When a nerve injury occurs, it is paramount the dental implant surgeon be able to recognize the type and extent of injury and provide the most appropriate postoperative care. Traumatic and iatrogenic nerve complications may involve total or partial nerve resection, crushing, thermal, stretching, or entrapment injuries. The resulting sensory deficits may range from a nonpainful, minor loss of sensation (hypoesthesia), to a more permanent and severe debilitating pain dysfunction (dysesthesia). Patients with neurosensory deficits often complain of symptoms that include interference with function, speaking, eating, kissing, facial soft tissue dysfunction, and inability to complete everyday tasks such as shaving and placing make-up. The sensory problems often result in an overall decreased quality of life and long-standing psychological problems.4 Most patients find accepting and coping with even minimal nerve injuries difficult to live with. The clinician is usually affected by increased complaints from the patients, embarrassment, with significant medicolegal implications.
In the field of oral implantology today, the clinician must have a thorough understanding of the etiology, prevention, and treatment of neurosensory impairments. The authors have developed postoperative guidelines for diagnosis and possible management of neurosensory deficits following dental implant surgery that are dependent on the history, type, and nature of the injury.
The individual nerve fibers of peripheral nerves are situated in fascicles, which are bundles or groups of nerve fibers. For example, the inferior alveolar nerve is classified as polyfascicular, meaning that it contains more than 10 fascicles surrounded by an abundance of interfascicular connective tissue. Within the fascicles, there are approximately 7000–12,000 axons in various fascicular arrangements.5 The number of fascicles varies along the intramandibular course of the inferior alveolar nerve because there are approximately 18–21 fascicles in the third molar region, decreasing to 12 fascicles in the mental foramen area.6 Because of the polyfascicular nature of the inferior alveolar nerve, it is better able to regain sensation after injury via compensatory innervation from the uninjured fascicles. Surrounding the polyfascicular makeup of this nerve is the perineurium, which consists of dense, multilayered connective tissue. The perineurium functions to maintain intrafascicular pressure and acts as a diffusion barrier in the protection of the individual nerve fibers. Two types of connective tissue, the inner and outer epineurium, surround the fascicles. The inner epineurium is composed of loose connective tissue with longitudinal collagen bundles. This tissue protects the nerve fibers against compressive and stretching forces, thus maintaining the structural continuity of the nerve. The outer epineurium is continuous with the mesoneurium, which is the outer loose areolar tissue that suspends the nerve trunk within the soft tissue and contains the blood supply to the nerve. The mesoneurium allows the nerve to have longitudinal movement within the surrounding tissue.
If any of these extraneural tissues (epineurium, perineurium, endoneurium, or mesoneurium) is injured, impaired neural transmission by the individual nerve fibers may result in a sensory disturbance. The neurosensory impairment is dependent on the individual fiber type that is involved. The A-alpha fibers are the largest fibers; mediate position and fine touch through muscle spindle afferents and skeletal muscle efferents. The A-beta fibers are solely for proprioception, and the A-delta carries the initial pain impulses along with temperature information. Unmyelinated C-fibers are slow conducting and function for the perception of “second” or slow pain with an additional temperature component. For dental implant surgeons the primary concern is loss of sensory functions such as touch, pressure, pain, and temperature following trauma (Fig. 9.2).
The trigeminal nerve is the fifth cranial nerve and largest of the 12 cranial nerves. This nerve originates from the brainstem at the midlateral surface of the pons with its afferent fibers transmitting innervation from the face, oral and nasal cavity, as well as the scalp. The trigeminal nerve also has visceral efferent fibers for lacrimal, salivary, and nasal mucosa glands. Somatic efferent fibers are present that innervate the masticatory muscles. The trigeminal nerve has three main branches: V1 (ophthalmic); V2 (maxillary); and V3 (mandibular).
