Evaluation and Grading of Peripheral Nerve Injuries

Peripheral nerve injury can be caused by many etiologies including ischemic, mechanical, chemical, thermal and inflammatory insults and affects sensory, motor and autonomic function. In this article we will review the classification of nerve injury, examination of a patient with a suspected nerve injury and useful supplementary diagnostic tools including electromyography, ultrasound and magnetic resonance neurography. The aforementioned are all critical parts in determining whether spontaneous recovery is possible or if, and when, surgical intervention including neurolysis, direct repair, grafting or nerve transfer should be considered.

Introduction

The peripheral nervous system (PNS) is the network of nerves stemming from the central nervous system (CNS) that innervates all the structures in the body. The nerves of the PNS send signals to recipient structures as well as feedback information from them, including motor units and sensory receptors. A peripheral nerve injury (PNI) refers to damage to these nerves outside of the CNS and can lead to sensory, motor, and sometimes autonomic deficits. Damage to the PNS can occur from ischemic, mechanical, chemical, thermal, or inflammatory insults. This damage can occur both in the acute or chronic setting; as part of a single or repetitive traumatic events, as well as through long-term compression. There are a number of classification systems used to grade nerve injuries, which can help guide management and provide prognostic value. A detailed clinical evaluation of the patient involving both history gathering and physical examination, paired with diagnostic imaging and electrodiagnostic workup is often necessary to accurately diagnose PNIs. Ultimately, timely diagnosis and treatment of PNIs is essential as nerve recovery can take significant time. Therefore, early intervention, when necessary, has a significant impact on their functional status.

Etiology

PNIs can arise from several different etiologies where the most common are inflammatory, compressive, and traumatic. Categorizing nerve injuries into these larger groups can ultimately help both diagnose and guide management.

Inflammatory nerve injuries are caused by autoimmune or infectious processes that lead to progressive weakness, paresthesia, and sensory dysfunction through nerve inflammation or damage. Chronic inflammatory demyelinating polyneuropathy and Parsonage-Turner Syndrome are 2 of the more common inflammatory conditions seen whereas Lyme disease, shingles, and leprosy are some of the more common infectious conditions worldwide. ^,

Compressive or entrapment injuries occur when nerves are subjected to chronic pressure, which can lead to ischemia, demyelination, and eventual axonal loss if untreated. These injuries often present with pain, numbness, and weakness in the distribution of the nerve. There is often a dose-response curve where the greater the duration and amount of pressure, the more significant nerve dysfunction is present. The most common examples of these are carpal tunnel syndrome and cubital tunnel syndrome. ^,

Traumatic injury is the most common mechanism of PNI and comprises several different injury types that are all caused by an external force. Common mechanisms include: stretch, crush, ballistic or blast, avulsion, and laceration. Obstetric and iatrogenic injuries also may fall into the traumatic injury category. They typically are a result of stretch injury during a complicated delivery or direct damage to the nerve during a medical procedure such as surgical dissection, vascular access, or prolonged extremity tourniquet use. PNI etiology can be multifactorial– for instance, traumatic injuries can occur in the setting of a coexisting entrapment neuropathy or even make a nerve more prone to developing injuries. Double crush injuries refer to the increased susceptibility of a nerve to develop a secondary compressive neuropathy distal to the area with already a pre-existing compressive insult. Another possibility is a reverse double crush, where an injury on a distal portion of the nerve leads to increased susceptibility of proximal compressive neuropathy.

Inflammatory Injuries

Inflammatory neuropathies can result from an autoimmune or infectious process. These forms of PNI may come on insidiously or along with an acute event. Additionally, they can present with any form of sensory, motor, or a combination of involvement. Parsonage-Turner Syndrome (PTS) is one example that can present with similar symptoms to traumatic PNI with unilateral neck, shoulder, and upper extremity pain with sensory loss and muscle weakness, but without a history of a traumatic event. While a traumatic PNI is usually linked to a clear incident leading to predictable nerve damage based on the injury’s location and nature, PTS may not follow classic peripheral nerve, brachial plexus or spinal level patterns. The initial cause of PTS is not well understood but is often associated with recent surgery, viral infection, or immunization. ^, Concurrent symptoms and the patient’s recent medical history become important for making the clinical diagnosis of PTS, which is most often treated conservatively with physical therapy, with most patients achieving full functional recovery at 3 years. Other inflammatory neuropathies include acute inflammatory demyelinating polyradiculoneuropathy, chronic inflammatory demyelinating polyradiculopathy, amyloidosis, multifocal motor neuropathy, and Lewis-Sumner syndrome.

