Nerve entrapment in the lateral pterygoid muscle Barry A. Loughner, Gainesville, Fla. UNIVERSITY
DDS, MS,n Lynn H. Larkin,
PhD,b and Parker E. Mahan, DDS, PhD,a
OF FLORIDA
The posterior trunk of the mandibular division of the trigeminal nerve normally descends deep to the lateral pterygoid muscle. In three of 52 dissections the three main branches of the posterior trunk (lingual, inferior alveolar, and auriculotemporal nerves) were observed to pass through the medial fibers of the lower belly of the lateral pterygoid muscle. The mylohyoid and anterior deep temporal nerves also were observed to pass through the lateral pterygoid muscle in other specimens. These nerve entrapments in the infratemporal fossa provide new information concerning the anatomic and clinical relationships between the mandibular nerve and the lateral pterygoid muscle. These findings support the hypothesis that a spastic condition of the lateral pterygoid muscle may be causally related to compression of an entrapped nerve that leads to numbness, pain, or both in the respective areas of nerve distribution. (ORAL
SURC
ORAL
MED
ORAL
PATHOL
1990;69:299-306)
E
ntrapment of a nerve occurs where the nerve passes through anatomic structures that have the potential of compressing the nerve. These anatomic sites usually are at predictable locations in the body.’ One unusual site is the infratemporal fossa, where the mandibular division of the fifth cranial nerve has intimate contact with the lateral pterygoid muscle (W. Clinically, it has been commonly understood that numbness of the cheek suggests compression of the buccal nerve in the LP. The buccal nerve mainly supplies general sensation to the skin and mucous membrane that are adjacent to the anterior part of the buccinator muscle. The buccal nerve typically passes between the two bellies of the LP shortly after
2Department of Oral Biology, Dental Occlusion and Facial Pain Center, College of Dentistry. bDepartment of Anatomy and Cell Biology, College of Medicine. Submitted in partial fulfillment of the requirement for the degree of master of science in the Department of Anatomy and Cell Biology, University of Florida, Ciainesville, Florida, 1987. Supported in part by funds of the Dental Occlusion and Facial Pain Center, College of Dentistry, University of Florida. Presented as a poster session at the annual meeting of the International Association of Dental Research, Chicago, Illinois, March 1987.
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it branches from the anterior trunk of the mandibular nerve. This normal passageway is a potential site of entrapment. If spasm of the LP occurs, the nerve could be compressed, and this compression could result in numbness of the cheek. It is believed that some cases of “temporomandrbular joint syndrome” or atypical facial pain may be due to entrapment neuropathies in the infratemporal fossa. Few investigations have been conducted concerning the anatomic substrates of entrapment of the trigeminal nerve. Since the first and second divisions of the trigeminal nerve do not travel near muscle at their proximal segments, only the third division is likely to be entrapped by muscle as it traverses the infratemporal fossa. Thus the objective of this study was to document the anatomic relationship between the mandibular nerve and the pterygoid muscles. In addition, an attempt is made to assess the structural abnormalities in relation to their possible role in producing negative sensorimotor symptoms. MATERIAL
AND METHODS
Twenty-five cadaver heads and two unpaired half heads from human adults embalmed in formalin were dissected. The specimens used in this study were obtained from the State Anatomical Board of Florida. The average age of the cadavers donated is 72 years. The whole heads were sectioned in the 299
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Fig. 1. Superior view of anterior trunk of the mandibular nerve. Note anterior deep temporal (ADT), posterior deep temporal (PDT), and masseteric (Mu) nerves. Also note anterior displaced disk (0) of mandibular condyle (Cl. LP, upper belly of lateral pterygoid muscle; B, buccal nerve.
midline with a band saw. Next, all specimens were sectioned along the posterior aspect of the petrous portion of the temporal bone to the sella turcica. The floor of the middle cranial fossa was removed to expose the anterior trunk of the mandibular division of the trigeminal nerve (Fig. 1). Medially, the eustachian tube, tensor veli palatine muscle, and levator veli palatine muscle were removed to expose the posterior trunk of the mandibular division of the trigeminal nerve and the medial aspect of the LP (Fig. 2).
trunk of the mandibular nerve. The mylohyoid nerve then descended through the lower belly of the LP. In addition to the nerve entrapments mentioned above, the middle meningeal artery was observed to be entrapped in the same three specimens that had entrapment of the lingual, inferior alveolar, and auriculotemporal nerves in the LP (Fig. 4). Also, the second part of the maxillary artery traveled deep to the LP in 23 specimens and in 13 of these specimens the maxillary artery passed through the lower belly of the LP (Fig. 6).
