Head trauma with contralateral traumatic optic neuropathy.

Introduction

Indirect traumatic optic neuropathy occurs in closed head trauma with a reported incidence varying from 0.5 to 5%. The neuropathy is typically seen on the same side as the blunt trauma.[1] We present a case of traumatic optic neuropathy involving the contralateral orbit, with a continuous fracture line running from the side that sustained the trauma to the opposite optic canal.

Comment

A 20-year-old male presented with loss of vision in the left eye seven days after sustaining trauma, to the right forehead, in a road traffic accident (RTA). The patient displayed no signs of any brain injury. On external examination, an abrasion on the right forehead and a right facial palsy, possibly due to direct impact to the right preauricular region, were seen [Figure 1a]. Ocular examination revealed visual acuity of 6/5 in the right eye and no perception of light in the left eye. Subconjunctival hemorrhage in the right eye and an afferent pupillary defect (APD) in the left eye were noted with the absence of any signs of intraocular trauma. The extraocular movements of both the eyes and the Goldman visual field of the right eye were within normal limits [Figure 1b]. There was no sign of trauma to the midfacial region or the left side of the face.

Figure 1a

Right-sided forehead abrasion and facial palsy along with subconjunctival hemorrhage; left eye is diverging

Figure 1b

Normal Goldman visual field of the right eye

Noncontrast computed tomography (NCCT) using a high-resolution algorithm in coronal and sagittal reconstructions revealed a continuous fracture line running obliquely from the right to the left side involving the superomedial margin of the right orbit, along the floor of the anterior cranial fossa to involve the left optic canal with a mildly thickened optic nerve [Figure 2]. Fracture of the left optic canal had no bony spicule protruding into it. There was a mild thickening of the intraorbital part of the left optic nerve. Both globes, extraocular muscles, and right optic nerve were normal. There was also an extension of the fracture line with involvement of the left foramen ovale and foramen spinosum.

Figure 2

A) Axial noncontrast computed tomography (NCCT) scan in bone window showing the fracture line (white arrow heads) extending from the right superomedial orbital margin (white arrow) to the left optic canal (black arrow). B) Coronal noncontrast computed tomography (NCCT) scan showing thickening of the left optic nerve (white arrow). C) Coronal noncontrast computed tomography (NCCT) scan in bone window showing fracture of the superior margin of the left optic canal (white arrow) with associated mucosal thickening of the sphenoid sinus (black arrow); also seen is the fracture of the lateral wall of left pterygoid bone (white arrow head) D) 3d Reconstruction noncontrast computed tomography (NCCT) scan shows the fracture line running obliquely (white arrow heads) from right to left along the floor of the cranial fossa to involve the left optic canal (white arrow) and also the left foramens of ovale and spinosum (black arrow)

Axial noncontrast computed tomography (NCCT) scan in bone window showing the fracture line (white arrow heads) extending from the right superomedial orbital margin (white arrow) to the left optic canal (black arrow)

Coronal noncontrast computed tomography (NCCT) scan showing thickening of the left optic nerve (white arrow)

Coronal noncontrast computed tomography (NCCT) scan in bone window showing fracture of the superior margin of the left optic canal (white arrow) with associated mucosal thickening of the sphenoid sinus (black arrow); also seen is the fracture of the lateral wall of left pterygoid bone (white arrow head)

3d Reconstruction noncontrast computed tomography (NCCT) scan shows the fracture line running obliquely (white arrow heads) from right to left along the floor of the cranial fossa to involve the left optic canal (white arrow) and also the left foramens of ovale and spinosum (black arrow)

Considering the late presentation at our center, no further treatment was offered to the patient.[23] At the follow-up after a month, the patient started developing disc pallor and after a period of three months, he had total optic atrophy and continued to have no light perception vision in the left eye.

The human orbit has multiple weak areas vulnerable to fracture. Fractures of such ’eggshell areas’ of anterior cranial fossa maybe produced by trivial injuries[4] as in our case. Conventionally, head trauma results in ipsilateral indirect traumatic optic neuropathy due to the unique arrangement and shape of the orbital bones. Holographic interferometric analysis of the human skull demonstrates that structural strain induced by frontal loading results in deformation of the ipsilateral orbital roof near the optic foramen.[5] Right orbital trauma is indicated by the presence of subconjunctival hemorrhage, facial palsy, and forehead abrasion on the right side The presence of a fracture line involving the right orbital margins and the right anterior cranial fossa confirm this. Unexpectedly, this fracture line continued to run through the opposite optic canal resulting in left optic neuropathy, sparing the right optic nerve, with the result that the patient maintained normal visual acuity and a normal visual field in the right eye. This case illustrates the possibility of traumatic optic neuropathy in one eye following trauma to the opposite side of the head and also highlights the requirement of a detailed examination of both eyes in all cases of trauma.