Traumatic Oculomotor Nerve Palsy

Oculomotor nerve palsy generally presents with mydriasis, blepharoptosis, and impairment of extraocular muscle movement. The incidence of primary traumatic oculomotor nerve palsy in craniocerebral trauma is approximately 1.2% [1]. The causes of oculomotor nerve palsy are congenital, traumatic, vascular, migrainous, and parainfectious. Especially in children, it is often caused by congenital factors, postnatal trauma, or infections [2]. Previous reports indicated that complete recovery is unusual [3]. Here, we report a case of a child with traumatic oculomotor nerve palsy accompanying an orbitozygomaticomaxillary fracture. To our knowledge, it is the first such case report to appear in a Korean plastic surgery journal and is of note because the patient experienced a near-complete recovery, contrary to the grave prognoses described in previous case reports. An 8-year-old girl was admitted to the hospital after a car accident. The patient had no specific past history. Right periorbital swelling was too severe for the patient to be able to open her right eye, and therefore the pupil size discrepancy was only recognized after four days. The right pupil was dilated up to 5.5 mm, compared with 2.0 mm dilation on the unaffected side. The complete impairment of eye adduction was also noted in the affected eye. However, results of the forced duction test were normal. Thus, her right eyeball was deviated to the inferolateral side in the neutral gaze (right exotropia) (Fig. 1). Complete blepharoptosis remained in the right upper eyelid after the periorbital swelling subsided seven days after the trauma. These findings were consistent with oculomotor nerve palsy. Visual acuity was normal at 20/20. The laboratory data, other aspects of the medical history, and the review of systems were in the normal range. There were also no specific neurological abnormalities except oculomotor nerve palsy. A facial computed tomography scan displayed a right orbitozygomaticomaxillary fracture and a nasal bone fracture, which were so minimal that they were not expected to affect oculomotor nerve function. Magnetic resonance images also revealed no abnormal findings associated with oculomotor nerve palsy. A cerebrospinal fluid test was not performed because there was no leakage of cerebrospinal fluid. One week after the trauma, an operation was performed to address the facial bone fracture. We employed steroid therapy to reduce periorbital swelling and possible endoneurial edema, in order to prevent secondary neuronal damage. Solu-Medrol (1 mg/kg, methylprednisolone) was injected