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Inferior oblique muscle palsy following maxillectomy for squamous cell carcinoma
Inferior Oblique Muscle Palsy Following Maxillectomy for Squamous Cell Carcinoma Allison A. Jensen, MD,a and Terri L. Young, MDa,b The patient is a 64-year-old male who presented for ophthalmologic consultation after a left maxillectomy and radiation therapy for squamous cell cancer. Immediately following the surgery, the patient noticed vertical and horizontal double vision. He then underwent reconstruction of his left inferior orbital rim with a Medpore implant and repair of left lower eyelid retraction. Ocular motility evaluation revealed a left inferior oblique muscle palsy, with sparing of the inferior rectus muscle function.
CASE REPORT A 64-year-old man with a history of squamous cell cancer of the left maxillary sinus underwent a left maxillectomy and radiation therapy (Figure 1). Immediately following this surgery the patient noted diplopia, and on examination he was found to have exotropia (XT) with a right hypertropia (RHT). He had reconstruction of his left cheek, maxilla, and orbital floor with placement of a Medpore implant (Porex Surgical Inc, College Park, Ga) in his left inferior orbital rim, as well as repair of his left lower eyelid entropion. His postoperative surgical course was complicated by recurrent left orbital cellulitis requiring multiple hospitalizations for intravenous antibiotics. The diplopia persisted after the Medpore implant procedure. Three months post maxillectomy and orbital rim repair the patient sought consultation for his diplopia (Figure 2). His ophthalmic examination revealed a visual acuity of 20/20 OU, with mild myopic astigmatic correction. Near visual acuity was J1⫹ OD and J2⫺ OS with bifocal correction in place. Anisocoria was noted with increased left eye pupillary diameter. The pupils were reactive, the left pupil less so, with no afferent pupillary defect. He had left inferior scleral show and lower eyelid ectropion. He had mild keratopathy from corneal exposure of the left eye. His extraocular motility evaluation in primary gaze revealed 20 PD of RHT and 18 PD of right XT with
From the University of Minnesota Academic Health Center, Departments of Ophthalmologyaand Pediatrics.b Supported in part by an unrestricted grant from Research to Prevent Blindness, Inc, New York, New York. Submitted December 27, 2000. Revisions accepted October 26, 2001. Reprint requests: Terri L. Young, MD, The Children’s Hospital of Philadelphia, Division of Ophthalmology, 34th and Civic Center Boulevard, Philadelphia, PA 19104-4399. J AAPOS 2002;6:51-53. Copyright © 2002 by the American Association for Pediatric Ophthalmology and Strabismus. 1091-8531/2002/$35.00 ⫹ 0 75/1/121325 doi:10.1067/mpa.2002.121325
Journal of AAPOS
preferred left eye fixation. In right gaze the RHT increased to 25 to 30 PD and the XT decreased to 12 PD. In left gaze the RHT decreased to 10 PD and the XT decreased to 9 PD. The RHT increased on right head tilt to 30 PD and decreased on left head tilt to 10 PD. His versions and ductions showed 2 to ⫺3 underaction of the left inferior oblique (IO) muscle with ⫹2 overaction of the left superior oblique (SO) muscle. The right inferior rectus (IR) muscle version testing showed underaction, but improved with normal excursions on duction testing, with normal saccadic velocities. The left IR muscle function was intact, with full excursions in downgaze centrally and laterally. Double Maddox rod testing revealed 15 of left intorsion. The presumptive diagnosis was left IO muscle paralysis with intorsion, left pupillary dilation, and IR muscle sparing consistent with a left partial third nerve palsy. There was concern for mild mechanical restriction of the inferior muscle complex due to post-surgical cicatricial changes in the inferior orbit. The patient elected to have strabismus surgery to eliminate his diplopia. This was delayed for an additional 6 months post orbital rim repair because of recurrent orbital infections. The extraocular motility evaluation was unchanged from his initial presentation. Forced duction testing was normal for the right eye, with mild restriction of elevation for the left eye. The patient underwent left SO muscle tenotomy, bilateral lateral rectus muscle recessions of 4.0 mm, and a right superior rectus muscle recession of 6.0 mm on an adjustable suture. Following minimal adjustment, he denied diplopia. Four months later, he had an