Lingual Nerve Injury

Steven B. Graff-Radford, DDS, Randolph W. Evans, MD


Headache. 2003;43(9) 

In This Article

Neurophysiology Postinjury


Peripheral nerve compression may result in a neuropathic pain syndrome or sensory deficit. The acute response to compression is edema and inflammation. The first stage is blood-nerve barrier changes resulting in subperineural and endoneural edema. This leads to connective tissue changes with perineural and endoneural thickening, followed by localized nerve fiber changes exhibited as demyelination. Wallerian degeneration then becomes apparent. The mechanism of compression includes both mechanical deforming forces and ischemic changes.[37,38,39,40,41,42] Epineural hematoma, due to a local anesthetic injection, may be a common cause of nerve injury.[43]

In nerve compression neuropathy, large myelinated fibers are lost and A delta and C fibers spared. There is an increase in circulating substance P and calcitonin gene-related peptide, and a decrease in dynorphin at the dorsal horn. There also may be activation of the N-methyl-D-aspartate (NMDA) receptor.[39] These changes are responsible for the dysesthesia or paresthesia. The response to peripheral or central nerve injury may involve neuroinflammation. This is defined as an infiltration of immune cells into the injured site.[40] An experimental neuritis provokes a local immune response, characterized by endoneural infiltration of granulocytes and CD4 and CD8 T lymphocytes.[41] This reaction occurs even without significant axonal damage. These findings support the presence of a distinct neroinflammatory event without significant nerve injury in generating persistent neuropathic pain and paresthesia.[42] As we begin to understand the inflammation/immune-induced tissue damage and repair and how it relates to neuropathic pain, the opportunities for targeting the neuroinflammatory system in chronic pain prevention and therapy can be developed. Nerve compression may occur with tracheal intubation, use of a laryngeal mask airway, tongue retraction, or jaw protrusion.[10,11,44,45,74]

Compartment Syndrome

The nerve injury seen in a compartment syndrome is similar to that seen in compression, but the effects are largely due to ischemia caused by diminished flow in the compartment. Increased venous pressure results from increased local tissue pressure, such as from inflammation or edema. There is a decrease in the arteriovenous gradient, diminished blood flow, and decreased oxygen delivery to the nerve. The reversibility is dependent on how long and how much pressure is applied. Early decompression or anti-inflammatory therapy may be useful in preventing long-term pain and numbness. Because the lingual nerve is often adjacent to the lingual plate, the pressure created by suturing the mucosa accompanied by postsurgical edema and bleeding may result in a compartmentlike syndrome.

Stretch Injury

Injury following stretch or traction varies considerably from fascicle to fascicle and along the nerve length. The injury may begin with axonal rupture followed by rupture of endoneural tubes, perineurium, and finally endoneurium. There is also a theory that the epineurium may be the first structure to rupture, followed by perineurium axons and then endoneurium.[46] The injury may occur in several places along the length of the nerve. Lundborg and Rydevik have studied the deleterious effects stretching may have on the physiologic function of a nerve. As little as 8% stretch produced changes in intraneural blood flow. Complete cessation in arterial blood flow occurred with 15% elongation.[37] Injuries to the lingual nerve from laryngoscope, intubation, and possibly jaw retraction have postulated stretching as a mechanism.

Chemical Injury

In dentistry, chemicals that create neural sensitization are commonly used. Some agents that have been implicated include eugenol, alcohol, phenol, and paraformaldehyde-containing endodontic filling materials.[47,75] Once the nerve is exposed to the chemical, an inflammatory response ensues. Depending on the nerve involved, a compartment syndrome or neuroinflammatory nerve injury may develop. Depending on the duration and severity of the damage, as well as other predisposing factors, a neuropathic pain may develop.

Nerve Injection Injury

Unexplained nerve injury following dental procedures, especially tooth removal, may be caused by intraneural injection, creating permanent damage.[48,49,50,51] Scarring and fibrosis that prevent axonal regeneration disrupt the fascicular architecture. There is a resultant conduction block, and dysesthesia may develop. Local anesthetic may produce persistent neurosensory deficit following enzymatic hydrolysis.[2,50,51,52] Neural hematoma also has been postulated as a cause of persistent sensory change. The anesthetic itself injected into the nerve along with the vasoconstrictors and preservatives may injure the nerve permanently.[53,54,55,56] Nickel suggests that under exceptional conditions, lidocaine metabolism may produce nerve dysfunction. If the lidocaine molecule is hydrolyzed while still bound to the receptor and the alcohol by-product persists, the metabolite may disrupt nerve conduction causing paresthesia.[56] Using 5% lidocaine in proximity to the peripheral nerve may cause permanent neural ablation.[57] The mechanism of neurotoxicity is unknown. Contaminating the anesthetic-containing Carpules with alcohol may cause nerve injury. Some anesthetics appear more likely to cause nerve injury. Articaine and prilocaine have been implicated, perhaps because of the higher concentrations injected.[52]

Stacy et al have proposed that after a needle encounters bone, it may develop a barb on its end. They noted barbs (inward and outward) occurred in 50% of 50 needles evaluated in dental student clinics and in 30% of the needles evaluated in the faculty clinic. They propose neural damage occurs as the needle is withdrawn through the nerve.[58] This is not unique to trigeminal nerves. Selander et al showed techniques where axillary blocks deliberately elicited paresthesia-caused damage to the perineurium, nerve fibers, and blood vessels. The damage was greatly reduced if a short-beveled needle was used, suggesting the barb in the needle would be less severe.[59] This has been supported by studies on nerve damage with short-beveled needles.[60] Harn and Durham reported a 3.6% chance of lingual nerve traumatization with a 15% chance of postinjection complication that could vary in severity.[49] In a closed-claims analysis, the presence of permanent peripheral nerve injury was described following local anesthetic injection and direct needle trauma.[61]

Transsection, Laceration, Rupture, or Avulsion

This injury is classified as a Sunderland type 5. The repair requires approximation of the 2 ends and suture. Scar tissue prevents the natural regrowth. Factors that minimize scar development may improve the prognosis. If the injury occurs intraosseously and the neurovascular canal is present, surgical repair should be delayed unless sensory testing over time shows no improvement.