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Updated: Mar 17, 2026
A Piglet Model of Neonatal Hypoxic-Ischemic Encephalopathy
Published on: May 16, 2015
Anoxic Brain Injury Secondary to Metabolic Encephalopathy
Lyndsey M Ferris1, Carla Engelke
1*OD, FAAO United States Air Force, Wilford Hall Ambulatory Surgical Center, Joint Base San Antonio-Lackland, Texas (LMF); Southern Arizona Veteran's Affairs Health Care System, Tucson, Arizona (CE); and Southern California College of Optometry at Marshal B. Ketchum University, Fullerton, California (CE).
Purpose:
To discuss the clinical case of a patient suffering visual dysfunction secondary to a metabolic brain injury, the patient's visual rehabilitative treatment, and outcomes.
Case Report:
A 24-year-old Caucasian male presented to the Southern Arizona Veteran's Affairs Healthcare System's Traumatic Brain Injury (TBI) eye clinic for evaluation and treatment of visual dysfunction secondary to an anoxic brain injury suffered 4 months before. Symptoms included persistent right homonymous hemianopia, oculomotor dysfunction, and a visual information processing deficit. After 5 weeks of vision rehabilitation, the patient was reassessed and displayed significant improvement in both signs and symptoms.
Conclusions:
The syndrome of inappropriate secretion of antidiuretic hormone (SIADH) is a metabolic syndrome that causes hyponatremia and, in severe cases, encephalopathy and anoxic brain injury. Damage to the visual pathways can produce visual field, ocular motility, and binocular vision deficits. Comprehensive treatment including rehabilitative vision therapy bolstering the natural neuroplasticity process can provide improvements in patients' quality of life.
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