Traumatic Nerve Injury
Our understanding of nerves and nerve injuries (NIs) has traditionally been based on war experiences. While caring for the injured during Wartime (1942), Sir Herbert Seddon created his NI classification system. However, it is not rare to find NI in non-combat-related trauma cases in recent times. These injuries have the ability to change one's life and are frequently accompanied with considerable morbidity, which can lead to significant disabilities. Because they most commonly affect young adults of working age, these disabilities have long-term consequences for the patients.
The peripheral nerve trunk is made up of three layers that enclose nerve fibers. To provide physical and metabolic stability, the innermost collagenous endoneurium layer encases the axonal fibers (myelinated or unmyelinated). The nerve fascicles are made up of these cells, which are bordered by a flattened cellular layer termed the perineurium. The fascicles are surrounded by the epineurium, the outermost collagenous layer. Understanding the classifications, clinical symptoms, and prognosis of NIs, as well as the best optimal care for each patient, requires knowledge of anatomy.
Traumatic Nerve Injury Epidemiology
NIs are found in around 4% of trauma patients. When nerve roots, plexuses, digital nerves, and small nerve injuries are included, this number rises to roughly 5% of all injuries. The average patient age is 34 years, and 60% of the patients are between the ages of 17 and 35. With a male-to-female ratio of around 5 to 1, males have a substantially higher incidence of NIs than females. NIs affect the upper limbs in 60 percent of cases, while nerve injuries in both the upper and lower limbs occur in 6% of instances. The radial nerve is the most often damaged nerve. However, the peroneal nerve is the most frequently damaged nerve in the lower limbs.
What Traumatic Brain Injury?
Traumatic brain injury (TBI) develops when the brain is affected by a sudden, external physical assault. It is one of the leading causes of adult mortality and disability. Traumatic brain injury is a wide term that encompasses a wide range of damage to the brain. The damage might be localized (limited to a single part of the brain) or diffuse (occurs in more than one area of the brain). A brain injury can vary in severity from a minor concussion to a severe lesion that leads to coma or death.
Traumatic Nerve Injury Pathophysiology
Pure conduction block injuries have few pathological effects (first grade, see Sunderland classification). Wallerian degeneration is an anterograde degenerative process that occurs distal to the injury site in all other grades of nerve injuries. The axonal and myelin fragmentation process begins hours after the damage. Due to varicose swelling, the neurotubules and neurofilaments lose their integrity, and the form of the axons becomes irregular. At 48 to 96 hours after injury, axonal continuity is destroyed, and impulse conduction stops. Axonal degeneration is noticeably slower than myelin degradation.
Within 24 hours after the damage, Schwann cells become activated. They phagocyte the axonal and myelin debris, along with migrating macrophages, to clean the damaged site over a period of weeks to months. The entire degenerative process takes 6 to 8 weeks, during which time the endoneurial tubes will have reduced in diameter despite swelling for the first two weeks following the damage. To promote axonal reinnervation, Schwann cell bands remain inside the endoneurial tubes.
The flexibility of the endoneurium causes a more pronounced local inflammatory reaction in grade III injuries, as well as the retraction of the cut nerve fibers. A thick fibrous scar forms as a result of the fibroblast growth, resulting in a fusiform swelling at the lesion site. This effect is exacerbated in fourth and fifth-grade injuries, where Schwann cells and axons are no longer confined to the fasciculi or endoneurial tubes. As a result, the proximal stump swells with Schwann cells and scar tissue, preventing axonal regrowth. The degeneration of proximal nerve fibers, on the other hand, might range from modest to reaching the cell body. The severity of the injury and its proximity to the cell body determine the amount of degradation.
