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Cortical Blindness (Plus Anton-Babinski Syndrome, Blindsight, & Riddoch Syndrome)
Published in Alexander R. Toftness, Incredible Consequences of Brain Injury, 2023
Cortical blindness may be permanent, but it may also be partially or completely recovered from (Bharati et al., 2017). The best outcomes seem to occur for younger people, especially those under the age of 40 (Aldrich et al., 1987). Overall, cortical blindness, whether partial or complete, can be startling at first, but the majority of people with disorders such as these find clever ways to adapt.
Postoperative blindness
Published in Hemanshu Prabhakar, Charu Mahajan, Indu Kapoor, Manual of Neuroanesthesia, 2017
Cortical blindness: The causes of cortical blindness include global or focal ischemia, cardiac arrest, hypoxemia, vascular occlusion, intracranial hypertension, exsanguinating hemorrhage, and emboli.3 Patients may present with the signs of stroke in the parieto-occipital region and agnosia, that is, inability to interpret sensory stimuli. The vision might recover within days, but impairment in spatial perception and in the relationship between sizes and distances may remain for a longer period.20
Practice Paper 9: Answers
Published in Anthony B. Starr, Hiruni Jayasena, David Capewell, Saran Shantikumar, Get ahead! Medicine, 2016
Anthony B. Starr, Hiruni Jayasena, David Capewell
Cortical blindness describes the loss of vision in a normal eye caused by bilateral damage to the visual cortex in the occipital lobe. The patient in this scenario has had bilateral posterior circulation strokes, which have caused his symptoms. Affected people have no vision, but can suffer with visual hallucinations and a vehement denial of visual loss (Anton’s syndrome).
Bilateral occipital lobe infarct neglect deficit (BLIND) syndrome
Published in Journal of Community Hospital Internal Medicine Perspectives, 2021
S Shanmugam, HL Haver, SM Knecht, R Rajjoub, O Ali, R Chow
Aldrich et al. notes that cortical blindness can be caused by multiple etiologies, including cerebrovascular infarct, surgery such as coronary artery bypass, aortic valve replacement, laryngeal surgery, craniotomy and cerebral angiography [1]. Mechanisms of cerebral dysfunction during surgery or angiography are usually described as an event of anoxia, hypoperfusion, or hemorrhage leading to infarction of the cerebral tissue [1]. Post-traumatic contusions, progressive multifocal leukoencephalopathy, adrenoleukodystrophy and seizures are nonvascular etiologies of cortical blindness that can present with findings consistent with Anton Syndrome [2]. For management, it is essential to distinguish vascular from nonvascular etiologies in patients with suspected Anton Syndrome. Vascular causes usually imply poor prognosis, while visual anosognosia and vision deficits due to nonvascular causes may improve and sometimes resolve completely [1,2,5].
Transient vision loss: a neuro-ophthalmic approach to localizing the diagnosis
Published in Expert Review of Ophthalmology, 2018
Helen Chung, Jodie M. Burton, Fiona E. Costello
Transient cortical blindness, visual field defects, changes in mental status, seizures, and headaches may be seen in PRES [2,36]. Common causes of PRES are pre-eclampsia/eclampsia, hypertensive encephalopathy, immunosuppressive drugs use, and uremic encephalopathy. The pathogenesis of PRES is not well understood, and remains somewhat controversial. Suggested mechanisms for PRES include failed autoregulation and vascular endothelial abnormalities [36]. Cranial MR imaging in PRES patients typically shows a pattern of relatively symmetric vasogenic edema involving the subcortical white matter in the parieto-occipital lobes [36]. Visual deficits tend to improve over days to weeks (chronic recovery) in PRES patients.
Consent for post-operative visual loss in prone spinal surgery: aligning clinical practice with legal standards
Published in British Journal of Neurosurgery, 2018
Fay Greenway, Isabel Tulloch, James Laban
Cortical blindness is due to ischaemia or extreme hypoperfusion resulting in occipital lobe infarction in the visual cortex. It usually manifests as bilateral visual loss, ranging from bilateral homonymous hemianopia to complete visual loss. It is thought to be the rarest cause of POVL in spine patients. The prognosis is better than the other causes of POVL, with most patients recovering vision to some degree.