intermittent XT of 12 PD and an intermittent right HT of 2 to 3 PD. He had limited abduction bilaterally and limited left eye infraduction (Figure 3). Double Maddox rod testing was negative for torsion. The patient had no complaints of diplopia. A few months after his successful strabismus repair, the patient died from metastases to the pulmonary system. An isolated IO muscle paresis causes a hypotropia of the affected eye with the nonparetic eye fixating, or a hypertropia of the unaffected eye with paretic eye fixation.1 The deviation increases on gaze into the field of action of the involved IO muscle (elevation of the adducted paretic eye) and increases with head tilt on the opposite side of the paretic IO muscle. Consequently patients have a head tilt towards the side of the paretic IO muscle and face turn towards the uninvolved side. This is a rare condition, and several other diagnostic possibilities should be considered February 2002
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Journal of AAPOS Volume 6 Number 1 February 2002
FIG 1. Coronal (A) and sagittal (B) computed axial tomographic scans of the head. Note coronal view demonstrates the IO and IR complex (arrow), and sagittal view shows a large left maxillary sinus defect.
initially. The differential diagnosis of a RHT first includes a right SO muscle palsy with a RHT that increases in left gaze and right head tilt. Secondly, it then includes a right
IR muscle palsy with a RHT that increases in right gaze and left head tilt. Thirdly, it includes a left double elevator palsy with limited elevation in all diagnostic fields of gaze
FIG 2. Preoperative photographs in diagnostic positions of gaze. Note right eye hypertropia and exotropia.
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FIG 3. Postoperative photographs in diagnostic positions of gaze. Note limited abduction bilaterally and improved right eye hypoduction with versions.
including adduction. Finally, it includes superior oblique tendon sheath syndrome of the right eye with limitation of elevation from an adductive position, positive forced duction testing, equal duction and version movements, and usually no SO muscle overaction. As described by Scott et al,2 an inhibitional palsy of the contralateral antagonist IR muscle in an isolated IO muscle palsy results from less innervational requirements of the antagonist (left SO muscle). Consequently, the yolk to the ipsilateral SO muscle (the contralateral right IR muscle) receives less innervation and appears to underact.2 This usually occurs when the paretic eye fixates. Supportive findings of inhibitional palsy of the right IR muscle were limited versions compared to duction testing excursions, normal forced duction testing of the right eye, normal saccadic velocities, and normal post-operative inferior rectus muscle versions. IO muscle palsies are rare. In most cases the etiology is congenital. With oculomotor nerve paralysis, the IO muscle is least likely to be involved.3 Typical clinical findings in oculomotor nerve paralysis of the inferior division are accommodative paralysis of the involved eye with pupillary dilation and IR muscle palsy in addition to IO muscle palsy. The parasympathetic neurons of the oculomotor nerve travel in the nerve with the IO muscle before branching off. This patient’s ocular findings may be ex-
plained by injury to this particular branch of the inferior division of the oculomotor nerve. A contusive insult is also possible and makes this case unusual with respect to the IR muscle sparing, given the proximity and mechanical destructive effects of a maxillectomy, orbital rim reconstruction, and recurrent infection.
DISCUSSION This patient developed a rare partial inferior division third nerve palsy after left maxillectomy to treat squamous cell carcinoma. The IO muscle was greatly affected while the IR muscle was spared. It seems unusual that given their close proximity both muscles were not equally affected, but this may be due to specific involvement of a branch of the oculomotor nerve that travels to the inferior oblique muscle only. References 1. Burian HM, von Norden GK. Binocular vision and ocular motility. St. Louis: Mosby, 1990. p. 381. 2. Scott WE, Sutton VJ, Grayson D. Inhibitional palsy of the inferior rectus in an isolated inferior oblique palsy. Amer Orthop J 1981;31: 91-4. 3. Reese PD, Scott WE. Superior oblique tenotomy in the treatment of isolated inferior oblique paresis. J Pediatr Ophthalmol Strabismus 1987;24:4-9.