Traumatic Nerve Injury Causes
Motor vehicle crashes (MVC) are the most common cause of nerve injury, followed by motorcycle crashes. Shrapnel and explosives, on the other hand, are the most common causes of nerve injury in battles. Vehicle vs. pedestrian injuries, gunshot wounds, falls, workplace injuries, stab wounds, recreational MVC (e.g., snowmobiles), and assaults are all common causes of nerve injury. According to one study, iatrogenic injuries induced by medical or surgical treatments account for 16% of surgically treated nerve injuries.
Acute nerve damage can occur for a variety of reasons. Among them are:
- Stretch-related injury. The most common type of nerve injury occurs when stretching forces exceed the nerve's flexibility. These injuries might be independent nerve injuries or are accompanied by extremity fractures. They normally do not impact the continuity of nerve elements, but in rare cases, such as brachial plexus avulsion injuries, they can cause complete loss of continuity.
- Laceration injury. The second most prevalent category is laceration injuries produced by sharp items (such as knives or swords). They usually result in a partial loss of continuity, but they can also result in a total loss of continuity.
- Compression injury. They are the third most prevalent type of nerve injury. They can cause total loss of motor and sensory nerve functioning, despite complete nerve continuity preservation. Ischemia and mechanical deformation caused by direct compression are thought to have a role in injuries. Mechanical deformation is the main cause of neurological impairments that persist longer and may not always show complete healing in more severe cases. Short-term ischemia of fewer than 8 hours, on the other hand, does not appear to induce any irreversible impairments and is not linked to any substantial histological abnormalities.
Nerve injury has also been linked to bone fractures. The injury might be primary (at the time of trauma) or secondary, iatrogenic or caused by scarring or callus formation. Radial nerve injury is the most frequent peripheral nerve injury related to bone fracture and is related to humeral shaft fracture. Traumatic nerve injury can also occur as a result of joint dislocation. Axillary nerve injury, for example, can occur as a result of glenohumeral joint dislocation due to the nerve's closeness to the joint capsule. Moreover, due to compression, strain, or ischemia, several nerves can be injured during specific procedures. Brachial plexus injury, for example, during the implantation of sternal retractors for sternotomy. A femoral nerve injury caused by a self-retaining retractor during abdominal surgery is another example.
Traumatic Nerve Injury Symptoms
The clinical presentation of nerve damage differs depending on the nerve involved (sensory, motor, or combined). A motor nerve damage causes muscle weakness, but a sensory nerve injury causes loss of sensation in the affected nerves' sensory distribution, as well as neuromatous or causalgia pain, or both.
Nerve injury can cause a wide range of complaints. The type and location of nerves affected determine which ones you may have. brain and spinal cord nerves can be injured. It can also affect your peripheral nerves, which run throughout your entire body.
Damage to the autonomic nervous system can cause the following symptoms:
- Inability to detect chest pain, such as that caused by ischemia or a heart attack
- Hyperhidrosis (excessive sweating) or anhidrosis (insufficient sweating)
- Dry mouth and eyes
- Bladder disorders
- Sexual impotence
Motor nerve damage can cause the following symptoms:
- Muscle wasting
- Twitching (fasciculation)
The following symptoms may be caused by sensory nerve damage:
- Tingling sensation
- Prickling or stinging
- Burning sensation
- Positional awareness deficits
People who have nerve damage may experience symptoms that reflect damage to two or even three separate types of nerves. You might, for example, feel weak and have your legs burn at the same time.
Traumatic Nerve Injury Classification
Seddon and Sunderland, in the1940s and the early 1950s, respectively, described the classification of nerve damage. Seddon divided nerve injury into three categories: neurapraxia, axonotmesis, and neurotmesis. This classification system was expanded by Sunderland to encompass five levels of nerve damage.
First-degree Nerve Injury
A first-degree injury, also known as neurapraxia, causes a transient conduction block and nerve demyelination at the damaged site. Above and below the level of damage, electrodiagnostic study results are normal, and no axonal degradation or denervation muscle alterations are evident. There is no Tinel sign. Complete motor and sensory recovery happens once the nerve has remyelinated in that location. It could take up to 3 months to heal.
