Infarction of the corpus callosum: a retrospective clinical investigation

Abstract

Objectives: The aim of this study was to investigate patients with ischemic infarctions in the territory of the corpus callosum to advance our understanding of this rare stroke subtype by providing comprehensive descriptive and epidemiological data.

Methods: From January 1, 2010 to June 30, 2014, all cases of acute ischemic stroke diagnosed by clinical manifestation and diffusion weighted imaging in Dalian Municipal Central Hospital were investigated. The patients presenting with corpus callosum infarctions were selected and further allocated into genu and/or body and splenium infarction groups. Proportion, lesion patterns, clinical features, risk factors and etiology of corpus callosum infarction were analyzed.

Results: Out of 1,629 cases, 59 patients (3.6%) with corpus callosum infarctions were identified by diffusion weighted imaging, including 7 patients who had ischemic lesions restricted to the corpus callosum territory. Thirty six patients had lesions in the splenium (61.0%). Corpus callosum infarction patients suffered from a broad spectrum of symptoms including weakness and/or numbness of the limbs, clumsy speech, and vertigo, which could not be explained by lesions in corpus callosum. A classical callosal disconnection syndrome was found in 2 out of all patients with corpus callosum infarctions. Statistical differences in the risk factor and infarct pattern between the genu and/or body group and splenium group were revealed.

Conclusion: Corpus callosum infarction and the callosal disconnection syndrome were generally rare. The most susceptible location of ischemic corpus callosum lesion was the splenium. Splenium infarctions were often associated with bilateral cerebral hemisphere involvement (46.2%). The genu and/or body infarctions were associated with atherosclerosis. The most common cause of corpus callosum infarction probably was embolism.

Fig 1. Representative images of pure and complex corpus callosum (CC) infarction.

(A) to (G) shows all individual cases presenting with ischemic lesions restricted to the CC. (A) and (B) DWI showing infarctions in CC genu, body and splenium. (C) infarctions situated in the right body and genu of CC. (D) ischemic lesions were detected in the left splenium. (E) small infarction in the left CC body. (F) bilateral splenium infarctions. (G) very small infarction of the left splenium. (H) and (I) provide representative examples of patients showing additional ischemic lesions outside the CC. (H) infarctions involving the left CC genu and body as well as the occipital-parietal areas. (I) lesions located in the occipital lobe, the left thalamus as well as the left CC genu and body.