RESULTS
DISCUSSION
In three of 52 specimens dissected, the lingual, inferior alveolar, and auriculotemporal nerves passed through the medial portion of the lower belly of the LP (Fig. 3). Two entrapments (bilateral) were found in the same specimen. The third entrapment was from another specimen (Fig. 4). Neither the chorda tympani nerve nor the nerve to the medial pterygoid muscle was entrapped in the LP. In another specimen the anterior deep temporal nerve branched from the anterior trunk of the mandibular nerve, proceeded laterally through fibers of the upper belly of the LP, and then entered the temporal muscle (Fig. 5). In another specimen the mylohyoid nerve left the XC& &\;eGlai nerve at the salmc location that the inferior alveolar nerve branched from the posterior
The infratemporal fossa is a space behind the maxilla that contains the LP. In the roof of the infratemporal fossa, the foramen ovale offers exits from the cranium for the third division of the fifth cranial nerve (mandibular nerve), which immediately divides in close association with the LP into two trunks consisting of terminal branches. The anterior trunk, which contains the anterior deep temporal, posterior deep temporal, and masseteric nerves, passes between the roof of the infratemporal fossa and the LP. The posterior trunk, which contains the lingual, inferior alveolar, and auriculotemporal nerves, descends medial to the LP. The results of this study provide a demonstration of entrapment of one or more branches of the mandibular nerve in the LP. The posterior trunk of the mandibular nerve was
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2. Medial view of posterior trunk of mandibular nerve. Note lingual (I,), inferior alveolar (IA), and two branches(arrowheads)of auriculotemporal nerve. AIso note middlemeningealartery (mm) betweentwo converging branchesof auriculotemporalnerve. SML, sphenomandibular ligament;B, buccalnerve; LP, lower belly of lateral pterygoid muscle;mp. stump of nerve to medialpterygoid muscle. Fig.
shown to be entrapped in three of the 52 dissections. Two of the entrapments were bilateral and thus the incidence of entrapment in all specimens was slightly less than 6%. Nerve entrapment in the infratemporal fossa is not the only possible cause of painful disorders of the mandibular nerve because mandibular nerve compression may result from inflammation, trauma, or neoplasms. On the other hand, some cases of primary trigeminal nerve injury unassociated with other neurologic or systemic diseases are difficult to diagnose. Pathologic changes have been found in entrapped peripheral nerves at routine autopsy on patients with no known diseases of the nervous system.3y 4 In a clinical study of 64 patients with isolated facial numbness, 11 appeared to have no underlying disease.’ An example
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Fig. 3. Medial view of entrapmentof posterior trunk of mandibularnerve. Note lingual /L). inferior alveolar (IA), and auriculotemporal (AT) nervespassingthrough lower belly of lateral pterygoid muscle(LP). S, styloid process; SML, sphenomandibularligament; B, buccal nerve.
of a primary nerve injury is trigeminal sensory neuropathy, which represents a dysfunction of the sensory portion of the fifth cranial nerve outside the brain stem. In a clinical study of 10 patients with trigeminal sensory neuropathy of undetermined etiology, numbness was a consistent complaint. In three cases the numbness was confined to the mandibular nerve.6 The present study suggests that a clinical case should not be considered undiagnosed until mandibular nerve entrapment in the LP is considered. On strictly theoretic grounds, spasm, hypertrophy, or both of the LP could compress the entrapped nerve branches. In addition, compression points may occur between the LP and the roof of the infratemporal fossa that would affect the nerves of the anterior trunk of the mandibular nerve. Each entrapped branch of the mandibular nerve may induce altered sensations during compression. Such compression may produce a partial lesion of the
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nerve that can lead to the distortion of signal patterns or to ectopic impulses set up in damaged nerve fibers. The resultant aberrant transmission from the periphery may disrupt normal processes in the somatosensory cortex.7 Compression of motor branches of the mandibular nerve can lead to paresis or weakness in the innervated muscle. l
present dissections the proximal trunk of the lingual nerve had an anomalous course through fibers of the LP in three of the 52 specimens. The chorda tympani nerve, which joins the lingual nerve at an acute angle at the inferior border of the LP, was not entrapped. The freedom from entrapment of the chorda tympani nerve suggests that taste sensation to the anterior two thirds of the tongue would not be affected by lingual nerve entrapment in the LP. In a previous study the lingual nerve was shown to be entrapped in the LP. Isberg and coworkers8 found that 3% of patients with disk displacement of the temporomandibular joint (TMJ) associated with severe pain complained of lingual numbness. When the TMJ was anesthetized locally, the numbness of the tongue was eliminated. It was hypothesized that spasm of the LP associated with the TMJ derangement was released by the local anesthetization of the joint. The release of the muscle spasm by anesthetizing the TMJ is based on the principle of Hilton’s law, which states that a nerve trunk innervating a joint also innervates the muscles that move that joint.9 Pain from the TMJ that had an internal derangement can initiate a mandibular muscle-splinting phenomenon. The afferent input facilitates the extensor and flexor muscles of the TMJ and results in splinting. Anesthetizing the TMJ stops the painful input, and the muscles relax. The entrapped lingual nerve is decompressed; a process that results in the cessation of numbness. The reversibility of numbness of the tongue suggests a first-degree nerve injury (neurapraxia). A first-degree nerve injury is defined as mild, transient compression usually producing no nerve degeneration or loss of neural continuity with the periphery. Decompression results in rapid recovery. Chronic, progressive compression of the lingual nerve may cause physical damage to the axons at the entrapment site and neighboring segments of the nerve. Such damage represents a second-degree nerve injury, and therefore numbness of the tongue may linger after decompression. ‘9 lo This possibility of lasting damage hints that early diagnosis is important.
