Trigeminal nerve branches are never far from the operating field of the oral and maxillofacial surgeon. Increasingly the surgeon is required to provide accurate diagnosis and grading of trigeminal nerve injury, and surgical management by oral and maxillofacial surgeons will become common. Although trauma and ablative procedures for head and neck pathology can cause injuries, dentoalveolar surgical procedures remain an important cause of injury to the fifth cranial nerve, with the third division being the main branch affected. Oral and maxillofacial surgeons should be aware of strategies of avoiding iatrogenic injury, and know when referral and surgical management are appropriate.
The fifth cranial nerve is the largest cranial nerve and the largest peripheral sensory nerve in the human body.
As oral and maxillofacial surgery broadens in scope, the surgeon will increasingly be required to diagnose and grade trigeminal nerve injury accurately and in the case of some surgeons surgically repair these injuries.
Injury to the branches of the trigeminal nerve is commonly associated with “negative” clinical symptoms of decrease in sensation (hypoesthesia, anesthesia), but may also be accompanied by distressing “positive” symptoms of prolonged or permanent painful or inappropriate sensation (dysesthesia) and hypersensitivity (hyperesthesia).
The areas most often affected (upper and lower lips, maxilla, mandible, tongue, and chin) are important in eating and touch and communication.
The fifth cranial nerve is the largest cranial nerve and the largest peripheral sensory nerve in the human body. The importance of this primary somatosensory cortex in daily function is well illustrated by the trigeminal nerve representing close to half of the sensory area in the postcentral gyrus. Patients with impaired function of the trigeminal nerve can present with significant functional deficits and a decreased quality of life.
The trigeminal nerve is the primary sensory neuron supplying the head and neck, and its branches are never far from the operating field of the oral and maxillofacial surgeon. As the specialty broadens in scope, the oral and maxillofacial surgeon will increasingly be required to diagnose and grade trigeminal nerve injury accurately and in the case of some surgeons surgically repair these injuries. In addition, litigation for iatrogenic damage to the trigeminal nerve is of increasing concern to oral and maxillofacial surgeons.
Injury to the branches of the trigeminal nerve is commonly associated with “negative” clinical symptoms of decrease in sensation (hypoesthesia, anesthesia), but may also be accompanied by distressing “positive” symptoms of prolonged or permanent painful or inappropriate sensation (dysesthesia) and hypersensitivity (hyperesthesia). The areas most often affected (upper and lower lips, maxilla, mandible, tongue, and chin) are important in eating, touch, and communication.
Injuries to the trigeminal nerve are caused by:
Trauma (avulsive motor vehicle trauma, missile injuries, interpersonal violence, military combat [these patients often suffer continuity loss of one or more peripheral branches])
Ablative tumor operations in the oral and maxillofacial region ( Fig. 1 )
Dentoalveolar surgical procedures
In general, third molar removal had the highest incidence of injury (40.8%), followed by endodontic therapy (35.3%), other surgical procedures (20.7%), and lastly implant placement (3.2%).
The data on injury to the first and second division of the trigeminal nerve are sparse. Tay and Zuniga in 2005 reported that the third molar was the most common cause of referral for trigeminal nerve injury. Where third division injuries are concerned, lingual nerve (LN) and inferior alveolar nerve (IAN) injuries are the most common. Renton and Yilmaz found that where IAN injury is concerned third molar surgery is the most common cause (60%), followed by local anesthetic injections (19%), implants (18%), and endodontic surgery (18%). Where LN injury is concerned, the same authors found that in their population, third molar removal was the leading cause (73%) followed by local anesthesia injections (17%).
Current literature accepts that the risk of injury to either the IAN or LN occurs in 0.4% to 22% of cases following third molar surgery. More recently Nguyen and colleagues found the incidence of IAN injury as 0.68% and LN injury as 0.15% in their study looking at 11,599 lower third molar extractions in 6803 patients.
Pogrel found that although the true incidence of injury to the IAN from injection was unknown, he estimated that permanent damage might occur in 1 in 25,000 IAN blocks. He found most patients entirely recovered with 85% recovering fully within 8 to 10 weeks, 5% taking longer, and 10% sustaining permanent deficits.
Lost or altered sensation resulting from peripheral trigeminal nerve injuries interferes with standard oral and facial functions and can result in a significantly reduced quality of life for patients. This can mean the difference between an acceptable return to function in the reconstructed tumor patient, detract from an otherwise successful trauma repair, and present as unacceptable morbidity in the elective wisdom tooth or implant patient. Thus, avoiding injury where possible, and offering a reconstruction of the trigeminal nerve where indicated, should be an integral part of the surgical service provided to patients. This is of particular importance in a clinical environment where more professionals are placing implants and there is increased awareness of injuries by patients, and increased reporting of incidents by professionals.
