Traumatic Cranial and Peripheral Nerve Injuries

Jennifer F. Russo

Charles B. Mikell

Christopher J. Winfree

INTRODUCTION

Traumatic injury to peripheral nerves is associated with significant disability and decreased quality of life. In this chapter, we discuss the classification, pathophysiology, evaluation, and treatment of peripheral nerve injuries, as well as the clinical manifestations of common peripheral and cranial nerve lesions. Understanding of the principles described in this chapter, by clinicians, is important for timely diagnosis and treatment of these common clinical entities.

EPIDEMIOLOGY

It has been estimated that approximately 3% to 10% of all patients presenting to a level 1 trauma center present with injury to a peripheral nerve. Motor vehicle accidents are most commonly cited as the leading cause, whereas industrial accidents, recreational vehicle use, falls, gunshot and stab wounds, as well as iatrogenic injuries also contribute. The potential economic and social impact of these injuries is compounded by the fact that they occur most commonly within the productive age range, with highest incidence reported between 20 and 40 years of age. Males are affected more often than females, and injury to the nerves of the upper extremity occur more commonly than do those to the nerves of the lower extremity. Peripheral nerve injuries are also commonly comorbid with traumatic injury to the brain, which can result in delayed diagnosis and intervention.

PATHOBIOLOGY

ANATOMY AND PHYSIOLOGY

Evaluation of traumatic peripheral nerve injury requires understanding of nerve structure. Peripheral nerves consist of a mixture of myelinated and unmyelinated, somatic and autonomic, nerve fibers. Each fiber is surrounded by an endoneurial sheath, which provides some tensile strength. Multiple fibers, of various types, are grouped together into fascicles and surrounded by the perineurium, a specialized structure composed of perineurial cells and collagen that serves to maintain homeostasis of the endoneurial fluid that surrounds individual fibers. This perineurial sheath provides most of the tensile strength and elasticity of the nerve and provides a diffusion barrier that resists and maintains intrafascicular pressure. Multiple fasciculi, in turn, are embedded in a connective tissue matrix called the epineurium, which protects the nerve from compression. The most superficial layer of the epineurium condenses to form an external epineural sheath, which gives the nerve a cord-like appearance on gross examination.

Both within and between nerve fibers, the number, size, and organization of fascicles varies significantly. As fascicles branch, split, and rejoin continuously along their course, sections through the nerve may alternatively reveal plexiform and cable-like structure, which has implications for both clinical presentation of nerve injuries, as well as surgical repair and functional regeneration. Further, variability in internal organization is partially responsible for observed differences in the prevalence of particular nerve injuries. That is, peripheral nerves with a higher proportion of epineural tissue to fasciculi may be more resistant to compression injuries, whereas peripheral nerves with greater numbers of fasciculi have greater tensile strength.

MECHANISMS OF INJURY

Traumatic nerve injuries may be acute or chronic and iatrogenic or idiopathic. They result from the application of kinetic energy to a nerve, which is transformed into damaging compressive or tensile forces. Chronic traumatic nerve injuries most often result from anatomic nerve entrapment leading to well-described clinical entities, such as carpal tunnel syndrome. These chronic syndromes, requiring unique medical and surgical treatment approaches, are discussed more thoroughly in Chapter 87.

Acute traumatic nerve injuries occur, most commonly, from traction/stretch, compression, contusion, laceration, or ischemia. Injury is derived primarily from direct application of mechanical forces and secondarily from vascular compromise. Multiple mechanisms of injury may be present, particularly when the lesion occurs during a catastrophic event, such as a motor vehicle accident. Identifying the type of insult incurred, when possible, is important for treatment planning, as various types of forces result in different patterns of injury.

INJURY CLASSIFICATION

Two major classifications systems are used most commonly to describe peripheral nerve injuries. The injury categories defined by these systems each have unique diagnostic characteristics, prognoses, and therapeutic approaches.

The classification system used most commonly in clinical settings was proposed by Seddon in 1942. Seddon’s system divides injuries into three main categories delineated by the extent of disruption to the structure of the nerve. The three categories are neurapraxia, axonotmesis, and neurotmesis (Table 48.1).

