J Oral MaxillofacSurg 50:1238-1239.1992
Trochlear Nerve Palsy Simulating an Orbital Blowout Fracture MITCHELL
M. RUBIN,
DMD*
Report of Case
Diplopia has multiple causes, including orbital hemorrhage and edema, incarceration of orbital fat, vertical displacement of the globe, decompensation of phorias, direct injury to an extraocular muscle, or injury to a cranial nerve supplying that muscle.’ Diplopia due to superior oblique paresis may follow minimal head injury.’ Posttraumatic fourth nerve palsies usually occur following oblique frontal impact. Thus, the lines of force are usually transmitted either from the right frontal to left occipital region, or from the left frontal to right occipital region.* Contusion of one or both of the dorsally exiting fourth cranial nerves may occur as the brain stem is shifted posteriorly against the cerebellar tentorium during head trauma.3 Closed head trauma is the most common cause of an acquired fourth nerve palsy. The correct diagnosis usually requires a moderate degree of patient cooperation and is difficult, if not impossible, to establish while the patient is stuperous. After the patient becomes alert and complains of vertical double vision, the diagnosis of unilateral trochlear nerve paresis is usually straightforward.4 The major function of the superior oblique muscle with the eye in primary position is to intort the globe and, secondarily, to depress and abduct. Weakness of this muscle thus causes a vertical diplopia that is worse on downward gaze or at near vision, rather than at upward gaze or at distant vision. To compensate for this problem, the patient soon learns to adopt an appropriate posture. Patients compensate for horizontal deviations of the eyes by turning the face: for vertical deviations by raising or lowering the chin; and for torsional deviations by tilting the head. A patient with a left superior oblique paresis thus tilts the head to the right, turns the face to the left, and points the chin down, to facilitate fusion or to minimize double vision.’
A 34-year-old white man was involved in an automobile accident in February 1991, in which he struck the right side of his head against the car interior. Police at the scene reported that he experienced a temporary loss of consciousness. He was brought to the emergency room awake, yet lethargic. Soft-tissue swelling and ecchymosis in the right temporal, preauricular, and mastoid regions was evident. Right orbital ecchymosis and infraorbital paresthesia were present. Ocular and neurologic examinations were normal. No infraorbital or frontozygomatic fractures were noted. A computed tomography scan of the head showed no intracranial abnormalities, and the patient was discharged from the emergency department at that time. Over the course of the next few days, the patient became acutely aware of vertical diplopia on downward gaze, and he developed a right head tilt. A few weeks following the accident, he sought a maxillofacial consultation regarding the continued diplopia and infraorbital paresthesia. Although it was possible that an occult right orbital floor fracture existed, the right eye appeared to move normally in all directions, pupillary heights were equal, and facial symmetry was present. The right infraorbital paresthesia was tentatively attributed to direct nerve damage at the infraorbital foramen; a neurosurgical consultation was suggested. The patient returned to the neurosurgeon who had initially evaluated him in the emergency department. Immediately on seeing the patient’s head tilt when entering the examination room, a fourth cranial nerve palsy of the left eye was diagnosed. The patient was then referred to a neuro-ophthalmologist,who confirmed the presence of a contralateral fourth cranial nerve palsy following a coup-contre-coup closed head injury. He suggested that a good chance of recovery existed within 3 months of the accident, and recommended strabismus surgery only if there was no improvement in 1 year. One year after the accident, the patient continues to have diplopia; however, he refuses surgery because his ability to function with the double vision has improved.
Discussion
* Attending Oral and Maxillofacial Surgeon, Nassau County Medical Center, East Meadow. NY; in private practice, Rockville Centre. New York. Address correspondence and reprint requests to Dr Rubin: South Shore Oral Surgery Associates. PC, Maple Medical Center, 24 Maple Ave, Rockville Centre. NY 11570.
