case_images: PMC8260950_01
case_images: MRI and serological monitoring of the disease course. (A-F) Sagittal FLAIR and axial T1 gadolinium (Gad) sequences. (A) Numerous lesions with Gad enhancement at first admission. (B) MRI at re-admission showing more than 100 Gad-enhancing lesions. (C) Decrease of lesion load 7 days after the first dose of cyclophosphamide. (D) Further decrease of lesion load mirroring clinical remission at 15 days and (E) at 30 days. (F) At 44 days after cyclophosphamide treatment, no more Gad enhancement was detectable. (G) Leukocyte and lymphocyte count as well as serological neurofilament light chain levels during treatment.
case_images: fneur-12-696807-g0001.jpg
case_images: PMC8260950_01_fneur-12-696807-g0001.jpg
case_images: F1
case_images: The MRZ reaction (MRZR), anti-AQP4, and anti-MOG antibodies as well as vasculitis screening and virological/microbiological analyses were all negative (see Table 1). 1 day later, intravenous corticosteroids (1,000 mg/day for five consecutive days) were initiated, and on the following day, numerous supra- and infratentorial gadolinium (Gad)-enhancing and non-enhancing T2w as well as two Gad-enhancing spinal lesions consistent with the diagnosis of multiple sclerosis (MS) were seen on MRI (Figure 1A). MRI revealed a fulminant progression of the lesion load and Gad enhancement with now more than 100 Gad-enhancing lesions (Figure 1B). Serum NfL was 340 pg/ml as measured by ELISA (Figure 1G). While the total lesion load was stable, only 16 lesions were still active (Figure 1C). The patient was discharged with mild residual neurological deficits and was closely monitored both clinically and radiologically (Figures 1D-F).