Second-degree Nerve Injury
Axonotmesis, or second-degree injury, is caused by more severe trauma or compression. This results in distal Wallerian degeneration and proximal neurodegeneration to at least the next node of Ranvier. Proximal degradation may extend beyond the next node of Ranvier in more severe traumatic nerve injury.
Denervation changes in the injured muscles are seen in electrodiagnostic tests of motor nerve injury, and motor unit potentials (MUPs) are detectable in situations of reinnervation. Axonal regeneration occurs at a rate of 1 mm per day, or 1 inch every month, and can be tracked using the Tinel sign. As long as the endoneurial tubes are intact, recovery is complete, with axons reinnervating their original motor and sensory targets.
Third-degree Nerve Injury
Sunderland invented the term third-degree injury to characterize an injury that was more serious than a second-degree injury. Wallerian degeneration develops, similar to a second-degree injury, and electrodiagnostic investigations reveal denervation changes with fibrillations in the afflicted muscles. MUPs are seen in situations of reinnervation.
The rate of regeneration is 1 mm every day, and the Tinel sign can be used to monitor progress. The endoneurial tubes are not intact due to the increased severity of the lesion, and regenerating axons may not reinnervate their native motor and sensory targets.
The pattern of recovery is mixed and incomplete. Sensory fibers can only be reinnervated if they reach their sensory end organs, and motor nerve fibers can only be reinnervated if they reach their muscle targets. Recovery can be off even within a sensory nerve if sensory fibers reinnervate a different portion of the nerves' sensory distribution. Because of the extended duration of denervation and permanent muscle degeneration, nerve regeneration may occur if the muscle target is far from the injured area, but the muscle may not be reinnervated.
Fourth-degree Nerve Injury
A fourth-degree injury causes a huge scar at the location of the nerve lesion, preventing any axons from advancing distal to the nerve injury. Denervation changes in the afflicted muscles are revealed by electrodiagnostic testing, but no MUPs are seen. A Tinel sign is present at the damaged site, but it does not progress beyond there. There is no improvement in function, hence surgery is needed to remove the neuroma and restore neural continuity, allowing for axonal regeneration and motor and sensory reinnervation.
Fifth-degree Nerve Injury
A full transection of the nerve is a fifth-degree injury. It requires surgery to restore neuronal continuity, just like a fourth-degree injury. The electrodiagnostic findings are consistent with fourth-degree damage.
Sixth-degree Nerve Injury
Mackinnon invented the phrase sixth-degree injury to describe a mixed nerve injury that encompasses all of the other degrees of damage. This type of injury frequently happens when certain nerve fascicles are functioning normally while others are healing, and some fascicles may require surgical intervention to enable axonal regeneration.
Traumatic Nerve Injury Diagnosis
Electrodiagnostic investigations are an important aspect of the workup for closed peripheral nerve injury. When nerve conduction studies (NCS) or electromyography (EMG) are used at different times after an injury, different clinically important information might be obtained. NCS aids in the localization of the lesion in the first week after injury due to conduction block across the lesion despite the preservation of conduction through the distal stump. Because preserved voluntary control of motor unit action potentials (MUAPS) in the target muscle implies an incomplete injury, EMG can identify whether the injury was complete or incomplete. Nerve conduction studies can identify a conduction block caused by neuropraxia from one caused by axonotmesis or neurotmesis after the first week because the distal stump would stop conducting if there was an anatomical discontinuity. EMGs can potentially indicate denervation by identifying fibrillation potentials, therefore testing beyond the first week is usually done at 3 to 4 weeks. Additional testing is performed at 3 to 4 months to further assess signs of early innervation and guide future management decisions. It's worth noting that several electrodiagnostic tests can be utilized to pinpoint the location of an injury. A preganglionic injury is defined as a mix of normal sensory nerve action potentials (SNAPs) and absent somatosensory evoked potentials (SSEPs) in the afflicted dermatome, as well as anesthesia.