The uppermost branch is the ophthalmic nerve, V1, which is the smallest of the three divisions of the trigeminal nerve. It supplies sensory branches to the ciliary body, cornea, conjunctiva, lacrimal glands, and nasal mucosa as well as to the skin of the nose, eyelid, and forehead. The ophthalmic division structures are rarely involved in neurosensory disturbances associated with dental implant procedures.
The middle branch of the maxillary nerve (V2) exits the middle cranial fossa through foramen rotundum and enters the pterygopalatine fossa, where it gives off branches to the maxillary teeth and gingiva, maxillary sinus, upper lip, lateral surface of the nose, the lower eyelid, the skin of the cheek and side of the forehead, nasal cavity, and mucosa of the hard and soft palate (Fig. 9.3).
The incisive canals fuse and form a common Y-shaped canal that exits lingual to the central incisor teeth (incisive foramen or incisive fossa). The nasopalatine nerve passes through these canals and provides sensation to the anterior palate. These nerves (also termed incisive nerves) terminate at the nasal floor and enter the oral cavity via the incisive canal, which is underneath the incisive papilla. To prevent trauma to these nerves, ideal presurgical planning of implant placement in the maxillary incisor region should be carefully evaluated (Fig. 9.4).
Removing the contents of the nasopalatine canal and grafting has been reported to have a high success rate.7,8 Although this nerve is often affected by the placement of implants or bone grafting in the incisor region, sensory disturbances are rare. Nerve damage reported in the literature caused by complete removal9 or flap surgery10 is of short duration. This is most likely due to cross innervation of the greater palatine nerve on the anterior palatal area.
The infraorbital nerve emerges from the infraorbital foramen and gives off four branches: the inferior palpebral, external nasal, internal nasal, and the superior labial branches, which are sensory to the lower eyelid, cheek, and upper lip. The inferior palpebral branches supply the skin and conjunctiva of the lower eyelid. The nasal branches supply the lateral nose soft tissue and the movable part of the nasal septum, and the superior labial branches supply the skin of the cheek and upper lip. Normally, the average distance of the inferior border of the orbital rim to the infraorbital foramen is 4.6 mm to 10.4 mm (Fig. 9.5).
Impairment of the infraorbital nerve may be very traumatic to patients. Damage to branches of the infraorbital nerve usually will result from retraction-related trauma (neuropraxia). Procedures involving the maxillary cuspid-bicuspid area are most susceptible to injuries. Anatomic variants of the infraorbital foramen have been shown to be up to 14 mm from the orbital rim. This is most likely seen in elderly female patients with extensive alveolar atrophy.
Anterior Superior Alveolar Nerve.
The anterior superior alveolar nerve branches from the infraorbital canal on the lateral face. This small canal may be seen lingual to the cuspid and is denoted as the canalis sinuosus. The canal runs forward and downward to the inferior wall of the orbit and, after reaching the edge of the anterior nasal aperture in the inferior turbinate, it follows the lower margin of the nasal aperture and opens to the side of the nasal septum.11 Studies have shown that in approximately 15% of the population, this area is described as foramina that are 1–2 mm in diameter. The canals present as a direct extension of the canalis sinuosus and may be clinically relevant when greater than 2.0 mm12 (Fig. 9.6).
Because the canine pillar region is a common area for dental implants, care should be taken to check for the presence of neurovascular bundles of the infraorbital canal. Insertion of implants in approximation to the canal may be problematic. Impingement into the canal may lead to a soft tissue interface and failure of the implant and temporary or permanent sensory dysfunction and possible bleeding issues.13 However, significant sensory impairments are rare because of cross innervation. Many clinicians are unaware of the canalia sinuosus and may misdiagnose this radiolucency as apical pathology of the maxillary cuspid.
The mandibular nerve is the largest of the trigeminal branches and is the most common branch involved with neurosensory disturbances following dental implant surgery. The mandibular nerve is the lowest branch of the trigeminal nerve, which runs along the floor of the cranium, exiting through the foramen ovale into the infratemporal fossa. It has two branches, the first being a smaller anterior branch containing the buccal and masseteric nerve. A larger posterior component divides the mandibular nerve into three main branches, the auriculotemporal, inferior alveolar (IAN), and lingual nerves (LN).