Lingual
inferior
Fig. 4. Medial view of entrapment of posterior trunk of mandibular nerve. Note lingual nerve (L), inferior alveolar nerve (ZAj, and middle meningeal artery (arrowheads) passing through lower belly of lateral pterygoid muscle (~9). Also note that chorda tympani (arrows) passes medial to lateral pterygoid muscle. S, styloid process; SML, sphenomandibular ligament; B, buccal nerve.
nerve
The lingual nerve originates from the posterior trunk of the mandibular nerve and normally descends medial to the LP. The lingual nerve then proceeds downward and forward between the ramus of the mandible and the medial pterygoid muscle and pab~ u&r iilr. 111u~osa of the lingual plate of bone next to the third molar tooth. It then crosses the floor of the mouth and terminates in the tongue. In the
alveolar
nerve
As it branches from the posterior trunk of the mandibular nerve in the infratemporal fossa, the inferior alveolar nerve normally descends medial to the LP. Then the inferior alveolar nerve enters the mandibular foramen and passes through the body of the mandible to innervate the teeth. A branch of the inferior alveolar nerve emerges from the mental foramen as the mental nerve, which supplies sensory
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5. Superior view of anterior trunk of mandibular nerve. Note entrapment of anterior deep temporal nerve /arrowheadsJ in upper belly of lateral pterygoid muscle (LP). PDT, posterior deep temporal nerve; Mu, masseteric nerve; B, buccal nerve; C, mandibular condyle.
Fig.
innervation to the chin and lower lip. The present study demonstrated entrapment of the inferior alveolar nerve in the lower belly of the LP. This anatomic variation represents another possible etiology in the differential diagnosis of facial numbness. Most causes of numbness of the chin, lower lip, or both must be considered as a potentially threatening manifestation of a grave disease. For example, metastatic breast cancer has an unexplained predilection for the inferior alveolar nerve and results in numbness of the mental nerve distribution. Metastasis to the dura of the trigeminal nerve or to the mandible are implicated in the pathogenesis.” The two most common causes of inferior alveolar nerve numbness are trauma from third molar tooth removal and mandibular fracture. The intramandibular plexiform arrangement of the nerve appears to be an important factor contributing to nerve damage and degeneration.12 In addition, the bony course that the inferior alveolar nerve travels may cause second-degree nerve injury that prevents successful regeneration.13 In the absence of trauma and tumors, muscular compression of the inferior alveolar nerve should be considered as an impinging mechanism in the differential diagnosis of facial numbness. Auriculotemporal
nerve
The auriculotemporal nerve originates from two branches of the posterior trunk of the mandibular nerve. Passing posteriorly, the two branches encircle the middle meningeal artery, converge, and then
continue deep to the LP, giving off secretomotor fibers to the parotid gland. The auriculotemporal nerve then travels laterally behind the neck of the mandibular condyle and supplies sensory innervation to the tragus, helix, external auditory meatus, and TMJ. Finally emerging from behind the joint, the nerve rises posterior to the superficial temporal artery and vein, passes over the zygomatic root of the temporal bone, and diverges into superficial temporal branches.14 Observations reported herein demonstrate entrapment of the auriculotemporal nerve between fibers of the lower belly of the LP. Myospasm or other local changes in the muscle such as myositis and myofibrositis could cause nerve compression that leads to paresthesia in any one or all of the branches supplying sensation to the external ear, TMJ, and temple. Furthermore, secretomotor fibers innervating the parotid gland also may be compressed, and this compression could result in functional impairment of salivation ipsilaterally. The auriculotemporal nerve communicates with the facial nerve at the posterior border of the ramus where the auriculotemporal nerve passes posterior to the neck of the condyle. If fibers cross over from the auriculotemporal nerve to the facial nerve and not vice versa, this communication may represent a pathway for sensory impairment of the facial nerve. That is, pain in the muscles of facial expression may occur from an entrapped and compressed auriculotemporal nerve as described above. Compression of a nerve at a proximal site may
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Fig. 6. Medial view of maxillary artery (arrowheads) entrapped in lower belly of lateral pterygoid muscle (LP). S, styloid process; SML, sphenomandibular ligament; 15, lingual nerve; IA, inferior alveolar nerve; AT, auriculotemporal nerve; B, buccal nerve; urrows. chorda tympani nerve.
make the nerve more susceptible to dysfunction at a distal site where an injury would normally resolve itself.15 This “double-crush” theory may be useful in consideration of a differential diagnosis for head pain. For example, it is common clinically to find a patient who has an internal derangement of the TMJ and accompanying spasm of the LP. An entrapped auriculotemporal nerve in the LP could be the etiology of a painful neuropathy in a distal auriculotemporal branch supplying sensory innervation to a deranged TMJ. If the mechanical derangement is corrected surgically but the myospams persist, postoperative joint pain may continue because of the painful neuropathy produced by the compression of the auriculotemporal nerve at the proximal entrapment site. Mylohyoid
nerve
Normally the nerve to the mylohyoid muscle branches from the inferior alveolar nerve as the
