This case describes bilateral corpus callosum infarction occurring in the setting of cerebral venous sinus thrombosis. Two aspects of this case are unusual: the location of the infarcts within the corpus callosum and the venous rather than arterial cause of the ischemia. 

Infarcts of the corpus callosum are rare. The literature explains that this is because the corpus callosum receives blood supply from multiple sources [10]. According to Ture et al. [4], the anterior cerebral artery supplies the front part, and the posterior cerebral artery helps supply the back. This rich, dual blood supply makes the corpus callosum relatively resistant to ischemia. In most cases where a callosal infarct does happen, studies have shown that it is usually caused by an arterial problem. For example, research by Sun et al. [2] and Chaudhari et al. [6] found that emboli from the heart or atherosclerosis in the feeding arteries are common culprits. In our patient, we initially considered this, but the imaging did not show a blockage in these arteries. 

In this patient, the cause of the stroke appeared to be venous rather than arterial. As discussed in the introduction, arterial causes like embolism or atherosclerosis are the most common reasons for callosal infarcts when they do occur [2,6]. However, in our patient, the CT angiogram did not show any blockages in the major arteries, such as the anterior cerebral or posterior cerebral arteries, that supply the corpus callosum. This prompted us to consider other mechanisms. 

Cerebral venous sinus thrombosis (CVST) can lead to stroke through a different mechanism than arterial blockages. When a vein or sinus like the superior sagittal sinus becomes thrombosed, it impairs the drainage of blood from the brain. This can cause blood to back up, leading to increased venous pressure. If the pressure becomes high enough, it can reduce the overall perfusion pressure and prevent oxygen from reaching the brain tissue, resulting in a venous infarct [7, 11]. This is what happened in the patient. 

The location of the thrombus is important for understanding why the corpus callosum was affected. While the corpus callosum receives blood from multiple arteries, its venous drainage ultimately connects to deep venous structures mainly the internal cerebral veins, which drain toward the vein of Galen and the straight sinus. The straight sinus then meets the superior sagittal sinus at the torcula. In our patient, the thrombus was not isolated to the superior sagittal sinus; it extended into the torcula and the left transverse sinus. As described by Ture et al. [4] in their anatomical study, the deep venous system is responsible for draining the white matter tracts. It is hypothesized that this extensive clot burden caused significant venous congestion in the deep system, which then led to reduced perfusion and infarction in the bilateral corpus callosum. 

Clinically, this case was also challenging because the patient's symptoms were non-specific. Kasow et al. [5] and Garcia-Sarreon et al. [8] have described classic "disconnection syndromes" associated with corpus callosum lesions, such as apraxia especially of the left hand, visual agnosia, pure alexia, and alien hand syndrome, where a patient's hand seems to move on its own. Our patient did not exhibit these specific findings. Instead, she presented with confusion and altered mental status. This is consistent with larger studies. Sun et al. [2] reviewed 127 cases of corpus callosum infarction and found that many patients present with generalized symptoms like confusion or cognitive decline rather than the classic syndromes. Our patient's presentation, therefore, fits with the more common yet less recognized clinical picture described in the literature. 

Another important educational value of this case is the importance of imaging in guiding the diagnosis. The initial MRI showed restricted diffusion in the bilateral corpus callosum, which is a sign of acute infarction. However, the pattern was unusual because it was bilateral and centrally located, rather than following the territory of a single artery like the anterior cerebral artery. According to the review by Li et al. [1], callosal infarcts are usually small and unilateral. Because our patient's imaging did not fit this typical arterial pattern, the team pursued further vascular imaging with CT angiography. This decision was critical, as it revealed the superior sagittal sinus thrombosis that was not visible on the initial MRI sequences. This highlights a key clinical pearl: when stroke patterns on MRI do not match arterial territories, unusual causes like CVST should be suspected [12]. 

Finally, we considered what might have triggered the thrombosis in this patient. The thrombophilia workup, including testing for Protein C, Protein S, Factor V Leiden, and antiphospholipid antibodies, was negative. This suggests that she does not have a chronic, inherited clotting disorder. However, the patient presented with severe urosepsis and hyperglycemia. Sepsis is known to create a pro-thrombotic state. Systemic inflammation can activate the coagulation cascade and cause dysfunction in the endothelial cells that line the blood vessels. Given that her infection was severe and her workup for other causes was negative, we believe the urosepsis was the most likely provoking factor for the development of CVST in this case, although it is impossible to prove causation definitively.