This nerve innervates the temporomandibular joint, skin above the ears, auricle, tongue and its adjacent gingiva, floor of the mouth, mandibular teeth and associated gingiva, mucosa and skin of the cheek, lower lip and the chin and the muscles of mastication.
Inferior Alveolar Nerve.
The inferior alveolar nerve is the largest branch of the mandibular nerve. Before entering the mandibular foramen on the lingual surface of the mandible, the mylohyoid nerve branches, giving innervation to the mylohyoid and anterior belly of digastric muscles. In the mandibular canal it runs downward and forward before dividing, in approximately the first molar region, into two terminal branches; the incisive and mental nerves.14 The mental nerve courses anteriorly until it exits through the mental foramen, which is sensory to the soft tissues of the chin, lip, and anterior gingiva. The incisive nerve continues anterior and innervates the mandibular anterior teeth. Accurately determining the exact location of the inferior alveolar nerve as it courses through the body of the mandible is imperative to avoid neurosensory disturbances secondary to implant placement (Fig. 9.7).
Histologically, this IAN consists of connective tissue and neural components in which the smallest functional unit is the individual nerve fiber. The IAN fibers may be either myelinated or unmyelinated. The myelinated nerve fibers are the most abundant; they consist of a single axon encased individually by a single Schwann cell. The individual nerve fibers and Schwann cells are surrounded by the endoneurium, which acts as a protective cushion made up of a basal lamina, collagen fibers, and endoneurial capillaries.
Nerve impairment to the inferior alveolar nerve (mental nerve) is a common clinical complication with major medicolegal implications. Because of its anatomic location, the mental nerve is the most common nerve to be damaged via implants or bone graft procedures. Trauma usually occurs from placement of implants directly into the foramen or into the inferior alveolar canal in the posterior mandible. Sensory nerve injury may result in altered sensation, complete numbness, and/or pain, which may interfere with speech, eating, drinking, shaving, or make-up application and lead to social embarrassment.
Within the infratemporal fossa, the lingual nerve divides from the posterior division of the mandibular nerve (V3) as a terminal branch. As the lingual nerve proceeds anteriorly, it lies against the medial pterygoid muscle and medial to the mandibular ramus. It then passes inferiorly to the superior constrictor attachment and courses anteroinferiorly to the lateral surface of the tongue. As it runs forward deep to the submandibular gland, it terminates as the sublingual nerve.
The lingual nerve is sensory to the anterior two thirds of the tongue, floor of the mouth, and lingual gingiva. It also contains visceral afferent and efferent fibers from cranial nerve seven (facial nerve) and from the chorda tympani, which relays taste information. With the prevalence of second molar implants, care should be taken to note the possible position of the lingual nerve on the medial ridge of the retromolar triangle, where it courses anteriorly along the superior lingual alveolar crest, which is slightly lingual to the teeth (Fig. 9.8).15
Due to the lingual nerve’s variable anatomic location, it may be iatrogenically traumatized during various implant surgical procedures. Usually the lingual nerve is not damaged from the actual osteotomy preparation of implants unless the lingual plate is perforated. This sensory nerve is most likely traumatized during soft tissue reflection during implant placement in the second molar area or incision/reflection over the retromolar pad for bone graft procedures. Additionally, the lingual nerve can suffer damage from lingual flap retraction and inferior alveolar nerve blocks. Studies have shown that lingual nerve impairment after nerve blocks occurs twice as often as inferior alveolar nerve damage.16 This is most likely due to the fact the lingual nerve is most commonly unifascular at the site of the injection. Sensory damage to the lingual nerve may cause a wide spectrum of complications ranging from complete anesthesia to paraesthesia, dysesthesia, drooling, tongue biting, change in taste perception, and change in speech pattern.
