Peripheral Neuropathies

Classification of Traumatic Peripheral Neuropathies

Seddon’s Clinical Classification of nerve injury is defined by mechanical trauma. Neurotmesis (“Cutting of Nerve”) refers to severance of all essential structures, including the axon; a visible disruption may not be apparent and the epineurium may be intact. Axonotmesis is a lesion to the axon severe enough to cause degeneration of the axon distal to the lesion, but with no interruption of continuity of the endoneurium. Neurapraxia (“nonacting nerve”) is injury to the nerve, causing some degree of paralysis but no peripheral degeneration.

Clinically Neuropraxia may result in decreased (or loss of) strength and absent tendon reflexes below the level of the lesion, slight sensory loss (confined to large diameter fibers) and no change in sympathetic function. There is no damage to the axon itself. Recovery is generally spontaneous and occurs within 3 months.

Axonotmesis result is variable loss of sensory, motor, and sympathetic function. Both myelinated and unmyelinated fibers may be involved. Muscle atrophy may occur and areflexia may be involved. These lesions generally occur as a result of closed-crush or percussion injuries. The axon is damaged, but the Schwann cell basal lamina remains intact along with the endoneurial connective tissue. Although Wallerian degeneration occurs distal to the lesion, regeneration is generally effective because Schwann cell integrity is maintained. Recovery is generally slow (several months to more than 1 year), with axonal regeneration occurring at a rate of 1 to 8 mm per day, depending on the specific nerve.

Neurotmesis commonly result from stab wounds, high-velocity projectiles, or nerve traction that disrupts the connective tissue components of the nerve along with complete transaction of the nerve trunk. Wallerian degeneration occurs distal to the lesion. Regeneration may occur, but because of damage to connective tissue and Schwann cells, sprouting may occur randomly. As a result, proper end-organ function may not be restored, and the formation of neuromas is not uncommon.

Pathogenesis of Peripheral Neuropathies

Primarily, after injury, the axon shrinks, fragments and becomes irregular in shape. Secondarily, if myelin is present, breaks down and associated cells undergo change. This myelin breakdown involves chemical alteration of myelin lipids and is accompanied by retraction of the myelin sheath from the axon at the nodes of Ranvier and breakdown of the sheath into ellipsoid or digestive chambers.

Fragments of axon and myelin debris are broken down by lysosomal vacuoles in Schwann cells and to some extent within macrophages that migrate in to the nerve during early stages of degeneration. Loss of protein within the first 24 hours is the basic chemical change of axonal and myelin degeneration. These changes reflect a cessation of normal axonal flow with disintegration of cell organelles.

At the time of and shortly after injury, there is a proliferation of Schwann cells, which then form columns of cells (bands of Bungner) that serve to guide the regenerating axons to their termination. The entire process of Wallerian degeneration prepares the nerve stump for regeneration and may also cause the elaboration of neurotrophic factors that promote this goal.

The Schwann cell continues to be active during the first 24 hours after injury and beyond. Reactive changes within the cell lead to proliferation through mitosis and formation of columns of cells (bands of Bungner) takes place along the endoneureal tube. Essentially the function of these columns is to guide the regenerating axonal sprouts to their target tissue. The Schwann cell may also provide trophic material (i.e., neural growth factor in umyelinated and autonomic fibers) through axoplasmic flow during the period of regeneration. The axonal sprouts grow from the proximal stump to the distal stump, the rate and progress dependent on the extent and/or type of injury.

Rates of regeneration vary from 1-8mm per day, depending on the specific nerve and location. As regeneration continues distally, axons may become myelinated and some eventually may reestablish peripheral connections.

Surgical Repair of Peripheral Nerve Injury

Surgical repair of peripheral nerve injuries is done by either nerve suturing (most effective) or use of a nerve graft. End-to end suturing of peripheral nerves is possible when the transected nerve ends can be closely approximated. If there is a considerable gap between the severed ends of the nerve, nerve suturing may not be effective and a graft may be considered.

There are many factors influencing the success of a nerve suture procedure. Success or failure depends on the age of the patient, location and/or level of the injury, extent or size of the defect, delay time from injury to repair, they type of nerve (motor or sensory), extent of paralysis, and surgical or technical factors.

Treatment Procedures

Patient Education

It is the most essential to maximize functional return and avoid secondary conditions resulting from sensory neglect.

Weakness/paralysis

- Treatment by neuromuscular electrical stimulation should begin as soon as possible after the injury because the rate of atrophy is greatest immediately following the injury. Denervated muscle has no motor point and so the current must pass through the bulk of the muscle to cause a contraction. As a result, interrupted galvanic currents is recommended. Stimulation should be strong enough to produce 15-20 strong contractions per session and the sessions should be repeated three to four times per day. This approach will help to retard muscular atrophy.

- Once there is regeneration and the muscles can be seen to contract, faradic currents to the motor point can be given in order to strengthen the muscle contraction. Patients are encouraged to continue contraction along with the muscle stimulation.

- Strengthening exercises to the partially denervated muscle generally can be given either by using a pattern of group of exercises (as in Proprioceptive Neuromuscular Facilitation) or by individual muscle contractions.

Sensory impairment

- Physiotherapy treatment of the sensory-impaired area should include extensive patient education about limb neglect. The patient should learn to regularly inspect the affected area in an attempt to reduce further trauma to the area. Monitoring the redevelopment and quality of returning sensations can be helpful in assessing the repair and regeneration of the injured nerve.

Vasomotor Disturbances

Though vasoconstrictor paralysis cannot be directly altered, the edema produced by the paralysis can be addressed.

- Reduction of edema can be accomplished by various techniques, including massage, compression and elevation. These techniques are means of assisting venous and lymphatic return from an extremity.

Soft Tissue Changes

Connective tissues and contractile tissue become progressively shorter when not stretched regularly.

- The most effective treatment program uses preventive measures such as ROM exercises. These exercises may initially be done by the therapist as passive or active-assisted exercises. However, as soon as possible the patient is taught how to do the appropriate exercises independently. Stretching should be given in a slow manner.

- Mobilization techniques can be utilized in order to increase any range that is restricted.

Orthotic Appliances

- Orthoses can be used to protect bony structures and articular structures as well as muscles, ligaments and nerves during periods of rehabilitation. The orthotic appliances assists in preventing deformities and limiting pathological motor patterns that can develop with muscular weakness and improper sensory input.