In the assessment of PNIs, magnetic resonance imaging (MRI) has proven increasingly useful, especially in brachial plexus injuries, where it is utilized to classify lesions based on their anatomical position along the plexus. The anatomy of the plexus can be well defined by MRI in this case. It's also a noninvasive test that doesn't involve a spinal tap, an intrathecal contrast injection, or exposure to radiation.
Although encouraging, a stand-alone MRI is still unable to distinguish between the various degrees of nerve injury. It can, however, exhibit signs of muscle denervation as early as four days after an injury, especially in the STIR sequence. Because of this, it can identify muscle denervation before EMG. Furthermore, animal studies have suggested that diffusion tensor imaging (DTI) and diffusion tensor tractography (DTT) can be used to diagnose and track nerve injury recovery, but this has yet to be demonstrated in humans.
Traumatic Nerve Injury Treatment
Non-surgical Treatment of Traumatic Nerve Injury
Initial treatment for patients with motor nerve injuries consists of patient education as well as the protection of the joints, particularly the surrounding ligaments and tendons, from further pressure. In certain circumstances, splints, slings, or both may be utilized to protect the joint and improve function. Radial nerve damage, for example, causes a wrist drop due to a loss of wrist and finger extension. A wrist-resting splint can be used to keep the hand in a more functional position by supporting it in a neutral wrist position.
Continued downward force at the glenohumeral joint without the muscle support of the rotator cuff muscles may cause glenohumeral joint subluxation in individuals with brachial plexus nerve injuries, especially when C5-6 is damaged. A sling can aid to relieve pain, unloading the joint, and avoiding complete shoulder dislocation.
Physiotherapy is initiated as soon as a nerve injury occurs to maintain a passive range of motion in the affected joints and muscular strength in the unaffected muscles.
There have been no conclusive studies to back up the use of electrical muscle stimulation to prevent muscle deterioration. Galvanic direct current stimulation is required to generate a muscular contraction in cases of muscle denervation. Thermal burn beneath the electrodes is a concern of galvanic stimulation, especially in individuals with impaired sensation. The researchers do not recommend direct current stimulation of denervated muscles because no research has proven that electrical muscle stimulation using surface electrodes can prevent total degeneration of muscle fibers, the neuromuscular junction, or both. There is no need to stimulate the muscle if the nerve does not recover in time to reinnervate it.
It is potentially conceivable to employ alternating current stimulation on reinnervated muscle. To activate the muscle with alternating current, however, a high number of reinnervated muscle fibers is required. The researchers recommend combining sensorimotor reeducation with exercise and biofeedback measures to enhance the strength of a reinnervated muscle.
Surgical Treatment of Traumatic Nerve Injury
The following are some of the indications for nerve surgery:
- Closed nerve injury. Surgery is suggested if there is no evidence of recovery at 3 months since the injury, either clinically or from electrodiagnostic studies; if there are signs of recovery as indicated by motor unit potentials (MUPs), patients should be evaluated to assess the progress of recovery and the need for surgery.
- Open nerve injury (laceration). All lacerations with a reported loss of feeling or motor weakness should be surgically explored as early as possible.
- Crush nerve injury. Surgical exploration of the nerve may be postponed for several weeks; however, if there are no signs of reinnervation after three months, either clinically or through electrodiagnostic studies (the absence of MUPs indicates the absence of reinnervation), surgical repair with nerve repair, transfer, or grafting is indicated.
Delay repair may be needed in contaminated or crushed nerve damage.
- Nerve Repair
Direct repair can be used to restore nerve continuity. This is done when the nerves' distal and proximal ends are directly coapted. If the repair cannot be done without tension, another kind of nerve repair should be undertaken (e.g., nerve graft or nerve transfer). Another type of repair (e.g., nerve graft or nerve transfer) should be utilized if the neighboring joint must be flexed or extended to allow coaptation of the distal and proximal ends of the nerve.