CASE REPORT A 64-year-old man with a history of squamous cell cancer of the left maxillary sinus underwent a left maxillectomy and radiation therapy (Figure 1). Immediately following this surgery the patient noted diplopia, and on examination he was found to have exotropia (XT) with a right hypertropia (RHT). He had reconstruction of his left cheek, maxilla, and orbital floor with placement of a Medpore implant (Porex Surgical Inc, College Park, Ga) in his left inferior orbital rim, as well as repair of his left lower eyelid entropion. His postoperative surgical course was complicated by recurrent left orbital cellulitis requiring multiple hospitalizations for intravenous antibiotics. The diplopia persisted after the Medpore implant procedure. Three months post maxillectomy and orbital rim repair the patient sought consultation for his diplopia (Figure 2). His ophthalmic examination revealed a visual acuity of 20/20 OU, with mild myopic astigmatic correction. Near visual acuity was J1⫹ OD and J2⫺ OS with bifocal correction in place. Anisocoria was noted with increased left eye pupillary diameter. The pupils were reactive, the left pupil less so, with no afferent pupillary defect. He had left inferior scleral show and lower eyelid ectropion. He had mild keratopathy from corneal exposure of the left eye. His extraocular motility evaluation in primary gaze revealed 20 PD of RHT and 18 PD of right XT with
From the University of Minnesota Academic Health Center, Departments of Ophthalmologyaand Pediatrics.b Supported in part by an unrestricted grant from Research to Prevent Blindness, Inc, New York, New York. Submitted December 27, 2000. Revisions accepted October 26, 2001. Reprint requests: Terri L. Young, MD, The Children’s Hospital of Philadelphia, Division of Ophthalmology, 34th and Civic Center Boulevard, Philadelphia, PA 19104-4399. J AAPOS 2002;6:51-53. Copyright © 2002 by the American Association for Pediatric Ophthalmology and Strabismus. 1091-8531/2002/$35.00 ⫹ 0 75/1/121325 doi:10.1067/mpa.2002.121325
Journal of AAPOS
preferred left eye fixation. In right gaze the RHT increased to 25 to 30 PD and the XT decreased to 12 PD. In left gaze the RHT decreased to 10 PD and the XT decreased to 9 PD. The RHT increased on right head tilt to 30 PD and decreased on left head tilt to 10 PD. His versions and ductions showed 2 to ⫺3 underaction of the left inferior oblique (IO) muscle with ⫹2 overaction of the left superior oblique (SO) muscle. The right inferior rectus (IR) muscle version testing showed underaction, but improved with normal excursions on duction testing, with normal saccadic velocities. The left IR muscle function was intact, with full excursions in downgaze centrally and laterally. Double Maddox rod testing revealed 15 of left intorsion. The presumptive diagnosis was left IO muscle paralysis with intorsion, left pupillary dilation, and IR muscle sparing consistent with a left partial third nerve palsy. There was concern for mild mechanical restriction of the inferior muscle complex due to post-surgical cicatricial changes in the inferior orbit. The patient elected to have strabismus surgery to eliminate his diplopia. This was delayed for an additional 6 months post orbital rim repair because of recurrent orbital infections. The extraocular motility evaluation was unchanged from his initial presentation. Forced duction testing was normal for the right eye, with mild restriction of elevation for the left eye. The patient underwent left SO muscle tenotomy, bilateral lateral rectus muscle recessions of 4.0 mm, and a right superior rectus muscle recession of 6.0 mm on an adjustable suture. Following minimal adjustment, he denied diplopia. Four months later, he had an intermittent XT of 12 PD and an intermittent right HT of 2 to 3 PD. He had limited abduction bilaterally and limited left eye infraduction (Figure 3). Double Maddox rod testing was negative for torsion. The patient had no complaints of diplopia. A few months after his successful strabismus repair, the patient died from metastases to the pulmonary system. An isolated IO muscle paresis causes a hypotropia of the affected eye with the nonparetic eye fixating, or a hypertropia of the unaffected eye with paretic eye fixation.1 The deviation increases on gaze into the field of action of the involved IO muscle (elevation of the adducted paretic eye) and increases with head tilt on the opposite side of the paretic IO muscle. Consequently patients have a head tilt towards the side of the paretic IO muscle and face turn towards the uninvolved side. This is a rare condition, and several other diagnostic possibilities should be considered February 2002
51
52
Jensen and Young
Journal of AAPOS Volume 6 Number 1 February 2002
FIG 1. Coronal (A) and sagittal (B) computed axial tomographic scans of the head. Note coronal view demonstrates the IO and IR complex (arrow), and sagittal view shows a large left maxillary sinus defect.
