EEG Correlates of Cortical Blindness in Anton's Syndrome

A 55-year-old man with a history of hypertension presented with a 4-day history of headache followed by rapidly progressive bilateral visual loss. On admission, the Glasgow Coma Scale score was 11 (E3V3M5). Neurological examination revealed absence of light perception in both eyes, while pupillary light reflexes were preserved and funduscopic examination was unremarkable. Despite objective blindness, the patient persistently denied visual impairment and provided elaborate but inaccurate descriptions of his surroundings. This combination of cortical blindness, anosognosia, and confabulation was consistent with Anton's syndrome.[ 1 ] Magnetic resonance imaging of the brain demonstrated acute bilateral occipital lobe infarctions within the posterior cerebral artery territories with additional involvement of the left thalamus, explaining the patient's cortical visual deficit. Electroencephalography (EEG) performed on the second day of hospitalization demonstrated generalized background slowing with marked attenuation of the posterior dominant rhythm over the occipital regions ([ Fig. 1 ]). Recurrent bursts of frontal intermittent rhythmic delta activity (FIRDA) were also observed. The background activity showed markedly reduced reactivity to eye opening and closing, reflecting disruption of normal occipital cortical function. No epileptiform discharges were present. Fig. 1 Electroencephalography (EEG) recording displayed in a standard double banana (anterior–posterior bipolar) montage. The tracing demonstrates diffuse attenuation and absence of a well-formed posterior dominant rhythm (PDR) over occipital regions. An eye closure–eye opening epoch is included: there is no significant emergence of posterior alpha activity during eye closure, and no clear reactivity with eye opening. Visual evoked potentials, recorded during the same evaluation, revealed markedly prolonged P100 latencies (180 ms on the right and 175 ms on the left; normal <120 ms) with reduced amplitudes bilaterally. These findings support dysfunction of the retrochiasmal visual pathways and are consistent with cortical visual impairment. Anton's syndrome is an uncommon manifestation of bilateral occipital lobe injury characterized by cortical blindness accompanied by denial of visual loss and confabulatory responses.[ 2 ] [ 3 ] While neuroimaging establishes the structural lesion, electrophysiological investigations provide important functional information about cortical integrity. In the present case, attenuation of the posterior dominant rhythm reflects disruption of occipital cortical networks responsible for the generation of alpha activity. The posterior dominant rhythm is normally generated through interactions between the visual cortex and thalamocortical circuits, and its attenuation indicates impaired occipital cortical function. Similar EEG findings have been reported in patients with bilateral occipital lobe injury and cortical blindness.[ 4 ] In addition, the presence of frontal intermittent rhythmic delta activity suggests involvement of deep midline structures and diffuse cerebral dysfunction. FIRDA is commonly associated with structural lesions affecting thalamocortical pathways, metabolic disturbances, or increased intracranial pressure. In this patient, the coexistence of FIRDA ([ Figs. 2 ] and [ 3 ]) with attenuation of the posterior dominant rhythm likely reflects disruption of both occipital cortical activity and thalamocortical integration, consistent with the thalamic involvement identified on neuroimaging. Fig. 2 An awake electroencephalography demonstrates generalized background slowing with prominent frontal intermittent rhythmic delta activity (FIRDA)(FIRDA; arrows ). The posterior dominant rhythm is markedly attenuated over the occipital leads, indicating bilateral occipital cortical dysfunction. Recording parameters: sensitivity 7 μV/mm, time base 30 mm/s, low-frequency filter 1 Hz, high-frequency filter 70 Hz, notch filter 50 Hz. Fig. 3 Electroencephalography segment displayed in montage (AP bipolar montage) demonstrating generalized background slowing with recurrent frontal intermittent rhythmic delta activity (FIRDA). Reduced posterior dominant rhythm is evident over the occipital electrodes. Recording parameters: sensitivity 7 μV/mm, time base 30 mm/s, low-frequency filter 1 Hz, high-frequency filter 70 Hz, and notch filter 50 Hz. Electrophysiological findings may also assist in differentiating cortical blindness from functional visual loss or disorders affecting the anterior visual pathways, in which posterior alpha activity and EEG reactivity are typically preserved. In patients presenting with visual loss and preserved pupillary reflexes, attenuation of the posterior dominant rhythm on EEG, particularly when accompanied by FIRDA, can provide an important electrophysiological clue to bilateral occipital cortical dysfunction. This case highlights the value of EEG and visual evoked potentials as complementary tools for functional assessment in patients with cortical blindness and suspected Anton's syndrome. Authors' Contributions A.V., S.S., N.B.P., N.J., S.S.F., and S.M. contributed to study design, manuscript writing, and revision. S.S. performed EEG acquisition and analysis. A.V. supervised the study and approved the final manuscript. N.B.P. and N.J. managed the clinical data. S.S.F. assisted with EEG data and figures. S.M. supported literature review and formatting. All authors approved the final version. Ethical Approval The authors confirm that they have read the journal's position on issues involved in ethical publication and affirm that this report is consistent with those guidelines. Publication History Article published online: 17 July 2026 © 2026. The Author(s). This is an open access article published by Thieme under the terms of the Creative Commons Attribution License, permitting unrestricted use, distribution, and reproduction so long as the original work is properly cited. (https://creativecommons.org/licenses/by/4.0/) Thieme Medical and Scientific Publishers Private Limited A-13A, Graphix Tower 1, 6th floor, Sector 62, Noida 201309, Uttar Pradesh, India