Neurapraxia is the least severe of the three injury types. It most commonly is caused by a mild insult resulting in focal demyelination with no associated axonal degeneration. It is characterized by transient focal conduction block across the lesion. The axon distal to the site of injury remains intact and the nerve remains in continuity. Clinically, this class of injury may manifest as weakness or sensory loss in the anatomic distribution of the affected nerve. Prognosis for this type of injury is excellent, with spontaneous recovery occurring within hours to, in the most severe cases, a few months. No specific therapeutic intervention is required.

Axonotmesis occurs most commonly during crush, stretch, or percussive injuries, such as gunshot wounds where injury is most commonly caused by indirect heat and shock wave from the bullet rather than transection. These injuries result in irreversible damage to axonal elements including the myelin sheath, leading to distal degeneration. Supporting structures such as the epineurium, perineurium, and, at times, the endoneurium remain intact.

TABLE 48.1 Seddon’s Nerve Injury Classifications and Prognosis

Class	Pathology	Mechanism	Treatment	Prognosis	Time Course
Neurapraxia	Demyelination	Compression Ischemia	Medical Physical therapy	Excellent	Hours to 3 mo
Axonotmesis	Axonal disruption Distal degeneration Epineurium intact	Crush Stretch Percussion	Variable: may require surgery	Variable: good to poor	Weeks to years
Neurotmesis	Complete loss of continuity Transection Distal degeneration	Sharp injuries Traction	Surgical: end-to-end neurorrhaphy, grafting or neurotization	Poor/nil without repair	Months to years with surgery No spontaneous recovery

Prognosis for axonotmetic injuries depends on several factors. These factors include the degree of disruption of the internal structure of the nerve, as well as distance from the end organ and the particular characteristics of the injured nerve. Spontaneous recovery is possible after axonotmetic injury, but the time course is considerably greater than that of neurapraxic lesions. Recovery is more commonly partial than complete.

Neurotmesis is defined by complete loss of continuity of the nerve. All connective tissue layers, the axon, and the myelin sheath are irreversibly damaged. Surgical intervention is required, as no spontaneous recovery is possible. The timing of surgery is dependent on the mechanism of injury, as blunt injuries continue to evolve through an inflammatory process over a period of weeks. Prognosis after surgery is variable but is generally poorer than that of spontaneous recovery.

A second important peripheral nerve injury classification system was proposed by Sunderland in 1951 (Table 48.2). Expanding on the work of Seddon, he described five classes of nerve injury, with class I describing neurapraxic lesions and class V equivalent to neurotmesis. For classes II to IV, Sunderland subdivided axonotmesis into three levels, of increasing severity and worsening prognosis, based on the extent of internal disruption, from axon only in class II to endoneurial sheath in class III and perineurium in class IV. Although this additional level of detail is helpful in a research setting, the clinical use is more limited, as all classes II to IV will require the same initial therapeutic approach. Nevertheless, this classification scheme highlights the importance of internal nerve structure for spontaneous recovery and functional regeneration.

TABLE 48.2 Sunderland’s Classification of Peripheral Nerve Injuries

Class	Pathology	Mechanism	Treatment	Prognosis	Time Course
I	Demyelination	Compression Ischemia	Medical Physical therapy	Excellent	Hours to 3 mo
II	Axonal disruption Distal degeneration	Crush Stretch Percussion	Variable	Good	Months to years
III	II + endoneurial disruption	Crush Stretch Percussion	Variable	Moderate	Months to years
IV	III + perineurial disruption	Crush Stretch Percussion Traction	Variable	Poor without repair	Months to years
V	Complete transection	Sharp injury Traction	Surgery	Poor/nil without repair	Months to years with surgery No spontaneous recovery

REPAIR AND REGENERATION

Characteristic pathologic changes in the nerve occur as a result of traumatic insult. In the mildest form, demyelination is observed at the injury site. When trauma results in axonal disruption, the distal nerve undergoes a process of degeneration that extends to the end organ. The duration of the degenerative process is dependent on the distance of the injury from the end organ. Morphologic and functional changes also take place within the proximal stump adjacent to the injury site.