initially. The differential diagnosis of a RHT first includes a right SO muscle palsy with a RHT that increases in left gaze and right head tilt. Secondly, it then includes a right
IR muscle palsy with a RHT that increases in right gaze and left head tilt. Thirdly, it includes a left double elevator palsy with limited elevation in all diagnostic fields of gaze
FIG 2. Preoperative photographs in diagnostic positions of gaze. Note right eye hypertropia and exotropia.
Journal of AAPOS Volume 6 Number 1 February 2002
Jensen and Young
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FIG 3. Postoperative photographs in diagnostic positions of gaze. Note limited abduction bilaterally and improved right eye hypoduction with versions.
including adduction. Finally, it includes superior oblique tendon sheath syndrome of the right eye with limitation of elevation from an adductive position, positive forced duction testing, equal duction and version movements, and usually no SO muscle overaction. As described by Scott et al,2 an inhibitional palsy of the contralateral antagonist IR muscle in an isolated IO muscle palsy results from less innervational requirements of the antagonist (left SO muscle). Consequently, the yolk to the ipsilateral SO muscle (the contralateral right IR muscle) receives less innervation and appears to underact.2 This usually occurs when the paretic eye fixates. Supportive findings of inhibitional palsy of the right IR muscle were limited versions compared to duction testing excursions, normal forced duction testing of the right eye, normal saccadic velocities, and normal post-operative inferior rectus muscle versions. IO muscle palsies are rare. In most cases the etiology is congenital. With oculomotor nerve paralysis, the IO muscle is least likely to be involved.3 Typical clinical findings in oculomotor nerve paralysis of the inferior division are accommodative paralysis of the involved eye with pupillary dilation and IR muscle palsy in addition to IO muscle palsy. The parasympathetic neurons of the oculomotor nerve travel in the nerve with the IO muscle before branching off. This patient’s ocular findings may be ex-
plained by injury to this particular branch of the inferior division of the oculomotor nerve. A contusive insult is also possible and makes this case unusual with respect to the IR muscle sparing, given the proximity and mechanical destructive effects of a maxillectomy, orbital rim reconstruction, and recurrent infection.
DISCUSSION This patient developed a rare partial inferior division third nerve palsy after left maxillectomy to treat squamous cell carcinoma. The IO muscle was greatly affected while the IR muscle was spared. It seems unusual that given their close proximity both muscles were not equally affected, but this may be due to specific involvement of a branch of the oculomotor nerve that travels to the inferior oblique muscle only. References 1. Burian HM, von Norden GK. Binocular vision and ocular motility. St. Louis: Mosby, 1990. p. 381. 2. Scott WE, Sutton VJ, Grayson D. Inhibitional palsy of the inferior rectus in an isolated inferior oblique palsy. Amer Orthop J 1981;31: 91-4. 3. Reese PD, Scott WE. Superior oblique tenotomy in the treatment of isolated inferior oblique paresis. J Pediatr Ophthalmol Strabismus 1987;24:4-9.