of the nerve.
  • Fibrils grow towards the distal cut end and few reach the neurilemmal tube.
  • Later, the Schwann cells (in about 3 months) and myelin sheath (formed by Schwann cells in 1 year) are developed.
  • Nerve diameter gradually increases and obtains size upto 80% of original size. New formed internodes are also shorter
  • The nerve cell body returns to normal anatomical shape by losing excess fluid and nucleus occupy center.
  • Nissl granules appear first followed by golgi apparatus.
Fig- Degenerative and Regenerative Changes after injury in a neuron

Degeneration in CNS-

Degeneration occurs in the same way as in peripheral neurons but regeneration does not occur due to absence of neurilemma. Formation of glial scar is seen at the site.


  • Direct injury- sharp cuts, lacerations, piercing injuries and nerve entrapment between fractured bony ends at the time of fracture.
  • General causes- metabolic diseases, collagen diseases, infections, excessive cooling, excessive heating, neurotoxic drugs, carelessly given intramuscular injections directly piercing the nerve, excessive traction or friction of nerve, prolonged ischemia and electric shock.
  • Late causes- growing tumor, excessive callus, malunion, fibrosis and adhesions.

Clinical features-

  • Paresis or paralysis of muscle innervated by injured nerves.
  • Loss of sensation to touch, pain, temperature and stereognosis.
  • Reduced or lost deep tendon reflexes.
  • Atrophy of innervated muscles.
  • Trophic changes like dry, thin and glossy skin.


  • Nerve conduction velocity (NCV) test
  • EMG (electromyography)
  • Electrodiagnostic test
  • Strength duration (S-D) curve
  • Sensory diagnosis-

The sequence to be followed is-

  • Vibration of 30 cycles per second (cps)
  • Moving touch
  • Constant touch
  • Vibration of 256 cps


Early stage (0-3 weeks)-

  1. Control pain-
  • Relaxed positioning
  • TENS over area of intact sensorium
  • Application of suitable orthosis
  1. To control oedema-
  • Limb elevation with supportive orthosis
  • Compressive bandaging
  • Gentle effleurage
  • Repetitive active or passive range of motion
  1. Prevention of further injury due to lack of sensation.

Recovery stage ( 3 weeks onwards)-

  1. Stretch adjacent joints to enhance range of motion.
  2. Assisted PNF pattern of movements with audio-visual feedback.
  3. Isometric contractions to achieve active efforts
  4. Functional education with or without orthosis
  5. Techniques of sensory re-education and motor control

Late stage-

  1. Static or dynamic orthosis during functional activities for stabilization.
  2. Altering biomechanics of the body to assist functional anatomy.


  • K Sembulingam and Prema Sembulingam ( Essential of medical physiology)
  • D. Venkatesh and H. H. Sudhakar ( Basics of medical physiology)
  • Glady Samuel Raj ( Physiotherapy in neuro conditions)
  • Patrica A. Downie ( Cash’s textbook of neurology for physiotherapists )
  • Jayant Joshi and Prakash Kotwal ( Orthopedics and applied physiotherapy)
  • J. Maheshwari and Vikram A. Mhaskar (Essential orthopedics)