Wallerian Degeneration

Original Editor - Anthonia Abraham
Top Contributors - Anthonia Abraham, Kim Jackson, Cindy John-Chu and Lucinda hampton

Clinically Relevant Anatomy

Wallerian degeneration is an active process of anterograde degeneration of the distal end of an axon that is a result of a nerve lesion. It occurs between 7 to 21 days after the lesion occurs. After the 21st day, acute nerve degeneration will show on the electromyograph. Although primarily an anterograde process, there is evidence that retrograde degeneration (Wallerian-like) can also be involved, affecting the neuron's cell body and proximal part of the axon.

Within a nerve, each axon is surrounded by a layer of connective tissue called the endoneurium. The axons are bundled together into groups called fascicles, and each fascicle is wrapped in a layer of connective tissue called the perineurium. Finally, the entire nerve is wrapped in a layer of connective tissue called the epineurium.

Mechanism of Injury

The pathological process of Wallerian degeneration is in 3 stages;

Axon Degeneration

Within approximately 30 minutes of injury, there is a separation of the proximal and distal ends of the nerve. After a short latency period, the transected membranes are sealed until degeneration which is marked by the formation of axonal sprouts. This occurs in less than a day and allows for nerve renervation and regeneration

Myelin Clearance

This occurs by the 7th day when macrophages are signaled by the Schwann cells to clean up axonal and myelin debris. Usually, the rate of clearance is slower in the Central Nervous System(CNS) than in the Peripheral Nervous System (PNS) due to the clearance rate of myelin. Another reason for the different rates is the change in permeability of the blood-tissue barrier in the two systems. In PNS, the permeability increases throughout the distal stump, but the barrier disruption in CNS is limited to just the site of injury. Also in the CNS, oligodendrocytes inhibit regeneration.

Regeneration

If soma/ cell body is damaged, a neuron cannot regenerate. However, if the injury is at the end of the axon, at a growth of 1mm per day, the distal segment undergoes granular disintegration over several days to weeks and cytoplasmic elements begin to accumulate.

Clinical Presentation

Presentations of nerve damage may include:

• Reduced or loss of function in associated structures to damaged nerves
• Gradual onset of numbness, prickling or tingling in feet or hands, which can spread upward into legs and arms
• Sharp, jabbing, throbbing, freezing, or burning pain
• Extreme sensitivity to touch
• Lack of coordination and falling
• Muscle weakness or paralysis if motor nerves are affected
• Neuromatous or causalgia pain

Diagnostic Procedures

• Electromyography

• Nerve conduction studies

• Pain assessment

• Sensation deficit and skin condition tests

• Muscle strength/loss

• Functional deficits
  

Outcome Measures

Depends on various criteria including pain and psychosocial skills but could include:

• Oxford scale
• Visual analogue scale
• Short form McGill pain questionnaire

(see Outcome Measures Database)

Management / Interventions

See Nerve Injury Rehabilitation

Wallerian Degeneration can instigate a nerve repair mechanism. Managing nerve damage can include the use of :Cryotherapy, Exercise, Neurorehabilitation, and Surgery.