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latter descends between the sphenomandibular ligament and the mandibular ramus. The mylohyoid nerve pierces the sphenomandibular ligament and passes forward in a groove to reach the mylohyoid muscle and the anterior belly of the digastric muscle. In the present findings an unusual entrapment of the mylohyoid nerve in the LP was observed in one specimen. This anatomic variation involved a more proximal branching from the inferior alveolar nerve. Since the mylohyoid nerve mainly is a motor nerve, compression may cause a poorly localized, deep pain from the muscles it innervates. Consequently, the mylohyoid muscle and the anterior belly of the digastric muscle may be tender to palpation. If chronic compression is present, then muscular paresis may occur.’ This symptom would be subclinical unless the nerve entrapment is bilateral; then swallowing difficulties may ensue. Sensory fibers may travel in the mylohyoid nerve. This occurrence has been used to explain some of the problems associated with inadequate mandibular block injections. ‘*, l6 Moreover, numbness under the chin has been reported from injury to the mylohyoid nerve from lingual retraction during a difficult mandibular third molar tooth extraction.” Similar sensory deficit under the chin may result from impingement of the mylohyoid nerve entrapped in the LP. Anterior
deep
temporal
nerve
The normal course of the anterior and posterior deep temporal nerves after they branch from the anterior trunk of the mandibular nerve is superior to the upper belly of the LP. These nerves are the motor innervation to the temporalis muscle. In one of the dissected specimens the anterior deep temporal nerve was entrapped in fibers of the upper belly of the LP. Since the posterior deep temporal nerve was not observed to be entrapped, any motor deficit would most likely be subclinical. Nevertheless, other motor-nerve entrapments such as in the posterior interosseous and suprascapular syndromes manifest dull, aching pain as an outstanding feature of prolonged compression. 18,l9 Therefore, impingement of the anterior deep temporal nerve could cause pain at the site of its distal distribution. Vascular
entrapment
Besides various nerve entrapments in the LP, the artery was obscrvcd to pass through fibers of the lower belly of the LP. Normally the maxillary artery has two pathways to the pterygomaxillary fissure. One pathway is lateral to the LP, and the rr~kiiai~
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other pathway is medial to the LP where the artery passes between the upper and lower bellies of the LP. If the maxillary artery and its accompanying sympathetic fibers are at all susceptible to compression in the infratemporal fossa, such compression seems more likely to occur at the entrapment site in the lower belly of the LP than in that of the upper belly. Such compression would not be expected to produce ischemia or efferent dysfunction because of collateral circulation of the anterior and posterior ethmoidal arteries or deep petrosal nerve, respectively. Nevertheless, a marked change in the caliber of an intracranial or extracranial blood vessel is thought to produce vascular headaches.20 The diameter of the maxilary artery entrapped in the LP could be reduced by compression. Furthermore, referred pain to the forehead and anterior scalp may occur as a result of pressure on nerve fibers within the adventitia of the maxillary artery.21 The middle meningeal artery was seen to be entrapped in the LP in the same three specimens that exhibited entrapment of the lingual, inferior alveolar, and auriculotemporal nerves. Anatomic studies suggest that an innervation of dural arteries is composed of both vasomotor efferents (automatic) and sensory afferent fibers.22* 23 Physiologic studies have shown that electric and mechanical stimulation of dural arteries produced pain in human subjects.24y 25 This finding implies that trigeminal afferent neurons innervate the middle meningeal artery and transmit nociceptive information from the vasculature to the brain. A recent study demonstrated that multireceptive units in the subnucleus caudalis of the cat respond to electric stimulation of the middle meningeal artery and to noxious stimulation of the skin of the face.26 One way to activate sensory fibers in the middle meningeal artery could be via compression in a spastic LP. Taken together, these data may indicate the basis of referred pain from dural arteries to the face. CONCLUSION
The explanation of undiagnosed paresthesia in the distribution of the mandibular nerve presented in this study involves nerve and vascular entrapment in the infratemporal fossa. This explanation has features similar to those of the thoracic outlet syndrome, which involves neurovascular compression at the base of the neck and its differential diagnosis is based on extensive diagnostic criteria.27 In this study the criteria discussed concerning mandibular nerve entrapment are based on anatomic relationships in cadavers and, are therefore speculative. Nevertheless, the dentist should maintain a high index of suspicion
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to the possible signs of neurovascular compression in the infratemporal fossa. When considering a diagnosis for head pain, a special inquiry should be made as to the status of the pterygoid muscles. Tenderness to palpation suggests a spastic condition. A provocation test of the LP may be useful. That is, protrusion of the mandible against isometeric pressure on the chin activates the lower belly of the LP. The resulting muscular contraction could elicit symptom(s) caused by compression of an entrapped nerve. Skill at performing a local anesthetic block of the auriculotemporal nerve could help in the evaluation of the condition of the LP. This injection may release spasm of the LP according to Hilton’s law resulting in decompression of entrapped nerves and/or arteries. Unfortunately, electrodiagnostic and nerve conduction studies would be difficult to apply in the infratemporal fossa. Behavioral studies using laboratory animals may add useful information to the understanding of peripheral nerve damage that produces pain in humans.28y 29 Further anatomical research correlated with clinical studies should be valuable to the diagnostician in identifying conditions that damage cranial nerves at a specific site.
REFERENCES 1. Gordon L, Ritland GD. Nerve entrapment syndromes. Corm Med 1974;38:97-102. 2. Kopell HP, Thompson WAL, eds. Peripheral entrapment neuropathies. Huntington, NY: RE Krieger Publishing Company, 1976;1-7. 3. Castaldo JE, Ochoa JL. Mechanical injury of peripheral nerves: fine structure and dysfunction. Clin Plast Surg 1984;11:9-16. 4. Neary D, Ochoa J, Gilliat RW. Sub-clinical entrapment neuropathy in man. J Neural Sci 1975;24:283-98. 5. Horowitz SH. Isolated facial numbness. Ann Intern Med 1974;80:49-53. 6. Blau JN, Harris M, Kennett S. Trigeminal sensory neuropathy. N Engl J Med 1969;281:873-6. 7. Sutherland S. Nerves and nerve injuries. New York: Churchill Livingstone, 1978;343-50.
