Case Report
Abducens Nerve Avulsion and Facial Nerve Palsy After Temporal Bone Fracture: A Rare Concomitance of Injuries Tej D. Azad1, Anand Veeravagu1, Carleton Eduardo Corrales2, Kevin K. Chow1, Nancy J. Fischbein3, Odette A. Harris1
Key words Abducens nerve - Cranial nerve avulsion - Cranial nerve palsy - Trauma -
Abbreviations and Acronyms CN: Cranial nerve MRI: Magnetic resonance imaging From the 1Department of Neurosurgery, Stanford University School of Medicine, Stanford, California; 2Department of Otology and Laryngology, Brigham and Women’s Hospital, Harvard Medical School, Boston, Massachusetts; and 3 Department of Radiology, Stanford University School of Medicine, Stanford, California, USA To whom correspondence should be addressed: Tej D. Azad, B.A. [E-mail:
[email protected]] Citation: World Neurosurg. (2016). http://dx.doi.org/10.1016/j.wneu.2015.11.076 Journal homepage: www.WORLDNEUROSURGERY.org Available online: www.sciencedirect.com 1878-8750/$ - see front matter ª 2016 Elsevier Inc. All rights reserved.
- BACKGROUND:
Avulsion of the abducens nerve in the setting of geniculate ganglion injury after temporal bone fracture is unreported previously. We discuss clinical assessment and management of a patient with traumatic avulsion of cranial nerve (CN) VI in the setting of an ipsilateral CN VII injury after temporal bone fracture and call attention to this unusual injury.
- CASE
DESCRIPTION: A 26-year-old man suffered a temporal bone fracture after a motor vehicle accident and developed diplopia and right-sided facial droop. Six weeks after the accident, the patient was readmitted with worsening diplopia and ipsilateral facial weakness. He demonstrated absent lateral gaze on the right suggestive of either restrictive movement or right.
- CN
VI DEFICIT: In addition, he had right-sided facial palsy graded as 6/6 HouseBrackmann. High-resolution computed tomography demonstrated a right-sided longitudinal otic capsule-sparing temporal bone fracture that propagated into the facial nerve canal and geniculate fossa. Magnetic resonance imaging revealed discontinuity of the right CN VI between the pons and the Dorello canal, as well as injury to the ipsilateral geniculate ganglion. CN VII was intact proximally, from the pons through the internal auditory canal. Consensus was reached to proceed with conservative management. At 13 months after injury, the patient reported 1/6 House-Brackmann with no improvement in CN VI function.
- CONCLUSIONS:
BACKGROUND The abducens nerve traverses a lengthy intracranial course from the brain stem, near the ventral midline at the junction of the pons and medulla, to the ocular surface of the lateral rectus muscle. The long span of cranial nerve (CN) VI makes it vulnerable to injury from skull base fractures and increased intracranial pressure.1 Although there are previous reports of abducens nerve palsies in the setting of temporal bone fracture2,3 as well as co-occurring injury of CN VI and VII,4 complete disruption of the somatic efferents of the abducens nerve caused by an avulsive injury has not been documented previously. We report here a case of traumatic avulsion of CN VI in the setting of CN VII palsy after temporal bone fracture, a novel constellation of injuries. Awareness of the potential for CN avulsion can be used to guide clinical evaluation and management of patients with this unusual injury after temporal bone fracture.
This case illustrates 2 subtle findings on imaging with potential therapeutic implications, notably the role of surgical intervention for facial nerve palsy.
CASE REPORT Patient History The patient was a 26-year-old man seen in the emergency department with complaint of severe headache, binocular diplopia, and right facial weakness, all which had progressively worsened after a motor vehicle accident 6 weeks earlier. In the accident, the patient sustained multiple injuries, including pneumocephalus attributable to right temporal bone fracture, intraventricular hemorrhage, left pneumothorax, right tibia and fibula fracture status post open reduction internal fixation, left rib fracture, and multiple facial fractures. No surgical intervention had been performed.
followed commands, and did not demonstrate dysarthria or aphasia. Facial sensation was intact to light touch in V1, V2, and V3 and tongue was midline. Findings of the ophthalmologic examination were notable for right esotropia and complete CN VI palsy (absent abduction), providing the basis for absent lateral gaze with right eye (Figure 1). Examination further revealed right paralytic lagophthalmos (5 mm) secondary to the CN VII palsy, which was graded as 6/6 House-Brackmann (Figure 2). Anisocoria also was noted, although no evidence of relative afferent pupil defect or CN III palsy was observed. The remainder of the neurologic and physical examination was unremarkable.
