Self-inflicted Blindness and Brown-Séquard Syndrome

Abstract

A 30-year-old paranoid schizophrenic man suffered a psychotic episode while flying on an airplane, locked himself in the bathroom, detached the temples of his sunglasses, and stabbed them deeply into both medial orbits. He then secured one temple into the door hinge and rammed the back of his neck repeatedly against it. The injuries caused no light perception from optic nerve trauma and a Brown-Séquard hemitransection of the spinal cord.

A 30-year-old Canadian man had a paranoid psychotic episode while flying from Canada to Melbourne, Australia. He became convinced that the cabin staff was plotting to kill him and decided to commit suicide. While locked in the airplane's bathroom, he removed the temples of his sunglasses, stabbed them deeply into both medial orbits and then jammed one of the temples into the hinge of the restroom door. He proceeded to hit the back of his neck against the temple, piercing his spine, and fell to the ground, partially paralyzed.

On presentation to our medical facility, he complained of blindness and left-sided weakness. Examination revealed no light perception in both eyes with dilated, nonreactive pupils. There were bilateral periocular hematomas, puncture wounds at both caruncles and a small right medial conjunctival laceration. Extraocular movements were intact on the left but a complete ophthalmoplegia was present on the right. Examination of the fundi was unremarkable. Neurological testing revealed a left hemiparesis and ipsilateral loss of vibration and position sense. On the right side of his body, caudal to the fourth cervical spinal segment (C-4), he had reduced temperature and pain sensation [spinothalamic fibers cross the spinal cord approximately two spinal levels above their point of entry (¹)]. These findings were consistent with a Brown-Séquard (spinal cord hemitransection) syndrome at C-2.

A cervical x-ray demonstrated the arm of the sunglasses extending into his spinal canal between the first and second cervical spinous processes (Fig. 1). The patient was taken to the operating room for exploration of the wounds. The temple was removed and intravenous methylprednisolone was administered for 48 hours. Magnetic resonance imaging (MRI) confirmed direct injury to both optic nerves at the orbital apices (Fig. 2) and to the cervical spinal cord (Figs. 3, 4). Visually evoked potentials (VEPs) were absent for the OD and poorly developed for the left.

FIG. 1.: Plain cervical spine x-ray shows C4 level penetration of the temple of the patient's glasses.

FIG. 2.: Axial T2 orbital MRI shows orbital fat herniated through medial canthal puncture wounds (arrows) and mixed signal and contour deformity at the orbital apices consistent with contusion of the optic nerves and surrounding soft tissues.

FIG. 3.: Sagittal T2 MRI shows high signal of reactive edema around the penetrating injury in the spinal cord (arrow). There is soft tissue edema in the suboccipital path of the wound.

FIG. 4.: Axial T2 MRI at the C1–2 level shows a band of low signal extending through the spinal cord (arrow) consistent with the fresh hemorrhage of a penetrating injury.

Three months later, his vision had improved to hand movements on the left but he remained at hand movements on the right. He now had a full range of extraocular movements bilaterally. His right pupil was nonreactive to light and the left showed a sluggish response. Funduscopic examination demonstrated bilateral optic disc pallor. VEPs confirmed some minor improvement in responses for the OS but responses from the right were still very depressed. There was moderate neurologic recovery from his spinal cord injury so that he was able to walk with a walking frame. Six months after returning to Canada, during a period of noncompliance with antipsychotic medication, he committed suicide by hanging himself.

This case is extraordinary for the devastating injuries inflicted with what would normally be considered an innocuous instrument—a pair of sunglasses. It is, we believe, the first documented case of a combination of self-inflicted bilateral optic nerve damage and Brown-Séquard syndrome.

Brown-Séquard syndrome is named after Charles-Edouard Brown-Séquard (1817–1894), a French physician who worked on both sides of the Atlantic—in New York, Richmond, Boston, and Geneva. He contributed to many fields of medicine, most notably to our understanding of spinal pathway anatomy and physiology. A founding physician at the National Hospital for Nervous Diseases, Queen's Square, London (²), he later succeeded Claude Bernard in the chair of experimental medicine at the Collège de France in Paris.

The features of Brown-Séquard syndrome, or hemitransection of the spinal cord, are most often caused by trauma or neoplasm (³). In most cases, the hemitransection is partial and not all the signs are found. Additional signs not seen in our case include an ipsilateral lower motor neuron paralysis resulting from destruction of the anterior gray column or nerve root, and a band of cutaneous anesthesia resulting from destruction of the posterior root of the spinal nerve at the level of the lesion.

Injury to the optic nerves may have occurred by several mechanisms. Direct trauma to both optic nerves resulting in ischemic neuropathy from disruption of the pial vessels supplying them is the most likely. A subperiosteal hematoma can compress the optic nerve at the canal but was not seen in the MRI (⁴). An intraconal hematoma or edema could have directly compressed the optic nerve, third, fourth, and sixth cranial nerves and would be the likely cause of the neurapraxia leading to the temporary complete right ophthalmoplegia.