DDS, MS,n Lynn H. Larkin,
PhD,b and Parker E. Mahan, DDS, PhD,a
OF FLORIDA
The posterior trunk of the mandibular division of the trigeminal nerve normally descends deep to the lateral pterygoid muscle. In three of 52 dissections the three main branches of the posterior trunk (lingual, inferior alveolar, and auriculotemporal nerves) were observed to pass through the medial fibers of the lower belly of the lateral pterygoid muscle. The mylohyoid and anterior deep temporal nerves also were observed to pass through the lateral pterygoid muscle in other specimens. These nerve entrapments in the infratemporal fossa provide new information concerning the anatomic and clinical relationships between the mandibular nerve and the lateral pterygoid muscle. These findings support the hypothesis that a spastic condition of the lateral pterygoid muscle may be causally related to compression of an entrapped nerve that leads to numbness, pain, or both in the respective areas of nerve distribution. (ORAL
SURC
ORAL
MED
ORAL
PATHOL
1990;69:299-306)
E
ntrapment of a nerve occurs where the nerve passes through anatomic structures that have the potential of compressing the nerve. These anatomic sites usually are at predictable locations in the body.’ One unusual site is the infratemporal fossa, where the mandibular division of the fifth cranial nerve has intimate contact with the lateral pterygoid muscle (W. Clinically, it has been commonly understood that numbness of the cheek suggests compression of the buccal nerve in the LP. The buccal nerve mainly supplies general sensation to the skin and mucous membrane that are adjacent to the anterior part of the buccinator muscle. The buccal nerve typically passes between the two bellies of the LP shortly after
2Department of Oral Biology, Dental Occlusion and Facial Pain Center, College of Dentistry. bDepartment of Anatomy and Cell Biology, College of Medicine. Submitted in partial fulfillment of the requirement for the degree of master of science in the Department of Anatomy and Cell Biology, University of Florida, Ciainesville, Florida, 1987. Supported in part by funds of the Dental Occlusion and Facial Pain Center, College of Dentistry, University of Florida. Presented as a poster session at the annual meeting of the International Association of Dental Research, Chicago, Illinois, March 1987.
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it branches from the anterior trunk of the mandibular nerve. This normal passageway is a potential site of entrapment. If spasm of the LP occurs, the nerve could be compressed, and this compression could result in numbness of the cheek. It is believed that some cases of “temporomandrbular joint syndrome” or atypical facial pain may be due to entrapment neuropathies in the infratemporal fossa. Few investigations have been conducted concerning the anatomic substrates of entrapment of the trigeminal nerve. Since the first and second divisions of the trigeminal nerve do not travel near muscle at their proximal segments, only the third division is likely to be entrapped by muscle as it traverses the infratemporal fossa. Thus the objective of this study was to document the anatomic relationship between the mandibular nerve and the pterygoid muscles. In addition, an attempt is made to assess the structural abnormalities in relation to their possible role in producing negative sensorimotor symptoms. MATERIAL
AND METHODS
Twenty-five cadaver heads and two unpaired half heads from human adults embalmed in formalin were dissected. The specimens used in this study were obtained from the State Anatomical Board of Florida. The average age of the cadavers donated is 72 years. The whole heads were sectioned in the 299
300
Loughner,
Larkin,
and Mahan
ORALSURG
ORAL
MLD
ORAI
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PAFHOI.
1990
Fig. 1. Superior view of anterior trunk of the mandibular nerve. Note anterior deep temporal (ADT), posterior deep temporal (PDT), and masseteric (Mu) nerves. Also note anterior displaced disk (0) of mandibular condyle (Cl. LP, upper belly of lateral pterygoid muscle; B, buccal nerve.
midline with a band saw. Next, all specimens were sectioned along the posterior aspect of the petrous portion of the temporal bone to the sella turcica. The floor of the middle cranial fossa was removed to expose the anterior trunk of the mandibular division of the trigeminal nerve (Fig. 1). Medially, the eustachian tube, tensor veli palatine muscle, and levator veli palatine muscle were removed to expose the posterior trunk of the mandibular division of the trigeminal nerve and the medial aspect of the LP (Fig. 2).
trunk of the mandibular nerve. The mylohyoid nerve then descended through the lower belly of the LP. In addition to the nerve entrapments mentioned above, the middle meningeal artery was observed to be entrapped in the same three specimens that had entrapment of the lingual, inferior alveolar, and auriculotemporal nerves in the LP (Fig. 4). Also, the second part of the maxillary artery traveled deep to the LP in 23 specimens and in 13 of these specimens the maxillary artery passed through the lower belly of the LP (Fig. 6).
RESULTS
DISCUSSION
In three of 52 specimens dissected, the lingual, inferior alveolar, and auriculotemporal nerves passed through the medial portion of the lower belly of the LP (Fig. 3). Two entrapments (bilateral) were found in the same specimen. The third entrapment was from another specimen (Fig. 4). Neither the chorda tympani nerve nor the nerve to the medial pterygoid muscle was entrapped in the LP. In another specimen the anterior deep temporal nerve branched from the anterior trunk of the mandibular nerve, proceeded laterally through fibers of the upper belly of the LP, and then entered the temporal muscle (Fig. 5). In another specimen the mylohyoid nerve left the XC& &\;eGlai nerve at the salmc location that the inferior alveolar nerve branched from the posterior
The infratemporal fossa is a space behind the maxilla that contains the LP. In the roof of the infratemporal fossa, the foramen ovale offers exits from the cranium for the third division of the fifth cranial nerve (mandibular nerve), which immediately divides in close association with the LP into two trunks consisting of terminal branches. The anterior trunk, which contains the anterior deep temporal, posterior deep temporal, and masseteric nerves, passes between the roof of the infratemporal fossa and the LP. The posterior trunk, which contains the lingual, inferior alveolar, and auriculotemporal nerves, descends medial to the LP. The results of this study provide a demonstration of entrapment of one or more branches of the mandibular nerve in the LP. The posterior trunk of the mandibular nerve was
Volume Number
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2. Medial view of posterior trunk of mandibular nerve. Note lingual (I,), inferior alveolar (IA), and two branches(arrowheads)of auriculotemporal nerve. AIso note middlemeningealartery (mm) betweentwo converging branchesof auriculotemporalnerve. SML, sphenomandibular ligament;B, buccalnerve; LP, lower belly of lateral pterygoid muscle;mp. stump of nerve to medialpterygoid muscle. Fig.
