Background:Cerebral amyloid angiopathy–related inflammation is a rare condition with approximately 100 reported cases. Its clinical manifestations are varied. We report here a novel presentation of this disease.Case presentation:A 61-year-old Caucasian man presented with rapidly progressive paralysis of the IX, X, XI and XII right cranial nerves associated with right central facial nerve palsy. Brain computed tomography angiography and cerebral catheter angiography found a focal fusiform enlargement of the distal cervical portion of the right internal carotid artery, related to a pseudo-aneurysm suggesting an evolution of a dissection and intra-cranial vessel dysplasia. Brain magnetic resonance imaging showed multiple asymmetrical subcortical regions of hyperintensity on T2 fluid-attenuated inversion recovery sequences. Punctiform cortical hyposignals on T2-weighted gradient echo magnetic resonance imaging sequences were mostly congruent with the white matter hyperintensities. There was a decreased cerebral perfusion at the frontal hyperintense fluid-attenuated inversion recovery region. Spectrometry identified a lactate–lipid peak. A brain biopsy showed intravascular amyloid deposits. Corticosteroid therapy was initiated, leading to a dramatic improvement of both clinical condition and magnetic resonance imaging brain lesions.Conclusion:This case report suggests that extra-cranial vasculitis and dysplasia can exceptionally be found in patients satisfying cerebral amyloid angiopathy–related inflammation criteria.
BACKGROUND: Identifying patients at risk of secondary neurologic deterioration (SND) after moderate traumatic brain injury (moTBI) is a challenge, as such patients will need specific care. No simple scoring system has been evaluated to date. This study aimed to determine clinical and radiological factors associated with SND after moTBI and to propose a triage score. METHODS: All adults admitted in our academic trauma center between January 2016 and January 2019 for moTBI (Glasgow Coma Scale [GCS] score, 9–13) were eligible. SND during the first week was defined either by a decrease in GCS score of >2 points from the admission GCS in the absence of pharmacologic sedation or by a deterioration in neurologic status associated with an intervention, such as mechanical ventilation, sedation, osmotherapy, transfer to the intensive care unit (ICU), or neurosurgical intervention (for intracranial mass lesions or depressed skull fracture). Clinical, biological, and radiological independent predictors of SND were identified by logistic regression (LR). An internal validation was performed using a bootstrap technique. A weighted score was defined based on beta (β) coefficients of the LR. RESULTS: A total of 142 patients were included. Forty-six patients (32%) showed SND, and 14-day mortality rate was 18.4%. Independent variables associated with SND were age above 60 years (odds ratio [OR], 3.45 [95% confidence interval {CI}, 1.45–8.48]; P = .005), brain frontal contusion (OR, 3.22 [95% CI, 1.31–8.49]; P = .01), prehospital or admission arterial hypotension (OR, 4.86 [95% CI, 2.03–12.60]; P = .006), and a Marshall computed tomography (CT) score of 6 (OR, 3.25 [95% CI, 1.31–8.20]; P = .01). The SND score was defined with a range from 0 to 10. The score included the following variables: age >60 years (3 points), prehospital or admission arterial hypotension (3 points), frontal contusion (2 points), and Marshall CT score of 6 (2 points). The score was able to detect patients at risk of SND, with an area under the receiver operating characteristic curve (AUC) of 0.73 (95% CI, 0.65–0.82). A score of 3 had a sensitivity of 85%, a specificity of 50%, a VPN of 87%, and a VPP of 44 % to predict SND. CONCLUSIONS: In this study, we demonstrate that moTBI patients have a significant risk of SND. A simple weighted score at hospital admission could be able to detect patients at risk of SND. The use of the score may enable optimization of care resources for these patients.
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