Most implant-related nerve impairments are the direct result of poor treatment planning and inadequate radiographic evaluation. Nerve trauma occurs when the implant clinician is not aware of the amount of bone or does not know the location of nerve canals or foramens. Preoperative planning is crucial to determine the amount of available bone in approximation to a nerve structure, location of vital structures, bone density, and location for proper placement of implants. A cone beam computed tomography (CBCT) examination is most commonly used for the three-dimensional planning in these areas.
Nerve injuries may result from various intraoperative and postoperative complications. Nerves may be mechanically injured by indirect or direct trauma via retraction, laceration, pressure, stretching, and transection. Thermal trauma may cause inflammation and secondary ischemia injuries with associated degeneration. And lastly, peripheral nerves have been shown to be susceptible to chemical injuries, where the nerve is directly traumatized by chemical solutions.
Administration of Local Anesthesia
Adequate local anesthesia is paramount for successful dental implant surgery and stress reduction protocol. However, although rare, the use of nerve blocks may result in trauma to various branches of the trigeminal nerve. The exact etiology of local anesthesia nerve damage is unclear, and various theories such as injection needle trauma, hematoma formation, and local anesthetic toxicity have been discussed. Although the true incidence is difficult to quantify, studies have shown permanent injury occurs in approximately 1 in 25,000 inferior nerve blocks. Most patients do recover fully without deficits, with full recovery in 85% of patients with complete remission in 8–10 weeks.17
Complications resulting from needle trauma are likely the most common theory on why nerve injury results after administering nerve blocks. First, it is not uncommon for the tip of the needle to become barbed (damaged) when contacting bone. Stace et al showed that 78% of needles became barbed after initial injection, increasing the possibility of damaging the nerve. Two-thirds of the needles developed outward-facing barbs, which have been shown to rupture the perineurium, damage the endoneurium, and cause transection of nerve fibers.18 The lingual nerve has been associated with the highest percentage of nerve impairment cases as a result of an anesthetic injection (∼70%)19. Because of the lingual nerve’s anatomic location, it is predisposed to nerve injuries because it is commonly contacted when using the pterygomandibular raphe as an injection landmark due to the nerve being positioned shallow in the tissue (∼3–5 mm from the mucosa).20
The anesthetic needle may also cause damage to the epineurial blood vessels, which may result in hemorrhage-related compression on the nerve fibers. The accumulation of blood may lead to fibrosis and scar formation, which may cause pressure-related trauma.21 The extent of impairment to the nerve is directly related to the amount of pressure exerted by the hematoma and recovery time of the axonal and connective tissue damage.
If the anesthetic is injected within the fascicular space, chemical irritation and damage may occur. Studies have shown articaine to comprise 54% of mandibular nerve block injuries,22 and it is 21 times more likely to cause injury in comparison to other nerve injuries.23 Theories concerning articaine toxicity include the high concentration of articaine solution24 and the increased resultant inflammatory reaction.25 Lidocaine has been shown to be the least toxic anesthetic followed by articaine, mepivacaine, and bupivacaine.26 Chemical trauma from local anesthetics has been shown to cause demyelination and axon degeneration of nerve fibers.27
Soft Tissue Reflection
Injury to nerves and nerve fibers may occur during the reflection, retraction, or suturing of the soft tissue. This is most noted when the mental nerve is dehiscenced or exposed on the mandibular ridge. Special caution should be exercised when making incisions over these areas because complete transection injuries may occur from incisions through the nerve or foramen. Stretching injuries (neuropraxia) may occur from excessive retraction, so care should be noted as to the proximity of neural vital structures within the retracted tissue. Complete transection of the nerve results from stretching the tissue to reduce tension over the flap without regard to the anatomic location of the nerve (Fig. 9.9).