Clinical Assessment Patient was Glasgow Coma Scale 15, alert and oriented, demonstrated normal motor and sensory examination of the extremities,
Imaging High-resolution computed tomography of the head was remarkable for an otic-capsule
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CASE REPORT TEJ D. AZAD ET AL.
ABDUCENS NERVE AVULSION, FN PALSY AFTER FRACTURE
Figure 1. Lack of lateral gaze in right eye attributable to cranial nerve VI injury.
sparing longitudinal fracture of the right temporal bone involving the mastoid air cells and anterior bony wall of the external auditory canal. In addition, the fracture line propagated into the fallopian canal, and there was evidence of an enlarged and disrupted right geniculate fossa compared with the left side (Figure 3). Magnetic resonance imaging (MRI) of the brain with and without contrast was ordered to further evaluate the cause of his deficits. MRI showed an asymmetrically prominent and enhancing right geniculate ganglion (Figure 4), but CN VII was intact proximally from the brainstem through the fundus of the internal auditory canal. MRI also revealed discontinuity of right CN VI between the pons and the Dorello canal (Figure 5). This finding was concerning for a traumatic nerve avulsion. In support of the injury to CN VI was the presence of denervation
Figure 2. The patient has lost the nasolabial fold, and he is unable to elevate the corner of his mouth as the result of injury to the buccal and marginal mandibular branches of the facial nerve.
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Figure 3. High-resolution computed tomography of the right ear (left) shows an enlarged geniculate fossa (arrow) compared with the left geniculate fossa (arrow on right).
atrophy involving the right lateral rectus muscle compared with the left. Management and Resolution MRI demonstrated no acute intracranial pathology; thus, no neurosurgical intervention was indicated nor undertaken. Follow-up was coordinated in conjunction with the otolaryngology and ophthalmology services regarding management of CN VI and VII palsies. Consensus was reached to proceed with conservative management. At 10 weeks after his motor
vehicle accident, the patient was able to move his upper lip, consistent with recovering CN VII function. The patient recovered facial nerve function to a 2/6 House-Brackmann at 14 weeks postaccident, consistent with ongoing resolution of swelling, edema, and possibly hemorrhage. No improvement of CN VI palsy has been observed at the 13-month follow up, as would be expected in the setting of a complete avulsion. CN VII function has recovered completely. Nerve conduction testing was considered but
Figure 4. Magnetic resonance imaging shows an enlarged, enhancing geniculate ganglion on the right compared to the left (arrows).
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CASE REPORT TEJ D. AZAD ET AL.
ABDUCENS NERVE AVULSION, FN PALSY AFTER FRACTURE
alleviate the symptoms of diplopia. Fresnel prism goggles can realign images in diplopic vision after CN VI injury and aid in rehabilitation. Another therapeutic option is botulinum injection to weaken the medial rectus. If resolution is not observed, strabismus surgery can be considered.6 When a motor nerve such as CN VI is injured, then assessment of imaging studies for denervation change can be helpful in determining whether function is likely to be regained or not.7
Figure 5. Oblique parasagittal reformations from a heavily T2-weighted image (fast imaging employing steady-state acquisition sequence) along the course of cranial nerve VI. The left abducens nerve (A) is normal while the right abducens nerve (B) is absent, consistent with its being avulsed. The arrows for both panel A and B identify the abducens nerve. However in B, the nerve is absent.
ultimately avoided because of the loss of the patient’s insurance coverage during the follow up period—thus, clinical observation and evaluation comprised the patient’s follow up.
DISCUSSION Pathogenesis Our patient’s CN VI palsy resulted from injury to the nerve along its course from the brainstem to the lateral rectus. CN VI exits the brainstem at the pontomedullary junction, where it is closely associated with CN VII. The nerve ascends through the subarachnoid space, penetrates the dura, courses vertically along the ridge of the petrous bone, and traverses the petrous apex, where it changes direction 120 forward. Here, CN VI passes beneath the petroclinoidal ligament and through the Dorello canal. Finally, the nerve passes through the sinus cavernous lateral to the internal carotid artery, enters the orbit via the superior orbital fissure, and innervates the lateral rectus. Our imaging results indicate that the avulsive injury in this patient occurred between the pons and the Dorello canal.