In the initial period immediately following injury, acute axonal degeneration, extending approximately 300 mm proximally and distally from the lesion site, is triggered by an influx of extracellular calcium. On electron microscopy, vacuoles resembling autophagosomes accumulate in the axon ends. Swelling and disruption of neurofilaments is observed.

These immediate changes are followed by fragmentation and phagocytosis of the myelin sheath. Within 2 days, whorls of myelin debris and small lipid droplets may be observed within the Schwann cells. Circulating macrophages are recruited and enter
the distal stump. Loss of axonal contact and the presence of macrophages stimulate Schwann cell proliferation and dedifferentiation. These dedifferentiated Schwann cells line up along the basal lamina to form bands of Büngner, which will act as guides to regenerating nerve axons.

Reinnervation occurs via two main mechanisms: collateral axonal sprouting from uninjured axons and axonal regeneration, which occurs spontaneously from the proximal stump following degeneration. Collateral sprouting is an early mechanism of functional motor recovery. It occurs with incomplete lesions, in which some of the axons remain intact. New axonal outgrowths are noted to arise from both nearby nodes and terminal branches. These fine axonal extensions travel along the remaining nerve structures to provide partial reinnervation to nearby motor targets. Generally, collateral sprouting is not sufficient to restore full power to the muscle but may be responsible for some early functional recovery.

Axonal regeneration is the primary mechanism by which reinnervation occurs, following distal degeneration, in axonotmetic and neurotmetic lesions. Regeneration begins from the proximal stump and extends along intact basal lamina toward the end organ at a variable rate of approximately 1 to 2 mm/day. Once the target organ has been reached, a process of maturation occurs to reestablish functional connection. The appearance of clinical evidence of reinnervation reflects both the distance from injury site to the end organ and the maturation process. Rate of regeneration appears to be slower for transected lesions than for crush injuries.

Successful regeneration and functional recovery rely on a number of factors. Inflammation and scar tissue provide major barriers to axonal growth. Gap lengths that are too long result in disorganized and highly tortuous axonal paths, which may coalesce within scar tissue to form a nonfunctional and potentially painful bulb referred to as a neuroma.

Even when regeneration does occur successfully, functional recovery is not guaranteed. Regenerating sprouts must be able to form mature connections with appropriate motor or sensory targets in order for recovery to occur. In highly mixed nerves, with an approximately equal amount of sensory and motor fibers, some regenerating motor fibers may be lost to sensory targets or vice versa. Nerves that contain one predominant modality generally have a better prognosis for functional recovery.

Finally, sensory targets maintain viability for a much longer period of time than does muscle tissue. Within 12 to 18 months, fibrotic changes take place in denervated muscle that make successful reinnervation unlikely. Sensory targets, on the other hand, maintain viability for up to 2 to 3 years. Therefore, patients may continue to experience recovery of sensation well beyond the period of motor recovery.

CLINICAL FEATURES

The clinical manifestation of traumatic peripheral nerve injury depends on the mode, location, and extent of the injury sustained. Signs and symptoms reflect both the location and severity of the lesion, as well as the composition of the injured nerve. Injury to a nerve that consists predominantly of motor fibers will manifest as weakness or paralysis and atrophy in the corresponding myotomal distribution. Injury to a predominantly sensory nerve, on the other hand, will present with sensory alteration or loss in the corresponding dermatomes. Autonomic and trophic function may also be affected resulting in decreased sweating, hair loss, and skin changes in the affected region. Partial lesions and faulty regeneration may result in the development of difficult to treat pain, often described as “pins and needles,” stabbing or burning in character. For some patients, a debilitating symptom complex called complex regional pain syndrome II, also referred to as causalgia, may develop, which is characterized by allodynia, autonomic dysregulation, and maladaptive neuroplastic changes in central nervous system (CNS) response to and processing of pain signals. This syndrome often does not respond well to conventional pain management strategies.

Some common associations are seen between various injury mechanisms and specific peripheral nerves. Awareness by clinicians, of these associations, may contribute to the earlier identification and treatment of potentially disabling injuries. Some of these common associations and their clinical presentations are discussed in the following section.