shown to be entrapped in three of the 52 dissections. Two of the entrapments were bilateral and thus the incidence of entrapment in all specimens was slightly less than 6%. Nerve entrapment in the infratemporal fossa is not the only possible cause of painful disorders of the mandibular nerve because mandibular nerve compression may result from inflammation, trauma, or neoplasms. On the other hand, some cases of primary trigeminal nerve injury unassociated with other neurologic or systemic diseases are difficult to diagnose. Pathologic changes have been found in entrapped peripheral nerves at routine autopsy on patients with no known diseases of the nervous system.3y 4 In a clinical study of 64 patients with isolated facial numbness, 11 appeared to have no underlying disease.’ An example
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Fig. 3. Medial view of entrapmentof posterior trunk of mandibularnerve. Note lingual /L). inferior alveolar (IA), and auriculotemporal (AT) nervespassingthrough lower belly of lateral pterygoid muscle(LP). S, styloid process; SML, sphenomandibularligament; B, buccal nerve.
of a primary nerve injury is trigeminal sensory neuropathy, which represents a dysfunction of the sensory portion of the fifth cranial nerve outside the brain stem. In a clinical study of 10 patients with trigeminal sensory neuropathy of undetermined etiology, numbness was a consistent complaint. In three cases the numbness was confined to the mandibular nerve.6 The present study suggests that a clinical case should not be considered undiagnosed until mandibular nerve entrapment in the LP is considered. On strictly theoretic grounds, spasm, hypertrophy, or both of the LP could compress the entrapped nerve branches. In addition, compression points may occur between the LP and the roof of the infratemporal fossa that would affect the nerves of the anterior trunk of the mandibular nerve. Each entrapped branch of the mandibular nerve may induce altered sensations during compression. Such compression may produce a partial lesion of the
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Larkin,
and Mahan
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ORAL PATHOL March 1990
nerve that can lead to the distortion of signal patterns or to ectopic impulses set up in damaged nerve fibers. The resultant aberrant transmission from the periphery may disrupt normal processes in the somatosensory cortex.7 Compression of motor branches of the mandibular nerve can lead to paresis or weakness in the innervated muscle. l
present dissections the proximal trunk of the lingual nerve had an anomalous course through fibers of the LP in three of the 52 specimens. The chorda tympani nerve, which joins the lingual nerve at an acute angle at the inferior border of the LP, was not entrapped. The freedom from entrapment of the chorda tympani nerve suggests that taste sensation to the anterior two thirds of the tongue would not be affected by lingual nerve entrapment in the LP. In a previous study the lingual nerve was shown to be entrapped in the LP. Isberg and coworkers8 found that 3% of patients with disk displacement of the temporomandibular joint (TMJ) associated with severe pain complained of lingual numbness. When the TMJ was anesthetized locally, the numbness of the tongue was eliminated. It was hypothesized that spasm of the LP associated with the TMJ derangement was released by the local anesthetization of the joint. The release of the muscle spasm by anesthetizing the TMJ is based on the principle of Hilton’s law, which states that a nerve trunk innervating a joint also innervates the muscles that move that joint.9 Pain from the TMJ that had an internal derangement can initiate a mandibular muscle-splinting phenomenon. The afferent input facilitates the extensor and flexor muscles of the TMJ and results in splinting. Anesthetizing the TMJ stops the painful input, and the muscles relax. The entrapped lingual nerve is decompressed; a process that results in the cessation of numbness. The reversibility of numbness of the tongue suggests a first-degree nerve injury (neurapraxia). A first-degree nerve injury is defined as mild, transient compression usually producing no nerve degeneration or loss of neural continuity with the periphery. Decompression results in rapid recovery. Chronic, progressive compression of the lingual nerve may cause physical damage to the axons at the entrapment site and neighboring segments of the nerve. Such damage represents a second-degree nerve injury, and therefore numbness of the tongue may linger after decompression. ‘9 lo This possibility of lasting damage hints that early diagnosis is important.