Implant Drill Trauma
Neurosensory impairment may result from direct or indirect trauma from the osteotomy sites. Direct trauma may occur from overpreparation of the osteotomy site or lack of knowledge of the true bur length. The implant clinician must know and understand the true length of the surgical burs used in the osteotomy site preparation. The marked millimeter gauge lines inscribed on the shank of the drills most often do not include the cutting edge of the drill and do not correspond to the actual depth of the drill. Most drills have a sharp, V-shaped apical portion to improve their cutting efficiency. The V-shaped apical portion of the drill (termed the “Y” dimension in engineering) is often not included in the depth measurements of the commercial drills and may measure as much as 1.5 mm longer than the intended depth.
When the bone is less dense, slippage of the handpiece may occur, leading to overpenetration. The implant clinician should use the initial implant osteotomy twist drill as a gauge for bone density type and for an evaluation of the position of the surgical drill relative to the mandibular canal. In implant dentistry today the overzealous use of immediate implants has been associated with an increase of drilling-related trauma. To gain primary stability, most immediate implant osteotomy sites require drill preparation and implant placement apical to the extraction site. When placing implants in the mandibular premolar area, violation of the canal may occur, causing nerve damage. Therefore in this anatomic area, immediate implant placement is not recommended unless adequate bone is available below the root apex.
The following are the types of surgical drill trauma that may lead to a neurosensory impairment:
The surgical drill may cause a nerve impairment from thermal damage even though the surgical drill does not violate the mandibular canal. Most commonly, this is the result of insufficient irrigation, which leads to overheating the bone. Thermal trauma may lead to nerve impairment via bone necrosis from overheating the bone during preparation. Nerve tissue has been shown to be more sensitive to thermal trauma than bone (osseous) tissue. Excessive temperatures have been shown to produce necrosis, fibrosis, degeneration, and increased osteoclastic involvement.28 To minimize this complication the bone density should be evaluated preoperatively via CBCT examination, tactile evaluation, and by location.
The surgical drill may also cause direct trauma to the neurovascular bundle by penetrating the mandibular canal or mental foramen. The neurosensory impairment will be directly proportional to the specific nerve fascicles that are damaged. Normally, the vein and artery, which are positioned more superiorly than the nerve, will be damaged when penetration of the canal results. Indirect trauma may also cause nerve damage from the excessive bleeding (hematoma), as well as thermal and chemical injuries from the penetration into the canal.
The most severe type of nerve injury, with the lowest probability of regeneration, is when the implant drill transects the canal. Because the nerve is usually completely severed, repair and regeneration is highly variable. This type of injury will usually result in anesthesia-type symptoms and neuroma formation with possible dysesthesia symptoms (Fig. 9.10).
Implant Encroachment on the Mandibular Canal.
Injuries to vital nerve structures due to implant positioning are most common in the posterior mandible. These may be caused by direct trauma (mechanical) and indirect trauma or infection (pressure). Placement of an implant into or near the mandibular canal is associated with many types of neurosensory impairments (Fig. 9.11).
Placement of an implant close to the mandibular canal may cause trauma due to compression or secondary ischemia. A 2.0-mm safety zone of the implant in proximity to the canal should always be adhered to. Studies have shown that implant pressure on the canal occurs with increasing stress as the bone density decreases.29 Khaja and Renton showed that placement of an implant too close to the canal may cause hemorrhage or deposition of debris into the canal, causing ischemia of the nerve. Even removing the implant or repositioning may not alleviate and decrease pressure-related symptoms. Additional studies have shown the presence of postoperative severe pain after implant placement in close approximation to the canal resulting in chronic stimulation and debilitating chronic neuropathy.30
Partial Penetration Into Mandibular Canal.
Placement of the implant body into the mandibular canal is associated with a high degree of morbidity. The sensory nerve fascicles are usually inferior to blood vessels within the canal, and the type and extent of injury is proportional to the fibers that are damaged. This is why in some cases the implant is directly within the canal; however, no neurosensory symptoms exist. Additionally, implant placement into the canal may cause hematoma formation (severing of the inferior alveolar artery or vein), leading to a nerve impairment.
