Cranial nerve (CN) injury after traumatic brain injury (TBI) is well described in the literature, with abducens palsy rates as high as 2.7% (1). Cranial nerve injury is more frequently associated with significant injuries, such as skull fracture and intracranial hemorrhage (1–6). The CN palsies after mild TBI and concussion, however, are much rarer. A large retrospective study of 19,800 patients with presenting Glasgow Coma Scores (GCS) of 14 to 15 found a CN incidence of 0.3% (7). The most commonly affected cranial nerves were olfactory (II) and facial (VII) followed by abducens (VI). Of the oculomotor nerves, CN VI was the most commonly injured. When combined, the three oculomotor nerves (III, IV, VI) were the most frequently injured among all cranial nerves.
This study describes a child with delayed onset abducens palsy after a concussion with normal imaging findings and spontaneous recovery.
An 11-yr-old previously healthy male presents to the concussion clinic 12 d after a bike injury with a chief complaint of double vision. He fell forward over the handlebars hitting his head on concrete. He was not wearing a helmet and had no loss of consciousness. He was evaluated in the emergency department where he underwent laceration repair with staples, and he was diagnosed with a concussion. His initial symptoms included headache, vomiting, and sleeping more than usual. He returned to ED on postinjury day 4 because of increased headaches and vomiting, and he had a negative computed tomography (CT) scan of the head. Approximately 9 d after his injury, he developed diplopia and his parents noticed his eyes were “crossing” more. Headaches and vomiting resolved on postinjury day 10 and did not return. At the time of his initial evaluation in the concussion clinic, his only symptoms were diplopia and fatigue.
He endorses a history of color blindness. He denies history of concussion, mood disorders, strabismus, amblyopia, or eye surgery. There is a strong family history of strabismus and eye surgery.
Physical examination was notable for palsy of left cranial nerve VI on extraocular movement testing with normal resting gaze. Testing of smooth pursuits, saccades, and gaze stability did not provoke symptoms. Diplopia and left eye lateral gaze deficit persisted throughout testing, but this was variable. He was able to cross midline intermittently (Figs. 1–4). Near point of convergence was 4 cm, and accommodation was 7 cm bilaterally. Neither provoked symptoms. Finger to nose testing was fast but inaccurate. Balance testing revealed difficulty with tandem walk backwards with eyes open and closed. He had been seen by ophthalmology earlier in the day who noted bilateral papilledema. Vital signs were normal. He had a 1.5-cm healing laceration to the posterior scalp as well as healing abrasions to his extremities. He was referred for expedited magnetic resonance imaging (MRI) and neurology referral. Treatment recommendations were eye patching for symptom relief as well as to advance back to cognitive activities as tolerated based on symptoms over the following several days. He was out of school for summer break. He was advised to avoid contact sports until cleared.
His MRI was normal and neurology evaluation on postinjury day 15 revealed interval resolution of his papilledema and 20/20 vision bilaterally. Repeat evaluation in the concussion clinic 4 wk after his injury demonstrated improvement in his oculomotor movements, but still with a partial left CN VI palsy. His only symptom at that time was intermittent diplopia. His other oculomotor and balance testing had returned to normal. He was prescribed a home oculomotor rehabilitation program at that time.
He was thereafter lost to follow-up clinically, but his mother called with an update at 7 wk and reported diplopia and crossed eyes had both completely resolved. He continues to do well as per his mother 2 yr after his injury. He has returned to sports, but he and his family have chosen to avoid contact sports to reduce his concussion risk.
Cranial nerve palsy after mild head injury is not a common encounter in the outpatient setting. Patients with CN injury typically require advanced imaging to determine the etiology of the neurologic deficit. Acute abducens palsy can be due to injury to the CN VI nucleus in the brainstem, injury along the course of the nerve, or nonlocalizing injury to the nerve from elevated intracranial pressure. Brainstem injury typically presents with other cranial nerve deficits. Localized injury to the abducens nerve may be suggested by the mechanism of injury and signs of trauma. Nonlocalizing abducens palsy from increased intracranial pressure is uniformly accompanied by headache and usually by papilledema as seen in this case. The differential diagnosis for posttraumatic CN palsy includes orbital fracture with muscular entrapment, intracranial mass or hemorrhage, peripheral nerve injury secondary to basilar skull or cervical fracture, and diffuse axonal injury within the brainstem. In this case, CT and MRI after his injury did not provide any structural etiology for his abducens palsy, and his clinical findings and symptom set were fairly benign other than diplopia. Papilledema and presumed increased intracranial pressure may have contributed to this patient’s CN injury, though this remains unexplained due to normal imaging.
The abducens nerve is particularly vulnerable to injury due to its long and angulated intracranial course. The most commonly accepted mechanism of injury theory is downward displacement of the abducens nerve within Dorello’s canal in the subarachnoid space with contusion against the petrous ridge (8). Fractures, hemorrhage, and other space-occupying lesions have been implicated in CN VI injury as well (1,3–6). One proposed theory in children is physeal fracture of the unfused spheno-occipital synchondrosis, which is the pediatric analogue to fracture of the clivus, a well-documented cause of CN VI palsy (9).
Delayed onset is seen in 42% of cases of traumatic abducens palsy (10). To our knowledge, the 9-d delay seen in this patient is the longest delay to onset of abducens palsy described in the literature. Vascular disruption due to ischemia or vasospasm may explain this delay, though etiology of delayed CN paresis remains largely unclear (3).
Spontaneous recovery with conservative treatment is common, with complete recovery rates ranging from 57% to 73% in recent large studies (10,11). Higher recovery rates were seen in those with unilateral palsy, partial palsies, and in men; all of which were present in this particular patient (11,12). One study found a median of 90 d to complete recovery with a range of 22 to 280 d, though patients in this study were not followed beyond 6 months (11). Injection of botulinum toxin into the ipsilateral lateral rectus is a treatment option for those with prolonged recovery, though the efficacy of this procedure is in question (12).
There are no evidence-based guidelines on return to sport after traumatic cranial nerve palsy, and return to contact sports should be determined on an individual basis. Consensus-based guidelines on return to sport after concussion may be applicable to some cases.
Cranial nerve palsy is rare in concussion patients, and delayed presentation is not uncommon. Recovery is spontaneous in most with a median recovery time of 90 d. This patient’s delayed abducens palsy at 9 d is the longest delay found in the literature. He was not found to have a structural cause of his injury, and he reportedly recovered in 5 wk. This case highlights the importance of full neuroophthalmological evaluation in the case of diplopia after a head injury.
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