case_images: PMC10702582_01
case_images: Skin changes and longitudinal MRI of brain and spinal cord. Localised painful rash with crusts on the neck and lateral face initially due to repetitive scratching in central neuropathic pain syndrome initially misdiagnosed as herpes zoster reactivation (A). Cerebral T2-weighted FLAIR MRI showing a new hyperintense parahippocampal lesion that evolved within 6 days from symptom onset (B) and presented gadolinium enhancement (C). T2 hyperintense lesions in both optic nerves consistent with optic neuritis (D). Hyperintense spinal cord lesions compatible with cervical longitudinally extensive transverse myelitis reaching from the atlas to the 6th vertebra upon admission to our tertiary care centre (E,F) and after 6 months (G,H).
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case_images: PMC10702582_01_fneur-14-1297341-g001.jpg
case_images: fig1
case_images: Over the next 3 days there was a marked clinical deterioration: The patient developed a vesiculopapular rash with secondary clustered crustation on her neck, ear and decolletage (Figure 1A) and became increasingly agitated and confused. A follow-up cerebral MRI revealed a right parahippocampal T2 lesion that was not evident on the initial MRI (Figures 1B,C). In addition, there were T2 hyperintense lesions in both optic nerves, which were consistent with optic neuritis (Figure 1D). MRI of the spinal cord revealed spinal cord T2 hyperintense lesion locations and extension compatible with transverse myelitis (Figures 1E,F). When we administered the second cycle of INE at the six-month follow-up, there were no new cerebral lesions and the inflammatory cervical myelopathy decreased in volume (Figures 1G,H).
case_images: Timeline of the disease course. After initial high-dose i.v. methylprednisolone therapy, seven plasma exchange sessions (PLEX) were performed, and concomitant prednisolone was tapered to a dose of 5 mg/d over 6 months. The first cycle of INE infusions was administered a few days after PLEX, with a 14-day interval. The overall EDSS improved from 7.5 to 4.0 at 6 months and remained stable over the 12-month follow-up period, with persistent deficits mainly representing visual impairment.
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case_images: PMC10702582_01_fneur-14-1297341-g002.jpg
case_images: fig2
case_images: A synopsis of the clinical course is shown in Figure 2.