Perforation Through the Entire Canal.
Complete transection of the nerve occurs when surgical error involves the preparation of an osteotomy too deep due to inaccurate measurements or slippage of the handpiece. This type of injury results in the most severe of response, a total nerve impairment (anesthesia) and neuroma formation. Usually this type of nerve injury results in a complete anesthesia and retrograde degeneration resulting in future dysesthesia.27 The extent of neurosensory impairment is proportional to the extent of fascicle injury and is dependent upon the time the implant is left to irritate the nerve fibers.
Placement of implants in approximation to the canal may cause neurosensory impairments via periimplant infections. Infectious processes after implant placement may result from heat generation, contamination, or prior existence of bone pathology. This may lead to spread of infection that may extend into the neural anatomy. Case reports have shown nerve impairment issues resulting from an implant infected by chronic peri-implantitis.31
Mandibular Socket Grafting.
After mandibular tooth extractions, grafting into the socket may effectively expose the inferior alveolar nerve to socket medicaments. This may lead to chemical neuritis and, if the irritation persists, an irreversible neuropathy may occur (Fig. 9.12). Additionally, care should be exercised when removing pathology and granulation tissue from extraction sockets in close proximity to the nerve canal (type 1 nerve).32 Overzealous curretting of the socket apex may lead to direct traumatic injury of the canal.
Delayed Nerve Damage (Canal Narrowing).
Nerve damage may result even when ideal implant placement is performed (>2.0 mm from the nerve canal). Shamloo et al reported an implant placement case in which the implant body caused compression and bone to be forced into the superior aspect of the mandibular canal (canal narrowing). This led to delayed healing and remodeling within the canal and resulted in excessive narrowing of the canal with compression of the nerve fibers. The narrowed aspect of the canal was shown to be approximately 0.2 mm, with an average diameter in the nonaffected sites being approximately 3.2 mm.33 The nerve impairment (paresthesia and anesthesia) occurred 2 years after implant placement surgery.
The incidence of nerve impairment has been shown to be patient specific. Studies have shown that females and older patients are at greater risk of nerve deficits. As patients age, neural cell body regeneration has been shown to be much slower.34 Women have been shown to have greater associated pain and nerve impairment in comparison to men because of lower pain thresholds, greater chance of seeking treatment in comparison to men, and an increased tendency to communicate their problems.35
There are many local and host-related factors that determine the neurologic response to a nerve injury. Older individuals exhibit slower and less dramatic cell body regeneration in comparison to younger individuals. The type of injury is the most significant local factor relating to the neurologic response after trauma. Injuries that occur at the proximal site of the peripheral nerve are usually more significant in comparison to those that occur at distal sites.9 In the event any of the extraneural tissues (epineurium, perineurium, endoneurium, or mesoneurium) are injured or traumatized, impaired neural transmission may result in a sensory disturbance. The resultant neurosensory impairment is dependent on the varying functional units of the individual fiber type involved. A-alpha fibers are the largest fibers and mediate position and fine touch by way of muscle spindle afferents and skeletal muscle efferents. The A-beta fibers are mainly proprioceptive in nature, and A-delta fibers mediate initial pain impulses along with temperature information. The C-fibers are unmyelinated and slow conducting, which allow the perception of pain and temperature.4
When complete transection of a nerve occurs, within 96 hours the proximal end of the nerve fiber shrinks approximately 20% to 50% in diameter and usually will not recover more than 80% of its original size.10 Shortly thereafter, axonal nerve sprouts will seek and extend out to the degenerating distal branch. Each axon may contain up to 50 collateral sprouts and advance approximately 1–3 mm per day and eventually attempt to reinnervate the target tissue. If the nerve sprouts are unable to reconnect, forward progress is stopped and Wallerian degeneration will occur. Wallerian degeneration is the process resulting from a damaged nerve fiber in which part of the axon is separated from the neurons cell body. This may also be known as anterograde or orthograde degeneration.35a Wallerian degeneration usually results in neuroma (benign growth) formation, which is associated with increased mechanical and chemical sensitivity, resulting in chronic neurosensory deficits.11
Quick, immediate treatment is highly recommended in neurosensory impairment cases. Nerve fiber atrophy has been shown to occur with trauma over 6 hours.36 After 3 months, permanent central and peripheral changes occur that make it unlikely the nerve will respond to surgical treatment intervention.37 Injuries older than 6 months rarely respond to any treatment and are usually permanent.38
After nerve injury, there exist two phases of healing, degeneration and regeneration.