Diagnosis and Evaluation Patients with CN VI palsy present with binocular horizontal diplopia exacerbated by gaze in the direction of the paretic lateral rectus muscle. Strabismus is nearly always present. Examination will reveal primary position esotropia with an ipsilateral abduction deficit. Often, the patient may angle his or her face toward the affected side to maintain binocularity and minimize diplopia. As illustrated in this case report, CN VI palsy is likely to present with additional injury intracranially or to the cervical spine. A comprehensive neurologic examination is requisite to identify all possible injuries. Important considerations are basilar skull fracture, intracranial hemorrhage, peripheral nerve injury, orbital wall fracture, and entrapment or injury to the medial rectus muscle.5 Appropriate imaging can be used to support clinical findings in evaluation of additional injuries. Management of CN VI Injury Management of CN injury is mostly symptomatic. For CN VI injury, occlusion of an eye with an eye pad may be useful to
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Prognosis Traumatic CN VI injury, typically caused by a stretching or compressive injury, has a spontaneous recovery rate of 84%, with average improvement 3 months after injury.8 Predictors of poor outcomes (no recovery) are complete palsy and bilateral palsy.9 At 13 months after our patient’s initial presentation, it seems unlikely that our patient will regain function of CN VI, consistent with our clinical and radiographic determination of an avulsive injury. CONCLUSIONS CN injuries can be subtle on highresolution computed tomography and MRI. This case illustrates how imaging findings can supplement careful clinical evaluation of a CN VI avulsion. Complete neurologic and ophthalmologic examination in conjunction with analysis of available neuroimaging studies was necessary to arrive at the optimal therapeutic regimen for this patient. REFERENCES 1. Antoniades K, Karakasis D, Taskos N. Abducent nerve palsy following transverse fracture of the middle cranial fossa. J Craniomaxillofac Surg. 1993;21: 172-175. 2. Ghorayeb BY, Yeakley JW, Hall JW 3rd, Jones BE. Unusual complications of temporal bone fractures. Arch Otolaryngol Head Neck Surg. 1987;113:749-753. 3. Ulug T, Ulubil SA. Bilateral traumatic facial paralysis associated with unilateral abducens palsy: a case report. J Laryngol Otol. 2005;119:144-147. 4. Chen J, Zhang D, Hou LJ. Dorsum sellae and bilateral temporal bone fracture associated with bilateral abducens and facial nerve palsy: letter to the editor. Acta Neurochir (Wien). 2015;157:1493-1494. 5. Advani RM, Baumann MR. Bilateral sixth nerve palsy after head trauma. Ann Emerg Med. 2003;41: 27-31.
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6. Azarmina M, Azarmina H. The six syndromes of the sixth cranial nerve. J Ophthalmic Vis Res. 2013;8: 160-171. 7. Kato K, Tomura N, Takahashi S, Watarai J. Motor denervation of tumors of the head and neck: changes in MR appearance. Magn Reson Med Sci. 2002;1:157-164. 8. Holmes JM, Droste PJ, Beck RW. The natural history of acute traumatic sixth nerve palsy or paresis. J AAPOS. 1998;2:265-268.
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9. Holmes JM, Beck RW, Kip KE, Droste PJ, Leske DA. Pediatric Eye Disease Investigator G. Predictors of nonrecovery in acute traumatic sixth nerve palsy and paresis. Ophthalmology. 2001;108: 1457-1460.
Received 16 September 2015; accepted 20 November 2015 Citation: World Neurosurg. (2016). http://dx.doi.org/10.1016/j.wneu.2015.11.076 Journal homepage: www.WORLDNEUROSURGERY.org Available online: www.sciencedirect.com
Conflict of interest statement: The authors declare that the article content was composed in the absence of any commercial or financial relationships that could be construed as a potential conflict of interest.
1878-8750/$ - see front matter ª 2016 Elsevier Inc. All rights reserved.
WORLD NEUROSURGERY, http://dx.doi.org/10.1016/j.wneu.2015.11.076