This page focuses on the neuropsychiatric manifestations associated with lesions of the corpus callosum.
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.
Corpus callosum
Page most recently updated 7 September 2026
● Lesion manifestations
▪ Posterior corpus callosum (splenium):
◦ Visual-language disconnection syndromes:
Alexia without agraphia (classically due to left occipital cortex infarction with splenial involvement, often in the territory of the left posterior cerebral artery)
Left visual field anomia (inability to name objects presented in the left visual field because visual information cannot reach dominant language regions)
▪ Body of the corpus callosum:
◦ Tactile anomia (inability to name objects placed in the left hand with the eyes closed, despite preserved recognition of the object through vision, due to failure of somatosensory information to reach dominant language networks)
◦ Difficulty with bimanual coordination requiring integration of information from both hands
▪ Diffuse callosal injury:
◦ Cognitive slowing and reduced processing speed
◦ Executive dysfunction
◦ Increased emotional reactivity (e.g., irritability, reduced frustration tolerance)
● Clinical pearls
▪ The corpus callosum is the brain’s major interhemispheric communication pathway; lesions can produce symptoms through disconnection, even when the cortical regions themselves remain structurally intact.
▪ Alexia without agraphia is the classic splenial disconnection syndrome. A left occipital lesion disrupts visual processing in the dominant visual cortex, while splenial damage prevents visual information from the intact right visual cortex from reaching dominant left occipitotemporal reading networks.
▪ Patients with ‘alexia without agraphia’ can:
◦ write normally;
◦ understand spoken language;
◦ recognise objects;
◦ but cannot read because visual information cannot access the dominant reading network.
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.