Callosal Aphasia after Stroke.

The corpus callosum, a midline brain structure that connects both hemispheres-the roles of which presumably include facilitating the language function-rarely causes aphasia (1,2). We had a 90-year-old, right-handed woman with hypertension and chronic cardiac failure that were managed by a cardiologist. She was referred to our hospital because of a sudden onset of transcortical motor aphasia with paraphasia, poor naming, poor verbal fluency, slightly-decreased prosody, and poor comprehension, but preserved repetition. She also had mild ideomotor apraxia of the left hand, but without left hemiplegia. Because of aphasia, other disconnection syndrome could not be obtained. Diffusion-weighted images of 3Tesla magnetic resonance imaging (MRI) showed lesions in the right corpus callosum and the adjacent medial frontal cortex with a short apparent diffusion coefficient (Picture A), the area being almost the same as that in previously reported cases (1). MR angiography showed spontaneous recanalization in the right anterior cerebral artery (Picture B). The callosal aphasia in most of the previous reported cases (1) was transcortical motor aphasia, as was noted in our case. Two mechanisms of aphasia were proposed in previous studies. The first mechanism involves damage to fibers from the frontal lobe language area, which pass through the genu/rostrum of the corpus callosum. This mechanism is supported by hypo-perfusion in the frontal/cingulate cortex on single-photon emission computed tomography (SPECT), which was noted in our case (Picture C, D). The second mechanism involves damage to the interconnecting fibers of the bilateral language cortices (transcallosal diaschisis), which pass through the body of the corpus callosum, noted as hypo-perfusion on SPECT in our case (Picture A, B). This mechanism was recently proposed based on functional MRI connectivity studies of the language regions in both hemispheres (2).

Picture.

The authors state that they have no Conflict of Interest (COI).