Lingual
inferior
Fig. 4. Medial view of entrapment of posterior trunk of mandibular nerve. Note lingual nerve (L), inferior alveolar nerve (ZAj, and middle meningeal artery (arrowheads) passing through lower belly of lateral pterygoid muscle (~9). Also note that chorda tympani (arrows) passes medial to lateral pterygoid muscle. S, styloid process; SML, sphenomandibular ligament; B, buccal nerve.
nerve
The lingual nerve originates from the posterior trunk of the mandibular nerve and normally descends medial to the LP. The lingual nerve then proceeds downward and forward between the ramus of the mandible and the medial pterygoid muscle and pab~ u&r iilr. 111u~osa of the lingual plate of bone next to the third molar tooth. It then crosses the floor of the mouth and terminates in the tongue. In the
alveolar
nerve
As it branches from the posterior trunk of the mandibular nerve in the infratemporal fossa, the inferior alveolar nerve normally descends medial to the LP. Then the inferior alveolar nerve enters the mandibular foramen and passes through the body of the mandible to innervate the teeth. A branch of the inferior alveolar nerve emerges from the mental foramen as the mental nerve, which supplies sensory
Volume Number
Nerve entrapment
69 3
in lateral pterygoid
muscle
303
5. Superior view of anterior trunk of mandibular nerve. Note entrapment of anterior deep temporal nerve /arrowheadsJ in upper belly of lateral pterygoid muscle (LP). PDT, posterior deep temporal nerve; Mu, masseteric nerve; B, buccal nerve; C, mandibular condyle.
Fig.
innervation to the chin and lower lip. The present study demonstrated entrapment of the inferior alveolar nerve in the lower belly of the LP. This anatomic variation represents another possible etiology in the differential diagnosis of facial numbness. Most causes of numbness of the chin, lower lip, or both must be considered as a potentially threatening manifestation of a grave disease. For example, metastatic breast cancer has an unexplained predilection for the inferior alveolar nerve and results in numbness of the mental nerve distribution. Metastasis to the dura of the trigeminal nerve or to the mandible are implicated in the pathogenesis.” The two most common causes of inferior alveolar nerve numbness are trauma from third molar tooth removal and mandibular fracture. The intramandibular plexiform arrangement of the nerve appears to be an important factor contributing to nerve damage and degeneration.12 In addition, the bony course that the inferior alveolar nerve travels may cause second-degree nerve injury that prevents successful regeneration.13 In the absence of trauma and tumors, muscular compression of the inferior alveolar nerve should be considered as an impinging mechanism in the differential diagnosis of facial numbness. Auriculotemporal
nerve
The auriculotemporal nerve originates from two branches of the posterior trunk of the mandibular nerve. Passing posteriorly, the two branches encircle the middle meningeal artery, converge, and then
continue deep to the LP, giving off secretomotor fibers to the parotid gland. The auriculotemporal nerve then travels laterally behind the neck of the mandibular condyle and supplies sensory innervation to the tragus, helix, external auditory meatus, and TMJ. Finally emerging from behind the joint, the nerve rises posterior to the superficial temporal artery and vein, passes over the zygomatic root of the temporal bone, and diverges into superficial temporal branches.14 Observations reported herein demonstrate entrapment of the auriculotemporal nerve between fibers of the lower belly of the LP. Myospasm or other local changes in the muscle such as myositis and myofibrositis could cause nerve compression that leads to paresthesia in any one or all of the branches supplying sensation to the external ear, TMJ, and temple. Furthermore, secretomotor fibers innervating the parotid gland also may be compressed, and this compression could result in functional impairment of salivation ipsilaterally. The auriculotemporal nerve communicates with the facial nerve at the posterior border of the ramus where the auriculotemporal nerve passes posterior to the neck of the condyle. If fibers cross over from the auriculotemporal nerve to the facial nerve and not vice versa, this communication may represent a pathway for sensory impairment of the facial nerve. That is, pain in the muscles of facial expression may occur from an entrapped and compressed auriculotemporal nerve as described above. Compression of a nerve at a proximal site may
304
Loughner,
Larkin,
and Mahan
Fig. 6. Medial view of maxillary artery (arrowheads) entrapped in lower belly of lateral pterygoid muscle (LP). S, styloid process; SML, sphenomandibular ligament; 15, lingual nerve; IA, inferior alveolar nerve; AT, auriculotemporal nerve; B, buccal nerve; urrows. chorda tympani nerve.
make the nerve more susceptible to dysfunction at a distal site where an injury would normally resolve itself.15 This “double-crush” theory may be useful in consideration of a differential diagnosis for head pain. For example, it is common clinically to find a patient who has an internal derangement of the TMJ and accompanying spasm of the LP. An entrapped auriculotemporal nerve in the LP could be the etiology of a painful neuropathy in a distal auriculotemporal branch supplying sensory innervation to a deranged TMJ. If the mechanical derangement is corrected surgically but the myospams persist, postoperative joint pain may continue because of the painful neuropathy produced by the compression of the auriculotemporal nerve at the proximal entrapment site. Mylohyoid
nerve
Normally the nerve to the mylohyoid muscle branches from the inferior alveolar nerve as the
ORAL
SURC
ORAL.
