Today, EdwardH Oldfield et al. of the University of Virginia Neurosurgery conducted a clinical study on the mechanism of stroke in pituitary adenomas. They concluded that most pituitary adenoma strokes occur without a clear cause, but rather the intrinsic characteristics of the pituitary adenoma itself lead to spontaneous infarction. Pituitary adenomas are characterized by hypermetabolism, lack of tumor angiogenesis, and sparse intra-tumor vascularity. The high incidence of ischemic infarction within pituitary adenomas is determined by the low vascular density of pituitary adenomas, which allows the tumor to establish a fragile balance between high metabolic demand and intra-tumoral perfusion, and any acute factor that disrupts the balance between perfusion and metabolism can cause spontaneous infarction or acute ischemia of the tumor.
Looking back at today’s intraoperative situation, I am skeptical of this idea.
On MRI, this pituitary adenoma had cystic changes, and intraoperatively it was confirmed that the tumor broke through the saddle septum and grew intracranially, compressing the third ventricle, with partial cystic changes in the apex of the tumor and visible obvious stroke necrosis changes. However, intraoperative blood supply to the tumor was seen to be abnormally rich, with a high density of intra-tumoral vessels and much intraoperative bleeding.
In fact, many of the stroke adenomas that we see intraoperatively, especially the invasive ones, tend to have a rich blood supply. On the contrary, we often see adenomas without stroke that have a soft texture, little blood supply and low vascular density.
Below is today’s surgical MRI: (postoperative results to be uploaded after review)