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Case Reports
. 2020 Apr 11;15(6):757-760.
doi: 10.1016/j.radcr.2020.03.009. eCollection 2020 Jun.

Thrombosis of a basilar perforator aneurysm associated with pontine infarction in a patient with systemic lupus erythematosus

Affiliations
Case Reports

Thrombosis of a basilar perforator aneurysm associated with pontine infarction in a patient with systemic lupus erythematosus

Takaki Murata et al. Radiol Case Rep. .

Abstract

Systemic lupus erythematosus (SLE) is an autoimmune disease that can affect multiple organ systems. Cerebral aneurysm formation is a rare central nervous system manifestation of SLE and tends to present as subarachnoid hemorrhage. Here, we report a 34-year-old woman with SLE complicated by a thrombosed aneurysm that had arose at the origin of a perforating artery, thereby causing obstruction of the artery and subsequent development of pontine infarction. Detailed examination of thin-slice CT and magnetic resonance imaging scans led to the correct diagnosis of uncommon cause of stroke.

Keywords: Basilar perforator aneurysm; CNS lupus; Cerebral infarction; Systemic lupus erythematosus.

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Figures

Fig 1
Fig. 1
Computed tomography (CT) without contrast enhancement was performed at 2 hours after symptom onset. Axial (A) and reformatted (B) coronal images revealed the presence of a small high-density lesion (arrows) close to the basilar artery (arrowheads).
Fig 2
Fig. 2
Diffusion-weighted imaging (DWI) (A) obtained at 2.5 hours after the onset of neurological symptoms revealed a faintly hyperintense lesion in the left side of the pons with corresponding low diffusivity on apparent diffusion coefficient (ADC) map (B) (arrow). Follow-up DWI (C) and ADC map (D) obtained 6 days later revealed clearly defined infarction in the left side of the pons with decreased diffusivity. Axial (E) and reformatted (F) coronal images from contrast-enhanced magnetization prepared rapid gradient echo imaging revealed the presence of a nonenhanced ovoid lesion (arrow) close to the enhanced basilar artery. Pontine infarction was observed as an area of decreased signal intensity on the same side as the ovoid lesion (arrowheads). The ovoid lesion was not observed using magnetic resonance angiography (G). Note the proximity of the ovoid lesion and pontine infarction and their position on the left side.
Fig 3
Fig. 3
Coronal reformatted images from dynamic contrast-enhanced CT obtained at 1 week before the onset of neurological symptoms. The early phase image (A) revealed the presence of an ovoid enhanced lesion close to the basilar artery. The delayed phase image (B) indicated that there was reduced attenuation of both the basilar artery and ovoid lesion. The similar densities as observed in both the early and delayed images indicate that the ovoid lesion was an aneurysm that had not yet thrombosed.
Fig 4
Fig. 4
Follow-up MRI at about 1 year later. Magnetic resonance angiography (A) revealed the presence of a high-intensity spot close to the basilar artery (arrow). Pre-contrast T1-weighted imaging (B) revealed the presence of a hyperintense nodular lesion (arrow) close to the basilar artery (arrowhead), indicating that the lesion was a basilar perforator aneurysm that still remained thrombosed.

References

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