CRANIAL NERVE LESIONS

Acute injury to cranial nerves often accompanies trauma to the head and neck. Significant injury may occur even with mild head trauma. One study by Coello and colleagues that evaluated cranial nerve function in 16,440 mild head trauma patients, defined by a Glasgow Coma Scale score of 14 or 15 at the time of presentation, over a period of 6 years, found a prevalence of associated cranial nerve injury of 0.3%, with the olfactory nerve being the most commonly affected, followed by the facial nerves and the nerves responsible for ocular movement. Injury to the lower cranial nerves (IX to XII) was noted to occur less frequently as a consequence of head trauma but to be more closely associated with iatrogenic injury during various medical and surgical interventions. The prevalence, location, and type of cranial nerve injuries observed most frequently result from the specific anatomic vulnerabilities of the affected nerve.

Cranial Nerve I: The Olfactory Nerve

The olfactory nerve, responsible for our ability to detect and distinguish smells, is one of the most commonly cited cranial nerves to be injured as a result of head trauma. Olfactory dysfunction has been reported to occur in up to 4% to 7% of all cases of head trauma. Injury may occur at multiple sites along the olfactory pathway. It is most often associated with acceleration-deceleration forces, such as those generated during motor vehicle accidents. Common injury sites include the olfactory nerve filaments as they cross the cribriform plate and are subject to shearing forces; the olfactory bulb, which may be contused against the frontal bone; and the cortical olfactory tracts, which may be damaged by edema, hemorrhage, or ischemic injury of the orbitofrontal and temporal lobes. Anosmia, the complete loss of odor detection, is the most common clinical finding, but parosmia, a decrease in olfaction acuity, is also observed, particularly with injury to the temporal lobe. The perception of taste, which is reliant on olfaction, is also commonly impaired in patients with injury to the olfactory nerve, and it is this symptom for treatment of which most patients present.

Despite the relative frequency with which injury to the olfactory nerve occurs following head trauma, deficits are rarely identified in the acute period. This may be because of the fact that trauma patients present with multiple injuries of varying severity and immediacy that require disproportionate allocation of resources. Nevertheless, loss of olfaction may have significant impact on quality of life, resulting in diminishment of enjoyment of food and other sensual experiences reliant on smell; loss of employment, when dependent on the sense of smell or taste; and decreased ability to detect environmental cues that may signal danger, such as the odor of volatile gas or fire. Awareness by clinicians of the association of head trauma with cranial nerve I dysfunction is important for early detection and diagnosis.

Cranial Nerve II: The Optic Nerve

Traumatic optic neuropathy, which may result in complete or partial loss of visual acuity in the affected eye, has been reported to occur in 1.4% to 5% of head trauma cases. Injury may be direct, resulting from anatomic disruption of nerve fibers by fracture fragments, penetrating trauma, or hematoma within the nerve sheath, or indirect, reflecting the transmission of forces to the optic canal during blunt head trauma. Early decompressive surgery may be required to prevent irreversible vision loss.

Additionally, injury to the optic nerve is recognized as a potential complication of facial fracture repair in patients with maxillofacial trauma, with a reported incidence of 0.3%. Mechanisms include direct intraoperative nerve injury, retinal vascular occlusion from orbital edema, and increased intraorbital pressure in the optic canal resulting in indirect injury to the nerve. This complication is most often reported after surgical intervention of the orbital floor, and ischemia is the most common final pathway leading to injury.

Unlike skeletal tissues, the optic nerve and retinal tissues are extremely sensitive to hypoxia and pressure, with irreversible ischemic damage occurring within 60 minutes to 2 hours. Because of this sensitivity, prompt identification of even subtle changes in visual acuity by the clinician is essential to provide potentially vision-sparing interventions in a timely manner.

Cranial Nerve III, IV, VI: The Oculomotor, Trochlear, and Abducens Nerve

Together, the oculomotor, trochlear, and abducens nerves innervate the muscles responsible for ocular movements. Damage to these nerves is a common complication of closed head injury. It may result in diplopia, impairments in eye movement, and ocular deviation. Injury to the nerves may occur at the nuclei in the brain stem, as the nerve exits the brain stem, and at the point where it pierces the dura mater. The site of injury reflects both the injury mechanism and the anatomic characteristics of the nerve. One or all of the nerves for oculomotor control may be affected, and clinical presentation will vary accordingly.