- Nerve graft
A nerve transplant may be advised if the proximal and distal nerve segments cannot be approximated without strain or if there is a gap between the proximal and distal ends of the nerve. The use of a donor’s nerve to close a nerve gap leads to a sensory loss in the donor’s nerves' distribution. With collateral sprouting from the adjacent sensory nerves, this area of sensory loss reduces over the course of 1-3 years.
Nerve grafts can be made from a variety of minor noncritical sensory nerves. Because of the considerable length of nerve graft material available, the sural nerve is employed in cases when there is a wide nerve gap. On the posterior calf, the sural nerve can be harvested either by a single longitudinal incision or many stepped incisions.
Because the donor site scar is minor and the consequent sensory loss is on the anterior portion of the forearm, the anterior branch of the medial antebrachial cutaneous (MABC) nerve is a favorable graft donor for shorter nerve gaps. Because all of the incisions are made in the same extremity, the MABC nerve is particularly useful for upper-extremity surgical reconstructions. Although the lateral antebrachial cutaneous (LABC) nerve provides approximately 6 cm of nerve graft material, the scar on the forearm is more visible than the MABC scar on the inner upper arm.
- Nerve transfer
A nerve-to-nerve transfer is a procedure in which a normal, noncritical nerve is coapted to the affected nerves' distal end. This is a particularly beneficial method in situations where there is a wide nerve gap, proximal nerve damage, or both. With proximal brachial plexus lesions and distal median, radial, and ulnar nerve traumas, excellent outcomes have been demonstrated.
For several days after surgery, the patient is immobilized in a heavy dressing. After 2-3 days, the surgical dressing (containing the drain and pain pump, if applicable) is removed.
The patient is then educated on range-of-motion (ROM) exercises for the joints proximal and distal to the immobilized area. A median nerve reconstruction at the wrist, for example, would be stabilized with a wrist-resting splint, and the patient's fingers, elbow, and shoulder ROM would be continued.
Following the surgical operation, the patient is directed to a hand physiotherapist for immobilization (e.g., splinting), postoperative care education, and exercises. The first goal of postoperative therapy is to restore the passive range of motion to immobilized joints and soft tissues. Exercises to maintain power in the unaffected muscles should be delivered to the patient. Sensory and motor reeducation are encouraged in the later phases to maximize the outcomes.
Traumatic Nerve Injury Complications
Infection, hematoma, seroma, and injury to nearby structures, including vascular structures or nerves, are all common complications of nerve surgery, especially in complex repairs involving mixed nerve injuries or scarred areas.
Traumatic Nerve Injury Prognosis
Predicting nerve injury recovery is difficult since it is dependent on several parameters, including injury acuity, the severity of the injury, scar formation, muscle length, patient age, and whether nerve endings approximation was performed if necessary. The severity of the injury, on the other hand, is negatively proportional to the degree of recovery.
Repair begins nearly immediately for first and second-degree injuries. Conduction block reversal and/or axonal regeneration usually result in a good to remarkable functional recovery within weeks to months. Axonal regeneration is expected to occur at a rate of 1mm/day, and the Tinel sign can be used to track its progression.
In higher degrees of injury, on the other hand, Wallerian degeneration must be complete before axonal regeneration may begin. Furthermore, disruption of nerve structure makes regeneration more complicated, allowing axons to stray out of their endoneurial tubes and into the improper endoneurial tubes or even surrounding tissues, which is particularly true for complete transaction injuries (Fifth degree), where no recovery is predicted without surgical repair and approximation.
The nerve can be injured in a variety of ways, with the majority of injuries involving a combination of methods. Clinically, the nerve can be evaluated in a variety of methods, but the basic and translational technologies behind new treatments are still being identified. When the clinical correlations of these processes are more known, therapeutic decisions will be guided in the future.