PMC9577094_01
Timeline of the case report scheme summarizing the disease, complications and progression of the patient. Study follow-up of the C-reactive protein (CRP) plasma levels.
fneur-13-991610-g0001.jpg
PMC9577094_01_fneur-13-991610-g0001.jpg
F1
Neurology due to a fever of 38 C and simultaneous progressive distal onset tetraparesis with areflexia. She also suffered mild respiratory symptoms, asthenia, and a cough from 1 week before (see Figure 1 for timeline scheme). No previous family history of autoimmune diseases, aneurysms, or stroke. As shown in Figure 1, neurological and respiratory worsening was in parallel with an increase in C-reactive protein (CRP) which peaked (>200 mg/dL) on day 7.
(A) Cranial CT scan showing left temporo-occipital intraparenchymal haematoma. (B) Diffusion-weighted MR image showing increased signal (diffusion restriction) and thickening of the splenium of the corpus callosum (green arrowhead), suggestive of a cytotoxic lesion of the corpus callosum (CLOCC). (C,D) 3D T1-weighted volumetric sequence without contrast (C) and with contrast (D) demonstrating the existence of a nodular image adjacent to the haematoma (white arrow). It presents as a signal void and after contrast administration, it enhances in an analogous way to vascular structures, compatible with a pseudoaneurysmal lesion.
fneur-13-991610-g0002.jpg
PMC9577094_01_fneur-13-991610-g0002.jpg
F2
A brain CT scan (day 14) demonstrated an acute left parietal lobar haematoma (Figure 2A). On day 18, an MRI confirmed the haematoma and showed a striking image of an irregular artery (Figures 2C,D). Interestingly, the MRI also revealed a non-specific focus of increased signal in the splenium of the corpus callosum (Figure 2B) on DWI sequences suggesting a cytotoxic lesion of the corpus callosum (CLOCC).
(A) Selective arteriography of RICA. The presence of a pseudoaneurysm is detected at the level of the distal temporo-occipital vasculature (black arrow). (B) Angular artery supraselective arteriography. The branch presenting the pseudoaneurysm shows an irregularity of the arterial wall suggesting arteritis (black arrow). (C) Glue cast after embolization (black arrow). (D) Selective arteriography of RICA after branch embolisation. Absence of pseudoaneurysm (black arrow). (E) Selective arteriography of LVA. Compensation of the left temporo-occipital territory through temporal branches of the left vertebral artery (black asterisk) is demonstrated. (F) Diffusion weighted MR image 1 month after treatment. Morphological and signal normalization of the splenium of the corpus callosum (green arrowhead). Absence of additional ischemic lesion after embolisation. RICA, Right internal carotid artery; LVA, Left vertebral artery.
fneur-13-991610-g0003.jpg
PMC9577094_01_fneur-13-991610-g0003.jpg
F3
Then, diagnostic cerebral arteriography (day 24) showed a 4-mm distal pseudoaneurysm located in a branch of the temporo-occipital artery of the left middle cerebral artery (MCA), at the M4 level (Figure 3A). The parental artery of the pseudoaneurysm was a very thin caliber with irregular morphology, such as mycotic or vasculitic angiographic appearance (Figure 3B). Moreover, a hypoperfused left parietal lobe was observed, due to the mass effect of the haematoma, and a parieto-occipital artery from the left posterior cerebral artery (PCA) was compensating for the blood flow (Figure 3E). Therefore, complete embolization of the pseudoaneurysm (day 25) was carried out by sacrificing the parental artery by using the synthetic glue N-butyl-cyanocrylate (Glubran , GME, Italy) through a 1.2F microcatheter (Magic , Balt group, France) (Figures 3C,D). As expected, following the procedure, blood circulation was compensated by a parieto-occipital artery from the left PCA (Figure 3E). A new MRI (Figure 3F) showed no ischemia, the CLOCC lesion had disappeared and the haematoma was reduced.