CC
A 24-year-old male is referred for evaluation and treatment of numbness and pain in his entire lower lip, chin, and gums.
HPI
The patient had a Le Fort I osteotomy, bilateral mandibular sagittal split osteotomy (BSSO), and genioplasty for correction of his midface deficiency, mandibular asymmetry, and microgenia 5 months earlier. Operative report from surgery did not indicate visualization of the inferior alveolar nerves (IANs) or mental nerves (MNs), and no injuries were noted to have occurred intraoperatively. After surgery, he continued to have complete numbness of his lower lip, chin, and mandibular labial gingiva bilaterally at 6 weeks. His left lower lip and chin numbness on the left side started to improve afterward and is now back to baseline sensation, but the right lower lip stayed completely anesthetic until 2 months ago, when he started experiencing painful sensations to any stimulation to this area. He reports having a very painful sensation when brushing his teeth, eating, washing his face, and shaving, and this sensation seems to be getting worse and lasting longer.
PMHX/PDHX/medications/allergies/SHX/FHX
The patient is in good general health. His only other previous surgery was removal of wisdom teeth at age 18 years. He takes no chronic medications and has no known allergies.
Examination
General. The patient is a well-developed, well-nourished young adult male with a normal facial profile. He is in no acute distress. His vital signs are normal, and his weight is 178 lb.
Maxillofacial. There is no facial edema. There is no temporomandibular joint or masticatory muscle tenderness. The nasal passages are patent, and the nasal septum is in the midline. There is no evidence of recent trauma to the lower lip. Unassisted maximal interincisal opening is 40 mm. There are orthodontic appliances on both dental arches, and the dental occlusion is class I. Intraoral surgical incisions are well healed. Oral hygiene is fair, with accumulated plaque on anterior mandibular dentition because of elicited pain while brushing. The tongue, palate, and pharynx are normal. There are no abnormal neck masses, and the carotid pulses are normal.
Cranial nerves (CNs). CNs II through XII are normal except for the right mandibular branch of CN V (CN V3). Neurosensory testing indicates abnormal findings at all three levels along this nerve distribution on the right side: level A (two-point discrimination and brush stroke direction), level B (contact detection), and level C (sharp or blunt and thermal discrimination). He also exhibits allodynia (painful response to a nonpainful stimulus) and hyperpathia (delayed painful response that increases in intensity with repeated stimulation [crescendo] and persists for a period of time after removal of the stimulus [afterglow]).
Imaging
A cone-beam computed tomography scan shows plates and screws stable at Le Fort site as well as plates with noncortical screws bilaterally at BSSO sites that are not superimposed on the IAN canal. The horizontal osteotomy for the genioplasty appears to be in proximity of the mental foramen ( Fig. 65.1 ).


Diagnostic blocks
Local anesthetic blocks (2% lidocaine with 1:100,000 epinephrine) was administered in the right pterygomandibular space to determine if allodynia is triggered centrally or peripherally. Relief of allodynia and hyperpathia after a few minutes of this procedure indicated that the source of this pain is distal to the site of injection. With this result, surgical exploration of this site and repair or reconstruction of this nerve would be an appropriate treatment option for symptomatic relief in this patient.
Labs
There are no studies indicated for the routine evaluation of a peripheral nerve injury, and this patient has no medical history or physical findings that require specific blood or urine investigation.
Assessment
This patient’s right IAN and MN injury findings are consistent with neurotmesis based on Seddon classification or grade V injury based on Sunderland classification (see Table 29.1 ), with recently developed allodynia and hyperpathia in the region of the right CN V3 distribution.
In an injury in which there has been persistent anesthesia for longer than 3 months, the prognosis for meaningful spontaneous improvement or full recovery of sensory function is dismal. When painful symptoms develop, it is important to treat them early (i.e., within 6–9 months after injury) to minimize the chance of a chronic, intractable pain syndrome. This can be a debilitating condition interfering with the normal daily activities of these patients and often develops in patients with neuropathic pain secondary to a known nerve injury that are left untreated beyond 12 months after the incident. The current patient is approaching that critical timeline; therefore, it is important that treatment for pain control be initiated forthwith.
