PMC5513951_01
Imaging during course of disease: (A) NMR imaging on day 3 after admission shows hyperintensity in FLAIR sequence (left), high degree of diffusion-positivity (DWI, middle), and lack of shine-through effect in ADC (right), indicating acute thalamic infarction. (B) cCT scan (day 10) showing increased sellar process.
fmed-04-00113-g001.jpg
PMC5513951_01_fmed-04-00113-g001.jpg
F1
NMR imaging on day 3 revealed infarction in the left thalamus, based on diffusion-weighted imaging and hyperintensity in the FLAIR sequence (Figure 1A), as well as an enlargement of the sellar region consistent with an adenoma of the pituitary gland. The cCT scan obtained on day 10 revealed sinusitis sphenoidalis and an increase in the space-occupying sellar process was observed, leading us to consider a fungal infection (Figure 1B).
Subarachnoidal hemorrhage from A. basilaris. (A) cCT on day 12 scan showing hemorrhage. (B,C) Digital subtraction angiography with intervention showing active bleeding (B) and insertion of flow diverting stent (C). (D) Late arterial phase of DSA indicating starting thrombosis immediately after flow diverter implantation. (E) Follow-up cCT on day 17 shows demarcation of ischemic areas.
fmed-04-00113-g002.jpg
PMC5513951_01_fmed-04-00113-g002.jpg
F2
Emergency cCT showed a massive subarachnoidal hemorrhage (Figure 2A), caused by active bleeding from a fusiform aneurysm of the basilar artery tip as revealed by digital subtraction angiography (Figure 2B). Bleeding could be stopped by insertion of a flow diverting stent (Figures 2C,D). On day 17, large demarcated infarction areas were seen by NMR in the mesencephalon, the cerebellum, and brain areas supplied by the A. cerebri anterior and posterior (Figure 2E).
Neuropathological findings. Macroscopic findings (A-C): (A) subarachnoid hemorrhage within the basal cisterns coating the midbrain and pons and extending to the cerebellopontine angle. (B) Macroscopic view of the vertebrobasilar vascular supply after preparation of the hematoma clearly showing an aneurysm at the basilar tip (red arrow). Higher magnification in (C) demonstrates the ruptured aneurysm. Microscopic findings (D-I): (D) hematoxylin & eosin (H&E) staining of the basilar aneurysm showing thickening and splitting of the wall due to intramural inflammatory infiltrates (arrow). (E) Same area as depicted in (D) the presence of hyphal structures in close association to the inflammatory infiltrates confirms the diagnosis of a mycotic aneurysm (Grocott histochemistry). (F) Higher magnification of (E) (Grocott histochemistry). (G) A pituitary adenoma visible in the sellar region (H&E staining) with immunohistochemical expression of adrenocorticotrophic hormone (H) proving the diagnosis of a corticotroph adenoma. (I) Hyphal structures within the dura adjacent to the corticotroph adenoma (Grocott histochemistry). Scale bar in (D) 200 microm, applies also for (E). Scale bar in (F) 20 microm. Scale bar in (G) 50 microm, applies also for (H). Scale bar in (I) 100 microm.
fmed-04-00113-g003.jpg
PMC5513951_01_fmed-04-00113-g003.jpg
F3
The cause of death was a rupture of an aneurysm of the basilar artery (Figures 3A-C). Microscopic analysis of the aneurysmatic vessel wall revealed inflammation and foci of hyphal structures with septae and dichotomous ramifications, which were best visualized by Grocott histochemical staining (Figures 3D-F), arguing for a mycotic aneurysm due to a hyphomycetal infection. The sellar region showed a pituitary adenoma with immunohistochemical expression of adrenocorticotrophic hormone (ACTH) in terms of a corticotroph adenoma (Figures 3G,H) with invasiveness concerning the adjacent bone and dura. There was also invasion of hyphae into the dura surrounding the sphenoid sinus (Figure 3I).