LAUSR

Editor – We read with interest the article published by Notghi and colleagues. The authors described a case of transverse myelitis, with symptoms manifesting 7 days post-administration of first dose of the AstraZeneca COVID-19 vaccination. The patient had a history of inactive pulmonary sarcoidosis. Due to the temporal association with the vaccine, lack of evidence supportive of active sarcoidosis on systemic imaging and the poor response to steroid therapy, the authors postulated that the myelitis is postvaccination rather than a vaccine triggered relapse of isolated neurosarcoidosis. Due to major implications, distinction is crucial. Post-vaccination immune-mediated response has been implicated in the pathogenesis of several neurological conditions including Guillain–Barré syndrome, acute demyelinating encephalomyelitis and transverse myelitis. Similarly, vaccine administration may trigger a flare-up of pre-existing inflammatory conditions. Recent reports have described a role of vaccination in triggering a relapse of chronic immune-mediated conditions including rheumatological diseases, minimal change disease and microscopic polyangiitis. Taking this point into account would make the temporal link not useful in discriminating between a purely vaccine-induced disease and a vaccine triggered relapse of inactive disease. From reading the article, we have also noted that the authors felt that lack of active systemic features of sarcoidosis make neurosarcoidosis unlikely. While patients with neurosarcoidosis often have other systems involvement, several studies have reported isolated neurosarcoidosis. We have also noted that some crucial investigations have not been performed in this case, including cerebrospinal fluid (CSF) angiotensin converting enzyme (ACE) and CD4/CD8 ratio. Although insensitive, CSF ACE may be reasonably specific for neurosarcoidosis. Additionally, combined elevation of CD4/CD8 ratio and CSF lymphocytosis may provide a specificity of 95% for neurosarcoidosis. Measuring CSF interleukins may also play a useful role in this clinical context. Finally, the observed clinical improvement is likely due to steroids starting to take effect rather than plasma exchange that would not be expected to exert a theraputic response by day 2 of the treatment cycle. We suggest close monitoring of this category of patients for features suggestive of re-emergence of quiescent disease, and we strongly advocate discussing such complex cases at specialised neuro-inflammatory multidisciplinary meetings to guide further management. TARIG ABKUR Senior specialist registrar in neurology, Southmead Hospital, Bristol, UK