This one 'struck a cord': When clinical history matters more than the MRI.

Kakkar, V.; Marzo-Ortega, H.

This one 'struck a cord': When clinical history matters more than the MRI.

All Authors

Kakkar, V.

Marzo-Ortega, H.

LTHT Author

Kakkar, Vishal
Marzo-Ortega, Helena

LTHT Department

NIHR Leeds Biomedical Research Centre
Rheumatology

Publication Date

2025

Item Type

Conference Abstract

Abstract

Introduction: Transverse myelitis (TM) is a rare inflammatory condition of the spinal cord with multiple potential triggers, including infections, autoimmune disorders, and, rarely, vaccinations. Post-vaccination TM has been primarily associated with live vaccines, including the earlier live herpes zoster vaccine. Shingrix (GlaxoSmithKline), a recombinant subunit vaccine, is now routinely offered to severely immunosuppressed patients over 50. To date, there are no published reports of TM following Shingrix. We describe a patient who developed thoracic myelitis following Shingrix administration, initially misattributed to functional neurological disorder, underscoring the importance of high-quality imaging, clinical intuition, and consideration of vaccine-associated complications. Case description: A 65-year-old retired male estate agent with ankylosing spondylitis (AS) and on anti-TNF therapy since 2010 presented to A&E with acute urinary retention, right leg sensory loss (L2-S1), and bilateral lower limb weakness (right > left). Cranial nerves were intact and anal tone preserved. Notably, he had received the Shingrix vaccine four days earlier and had suffered a close bereavement two months prior. Initial lumbar and sacroiliac MRI showed fused SI joints and degenerative changes without compressive lesions. Head MRI and EMG were normal. Neurology diagnosed functional neurological disorder, advising physiotherapy and psychological input. However, his partner, concerned by the diagnosis, contacted our rheumatology team for advice based on the longstanding relationship due to his AS. After review, and based on our prior knowledge of this patient, our team felt that the neurological diagnosis given was out of character with this gentleman's personality. Suspecting an inflammatory condition, an intramuscular 120 mg methylprednisolone acetate injection was prescribed together with a reducing prednisolone regime. A second neurology opinion reaffirmed the original diagnosis based on existing imaging. Following steroid treatment, there was partial improvement in motor and bladder symptoms, though sensory deficits remained. At the insistence of the partner and with rheumatology support, the patient was referred to a tertiary neurology centre. Repeat MRI revealed a short segment of myelitis at the C3 level, correlating with a T8 sensory level and mild spastic paraparesis. It was determined the initial MRI had insufficient imaging at this level. The final diagnosis was post-Shingrix vaccination transverse myelitis, made five weeks after initial presentation. He was treated with oral methylprednisolone (500 mg/day for 5 days) and solifenacin for detrusor hyperreflexia. Two months later, he shows slow recovery with improved bladder and sensory symptoms, but persistent motor weakness. He remains under joint care of rheumatology, neurology, and urology teams. Discussion(s): This case highlights a rare and potentially first-reported instance of TM following administration of the Shingrix vaccine. While TM has been previously linked to the live shingles vaccine, the recombinant formulation was presumed safer in immunocompromised populations. The temporal relationship between vaccination and symptom onset, combined with the lack of other plausible causes, supports a vaccine-related immune-mediated aetiology. There have been previous examples of recombinant vaccines associated with TM. Taken together, this suggests that recombinant vaccinations, while generally safe, may in rare cases trigger neuroinflammatory responses, especially in susceptible individuals. With the Shingrix vaccine, this has also previously been reported as a possible risk factor for inducing Guillain-Barre syndrome. Diagnostic challenges were considerable in this case, particularly given the patient's history of a recent bereavement, and initial imaging being reported as non-diagnostic. Furthermore, the symptoms were misattributed to a functional neurological disorder with this diagnosis upheld by two different consultants. However, this patient was well known to our rheumatology team, whose familiarity with his baseline status and clinical context contributed significantly to pushing for further investigation. The rheumatology team, recognising that the presentation deviated from functional patterns, actively encouraged the family to persist with seeking reassessment. Subsequent review at the tertiary neurology centre revealed a short segment myelitis at the C3 level, which had not been fully captured in earlier scans. Corticosteroid therapy led to neurological improvement. This case highlights the value for continuity of care, attentive listening to patients and families, and an openness to re-evaluate initial conclusions in light of evolving evidence. In addition, the caveats of incomplete or suboptimal investigations led to a misdiagnosis. Finally, this case calls for vigilance around post-vaccination neurological symptoms, even with recombinant vaccines like Shingrix, and supports reporting of such cases to pharmacovigilance systems and the wider medical community. Key learning points: * First reported case of Shingrix-associated TM: This may be the first published case linking Shingrix, a recombinant herpes zoster vaccine, to transverse myelitis. * Continuity of care matters: The patient was well known to our rheumatology team, whose prior knowledge of his baseline functional status and character helped distinguish this from a functional presentation. This relationship encouraged the family to persist in their advocation for further assessment and the importance of a "second opinion", leading to further investigation and a revised diagnosis. * Recombinant vaccines and TM: While Shingrix has not previously been associated with TM, similar associations have been reported with recombinant COVID-19 vaccines, suggesting possible shared immunogenic pathways. * History matters more than MRI: Early imaging failed to detect the lesion, emphasising the need to align imaging with evolving clinical symptoms and maintain diagnostic flexibility. * Beware premature functional diagnoses: Initial labelling of the symptoms as functional delayed appropriate therapy. Organic pathology must be excluded thoroughly, especially in patients with complex histories. * Multidisciplinary input is essential: Collaboration between neurology, rheumatology, neuroradiology, and the patient's family was key to reaching the correct diagnosis. * Treatment response: High-dose corticosteroids led to partial recovery, reinforcing the immune-mediated nature of the disease. * Learning objectives: * Recognise signs of TM, even when imaging is initially unrevealing. * Consider recombinant vaccines as possible, albeit rare, triggers of TM. * Value long-term clinician-patient relationships in shaping clinical judgment. * Strengthen collaboration across specialties and with families. * Report suspected vaccine-related adverse events to support pharmacovigilance and broader learning.