This is the case of a 26-year-old male who developed Anton Babinski syndrome (ABS), quadriplegia, and delayed post-hypoxic leukoencephalopathy (DPHL) after an opioid overdose. He exhibited cortical blindness, visual anosognosia, and confabulation upon awakening. Several days later, he experienced acute psychosis and agitation. T2-FSE MRI revealed extensive supratentorial leukoencephalopathy involving both cerebral hemispheres, extending to the posterior corpus callosum due to cerebral anoxia. This case report will discuss different types of encephalopathy from opioid abuse, ABS, visual anosognosia, and confabulation\'s pathogenic mechanisms. It underscores the necessity of researching substance-induced neuropsychiatric disorders and their pathogenic mechanisms for effective treatments.

Anton-Babinski syndrome is a rare extension of cortical blindness following injury to the occipital lobe. The patient behaves as sighted but has visual function derangements. The posterior cerebral artery (PCA) stroke represents 5% to 10% of total strokes. The COVID-19 pandemic has shown a rise in stroke cases. We present a case of this rare PCA stroke, first diagnosed by an ophthalmologist. This case had an inconsistent initial presentation, but subsequent computed tomography of the brain and other neurological investigations confirmed the diagnosis. If such cases are diagnosed early, they could have better management. Timely intervention can decrease morbidity as well as mortality.

[This corrects the article DOI: 10.3389/fneur.2022.887287.].

UNASSIGNED: We describe the case of a 57-years-old patient who presented an Anton-Babinski syndrome in the context of a stroke-like migraine attack after radiation therapy (SMART).
UNASSIGNED: The patient was brought to the emergency room following a sudden loss of vision in the context of a pre-existing left-sided hemianopia after excision of a right occipital astrocytoma followed by radio-chemotherapy 35 years prior to his admission in our services. At admittance, he also presented hyperthermia, hypertension, and a GCS of 7. The MRI showed a leptomeningeal enhancement in the left temporal, parietal, and occipital lobes. After exclusion of other differential diagnoses, we diagnosed a cortical blindness in the context of a SMART syndrome affecting the left hemisphere. While the symptoms improved under corticosteroid therapy, the patient successively presented an Anton-Babinski syndrome, a Riddoch syndrome and a visual associative agnosia before finally regaining his usual sight.
UNASSIGNED: This is, to our knowledge, the first report of an Anton-Babinski syndrome in the context of a SMART syndrome. A dual etiology is mandatory for cortical blindness in SMART syndrome since the latter affects only one hemisphere. A SMART syndrome affecting the contralateral hemisphere in respect to the radiation site seems to be uncommon, which makes this case even more exceptional.

Vivid visual hallucinations are common in the geriatric population and can be due to a number of causes such as dementia, delirium, stroke, adverse effects of medication, or ocular disease. We will examine an interesting patient case report, which allowed us to explore two lesser-known causes of these types of hallucinations: Charles Bonnet Syndrome and Anton-Babinski Syndrome. Treatment of these syndromes focuses on supportive care as well as extensive education for the patient and family concerning the benign nature of the visual hallucinations. Many patients, however, end up undergoing extensive diagnostic studies and treatments that are not necessary. This occurs as a result of a lack of education when it comes to the diagnosis and management of these conditions. By raising awareness among healthcare providers, we can prevent unnecessary and potentially harmful workups and treatments for patients suffering from these syndromes.

Anton-Babinski syndrome is a rare disease featuring bilateral cortical blindness and anosognosia with visual confabulation, but without dementia or any memory impairment. It has a unique neuropsychiatric presentation and should be highly suspected in those with odd visual loss and imaging evidence of occipital lobe injury. In the case discussed herein, a 90-year-old man presented with bilateral blindness, obvious anosognosia, and vivid visual confabulation, which he had had for 3 days. Brain computed tomography demonstrated recent hypodense infarctions at the bilateral occipital lobes. Thus, the patient was diagnosed with Anton-Babinski syndrome. Because of his age and the thrombolytic therapy during the golden 3 hours after ischemic stroke, the patient received aspirin therapy rather than tissue plasminogen activator or warfarin. He gradually realized he was blind during the following week, but died of pneumonia 1 month later. In the literature, it is difficult to establish awareness of blindness in patients with Anton-Babinski syndrome, but optimistically, in one report, a patient was aware of blindness within 2 weeks, without vision improvement. Our case illustrates that elderly patients with Anton-Babinski syndrome can partially recover and that 1 week is the shortest time for the establishment of awareness of blindness for sufferers without vision improvement.