Journal of Emergencies, Trauma, and Shock

: 2019  |  Volume : 12  |  Issue : 3  |  Page : 222--224

Bilateral abducens nerve palsy after closed head trauma without acute intracranial pathology

Farris Serio, Jonathon Choi, Andrew Mccague 
 Natividad Medical Center, Salinas, CA, USA

Correspondence Address:
Dr. Andrew Mccague
Natividad Medical Center, 1441 Constitution Blvd, Salinas, CA 93906


Bilateral abducens nerve palsy due to closed head trauma is exceedingly rare. We present the case of a 51-year-old woman with posttraumatic bilateral abducens nerve palsy and persistent deficits at 1-year follow-up. This case demonstrates a rare example of cranial nerve palsy in the setting of a closed head injury without intracranial pathology.

How to cite this article:
Serio F, Choi J, Mccague A. Bilateral abducens nerve palsy after closed head trauma without acute intracranial pathology.J Emerg Trauma Shock 2019;12:222-224

How to cite this URL:
Serio F, Choi J, Mccague A. Bilateral abducens nerve palsy after closed head trauma without acute intracranial pathology. J Emerg Trauma Shock [serial online] 2019 [cited 2021 Mar 3 ];12:222-224
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Full Text


Motor vehicle accidents account for millions of injuries annually, but only a small fraction of these traumas result in cranial nerve (CN) palsies. Of these palsies, abducens nerve palsy is reported in only 0.3%–2% of cases.[1] Most of these cases have been attributed to an intracranial mass effect or fracture.[2] This case demonstrates a rare example of bilateral abducens palsy without evidence of an acute intracranial lesion or intracranial fracture.

 Case Report

We present the case of a 51-year-old woman who was transferred to our trauma center from a local hospital following a single car motor vehicle accident. Glasgow Coma Scale score was 15. She was found to have a Type 3 odontoid fracture on computed tomography (CT) C-spine [Figure 1]. She was also found to have a small chin laceration with bilateral lateral gaze. Additional workup included CT angiogram of her neck which was negative for cerebrovascular injuries. CT head was negative. CT chest showed mild bilateral pulmonary contusions. CT abdomen and pelvis was negative. No other evidence of a head injury was revealed, and neck stability was maintained by a soft C-Collar. Toxicology screen was negative and the only abnormality on initial labs was a leukocytosis of 16,800 white blood cells per microliter.{Figure 1}

The patient's medical history, allergies, medications, family history, and social history were noncontributory.

She was seen by a neurosurgeon at the outside hospital who recommended transfer to our trauma center.

On arrival to our facility, assessment revealed persistent bilateral abducens palsy. Magnetic resonance imaging and magnetic resonance angiography were negative for vascular injury.

She was admitted to the trauma service where she worked with physical therapy and occupational therapy, her pain was controlled, and she was given a regular diet. She was given follow-up instructions to refer neurosurgery, ophthalmology, ENT, and trauma clinics.

Her postdischarge course was uncomplicated. At the 1-month follow-up in the trauma clinic, she had visited ENT, ophthalmology, and neurosurgery clinics where conservative management was instituted. At 3-month follow-up, her cervical fracture had healed, and her bilateral lateral gaze palsy had resolved [Figure 2].{Figure 2}


Bilateral abducens nerve palsies are an exceedingly rare sequelae of closed head trauma. Within the last 50 years, there have been fewer than thirty articles published on this subject and of those reports, many were attributed to intracranial pathology causing increased pressures or to cranial fractures.[3] However, in our patient, there was no intracranial pathology that might explain her deficits.

The abducens nerve takes a long trajectory to reach the lateral rectus muscles. From its nucleus in the pons, it courses along the posterior aspect of the clivus before tracking through the superior orbital fissure to the lateral rectus muscle.[4] Because of this indirect route and the many angulations along this course, it is vulnerable to traction forces.[4]

Injuries to CN VI present as deficits in lateral gaze. These deficits must be differentiated between central deficits, nerve fiber deficits, and muscular deficits.[2] In our patient, there was no evidence of intracranial pathology on imaging and her physical examination was benign, suggesting that her deficits were not the result of a central lesion. Additionally, there was no evidence of muscular entrapment or avulsion that might have caused motor unit deficits, making CN VI the most likely site of her lesion.

While there have been reports of hematomas or other expanding mass lesions causing CN VI palsy, the lack of intracranial pathology in our patient suggests that her deficits were due directly to the mechanism of her trauma.[2] Additionally, the Type 3 odontoid fracture that she suffered suggests either a shearing or distractive mechanism of injury.[5] These findings, coupled with her physical symptoms, suggest damage to the bilateral abducens nerves by tractional forces.

Prognosis for this condition is highly variable, with spontaneous resolution reported in 12%–73% of unilateral CN VI palsies, with an average time to recovery of 90 days.[6] Yanamadala et al. suggest that a full recovery occurs in a majority of traumatic abducens nerve palsies; however, complete palsy and bilateral palsy are predictors of poor prognosis.[2] Both factors were present in our patient and at 1-year follow-up, her palsy was persistent.

Management of this condition is variable, with acute management consisting of patching one eye to alleviate the symptoms of strabismus and chronic management involving botulinum toxin injection of the antagonizing medial rectus muscle during the recovery period.[7],[8] In addition, there is conflicting evidence in the literature on the efficacy of treatment with botulinum versus watchful waiting.[8] Our patient was referred to a tertiary center for the management of her lateral gaze deficit, but there were no records to indicate that she received treatment at that facility or that any treatment more than the initial patching was prescribed. She eventually improved with conservative management.


This case highlights the potential for serious but rare sequelae after closed head trauma, even without intracranial pathology on imaging. Based on our patient's injuries, any tractioning of CN VI along its course within the head might have resulted in the observed deficits. Furthermore, her persistent deficits at 1 year agree with the observation that bilateral palsy may be associated with worse prognosis.[2]

Declaration of patient consent

The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.

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Conflicts of interest

There are no conflicts of interest.


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