Cranial nerve III, the oculomotor nerve, innervates many of the muscles responsible for eye movement, including the medial rectus, superior rectus, inferior rectus, inferior oblique, levator palpebrae superior, and the pupillary constrictor. Additionally, the oculomotor nerve carries parasympathetic fibers to the eye. Complete lesion of this nerve results in a “down and out” deviation of the eye, ptosis, dilation of the pupil, and loss of pupillary constriction to light but not accommodation. Partial lesions may result in any combination of these findings, depending on the specific nerve fibers affected. Because the parasympathetic fibers run along the outside of the nerve, compressive lesions, such as an expanding hematoma or progressive uncal herniation secondary to intracranial hemorrhage or edema, tend to present with pupillary changes first, which may progress to oculomotor palsy with increasing pressure. Aneurysms of the posterior communicating artery may also compress the third cranial nerve and should be considered when evaluating a patient with oculomotor nerve palsy. Injuries that cause third nerve ischemia, on the other hand, are more likely to affect the motor fibers before disrupting the parasympathetic components. This distinction may help the clinician to identify the etiology of idiopathic third nerve palsy.

The trochlear nerve provides innervation to the superior oblique muscle. Lesion of this nerve results in an inability to move the eye medially and inferiorly. The resulting diplopia may be resolved by inclining the head toward the unaffected eye. Trochlear nerve palsies occurring in isolation have been observed following dorsal midbrain hemorrhage and as a complication of dental anesthesia during upper molar surgery but are extremely rare. Generally, injury to the fourth cranial nerve is accompanied by other oculomotor and neurologic deficits.

The abducens nerve innervates the lateral rectus muscle, which is responsible for abduction of the eye. Injury to this nerve results in severe double vision in almost all gaze directions and medial deviation. Traumatic injury to the sixth cranial nerve has been associated with cranial base fracture and the development of clival epidural hematoma, as well as cervical hyperextension, atlantooccipital dislocation, and hyperflexion. The sixth cranial nerve vulnerability to injury is thought to be a result of its long and delicate intracranial source. After exiting the pons, it ascends vertically within the subarachnoid space for 15 mm before piercing the dura mater. From there, the nerve travels over the ridge of the petrous bone, change directions abruptly at a 120-degree angle to enter Dorello canal, a triangular space defined by the apex of the petrous bone, the posterior clinoidal process, and a thickened portion of the dura mater, which connects the two, referred to as Gruber ligament. The nerve is tethered by the dura on either side of the canal. From Dorello canal, the nerve passes through the cavernous sinus and the superior orbital fissure to reach the lateral rectus muscle. Traumatic injury to the abducens nerve is thought to occur most commonly by downward displacement against the petrous ridge at the point at which it turns to enter the canal.

Cranial Nerve V: The Trigeminal Nerve

The trigeminal nerve supplies sensation to the face through three major peripheral branches, the ophthalmic (VI), maxillary (V2), and mandibular (V3) nerves. V1 and V2 are purely sensory, whereas V3 also carries motor fibers to the muscles of mastication. V1 is also responsible for the corneal reflex. Traumatic injury to the branches of the trigeminal nerve is uncommon but may result from dental or cranial trauma or as a side effect of dental and surgical procedures in the region. Several cases of damage to the lingual nerve, which is a branch of the mandibular division, which provides sensation to the anterior two-thirds of the tongue, and which is joined by the chorda tympani from cranial nerve VII, have been reported with the use of supraglottic airway devices. Compression of the nerve branch by the device results in temporary loss of sensation and taste (from the gustatory fibers of cranial nerve VII) in the anterior tongue, which, although potentially upsetting to the patient, generally resolves spontaneously within 6 to 9 weeks. The patient experiencing these symptoms postoperatively should be reassured regarding chance of recovery.

