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Table of Contents    
Year : 2019  |  Volume : 67  |  Issue : 3  |  Page : 930-931

Acute corpus callosum infarct

1 Department of Neurology, Institute of Neurosciences, Indraprastha Apollo Hospitals, New Delhi, India
2 Department of Radiology, Indraprastha Apollo Hospital, New Delhi, India

Date of Web Publication23-Jul-2019

Correspondence Address:
Dr. Pushpendra N Renjen
C-85, Anand Niketan, New Delhi - 110 021
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/0028-3886.263234

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How to cite this article:
Chaudhari D, Renjen PN, Arora AS. Acute corpus callosum infarct. Neurol India 2019;67:930-1

How to cite this URL:
Chaudhari D, Renjen PN, Arora AS. Acute corpus callosum infarct. Neurol India [serial online] 2019 [cited 2023 Sep 26];67:930-1. Available from:

A 62-year old diabetic gentleman presented to the emergency room with a sudden-onset weakness of the right side of body along with slurring of speech for 1 day. He had a history of a few episodes of hypotension (BP <100/60) two days back. He also had a history of two episodes of transient ischemic attacks over the last 1month in the form of heaviness of the right side of body and weakness of bilateral hand grip. His physical examination revealed significant motor deficit of the right upper and lower extremities. The initial non-contrast computed tomography (CT) scan performed during admission showed multiple areas of ischemic demyelination in bilateral periventricular white matter along with a small focal hypodensity seen in the corpus callosum (CC) (more on the left side). In view of the atypical location of these hypodensities, magnetic resonance imaging (MRI) of the brain with MR angiogram (MRA) was done on the next day. MRI was suggestive of altered signal within both sides of the genu and body of the CC [Figure 1]. MRA revealed bilateral petrous–cavernous internal carotid artery (ICA) with critical stenosis (left > right). The right A1 artery was absent, and both anterior cerebral arteries (ACAs) were getting blood supply from the left side only [Figure 2]. The callosomarginal branches were not clearly visualized, which was suggestive of watershed infarcts, probably due to the hypotensive episode.
Figure 1: MRI brain showing altered signals on both sides of the genu and body of the corpus callosum

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Figure 2: MRA showing absent right A1 artery, and the callosomarginal branches are not clearly visualized

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Infarcts of the CC are not common and are attributed to a rich blood supply from three main arterial systems: the anterior communicating artery, the pericallosal artery, and the posterior pericallosal artery.[1] The clinical manifestations of the acute CC infarction lack specificity and are difficult to clinically diagnose because they often merge with the manifestations of other infarctions.[2] A detailed description of the vascular supply to the CC was published by Ture et al., including variations in the main arterial supply.[3] The pericallosal branch of the anterior cerebral artery is most often the main vascular supply to the body. The subcallosal and medial callosal arteries, branches of the anterior communicating artery, provide the main supply for the anterior portion of the CC. The posterior pericallosal artery, a branch of the posterior cerebral artery, supplies the splenium.[1]

In a recent study, it was found that CC infarction is generally rare. The most susceptible location of an ischemic CC lesion lies in the splenium. Splenium infarctions are often associated with bilateral cerebral hemispheric involvement in 46.2% patients. The genu and/or body infarctions are associated with atherosclerosis. The most common cause of CC infarction is probably embolism.[4] A CC infarct can be associated with the disconnection syndrome, even though our patient did not have any peculiar clinical manifestations, such as the frontal alien hand syndrome (AHS), agraphia, or impaired visual recognition. The disconnection syndrome is a neurological disorder due to the blocking of impulse transmission along a cerebral fiber pathway, mainly an interruption in the uncinate temporal–frontal fasciculus and the occipito- and temporoparietal tract. It manifests as apraxias of the left hand, pseudoneglect, alien left hand, astereognosis, agraphia, alexia, visual apraxias, and hemianopsia.[5]

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 » References Top

Kasow DL, Destian S, Braun C, Quintas JC, Kagetsu NJ, Johnson CE. Corpus callosum infarcts with atypical clinical and radiologic presentations. Am J Neuroradiol 2000;21:1876-80.  Back to cited text no. 1
Murthy SB, Chmayssani M, Shah S, Goldsmith CE, Kass JS. Clinical and radiologic spectrum of corpus callosum infarctions: Clues to the etiology. J Clin Neurosci 2013;20:175-7.  Back to cited text no. 2
Ture U, Yasargil MG, Krisht AF. The arteries of the corpus callosum: A microsurgical anatomic study. Neurosurgery 1996;39:1075-85.  Back to cited text no. 3
Li S, Sun X, Bai YM, Qin HM, Wu XM, Zhang X, et al. Infarction of the corpus callosum: A retrospective clinical investigation. PLoS One 2015;10:e0120409.  Back to cited text no. 4
Park MK, Hwang SH, Jung S, Hong SS, Kwon SB. Lesions in the splenium of the corpus callosum: Clinical and radiological implications. Neurol Asia 2014;19:79-88.  Back to cited text no. 5


  [Figure 1], [Figure 2]


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