MED
ORAL PATHOL March 1990
latter descends between the sphenomandibular ligament and the mandibular ramus. The mylohyoid nerve pierces the sphenomandibular ligament and passes forward in a groove to reach the mylohyoid muscle and the anterior belly of the digastric muscle. In the present findings an unusual entrapment of the mylohyoid nerve in the LP was observed in one specimen. This anatomic variation involved a more proximal branching from the inferior alveolar nerve. Since the mylohyoid nerve mainly is a motor nerve, compression may cause a poorly localized, deep pain from the muscles it innervates. Consequently, the mylohyoid muscle and the anterior belly of the digastric muscle may be tender to palpation. If chronic compression is present, then muscular paresis may occur.’ This symptom would be subclinical unless the nerve entrapment is bilateral; then swallowing difficulties may ensue. Sensory fibers may travel in the mylohyoid nerve. This occurrence has been used to explain some of the problems associated with inadequate mandibular block injections. ‘*, l6 Moreover, numbness under the chin has been reported from injury to the mylohyoid nerve from lingual retraction during a difficult mandibular third molar tooth extraction.” Similar sensory deficit under the chin may result from impingement of the mylohyoid nerve entrapped in the LP. Anterior
deep
temporal
nerve
The normal course of the anterior and posterior deep temporal nerves after they branch from the anterior trunk of the mandibular nerve is superior to the upper belly of the LP. These nerves are the motor innervation to the temporalis muscle. In one of the dissected specimens the anterior deep temporal nerve was entrapped in fibers of the upper belly of the LP. Since the posterior deep temporal nerve was not observed to be entrapped, any motor deficit would most likely be subclinical. Nevertheless, other motor-nerve entrapments such as in the posterior interosseous and suprascapular syndromes manifest dull, aching pain as an outstanding feature of prolonged compression. 18,l9 Therefore, impingement of the anterior deep temporal nerve could cause pain at the site of its distal distribution. Vascular
entrapment
Besides various nerve entrapments in the LP, the artery was obscrvcd to pass through fibers of the lower belly of the LP. Normally the maxillary artery has two pathways to the pterygomaxillary fissure. One pathway is lateral to the LP, and the rr~kiiai~
Volume Number
69 3
other pathway is medial to the LP where the artery passes between the upper and lower bellies of the LP. If the maxillary artery and its accompanying sympathetic fibers are at all susceptible to compression in the infratemporal fossa, such compression seems more likely to occur at the entrapment site in the lower belly of the LP than in that of the upper belly. Such compression would not be expected to produce ischemia or efferent dysfunction because of collateral circulation of the anterior and posterior ethmoidal arteries or deep petrosal nerve, respectively. Nevertheless, a marked change in the caliber of an intracranial or extracranial blood vessel is thought to produce vascular headaches.20 The diameter of the maxilary artery entrapped in the LP could be reduced by compression. Furthermore, referred pain to the forehead and anterior scalp may occur as a result of pressure on nerve fibers within the adventitia of the maxillary artery.21 The middle meningeal artery was seen to be entrapped in the LP in the same three specimens that exhibited entrapment of the lingual, inferior alveolar, and auriculotemporal nerves. Anatomic studies suggest that an innervation of dural arteries is composed of both vasomotor efferents (automatic) and sensory afferent fibers.22* 23 Physiologic studies have shown that electric and mechanical stimulation of dural arteries produced pain in human subjects.24y 25 This finding implies that trigeminal afferent neurons innervate the middle meningeal artery and transmit nociceptive information from the vasculature to the brain. A recent study demonstrated that multireceptive units in the subnucleus caudalis of the cat respond to electric stimulation of the middle meningeal artery and to noxious stimulation of the skin of the face.26 One way to activate sensory fibers in the middle meningeal artery could be via compression in a spastic LP. Taken together, these data may indicate the basis of referred pain from dural arteries to the face. CONCLUSION
The explanation of undiagnosed paresthesia in the distribution of the mandibular nerve presented in this study involves nerve and vascular entrapment in the infratemporal fossa. This explanation has features similar to those of the thoracic outlet syndrome, which involves neurovascular compression at the base of the neck and its differential diagnosis is based on extensive diagnostic criteria.27 In this study the criteria discussed concerning mandibular nerve entrapment are based on anatomic relationships in cadavers and, are therefore speculative. Nevertheless, the dentist should maintain a high index of suspicion
Nerve entrapment
in lateral pterygoid
muscle
305
to the possible signs of neurovascular compression in the infratemporal fossa. When considering a diagnosis for head pain, a special inquiry should be made as to the status of the pterygoid muscles. Tenderness to palpation suggests a spastic condition. A provocation test of the LP may be useful. That is, protrusion of the mandible against isometeric pressure on the chin activates the lower belly of the LP. The resulting muscular contraction could elicit symptom(s) caused by compression of an entrapped nerve. Skill at performing a local anesthetic block of the auriculotemporal nerve could help in the evaluation of the condition of the LP. This injection may release spasm of the LP according to Hilton’s law resulting in decompression of entrapped nerves and/or arteries. Unfortunately, electrodiagnostic and nerve conduction studies would be difficult to apply in the infratemporal fossa. Behavioral studies using laboratory animals may add useful information to the understanding of peripheral nerve damage that produces pain in humans.28y 29 Further anatomical research correlated with clinical studies should be valuable to the diagnostician in identifying conditions that damage cranial nerves at a specific site.
REFERENCES 1. Gordon L, Ritland GD. Nerve entrapment syndromes. Corm Med 1974;38:97-102. 2. Kopell HP, Thompson WAL, eds. Peripheral entrapment neuropathies. Huntington, NY: RE Krieger Publishing Company, 1976;1-7. 3. Castaldo JE, Ochoa JL. Mechanical injury of peripheral nerves: fine structure and dysfunction. Clin Plast Surg 1984;11:9-16. 4. Neary D, Ochoa J, Gilliat RW. Sub-clinical entrapment neuropathy in man. J Neural Sci 1975;24:283-98. 5. Horowitz SH. Isolated facial numbness. Ann Intern Med 1974;80:49-53. 6. Blau JN, Harris M, Kennett S. Trigeminal sensory neuropathy. N Engl J Med 1969;281:873-6. 7. Sutherland S. Nerves and nerve injuries. New York: Churchill Livingstone, 1978;343-50.
