P251 A rare case of cauda equina syndrome complicating axial spondyloarthropathy

Abstract

Abstract Background/Aims Cauda equina syndrome is a rare but disabling neurological complication of axial spondyloarthropathy (axSpA) that occurs many years after disease onset, and often in the absence of inflammatory symptoms. Its insidious onset in long-standing axSpA means that this is a condition that can easily be missed, and this case report describes such an instance. Methods: Case report An 82-year-old man diagnosed with HLA-B27 positive axSpA in 1972 developed symptoms of lumbar pain and thigh pain in 2012. He had nerve conduction studies which demonstrated an axonal sensory and motor peripheral neuropathy thought to be multifactorial in cause. He was unable to have a spinal MRI scan due to back pain. Over the years he had ongoing lumbar and sacral pain with increased lower limb weakness, and he became wheelchair bound. In 2014 he started adalimumab, then switched to golimumab. He felt some improvement in pain but never mobility. Over the next few years, he started to experience gastro-urological symptoms including diarrhoea, tenesmus, incontinence, and urinary retention. In March 2021 he presented to hospital with shortness of breath. He was found to have a pleural effusion and enlarged mediastinal lymph nodes consistent with lymphoma and/or lung malignancy. It was also noted that a spinal MRI scan had been requested a few months ago by his GP for ongoing sciatic pain, constipation, and tenesmus. This scan had showed an ankylosed spine, but also abnormal tissue occupying the thecal sac between S1 and S2 and the presence of arachnoiditis. It then came to light that the patient had also undergone a spinal MRI scan in 2014 after being admitted due to a fall. This scan had shown chronic distal cauda equina distortion and even then, had presence of an enlarged thecal sac at S1/2 and chronic arachnoiditis. These results had been overlooked. Results Cauda equina syndrome complicating long-standing axSpA was first reported in 1961. The pathophysiology in axSpA is not well understood but seems to occur in longstanding disease suggesting chronic progressive dural stiffening causes a damaging rise in CSF pressure that is transmitted to the sacral nerve roots. It is not considered to be due to active inflammation, and anti-TNF treatment can be non-beneficial. MRI imaging may show nerve clumping and distortion of the thecal sac. Management for this condition is not well established and surgical intervention may not be successful. The resulting neurological deficit can be severe and irreversible and high index of suspicion is needed to investigate and diagnose it. Conclusion Neurological symptoms should not be overlooked by the rheumatology team or attributed to a joint issue. Safety netting should be in place for following up the results of imaging investigations. Disclosure S. Byravan: None. F. Javaid: None. R. Neame: None.