Lethargy and physical signs suggesting an orbital blowout fracture may combine to delay the diagnosis of fourth nerve palsy. An oblique frontal blow has been suggested as a common cause of contralateral trochlear nerve trauma. The resultant findings can mimic a blowout fracture of the contralateral orbit.4 The ocular motility pattern, including the results of forced-duction
0 1992 American Association of Oral and Maxillofacial Surgeons 0278-2391/92/5011-0020$3.00/O
1238
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GRAY, MILLER, AND LOF-TUS
testing, must be consistent with the radiographic findings of a blowout fracture before repair is undertaken for the relief of diplopia.3 If the diplopia is due to an isolated extraocular muscle or cranial nerve palsy, the patient should be evaluated without orbital surgery (assuming the fracture is not markedly displaced). Under such circumstances, the diplopia is very likely to resolve spontaneously. However, if it persists, strabismus surgery can be performed at a later date. ’ Treatments for fourth nerve palsy have been classified according to increasing degree of intervention. The first modality involves supervised medical observation, and the second consists of ocular occlusion to eliminate one of the images. Sometimes a patch is used, but most often translucent tape is placed over the entire lens of one eye, or over the lower segment if the patient complains of diplopia only in downward and near gaze. The use of vertical prisms improves some patients. If diplopia persists, surgical correction involves weakening the antagonistic muscle in the eye that has the superior oblique involvement, ie, the ipsilateral inferior oblique muscle. Weakening can be accomplished by recessing the muscle 10 mm on the globe, along its direction of action.5 Tucking of the paretic superior oblique muscle is found to be of less value than inferior oblique and vertical rectus muscle surgery.6 The surgery should be deferred for 1 year to allow for possible further recovery or even adequate adaptation that may
occur during that interval.6 Although some studies of untreated unilateral posttraumatic fourth nerve palsy indicate that the condition is usually permanent,2,5 others report that spontaneous improvement generally occurs. ’ The case presented here suggests some caution in interpreting the “typical signs” of a blowout fracture. Even when a blowout fracture is confirmed, the possibility that vertical diplopia may be the result of an associated fourth nerve palsy should be considered. If the motility pattern is more compatible with paretic than restrictive strabismus, orbital exploration is not recommended.4
References 1. Wojno TH: The incidence of extraocular muscle and cranial nerve palsy in orbital floor blowout fractures. Ophthalmology 94682, 1987 2. Burger LJ, Kalvin NH, Smith JC: Acquired lesions of the fourth cranial nerve. Brain 93:567, 1970 3. Ruttum MS, Harris GT: Orbital blowout fracture with ipsilateral fourth nerve palsy. Am J Ophthalmol 100:343, 1985 4. Keane JR: Fourth nerve palsy opposite a black eye. J Clin Neuro Ophthalmol 1:209, 198 I 5. Younge BR, Sutula F: Analysis of trochlear nerve palsies. Diagnosis, etiology and treatment. Mayo Clin Proc 52: 11, 1977 6. Kawam E, Scott AB, Jampolsky A: Acquired superior oblique palsy, diagnosis and management. Arch Ophthalmol 77:76, 1967
Oral MaxlllofaC Surg 50:1239-1242,1992
J
Benign Fibrous Histiocytoma of the Oral/Perioral Regions: Report of a Case and Review of I7 Additional Cases PETER B. GRAY, DMD,* ARTHUR S. MILLER, DMD,t AND MICHAEL J. LOFTUS, DDS*
* Chief Resident, Department of Oral and Maxillofacial Surgery, Hahnemann University Hospital, Philadelphia, PA. 7 Department Chairman, Oral Pathology Section, Temple University School of Medicine, Philadelphia, PA. # Acting Chairman, Department of Oral and MaxilJofacial Surgery, Hahnemann University Hospital, Philadelphia, PA. Address correspondence and reprint requests to Dr Gray: Department of Oral and Maxillofacial Surgery, Hahnemann University Hospital, Broad & Vine Sts, Philadelphia, PA I9 102. 0 1992 American Association of Oral and Maxillofacial Surgeons 0278-2391/92/501
l-0021$3.00/0
Fibrous histiocytomas are uncommon tumors of the superficial and deep soft tissues that are reported to have a common origin from the tissue histiocyte.’ The neoplastic growth can assume many forms, and this has led to a diversity of applied names.’ This group of lesions has been shown to have a wide spectrum of clinical behaviors, from those with totally benign characteristics to those with malignant features. The latter may demonstrate multiple recurrences and widespread metastases.3“’ Benign fibrous histiocytomas occur most