Chronic Compressive Injuries

Compressive or entrapment nerve injury may occur in the acute traumatic situation (or commonly a neuropraxia secondary to resting an extremity on an object for too long), however, these injuries are also extremely common in the chronic setting. Chronic compression neuropathies can lead to progressive weakness, numbness, and pain over time. They are most often secondary to local soft tissue hypertrophy, as is the case in carpal tunnel syndrome, or from surrounding muscular, osseous or vascular structures, as in thoracic outlet syndrome. These chronic compressive injuries typically present over a prolonged period and show a progressive decline in function or worsening of pain/numbness. In most cases, decompression of the involved nerve from the offending agent can lead to significant return of function.

Traumatic Injuries

Traumatic PNI are a heterogenous group that can cause significant motor or sensory impairment. They typically arise immediately after an injury and can be part of a larger complex management in the cases of polytrauma. Traumatic injuries present a unique challenge as the injury may be known (i.e. car accident, knife wound, blunt extremity trauma) but the degree of nerve injury is not. Traumatic injuries can be broadly grouped into the following mechanisms: stretch/traction, compression/crush, lacerations, ballistic, and avulsions. Classifying traumatic injuries based on their mechanisms can help guide management.

Crush nerve injuries commonly occur from motor vehicle accidents or industrial workplace accidents. While these injuries may be severe, they often do not result in nerve transection and can be managed nonoperatively initially to monitor for spontaneous recovery.

Laceration or penetrating injuries may present with either complete or partial transection of the nerve and suspicion should be high for some form of nerve discontinuity in these cases. Management is these cases frequently involves immediate exploration of the nerve as primary repair of the nerve in the case of a complete transection portends the best prognosis.

Ballistic injuries occur secondary to shrapnel or other projectiles commonly due to gunshot wounds. In these cases, there is significant blunt trauma both from the projectile itself, and around the path of the projectile (cavitation), which leads to more extensive soft tissue damage than would be expected. Historically, many of these injuries were not explored in the acute setting as the thought was that the PNI would be primarily neuropraxic from local concussive injury. More recently, however, some have suggested management has move towards acute exploration as high-grade injuries are thought to be more common in ballistic injuries than previously expected.

Stretch-related injury occurs when traction forces overcome the nerve’s elastic properties. This type of injury often occurs in nerves near the bone of an extremity that fractures, or at a point where the nerve may be stretched along a fixed structure (frequently seen after significant neck trauma). Many of these injuries will be neuropraxic in nature and recover on their own in time, however, severe injury can result in nerve rupture necessitating surgical intervention.

Avulsion injury is a severe form of stretch injury where the nerve root is torn away from the spinal cord. These injuries result in the complete loss of both motor and sensory function and most often occur at the brachial plexus. In these types of PNI, surgical intervention in the form of nerve and tendon transfers is the primary treatment and offers some functional recovery.

Differentiating types of nerve trauma are essential because certain types of traumas result in predictable nerve injury patterns based on the mechanism. For example, an upper brachial plexus injury results in damage to the C5 and C6 root levels. These nerves supply the axillary, suprascapular, and musculocutaneous nerves to the upper limb. The most common mechanism of injury is traction on the infant neck during delivery or when the neck is deviated during a traumatic injury. Damage results in loss of sensation in the arm and atrophy of the deltoid, biceps, and brachialis muscles.

A similar, but less common pattern is a lower brachial plexus injury pattern which results in damage to C8 and T1. The most common mechanism of injury is hyper-abduction trauma to the arm, either from grabbing something while falling or excessively stretching an arm that is raised overhead. These nerve roots form the ulnar and part of the median nerve, and innervate the medial side of the arm, forearm, and hand. There is resulting weakness and atrophy of the intrinsic hand muscles resulting in a characteristic “claw hand” where finders are flexed at the interphalangeal joints and extended at the metacarpophalangeal joints. Horner’s syndrome may also be seen due to damage to the sympathetic fibers traveling through T1.