There are two types of nerve degeneration: segmental degeneration and Wallerian degeneration. Segmental demyelination occurs when the myelin sheath is damaged and causes a slowing of the conduction velocity, which may prevent the transmission of nerve impulses. The resulting effects will clinically be paresthesia, dysesthesia, or hyperesthesia. The second type of degeneration is termed Wallerian degeneration, in which the axons and myelin sheath distal (away from central nervous system [CNS]) to the injury undergo complete disintegration (Fig. 9.13). The axons proximal to the site of injury (towards the CNS) undergo less degeneration, but many nodes of Ranvier (periodic gaps in the myelin sheaths of axons that facilitate the rapid conduction of nerve impulses) are affected. Wallerian degeneration usually occurs after complete transection of the nerve and results in dysesthesia type of symptoms.
Usually, regeneration occurs immediately after nerve injury. The proximal nerve area sprouts out new fibers that grow at a rate of 1.0–1.5 mm per day. This will continue until the site innervated by the nerve is reached or blocked by fibrous connective tissue, bone, or object (e.g., dental implant). During the regeneration process, new myelin sheaths form as axons increase in size. In some situations the continuity of the Schwann cells is disrupted, and connective tissue may enter the area. The growth may find an alternative path, or it may form a traumatic neuroma, which is usually characterized by significant pain. Studies have shown that the administration of steroids may minimize the formation of neuromas, especially the administration of high doses within the first week of nerve injury (Fig. 9.14).2
Neurosensory Deficit Classification
There are two widely accepted classifications of nerve injuries. In 1943 Seddon postulated a three-stage classification, which was later reclassified by Sunderland in 1951 into five different subclassifications. These nerve injury classifications are described by the resultant morphophysiologic type of injury, which is based on the time course and amount of sensory recovery (Fig. 9.15).
Neuropraxia, or first-degree injury, is characterized by a conduction block with no degeneration of the axon or visible damage of the epineurium. Usually, this type of injury is consistent with stretching or manipulation (reflection of tissue) of the nerve fibers, which results in injury to the endoneurial capillaries. The degree of trauma to the endoneurial capillaries will determine the magnitude of intrafascicular edema, which results in various degrees of conduction block. Usually, resolution of sensation and function will occur within hours to weeks.
Axonotmesis (second-, third-, or fourth-degree injury) consists of degeneration or regeneration axonal injuries. The injury classification depends on the severity of axonal damage. This type of injury involves the endoneurium, with minimum disruption to the perineurium and epineurium. The most common type of injuries are traction, stretching, and compression, which can lead to severe ischemia, intrafascicular edema, or demyelination of the nerve fibers. Initially, complete anesthesia is most common, which is followed by paresthesia as recovery begins. Improvement of the related sensory deficits occurs within approximately 2–4 months with complete recovery usually within 12 months. In some cases, painful dysesthesias are possible with resulting neuroma formation.
Neurotmesis (fifth-degree injury) is the most severe type of injury, resulting from severe traction, compression, or complete transection injuries. Initially, patients exhibit anesthesia, followed by paresthesia with possible dysesthesia. A very low probability of neurosensory recovery exists, with immediate referral for a neurosurgical evaluation recommended.39,40 The axon and encapsulating connective tissue will lose their continuity. There is usually complete loss of motor, sensory and autonomic function. Neuroma formation is common if transection has occurred.