Trochlear Nerve Palsy Simulating an Orbital Blowout Fracture MITCHELL
M. RUBIN,
DMD*
Report of Case
Diplopia has multiple causes, including orbital hemorrhage and edema, incarceration of orbital fat, vertical displacement of the globe, decompensation of phorias, direct injury to an extraocular muscle, or injury to a cranial nerve supplying that muscle.’ Diplopia due to superior oblique paresis may follow minimal head injury.’ Posttraumatic fourth nerve palsies usually occur following oblique frontal impact. Thus, the lines of force are usually transmitted either from the right frontal to left occipital region, or from the left frontal to right occipital region.* Contusion of one or both of the dorsally exiting fourth cranial nerves may occur as the brain stem is shifted posteriorly against the cerebellar tentorium during head trauma.3 Closed head trauma is the most common cause of an acquired fourth nerve palsy. The correct diagnosis usually requires a moderate degree of patient cooperation and is difficult, if not impossible, to establish while the patient is stuperous. After the patient becomes alert and complains of vertical double vision, the diagnosis of unilateral trochlear nerve paresis is usually straightforward.4 The major function of the superior oblique muscle with the eye in primary position is to intort the globe and, secondarily, to depress and abduct. Weakness of this muscle thus causes a vertical diplopia that is worse on downward gaze or at near vision, rather than at upward gaze or at distant vision. To compensate for this problem, the patient soon learns to adopt an appropriate posture. Patients compensate for horizontal deviations of the eyes by turning the face: for vertical deviations by raising or lowering the chin; and for torsional deviations by tilting the head. A patient with a left superior oblique paresis thus tilts the head to the right, turns the face to the left, and points the chin down, to facilitate fusion or to minimize double vision.’
A 34-year-old white man was involved in an automobile accident in February 1991, in which he struck the right side of his head against the car interior. Police at the scene reported that he experienced a temporary loss of consciousness. He was brought to the emergency room awake, yet lethargic. Soft-tissue swelling and ecchymosis in the right temporal, preauricular, and mastoid regions was evident. Right orbital ecchymosis and infraorbital paresthesia were present. Ocular and neurologic examinations were normal. No infraorbital or frontozygomatic fractures were noted. A computed tomography scan of the head showed no intracranial abnormalities, and the patient was discharged from the emergency department at that time. Over the course of the next few days, the patient became acutely aware of vertical diplopia on downward gaze, and he developed a right head tilt. A few weeks following the accident, he sought a maxillofacial consultation regarding the continued diplopia and infraorbital paresthesia. Although it was possible that an occult right orbital floor fracture existed, the right eye appeared to move normally in all directions, pupillary heights were equal, and facial symmetry was present. The right infraorbital paresthesia was tentatively attributed to direct nerve damage at the infraorbital foramen; a neurosurgical consultation was suggested. The patient returned to the neurosurgeon who had initially evaluated him in the emergency department. Immediately on seeing the patient’s head tilt when entering the examination room, a fourth cranial nerve palsy of the left eye was diagnosed. The patient was then referred to a neuro-ophthalmologist,who confirmed the presence of a contralateral fourth cranial nerve palsy following a coup-contre-coup closed head injury. He suggested that a good chance of recovery existed within 3 months of the accident, and recommended strabismus surgery only if there was no improvement in 1 year. One year after the accident, the patient continues to have diplopia; however, he refuses surgery because his ability to function with the double vision has improved.
Discussion
* Attending Oral and Maxillofacial Surgeon, Nassau County Medical Center, East Meadow. NY; in private practice, Rockville Centre. New York. Address correspondence and reprint requests to Dr Rubin: South Shore Oral Surgery Associates. PC, Maple Medical Center, 24 Maple Ave, Rockville Centre. NY 11570.