A baseline complete neurosensory examination consisting of a thorough history and physical should be conducted with care taken to document the patient’s sensory deficit or pain accurately. Is the patient experiencing “positive” symptoms, such as painful or unpleasant sensation (dysesthesia)? Alternatively, are the symptoms more in the “negative” category with absent, decreased, or altered sensation (paresthesia, hypoesthesia, anesthesia)? Is the pain constant (suggesting a long-term injury or neuroma formation)? Is the pain intermittent? If so, are there instigating factors? Is it spontaneous and how long does each episode last? Next, a visual analog scale should be used to quantify the pain on a scale of 1 to 10. Determine further whether there are any relieving or exacerbating factors. Have any medications or treatments been tried and have any succeeded? Lastly, establish from the patient what the effect of the injury is on their quality of life and activities of daily living.
Thus, the patient can be placed in one of three groups based on whether they perceive a neurosensory or functional deficit from the injury, and secondly, whether they are concerned about it or motivated to seek some intervention.
Not aware: does not care
Aware: does not care
The “aware and cares” patient is the one for whom medical or surgical intervention is an absolute requirement.
The physical examination should take place in a quiet room with the patient relaxed, seated comfortably, and with their eyes closed when tests are administered. Clinical photography is instrumental in mapping the affected areas and recording any trophic changes, or traumatic injuries and any obviously visible pathology. It is good practice to begin the examination with the “normal” side to establish a baseline. Any difference in sensory testing is then graded using Zuniga’s clinical Neurosensory Test (NST). If the patient has reduced or no sensation, then levels of function are tested in a stepwise approach ( Fig. 4 ).
Boley gauge, or college pliers and a millimeter rule or Axotouch (two-point discriminator [AxoGen, Alachua, FL]) ( Fig. 5 )
Ethyl chloride spray
Level A testing (light touch and direction discrimination)
Fibers evaluated: Larger diameter A-alpha and A-beta (5–12 μm diameter).
Method: The cotton fibers are drawn into a wisp, and 10 strokes are applied with the patient being asked to determine the direction of the strokes. Begin on the normal side and then repeat on the altered side. Record how many attempts are correctly identified (9/10 is a normal score).
Two-point discrimination is then performed using an Axotouch two-point discriminator, Boley gauge, or college pliers and millimeter ruler. The patient is asked the smallest distance at which they can discriminate two separate points (normal IAN distribution is 4 mm; normal LN is 3 mm). Compare the normal side with the altered side. Only if there are abnormal results does one proceed to level B testing.
Allodynia (abnormal pain response to a nonnoxious stimulus) is experienced as pain that ceases with the removal of the stimulus.
Level B testing (static and light touch)
Fibers evaluated: Smaller A-beta fibers (4–8 μm diameter).
Method: Lightly touch the skin without indentation using the wooden end of a cotton swab. If there is no response increase the pressure until the skin is slightly indented. Start on the normal side and compare with the altered side. Record whether light or heavy pressure is required. More accuracy is obtained by using Semmes-Weinstein filaments in a stepwise fashion, recording which filament is felt when it is deformed (increasing pressure is required to deform the larger filaments). If the sensation is not present even at higher pressures, then proceed to level C testing.
Hyperpathia (exaggerated response to a potentially noxious stimulus) is present if the patient has delayed-onset pain, or increasing intensity on repeated stimuli.
Level C testing (noxious stimulus)
Fibers evaluated: Partial myelinated A-delta fibers and nonmyelinated C fibers.
Method: Lightly touch the skin with a dental needle. If there is no response increase the pressure until light indentation of the skin. The temperature perception of hot and cold stimuli can also be tested with ethyl chloride on a cotton tip or warm gutta-percha.
Hyperalgesia (abnormally increased sensitivity to pain) is present if the patient has pain out of all proportion in comparison with the normal side.
Diagnostic nerve blocks can be performed at the end of the examination. They are useful in patients who present with constant pain, or dysesthesia. A lack of response to the local anesthetic may indicate a central mechanism to the pain or collateral macrosprouting from adjacent nerves.
No clinical examination, however, is perfect. The NST has been shown to exhibit high positive predictive values (95%) and negative predictive values (100%) for LN injuries and moderate positive predictive values (77%) and negative predictive values (60%) for IAN injuries. This negative predictive value of 60% indicates that the NST may be less efficient at ruling out IAN injury. At higher sensory impairment scores, the NST tends to underestimate the degree of nerve injury for IAN and LN. Conversely, at lower sensory impairment scores, the NST tends to minimize the degree of damage. Besides, patients with different degrees of nerve injury may have similar NST scores, and there may be variation with age, duration, and cause of injury. Lastly, there may be added inaccuracy in examinations done less than 1-month postinjury.
Although clinically useful in providing diagnosis and prognosis, as noted by Zuniga and colleagues, the NST has the following shortcomings:
There may be delays in treatment of higher class injuries that would have benefitted from earlier intervention.
There may be inaccuracies in delineating the anatomy and exact location of injuries.
There may be underestimation or overestimation of injuries, especially with variation in patient age, duration of injury, and cause of injury.
The Medical Research Council Scale (MRCS) for sensory recovery is currently the reference standard to identify functional sensory recovery after surgical repair ( Table 1 ). The MRCS was originally developed in the United Kingdom to evaluate sensory injuries in the upper extremity, but has since been adapted for use in the head and neck region. The patient is scored according to their NST result with grades from S0 (no sensation) to S4 (normal sensation). S3 is defined as “useful sensory function” and S4 “complete sensory function.”