Loss of Vision Because of Bilateral Lateral Geniculate Body Infarction After Traumatic Brain Injury

PRACTICAL IMPLICATIONS

In patients with TBI, LPG infarction as a consequence of descending transtentorial herniation should be considered as a possible etiology of bilateral blindness.

Case

An 18-year-old female patient with a history of borderline personality disorder was admitted to our hospital after jumping from a fifth storey window. CT revealed traumatic brain injury (TBI) with acute subdural hematoma (SDH) on the left side with 15 mm maximum diameter, consecutive midline shift, compression of the left second ventricle and third and fourth ventricle, and severe to complete bilateral descending transtentorial herniation. No fractures of the skull were noted. CT angiography revealed compression of the left posterior cerebral artery (PCA). In addition, complicated fractures to the left lower leg and both ankles, the sternum, the seventh and eighth right rib, dislocated fractures of the lumbar vertebrae 2 and 3 involving the dura, and nondislocated fractures of several other vertebrae were present. Initially, decompressive hemicraniectomy was performed and the SDH was surgically evacuated. The fractures were surgically treated as appropriate, and the patient was admitted to an intensive care unit. Follow-up CT later on the day of admission and on the following day revealed progressive SDH at the left tentorium cerebelli, measuring 5 and 12 mm in widest diameter respectively, but partial regression of descending transtentorial herniation. Six days after admission, the patient's conscious state improved. In detailed neurologic examination, the patient now revealed complete bilateral loss of vision. A consecutive CT on day 7 showed complete regression of descending transtentorial herniation, regression of the tentorial SDH, but left-sided territorial infarction of the PCA. Because the left-sided territorial PCA infarction could only explain right-sided homonymous hemianopia, we undertook further diagnostic tests.

Ophthalmologic examination excluded vitreous hemorrhage, retinal infarction, retinal fat embolism syndrome, or traumatic retinal detachment, respectively. Brain MRI with targeted optic nerve imaging 3 weeks after initial trauma did not confirm damage to the optic nerves or chiasma because of bony fragments or hematoma secondary to trauma or because of shearing forces inflicted by deceleration (known as traumatic optic neuropathy). However, MRI demonstrated diffuse bilateral subacute infarctions, especially of the uncus, hippocampus, substantia nigra, hypothalamus, and dorsal thalamus with involvement of both lateral geniculate bodies (LGBs), which was more pronounced on the right (Figure). Visually evoked potentials (VEPs) confirmed bilateral deafferentation of the visual pathway. We therefore hypothesized that our patient's blindness was caused by bilateral LGB infarction and thus bilateral deafferentation of the visual pathway. After completion of surgical therapy, we transferred the patient to a rehabilitation facility on day 29 after admission. Six weeks later, the patient's vison did not recover and VEP still demonstrated loss of cortical potentials.

Figure. MRI Findings 21 Days After Admission.

Coronal T2-weighted fluid-attenuated inversion recovery (T2-FLAIR) 3 weeks after initial severe to complete (central) bilateral descending transtentorial herniation reveals subacute infarction of the right (A) lateral geniculate body with strong T2-FLAIR hyperintensity and implied on the left side (B) with slight T2-FLAIR hyperintensity. White arrows indicate the location of lateral geniculate body infarction. Further secondary posttraumatic complication partially depicted bilateral subacute infarction of the uncus, hippocampus, hypothalamus, dorsal thalamus and substantia nigra, subacute infarction of the left posterior cerebral artery vascular territory after initial displacement/occlusion, and small residual left occipital subdural hematoma.

Discussion

Bilateral infarction of the LGB is a rare condition. Some reports on bow tie- or hourglass-shaped visual defects after the lesion exist.¹ However, it has also been described as a cause for complete blindness after watershed infarction in hypotensive patients. Underlying problems were septic shock because of influenza² or gastrointestinal infection,³ anaphylactic shock,⁴ and distributive shock because of pancreatitis.⁵

Descending transtentorial herniation with compression of perforating arteries arising from the top of basilar artery, the circle of Willis or PCA, and direct pressure necrosis are the most likely reason for the diffuse infarction involving LGB on both hemispheres. This unusual posttraumatic lesional pattern must have led to a complete loss of vision in our patient.

In patients with TBI, LPG infarction as a consequence of descending transtentorial herniation should be considered as a possible etiology when patients reveal bilateral loss of vision. Unfortunately, there is no specific therapy available and, judging from the literature available, the likelihood of regaining vision is low.

Appendix. Authors

Study Funding

No targeted funding reported.

Disclosure

The authors report no disclosures relevant to the manuscript. Full disclosure form information provided by the authors is available with the full text of this article at Neurology.org/cp.