Lesions in the calcarine cortex (primary visual cortex, V1) are typically associated with loss of primary visual processing rather than complex visual recognition disorders. These deficits alone are less commonly classified as neuropsychiatric, but involvement of adjacent visual association cortical regions can produce higher-order visual disturbances, which are discussed separately on the pages for those regions.
Cognitive, behavioural, and psychiatric effects of lesions may also arise through mechanisms other than network disruption; the potential contribution of these mechanisms can be considered using the Neuropsychiatric Effects of CNS Structural Abnormalities (NECSA) classification.
Calcarine cortex
Page most recently updated 7 September 2026
● Lesion manifestations
▪ Unilateral lesions:
◦ Contralateral homonymous visual field loss
▪ Bilateral lesions:
◦ Cortical blindness
◦ Anton syndrome (when blindness is accompanied by denial due to involvement of visual awareness networks beyond V1)
● Clinical pearls
▪ Lesions in the calcarine cortex (primary visual cortex, V1) are typically associated with loss of primary visual processing rather than complex visual recognition disorders. These deficits alone are less commonly classified as neuropsychiatric, but involvement of adjacent visual association cortical regions can produce higher-order visual disturbances, which are discussed separately in the sections for those regions.
▪ Bilateral V1 injury can produce cortical blindness despite preserved eyes and optic nerves, due to disruption of cortical visual input.
▪ Denial of blindness (Anton syndrome) reflects disruption of awareness networks beyond V1.
Clinical reminder: consider NECSA mechanisms
(Neuropsychiatric Effects of CNS Structural Abnormalities)
When a structural lesion is identified in a patient presenting with neuropsychiatric symptoms, consider which NECSA mechanisms may explain these symptoms:
● Network disruption
Disruption of functional networks due to the presence of the lesion
● Electrical disturbance
Ictal, preictal, postictal, or interictal effects due to epileptic activity associated with the lesion (particularly if involving or adjacent to cortex)
● Chemical (endocrine) effects
Hormone excess or deficiency caused by the lesion (particularly if involving the pituitary gland or hypothalamus)
● Side effects of treatment
Effects of medications, surgery, radiotherapy, or other interventions
● Alternative explanations
The lesion may be incidental, or symptoms may arise from another cause (e.g., psychological response to illness or a comorbid psychiatric condition)
Selected references and further reading — Lesional lens
Rohlfing T, Zahr NM, Sullivan EV, Pfefferbaum A. The SRI24 multichannel atlas of normal adult human brain structure. Hum Brain Mapp. 2010;31(5):798–819.
Clark DL, Boutros NN, Mendez MF. The brain and behavior: an introduction to behavioral neuroanatomy. 4th ed. Cambridge: Cambridge University Press; 2018.
Brazis PW, Masdeu JC, Biller J. Localization in clinical neurology. 7th ed. Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins; 2016.
Blumenfeld H. Neuroanatomy through clinical cases. 3rd ed. New York: Oxford University Press; 2021.
Hassan I. The neuropsychiatric effects of CNS structural abnormalities (NECSA) classification: an aid to differential diagnosis. Aust N Z J Psychiatry. 2015;49(10):943.
Arciniegas DB, Yudofsky SC, Hales RE, editors. The American Psychiatric Association Publishing textbook of neuropsychiatry and clinical neurosciences. 6th ed. Washington (DC): American Psychiatric Association Publishing; 2018.
Agrawal N, Faruqui R, Bodani M, editors. Oxford textbook of neuropsychiatry. Oxford: Oxford University Press; 2020.