Traumatic PNI may present as isolated nerve injuries with a simple and clear mechanism, or as a cluster of symptoms secondary to multiple nerves being involved. Understanding the mechanism of injury, time period from when the injury occurred to when symptoms developed, and the functioning of the patient is critical to determining both diagnosis and treatment.

Classification of PNI

Classifying PNI helps surgeons to standardize diagnoses, predict prognosis of the injury, and to enable effective communication among healthcare professionals ( Table 1 ). Accurate classification of injury helps to set expectations for both the healthcare team and the patient, ensuring that a treatment framework guides healthcare decisions. The first system to gain wide use for classifying PNI emerged in 1943 when Sir Herbert Seddon published his 3-category system based on structural continuity and recovery potential, in which PNI were classified as neurapraxia, axonotmesis, or neurotmesis.

Table 1

Peripheral Nerve Injury Grading Characteristics, Prognosis, and Recommended Surgical Intervention

Degree of Injury		Pathology					Potential for Recovery	Recovery Rate	Surgical Intervention
Sunderland	Seddon	Myelin	Axons	Endoneurium	Perineurium	Epineurium
I	Neurapraxia	+	–	–	–	–	Full	Up to 12 weeks	None
II	Axonotmesis	+	+	–	–	–	Full	1 mm/day	None
III	Neurotemesis	+	+	+	–	–	Partial, often incomplete	1 mm/day	None or Neurolysis
IV		+	+	+	+	–	Poor to none	Limited	Primary repair, graft, or distal nerve transfer
V		+	+	+	+	+	None due to rupture	None	Primary repair, graft, or distal nerve transfer

+ = injured anatomic structure.

Figure 1 demonstrates a peripheral nerve in cross-section, with the layered connective tissues of the endoneurium, perineurium, and epineurium that provide a protective sheathe to axons. It also displays the myelin sheath, which insulates axons to speed up nerve signal transmission. An anatomical understanding of the multilayers of a nerve is important for classification as the Seddon system describes injuries based on these anatomical layers

Neurapraxia is the mildest form of PNI in which the conduction of nerve impulses is lost in an injured area, resulting in either partial or total loss of motor and sensory function. Neurapraxia is often caused by either focal ischemia or direct damage to the myelin sheath of the nerve, however the axons are spared. Recovery is typically full due to the nerve structure remaining intact.

Axonotmesis involves damage to the nerve’s axon fibers, with Wallerian degeneration occurring distal to the injury. In this type of injury the surrounding connective tissue framework is preserved and provides a scaffold for nerve regrowth. This type of injury is often seen in crush or stretch injuries and can lead to more pronounced motor and sensory impairments with a longer recovery. Despite the damage to axons themselves, in many cases a complete recovery without surgical intervention can be possible.

The most severe injury is neurotmesis, which involves damage to the entirety of the peripheral nerve leading to total sensory and motor loss. These injuries are often caused by significant trauma and require surgical intervention as the recovery potential without intervention is low.

In 1951, Dr. Sidney Sunderland expanded upon Seddon’s work and developed a 5-degree classification system. Grade I retains Seddon’s definition of neurapraxia, while grade II is most like axonotmesis. Both grades I and II are expected to recover completely through conservative treatment. Grade III refers to damaged axons, myelin sheath, and endoneurium but an unharmed perineurium. Grade III injuries will often heal spontaneously but often lack complete recovery, due to scar tissue, conduction block and improper nerve regrowth. Grade IV involves damage to nerve bundles, axons, endoneurium, and perineurium with an intact epineurium. Like grade III injuries, spontaneous regrowth is severely limited by scar tissue and the formation of a neuroma in situ resulting in minimal functional recovery. Degree V injury corresponds to neurotmesis with rupture of both the nerve bundle and epineurium, requiring surgical repair. Figure 2 A and B demonstrate a case where there was higher grade injury resulting in neuroma formation. In this case the neuroma was excised, and the nerve was reconstructed with a graft.