Facial Neuropathology of Traumatic Origin
Injuries to sensory nerves of the maxillofacial region occasionally occur as the result of facial fractures, during the treatment of oral pathologic conditions, or when maxillofacial reconstructive surgery is performed. Fortunately most injured nerves spontaneously recover, However, in the past little was done to treat persistent sensory nerve disorders. Recent advances in the undersea of how nerves heal and in the surgical means of repairing
peripheral nerves provide patients with the possibility of regaining normal nerve function.
The three branches of the trigeminal nerve injured most commonly, for which the altered sensation is clinically significant, are (1) the inferior alveolar-mental nerve, (2) the lingual nerve, and (3) the infraorbital nerve. When
the ,inferior alveolar-mental nerve- is injured, the usual causes are the following:
1. Mandibular (body) fractures
2. Preprosthetic surgical procedures
3. Sagittal split osteotomy surgery
4. Mandibular resection for oral neoplasms
S. Removal of impacted lower third molars
Lingual nerve damage occurs in the course of surgery to remove oral malignancies or impacted third molars. Injury to the infraorbital nerve is most common during zygomaticomaxillary complex fractures.
Classification, Research and clinical experience have shown that surgical intervention to repair damaged
nerves is more successful when performed soon after the ‘injury has occurred. Thus an understanding of the various types of nerve damage, especially their prognoses, is important because it enables the clinician to decide when referral for peripheral nerve surgery is warranted.
The three types of nerve injuries are (1) neurapraxia, (2) axonotmesis, and (3) neurotmesis (Fig.4-10). Although a determination as to which type of nerve damage has occurred is usually made retrospectively, knowledge of
the pathophysiology of each type is important for gaining an appreciation of nerve healing.
Neurapraxia, the least severe form of peripheral nerve injury, is a contusion of a nerve in which continuity of both the epineurial sheath and the axons is maintained. Blunt trauma or traction (i.e., stretching) of a nerve, inflammation around a nerve, or local ischemia of a nerve can produce a neurapraxia. Becausethere has been no loss in axonal continuity, spontaneous full.recovery of nerve function usually occurs in a few days or weeks.
Axonotmesis has occurred when the continuity of the axons but not the epineurial sheath is disrupted. Severe blunt trauma, nerve crushing, or extreme traction of a nerve can produce this type of _injury. Because the
epineural sheath is still intact, axonal regeneration can (but does not always) occur with aresolution of nerve dysfunction in 2 to 6 months.
Neurotmesls, the most severe type of nerve injury, involves a complete loss of nerve continuity. This form of damage can be produced by badly displaced fractures, severance by bullets or’ knives during an assault, or by
iatrogenic transection. Prognosis for spontaneous recovery of nerves that have undergone neurotmesis is poor, except if the ends of the affected nerve have -been left in close approximation and properly oriented.
Nerve healing. Nerve healing usually has two phases:
(1) degeneration and (2) regeneration. Two types of degeneration can occur The first is segmental demyelination,in which the myelin sheath is dissolved in isolated segments. This partial ‘tIemyelination causes a slowing of conduction velocity and may prevent the transmission of some nerve impulses. Symptoms include paresthesia (a spontaneous and subjective altered sensation that a patient does not find painful), dysesthesia (a spontaneous and subjective altered sensation that a- patient finds
painful), hyperesthesia (excessive sensitivity of a nerve to stimulation), and hypesthesia (decreased sensitivity of a never to stimulation). Segmental demyelination can occur after neurapraxic injuries or with vascular or connective tissue disorders (rig. 4-11).
Wallerian degeneration “is the second type of degeneration occurring after nerve trauma, In this process the axons and myelin sheath otthe nerve distal to the site of nerve trunk Interruption” (away from the ce1ltral nervous system) undergo disintegration in their entirety. The
axons proximal to the site of injury (toward the central nervous’system) also undergo some degeneration, occasionally all the way to the cell body but generally just for a few nodes of Ranvier. Wallerian degeneration stops all nerve conduction distal to the proximal axonal stump. This type of degeneration follows nerve transsection and other destructive processes that affect peripheral nerves (see fig. 4-11).
“The terms axial and proximal used in the description of nerves acid hones refer to positions farthest away from (i.e., distal) or nearest (i.e.,proximal) the central nervous system. In this case, distal is not used in till” same sense as common when referring to teeth and the dental rach.
Regeneration of a peripheral nerve can begin almost immediately after nerve injury. Normally the proximal nerve stump sends out a group of new fibers (the growth cone) that grow down the remnant Schwann cell tube.
Growth progresses at a rate of 1 to 1.5 mm per day and continues until the site innervated by the nerve is reached or growth is blocked by fibrous connective tissue or bone. During regeneration new myelin sheaths may
form as the axons increase in diameter. As functional contacts are made, the patient- will experience altered sensations in the previously anesthetic area, which take the form of paresthesias or dysesthesias.
Problems can occur during regeneration that prevent normal nerve healing. If the continuity of the Schwarm cell tube is disrupted, connective tissue may enter the tube while it is partially vacant. When the growth onereaches the connective tissue obstruction, it may find a way around it and continue on, or it may form a mass of aimless nerve fibers that constitutes a traumatic neuroma subject to pain production when disturbed (Fig. 4-12).