The corpus callosum (from Latin: “tough body”), also known as the colossal commissure, is a wide, flat bundle of neural fibers beneath the cortex in the eutherian brain at the longitudinal fissure. It connects the left and right cerebral hemispheres and facilitates interhemispheric communication. It is the largest white matter structure in the brain, consisting of 200–250 million contralateral axonal projections.
The band of white matter connecting the two cerebral hemispheres.
Plays a crucial role in interhemispheric communication.
It is particularly important because various tumors and vascular lesions can be located in and around the corpus callosum, and it is a route through which pass several surgical approaches. Performing accurate surgery in this region and avoiding damage to normal structures require that the neurosurgeon have adequate knowledge of the anatomy of the intricate blood supply to this area.
Callosal disconnection syndrome, or split brain is an example of a disconnection syndrome from damage to the corpus callosum between the two hemispheres of the brain. Disconnection syndrome can also lead to aphasia, left-sided apraxia, and tactile aphasia, among other symptoms.
The pericallosal and posterior pericallosal arteries were found to be the main sources of blood supply to the corpus callosum. In 80% of the specimens, the anterior communicating artery gave rise to either a subcallosal artery or a median callosal artery, each of which made a substantial contribution to the blood supply of the corpus callosum 1).
Short callosal arteries were present in 58 hemispheres (96.6%) and supplied the superficial surface of the corpus callosum along its midline and were a primary arterial source to this structure. Long callosal arteries were found in 28 hemispheres (46.6%) and contributed to the pial plexus. The cingulocallosal arteries were present in all hemispheres and supplied the corpus callosum, cingulate gyrus, and also contributed to the pericallosal pial plexus. The recurrent cingulocallosal arteries were present in 17 hemispheres (28.3%) and also contributed to the pericallosal pial plexus. The median callosal artery, an anatomical variation, was present in 10 brains (33.3%). This vessel supplied the corpus callosum and the cingulate gyrus 2).
Variations in morphometry exist. There is a paucity of data on CC dimensions in Nigeria, and no standardized reference is available. The study aimed to determine the CC dimensions among the adult population in southeast Nigeria. The result will provide reference ranges and form a benchmark for comparisons of CC-related pathologies. A retrospective study of CC morphometric dimensions in normal subjects who had cranial MRI over two years in Memfys Hospital, Enugu, Southeast Nigeria, using a 1.5T GE© 16 channel machine. The CC was segmentalized into seven subregions using the modified Witelson method with special computer software. All measurements were taken twice from the T1 mid-sagittal image, and the mean was used for computation. The results were analyzed using descriptive and inferential statistics. A total of 200 subjects were recruited for the study. The mean length and height of the CC were 75.58 ± 4.52 mm and 24.64 ± 3.40 mm, respectively. The width dimensions of the genu, body, rostrum and splenium were 10.88 ± 1.81 mm, 5.66 ± 1.32 mm, 3.65 ± 1.25 mm, and 10.02 ± 1.70 mm, respectively. No gender variations were noted among the different dimensions of CC (P = 0.90). The length and height of CC increase gradually with age and show a positive correlation. The width dimensions of the genu and splenium increase till middle age and subsequently decreases in line with brain atrophy (p = 0.0000& p = 0.004). Using Pearson’s correlation test, no correlation was noted in the dimensions of the body and rostrum of the corpus callosum when related to age and sex. (P = 0.92 & p = 0.66). Reference ranges of CC dimensions in the subregion were presented, and variations exist in its different morphometric dimensions which are affected by brain atrophy. Gender does not influence the dimensions in these subpopulations 3)
Corpus callosum abnormality
Corpus callosum and epilepsies
Epilepsies are reported in up to two thirds of patients with complete or partial CC agenesis (AgCC). However, AgCC per se is not indicative for seizure disorders. Moreover, additional malformations of cortical development (MCD) are causal. Microstructural CC abnormalities are detected by advanced imaging techniques, are part of diffuse white matter disturbances and are related to cognitive deficits. The etiological significance remains unexplained. However, they are also found in non-epileptic benign and transient disorders. In drug-resistant epilepsies with violent drops to the floor (“drop seizures”) callosotomy may be beneficial in seizure reduction. Since the EEG after callosotomy exhibits a single seizure focus in up to 50% of patients, consecutive resective surgical methods might be successful.
CC is part of cerebral white matter and anomalies cannot act per se as seizure onset zone. Imaging techniques demonstrate additional lesions in patients with epilepsies. CC is the major pathway for seizure generalization. Therefore, callosotomy is used to prevent generalized drop seizures 4).
Corpus callosum lesion
Agenesis of the corpus callosum
Agenesis of the corpus callosum.
Corpus callosum dysgenesis
Arteriovenous malformation of the corpus callosum
Arteriovenous malformation of the corpus callosum.
Corpus callosum tumor
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Kahilogullari G, Comert A, Arslan M, Esmer AF, Tuccar E, Elhan A, Tubbs RS, Ugur HC. Callosal branches of the anterior cerebral artery: an anatomical report. Clin Anat. 2008 Jul;21(5):383-8. doi: 10.1002/ca.20647. PubMed PMID: 18521950.
Ajare EC, Campbell FC, Mgbe EK, Efekemo AO, Onuh AC, Nnamani AO, Okwunodulu O, Ohaegbulam SC. MRI-based morphometric analysis of corpus callosum dimensions of adults in Southeast Nigeria. Libyan J Med. 2023 Dec;18(1):2188649. doi: 10.1080/19932820.2023.2188649. PMID: 36946121.
Unterberger I, Bauer R, Walser G, Bauer G. Corpus callosum and epilepsies. Seizure. 2016 Apr;37:55-60. doi: 10.1016/j.seizure.2016.02.012. Epub 2016 Mar 3. Review. PubMed PMID: 27010176.