Lethargy and physical signs suggesting an orbital blowout fracture may combine to delay the diagnosis of fourth nerve palsy. An oblique frontal blow has been suggested as a common cause of contralateral trochlear nerve trauma. The resultant findings can mimic a blowout fracture of the contralateral orbit.4 The ocular motility pattern, including the results of forced-duction
0 1992 American Association of Oral and Maxillofacial Surgeons 0278-2391/92/5011-0020$3.00/O
1238
1239
GRAY, MILLER, AND LOF-TUS
testing, must be consistent with the radiographic findings of a blowout fracture before repair is undertaken for the relief of diplopia.3 If the diplopia is due to an isolated extraocular muscle or cranial nerve palsy, the patient should be evaluated without orbital surgery (assuming the fracture is not markedly displaced). Under such circumstances, the diplopia is very likely to resolve spontaneously. However, if it persists, strabismus surgery can be performed at a later date. ’ Treatments for fourth nerve palsy have been classified according to increasing degree of intervention. The first modality involves supervised medical observation, and the second consists of ocular occlusion to eliminate one of the images. Sometimes a patch is used, but most often translucent tape is placed over the entire lens of one eye, or over the lower segment if the patient complains of diplopia only in downward and near gaze. The use of vertical prisms improves some patients. If diplopia persists, surgical correction involves weakening the antagonistic muscle in the eye that has the superior oblique involvement, ie, the ipsilateral inferior oblique muscle. Weakening can be accomplished by recessing the muscle 10 mm on the globe, along its direction of action.5 Tucking of the paretic superior oblique muscle is found to be of less value than inferior oblique and vertical rectus muscle surgery.6 The surgery should be deferred for 1 year to allow for possible further recovery or even adequate adaptation that may
occur during that interval.6 Although some studies of untreated unilateral posttraumatic fourth nerve palsy indicate that the condition is usually permanent,2,5 others report that spontaneous improvement generally occurs. ’ The case presented here suggests some caution in interpreting the “typical signs” of a blowout fracture. Even when a blowout fracture is confirmed, the possibility that vertical diplopia may be the result of an associated fourth nerve palsy should be considered. If the motility pattern is more compatible with paretic than restrictive strabismus, orbital exploration is not recommended.4
References 1. Wojno TH: The incidence of extraocular muscle and cranial nerve palsy in orbital floor blowout fractures. Ophthalmology 94682, 1987 2. Burger LJ, Kalvin NH, Smith JC: Acquired lesions of the fourth cranial nerve. Brain 93:567, 1970 3. Ruttum MS, Harris GT: Orbital blowout fracture with ipsilateral fourth nerve palsy. Am J Ophthalmol 100:343, 1985 4. Keane JR: Fourth nerve palsy opposite a black eye. J Clin Neuro Ophthalmol 1:209, 198 I 5. Younge BR, Sutula F: Analysis of trochlear nerve palsies. Diagnosis, etiology and treatment. Mayo Clin Proc 52: 11, 1977 6. Kawam E, Scott AB, Jampolsky A: Acquired superior oblique palsy, diagnosis and management. Arch Ophthalmol 77:76, 1967
Oral MaxlllofaC Surg 50:1239-1242,1992
J
Benign Fibrous Histiocytoma of the Oral/Perioral Regions: Report of a Case and Review of I7 Additional Cases PETER B. GRAY, DMD,* ARTHUR S. MILLER, DMD,t AND MICHAEL J. LOFTUS, DDS*
* Chief Resident, Department of Oral and Maxillofacial Surgery, Hahnemann University Hospital, Philadelphia, PA. 7 Department Chairman, Oral Pathology Section, Temple University School of Medicine, Philadelphia, PA. # Acting Chairman, Department of Oral and MaxilJofacial Surgery, Hahnemann University Hospital, Philadelphia, PA. Address correspondence and reprint requests to Dr Gray: Department of Oral and Maxillofacial Surgery, Hahnemann University Hospital, Broad & Vine Sts, Philadelphia, PA I9 102. 0 1992 American Association of Oral and Maxillofacial Surgeons 0278-2391/92/501
l-0021$3.00/0
Fibrous histiocytomas are uncommon tumors of the superficial and deep soft tissues that are reported to have a common origin from the tissue histiocyte.’ The neoplastic growth can assume many forms, and this has led to a diversity of applied names.’ This group of lesions has been shown to have a wide spectrum of clinical behaviors, from those with totally benign characteristics to those with malignant features. The latter may demonstrate multiple recurrences and widespread metastases.3“’ Benign fibrous histiocytomas occur most
