Etiology and classification
1.Pathogenesis
(1) Impact on the head or shoulder during high speed motion; impact on the head or shoulder from a fall of a heavy object from a high place after an explosion; collapse, heavy object crushing the neck and shoulder, and violent separation of the baby’s head from the shoulder during difficult delivery of the fetus. This kind of violence most often causes injury to the upper trunk of the brachial plexus nerve, and if the violence is heavy or lasts long it can still involve the middle trunk, and in severe cases, the whole brachial plexus nerve can be involved.
(2) Horizontal or upward persistent strain injury of the limb, such as the affected limb is involved in the belt or transport belt, often cause C8, T1 nerve root or lower trunk injury, the violence is severe or long duration can involve the middle trunk and upper trunk. Because C5-7 nerve roots are often reinforced by fibrous tissue and fascia at the vertebral foramen, while C8 and T1 lack such reinforcement, they often cause radical avulsion injury of the lower trunk of the brachial plexus, and if the violence is severe or persistent, they cause radical avulsion injury of the middle trunk or the whole brachial plexus. When the upper arm is on the lateral side of the body and the violence continues downward traction, the limb is simultaneously internally rotated resulting in increased tension on the axillary and radial nerves making them susceptible to tearing. When the upper arm is abducted by 90 degrees and then externally rotated, the musculocutaneous nerve is stretched and prone to tearing.
(3) In conclusion, the position of the limb, the direction of violence, and the duration of the injury result in nerve avulsion rupture or contusion at different sites (including pre and postganglionic). Although the C5 and C6 nerve roots are reinforced by fibrous tissue and fascia at the foramen, which reduces the chance of avulsion, once the violence is severe, not only the reinforced fibrous tissue at the foramen is pulled off, but also the preganglionic filamentous structure is eventually pulled off, resulting in a double injury of postganglionic combined with preganglionic. In addition to the above-mentioned direct and indirect violence, it is more common to see mixed violence, such as in shoulder dislocation or fracture, where the brachial plexus nerve is not only stretched, but also directly compressed or injured by the dislocated humeral head or fracture fragment.
2.Pathological classification of nerve injury
The current classification and grading of nerve injury pathology is still in accordance with.
Seddon (1943) proposed three types (- Am J Orthop. 2000 Mar;29(3)).
(1) neurapraxia: the nerve conduction dysfunction is a temporary physiological block, the nerve fibers do not show significant anatomical and morphological changes, the distal segment nerve fibers do not show degenerative changes, and the nerve conduction function usually recovers on its own within a few days to a few weeks.
(2) Axonotmesis: Axon rupture occurs in the sheath, the nerve sheath is intact, and the distal nerve fibers are degenerated.
(3) neurotmesis: the nerve bundle or nerve trunk is completely broken, or separated by scar tissue, and the nerve needs to be surgically sutured, and the nerve can recover function or incomplete function after suturing.
Sunderland’s (1968) five-degree classification.
First-degree injury: mainly in the nerve membrane blood supply or ion exchange temporary damage and temporary interruption of nerve conduction function, while the continuity between nerve fibers and their cell bodies and end organs and their structure remain intact, the distal segment of the nerve injury does not appear cis-degeneration (Wallerian), and the response to electrical stimulation is normal or slightly slowed. The function of the nerve with the first degree of injury is usually fully restored within 3-4 weeks.
Second-degree injury: The main manifestation is axonal disruption, i.e., degeneration and necrosis of the axon at the site of injury, but the structure around the axon remains intact, and the distal segment of the injured axon shows cis-degeneration (Wallerian degeneration), but does not damage the nerve. Due to axonal disruption, temporary nerve conduction dysfunction occurs, with loss of sensation in the innervated area, motor muscle paralysis, and atrophy. Because the proximal nerve axon can be regenerated by the original endoneurial canal, the nerve can recover on its own with a good prognosis. The recovery time depends on the distance of the axon from the injury to the sensory and motor end organs of the innervated area, and generally grows to the distal segment at a rate of 1 mm per day.
Third-degree injury: The pathological features include not only axonal disruption, cis-degeneration of the distal segment of the injured nerve fiber, but also damage to the endoneural canal, which is incomplete. However, the continuity of the nerve bundle remains intact. As a result of injury within the nerve bundle, internal hemorrhage, edema, and obstruction of blood flow, ischemia causes protein exudation within the nerve bundle and fiber scar formation, which affects nerve regeneration and recovery. Therefore, although the nerve can be regenerated and recovered from the third degree injury, the recovery is often incomplete.
Fourth-degree injury: The nerve bundle is severely damaged or extensively fractured, and the outer membrane of the nerve is sometimes affected, but the continuity of the nerve trunk remains intact. The nerve is damaged due to ischemic degeneration and necrosis of the nerve fibers, massive protein exudation, cellular infiltration, and proliferation of connective tissue that eventually turns into cords replaced by connective tissue, with the proximal end forming a neuroma with localized residual neuromasts (Schwann cells) and regenerating axons. The distal segment of the injured nerve still undergoes cis-degeneration. In the fourth degree of injury, the nerve bundle is more severely disrupted than in the third degree of injury, and the number of regenerating axons is correspondingly greatly reduced. The regenerating axons are free to enter the interstitial space of the bundle within the nerve bundle, so that many regenerating axons are absent or cease to grow, with the result that only a few axons reach the nerve terminal region and form useful connections. Motor muscle function and sensory, sympathetic function in the innervated areas are largely lost. Therefore, surgery is required to remove the scarred segment of the nerve and perform nerve repair for this degree of injury.
Fifth-degree injury: The entire nerve trunk is completely severed, with the severed ends completely separated or connected only by scarred cords of fine fibrotic tissue. The result is a complete loss of function of the motor muscles, sensory and sympathetic nerves innervated by the injured nerve. Fifth-degree nerve injury requires surgical repair.
3, tissue changes at the site of nerve injury.
Clinical significance: there are two types of tissue growth at the nerve dissection, one is the growth of axonal flow within the nerve axon —- i.e. nerve fiber, and the other is the proliferation of connective tissue of interstitial cells around the nerve axon (sheath, fascicle, endoneurium).
There are three conditions depending on the growth rate of both.
Axoplasmic flow growth > connective tissue growth, good nerve regeneration.
Axial flow growth = nerve connective tissue growth, fair nerve regeneration.
Axial flow growth < neural connective tissue growth, poor nerve regeneration.
Clinical tasks.
(1) Promote nerve axoplasmic flow growth (various drug applications to promote active nerve cells and accelerate enzyme and energy metabolism, select the period of active growth for surgery).
(2) Inhibit the growth of neural connective tissue by.
1.Cut the nerve severed end at a time with a new sharp blade or cryosurgical technique to minimize tissue reaction.
2, Place the nerve suture site within normal soft tissue with a rich blood supply and slowed connective tissue growth.
3.Apply silicone rubber or intravenous cannula to inhibit the growth of surrounding connective tissue into it.
4.Apply microsurgical suturing technique.
5.The oblique suture method of the sheath and the sleeve suture method to reduce the circumferential stenosis at the anastomosis.
4.Pathological types of brachial plexus nerve injury
(1) Brachial plexus nerve shock injury, or brachial plexus shock
(2) Brachial plexus nerve conduction dysfunction
(3) Brachial plexus nerve compression demyelination injury
(4) Brachial plexus nerve rupture injury
(5) radical avulsion injury of the brachial plexus nerve