Nerve injury and Wallerian degeneration

Nerves can be damaged either by crushing or getting cut. The extent of damage depends on the type and site of injury. Neurons of central nervous system do not multiply, however the neurons present in the peripheral nervous system shows some repair mechanisms and can be functional again. 

Nerve injury can be classified as: 

1. First degree nerve injury (Neuropraxia)
2. Second degree nerve injury (Axonotemesis)
3. Third degree nerve injury (Neurotmesis)

First degree nerve injury, aslo called Neuropraxia

In this type of injury there is only pressure on the axon causing it to be compressed. The structure of the neuron remains intact. The recovery from this type of injury is possible with in few hours to few days and the functions are temporarily lost.

Second degree nerve injury, also called Axonotemisis

In this type of injury the axon is damaged but the endoneural sheath is intact. This is due to a crushing injury which causes prolonged and severe pressure on the neuron. Regeneration is possible and complete.

Third degree nerve injury, also called Neurotmesis

In this type of injury the axon and endoneural tube are both divided. Regeneration is complex and depends on the alignment of endoneural tube. If alignment of the cut ends is proper, regeneration is possible.

Wallerian Degeneration

When a nerve fiber is damaged, the part of distal to the site of injury undergoes some changes which is known as Wallerian Degeneration. It is named after a person Waller who first described these changes.

The changes occurring in the proximal part of the nerve fiber after the injury:

• The cell body undergoes swelling with degeneration of Nissl granules. 
• The neurofibrils disappear and are associated with a reduction in the number of Golgi apparatus.
• The nucleus is pushed to the periphery which is is called chromatolysis.

The changes occurring in the distal part of the nerve fiber after the injury:

• The peripheral cut end conducts the impulses up to 3 days after the injury
• Axis cylinder swells and breaks down into small rodlets.
• On the 8th day after injury the myelin sheath begins to disintegrate and is replaced by fatty droplets
• On the 32nd day the myelin sheath is completely disintegrated
• The broken rodlets and fat droplets are eaten up by macrophages by phagocytosis
• The hollow tube of the neurilemma with phagocytes is known as the ghost tube.
• If the neurilemma  remains intact, the cells of Schwann multiply rapidly and can bridge a gap of about 3 mm
• If the gap at the site of injury is greater than 3 mm, repair occurs by the formation of scar tissue.

Regeneration of Damaged Nerve Fiber

If the cut end of the neurilemma is close to each other and in proper alignment there is sprouting of fine branches from axis cylinder. These branches reach out to the cut end and starts growing rapidly. The newly formed fibers are thin and unmyelianted which gets myelinated slowly by the Schwann cells.

Degeneration in CNS

Since the neurons in the CNS do not have neurilemma, degeneration doesnot occur in them. The site of injury is covered by neuroglia with the formation of the glial scar.

Neurotrophins

• They are proteins required for the growth and survival of neurons. 
• They are produced by muscle and other structures innervated by the neuron and astrocytes.

Neurotrophins are as follows: 

• Nerve growth factor (NGF) 
• Brain-derived neurotrophic factor (BDNF) 
• Neurotrophin 3 (NT-3)
• Neurotrophin 4/5 (NT-4/5)

Nerve Growth Factor 

It is a protein necessary for the growth and maintenance of the sympathetic neurons.

They are up by neurons and transported to the cell body.

Other factors affecting the neuronal growth are as follows:

• Ciliary neurotrophic factor (CNTF)
• Glial cell line-derived neurotrophic factor (GDNF)
• Leukemia inhibitory factor (LIF) 
• Insulin-like growth factor I (IGF-I) 
• Transforming growth factor (TGF) 
• Fibroblast growth factor (FGF)
• Platelet-derived growth factor (PDGF)