Treatment
The primary goal of intervention in patients with neuropathic pain is for symptomatic relief. Multiple pharmacologic treatment options are available for treatment of neuropathic pain specifically associated with the trigeminal nerve. First-line treatment for trigeminal neuralgia pain treatment is use of low-dose carbamazepine (anticonvulsant) twice daily. Other commonly used pharmacologic interventions for neuropathic pain include other anticonvulsants (gabapentin and pregabalin), tricyclic antidepressants (amitriptyline), serotonin norepinephrine reuptake inhibitors (duloxetine, venlafaxine), and some muscle relaxants (baclofen). All these interventions require several weeks of use before showing any signs of relief and can lead to a variety of unwanted side effects. Our patient was started on low-dose carbamazepine, and he experienced minimal improvement in his allodynia symptoms after 6 weeks of use. This improvement, however, was not significant enough for him to want to continue with this treatment, and he returned to further discuss his treatment options.
The most difficult determination in the surgical approach to an IAN injury from sagittal split ramus osteotomy (SSRO) is locating the site of the injury. Proximally, the IAN can be injured during the SSRO from surgical incisions, stretching of the soft tissue, osteotomies, stretching or crushing injury caused by mandibular segments at the new position, or injury from fixation devices. Distally, this nerve can be injured at the mental foramen from surgical exposure or osteotomies made for genioplasty.
Ideally, exposure of the nerve should be made through a single surgical incision, allowing visibility and for access for surgical manipulations, including neurorrhaphy or reconstruction of a nerve gap (see Table 29.2 ). Historically, the transcervical approach for this procedure has been described, but it is not these authors’ approach of choice for this procedure.
In the current patient, transoral surgical approach was used to expose the IAN and MN. The patient was advised of all possible complications and possible outcomes and planned to undergo procedures after obtaining informed consent. The patient was taken to the operating room, and general oral endotracheal anesthesia was administered. The face and perioral region were sterilely prepped and draped. A pharyngeal pack was inserted, and the mouth was thoroughly rinsed with chlorhexidine solution. Right-sided IAN blocks and infiltration of local anesthesia were performed with 2% lidocaine and 1:100,000 epinephrine. An incision was made along the previously made SSRO incision scar on the right side and extended anteriorly along the vestibule to have exposure of the right IAN and MNs. A full-thickness mucoperiosteal flap was elevated. The incision was then extended anteriorly to expose the genioplasty hardware. Right SSRO and genioplasty hardware were removed. The left MN was identified and found to be intact ( Fig. 65.2 A). The proximal portion of the IAN entering the mandibular foramen was found to be intact. The remaining IAN was exposed by removal of overlying lateral mandibular bone with a high-speed drill, fine osteotomes, and curettes. There was a complete discontinuity defect of the right IAN at its junction with the MN ( Fig. 65.2 B). Inspection under magnification (foot-controlled operating microscope with ports for the surgeon, assistant, or camera or surgical loupes of ×2.5 to ×5.0, depending on surgical needs and the surgeon’s preference) revealed that the proximal stump of the IAN had formed scarring and possible neuroma. Distally, the MN was found to be intact with its three branches proceeding into the buccal mucosa. Stump ends of the IAN and MN were prepared for reconstruction by making a sharp straight incision 2 mm proximal to the ends where scarring and distortions were noted. These stump ends were sent for pathological evaluation (later verified by the pathologist’s report as neuroma). This left a significant nerve gap of 2 cm. A processed heterogenous nerve graft was placed in between these two segments. This nerve graft was secured to the proximal segment of the nerve using interrupted 8-0 nylon sutures placed circumferentially through the epineural layer of IAN to the nerve graft. This process was then repeated to secure the distal segment of this nerve graft to the MN. The reconstructed nerve was entubulated by a processed nerve cuff. (A nerve cuff enhances the healing process in the nerve by preventing percolation of blood and ingrowth of scar tissue between the nerve stumps.)


Alternately, the nerve gap can be reconstructed using an autogenous nerve graft. Commonly used donor nerves are the great auricular nerve (GAN) in the neck or the sural nerve (SN) in the lower extremity ( Fig. 65.3 ).