Cranial Nerve VII: The Facial Nerve

The facial nerve provides most of the motor innervation for the muscles of expression in the face. It also, via the nervus intermedius, relays afferent taste sensation from the anterior two-thirds of the tongue and carries sympathetic fibers to the lacrimal and salivary glands. Depending on the location of the injury, motor, autonomic, and gustatory deficits may be seen. Lesions of the intracranial portion of the nerve near the origin or close to the geniculate ganglion by the internal acoustic meatus, may affect all three components, whereas those in the facial canal of the temporal bone between the geniculate ganglion and the origin of the chorda tympani near the stylomastoid foramen may spare lacrimation. Lesions occurring after the stylomastoid process in the extracranial portion of the nerve result primarily in motor deficits. Symptoms may be mild to severe depending on the severity of injury.

Injury to the facial nerve may present as complete paralysis of the facial muscles, with flattening of the facial folds around the nose, lips, and forehead; widening of palpebral fissures; and incomplete closure of the eyelid on the affected side, which can result in corneal scarring from desiccation particularly if the injury also affects lacrimation. Decreased salivation and loss of taste in the anterior two-thirds of the tongue may also be present if the chorda tympani is affected. Less commonly, patients with seventh nerve injuries may experience sensitivity to loud sounds, or hyperacusis, as the facial nerve supplies motor input to the stapedius muscle, which has a dampening effect on the tympanic membrane. During regeneration, synkinesis may develop, which is the movement of unrelated facial muscles during attempts at isolated muscle movements, such as lip twitch with blinking, if aberrant reinnervation occurs. Importantly, lesions of the peripheral facial nerve can be distinguished from central motor pathway lesions by assessing involvement of the forehead. Central lesions spare forehead motion due to bilateral representation in the CNS, whereas peripheral lesions do not.

Traumatic injury to the facial nerve may result from temporal bone fracture, penetrating injuries, such as knife or gunshot wounds, as a result of surgery for other indications, including resection of acoustic neuroma, or in the neonate at the time of delivery by the application of forceps. The superficial peripheral branches are particularly vulnerable to injury. Studies suggest that approximately 7% to 10% of temporal bone fractures result in facial nerve dysfunction. Trauma to the temporal bone may result in both an initial direct injury to the nerve followed by a secondary ischemic injury, as edema causes increased pressure in the fallopian canal containing the nerve. Decompressive surgery may be necessary to prevent progression of injury and should be undertaken as early as possible. Likewise, penetrating injuries most often result in nerve transection and early surgical exploration is desirable. Surgical approach is dependent on the location of the injury.

Cranial Nerve IX: The Glossopharyngeal Nerve

Trauma to cranial nerves IX, X, XI, and XII is most often iatrogenic. The glossopharyngeal nerve carries both sensory and motor fibers. The sensory fibers transmit information from the upper part of the pharynx and taste from the posterior one-third of the tongue. The motor component innervates the constrictor muscles of the pharynx and the stylopharyngeus as well as secretory glands in the pharyngeal mucosa. Traumatic injury to the nerve occurs most commonly with fractures through the jugular foramen where it exits the skull together with the vagus and accessory nerves. Lesions resulting from trauma are rarely isolated and occur most commonly with injuries of the X and XI cranial nerves. Clinically, glossopharyngeal dysfunction presents with diminished taste in the posterior one-third of the tongue and loss of gag reflex on the side of the lesion. The presence of dysphagia or dysarthria may signal concomitant injury to the vagus nerve, as these symptoms are rarely present in isolated glossopharyngeal injuries.

Cranial Nerve X: The Vagus Nerve

The vagus nerve provides motor, sensory, and autonomic innervation to a wide variety of targets. Motor fibers originating in the nucleus ambiguous in the brain stem innervate the somatic muscles of the pharynx and larynx, which coordinate the initial phase of swallowing. Autonomic fibers from the dorsal motor nucleus provide innervation to the heart, lungs, esophagus, and stomach. Sensory fibers from the upper gastrointestinal tract and oropharynx travel within the vagus nerve to the spinal nucleus, and sensation from the thoracic and abdominal organs is transmitted to the tractus solitarius. Dysarthria and dysphagia may occur with injury, and the palate on the affected side will be low at rest. Deviation of the uvula toward the unaffected side with phonation may be observed as the unopposed contralateral muscles contract.

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