Alexandre Majoulet1, Isabelle Audo2,3, Cécile Goujard4,5, Mathilde De Menthon4, Fabrice Chaix6, Pierre Safar7, Marc Labetoulle1,5, Antoine Rousseau8,9. 1. Department of Ophthalmology Assistance Publique - Hôpitaux de Paris, Service d'ophtalmologie, Hôpital Bicêtre, 78, Rue du Général Leclerc, 94275, Le Kremlin Bicêtre, France. 2. INSERM, CNRS, Institut de la Vision, Sorbonne Université, 75012, Paris, France. 3. CHNO des Quinze-Vingts, IHU FOReSIGHT, INSERM-DGOS CIC1423, 28 rue de Charenton, 75012, Paris, France. 4. Department of Internal Medicine and Clinical Immunology, Assistance Publique - Hôpitaux de Paris, Bicêtre Hospital, Le Kremlin Bicêtre, France. 5. Paris Saclay University, Le Kremlin Bicêtre, France. 6. Department of Internal Medicine, Centre Hospitalier de Polynésie Française, 98713, Papeete, Tahiti, France. 7. Department of Vision Rehabilitation, Fondation Hospitalière Sainte-Marie, Paris, France. 8. Department of Ophthalmology Assistance Publique - Hôpitaux de Paris, Service d'ophtalmologie, Hôpital Bicêtre, 78, Rue du Général Leclerc, 94275, Le Kremlin Bicêtre, France. antoine.rousseau@aphp.fr. 9. Paris Saclay University, Le Kremlin Bicêtre, France. antoine.rousseau@aphp.fr.
Abstract
PURPOSE: To report a case of typical delayed-onset hypoxic cortical blindness that occurred few days after resuscitation from drowning in a young male. METHODS: Neurological and ophthalmological examination were performed including optical coherence tomography (OCT), Goldmann perimetry, pattern electroretinogram (pERG), pattern and flash visual evoked potentials (pVEP and fVEP) and brain magnetic resonance imaging (MRI). RESULTS: At presentation, at day 12 post-hypoxic incident, best corrected visual acuity (BCVA) was reduced to hand motion OU with an abolished optokinetic nystagmus, a normal fundus and no relative afferent pupillary defect. Macular and peripapillary OCT were normal. Goldmann perimetry revealed bilateral centrocecal scotoma. pERG was normal while pVEPs were undetectable and fVEPs were abnormal with delayed, decreased and disorganized responses, without interhemispheric asymmetry. Brain MRI disclosed a bilateral cortical-subcortical occipital hypersignal with laminar necrosis and thus confirmed the diagnosis of delayed-onset hypoxic cortical blindness. Visual rehabilitation, including visual stimulation in the scotomatous areas, was associated with a dramatic and rapid visual improvement with a BCVA of 20/32 OU, an ability to read after 2 weeks (day 30 post-hypoxic incident), and a reduction in the size of the scotoma. CONCLUSION: Delayed-onset hypoxic cortical blindness is a rare presentation of cortical blindness that develops few days after a cerebral hypoxic stress. While initial presentation can be catastrophic, visual improvement may be spectacular and enhanced with visual rehabilitation.
PURPOSE: To report a case of typical delayed-onset hypoxic cortical blindness that occurred few days after resuscitation from drowning in a young male. METHODS: Neurological and ophthalmological examination were performed including optical coherence tomography (OCT), Goldmann perimetry, pattern electroretinogram (pERG), pattern and flash visual evoked potentials (pVEP and fVEP) and brain magnetic resonance imaging (MRI). RESULTS: At presentation, at day 12 post-hypoxic incident, best corrected visual acuity (BCVA) was reduced to hand motion OU with an abolished optokinetic nystagmus, a normal fundus and no relative afferent pupillary defect. Macular and peripapillary OCT were normal. Goldmann perimetry revealed bilateral centrocecal scotoma. pERG was normal while pVEPs were undetectable and fVEPs were abnormal with delayed, decreased and disorganized responses, without interhemispheric asymmetry. Brain MRI disclosed a bilateral cortical-subcortical occipital hypersignal with laminar necrosis and thus confirmed the diagnosis of delayed-onset hypoxic cortical blindness. Visual rehabilitation, including visual stimulation in the scotomatous areas, was associated with a dramatic and rapid visual improvement with a BCVA of 20/32 OU, an ability to read after 2 weeks (day 30 post-hypoxic incident), and a reduction in the size of the scotoma. CONCLUSION: Delayed-onset hypoxic cortical blindness is a rare presentation of cortical blindness that develops few days after a cerebral hypoxic stress. While initial presentation can be catastrophic, visual improvement may be spectacular and enhanced with visual rehabilitation.
Authors: Michael Bach; Mitchell G Brigell; Marko Hawlina; Graham E Holder; Mary A Johnson; Daphne L McCulloch; Thomas Meigen; Suresh Viswanathan Journal: Doc Ophthalmol Date: 2012-10-17 Impact factor: 2.379
Authors: J Vernon Odom; Michael Bach; Mitchell Brigell; Graham E Holder; Daphne L McCulloch; Atsushi Mizota; Alma Patrizia Tormene Journal: Doc Ophthalmol Date: 2016-07-21 Impact factor: 2.379