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A 47-year-old female presented with subacute onset progressive backache, severe lancinating pain radiating to lower limbs, and bowel/bladder dysfunction over a period of 2 months duration. On examination, she had flaccid paraplegia, areflexia, and sensory loss in lower limbs. Diagnosis of severe cauda equina syndrome was considered. Magnetic resonance imaging (MRI) lumbosacral (LS) spine T2 sagittal images showed thickening and clumping of LS roots leading to the obliteration of cerebrospinal fluid (CSF) space. Contrast-enhanced MRI demonstrated intense enhancement of LS nerve roots and meninges [Figure [Figure1a1a and andb].b]. Lumbar puncture resulted in dry tap due to LS root hypertrophy and CSF space obliteration. Positron emission tomography-computed tomography (PET-CT) showed linear hypermetabolic ill-defined soft tissue in spinal canal, raising suspicion of malignancy [Figure 1c]. Histopathology and immunohistochemistry of meningeal biopsy arachnoid matter were suggestive of undifferentiated carcinoma [Figure 2]. Diagnosis of leptomeningeal carcinomatosis was confirmed. However, the primary source of malignancy was not detected in this patient.
Diffuse cauda equina enhancement is seen in leptomeningeal carcinomatosis and lymphomatosis as well as many nonneoplastic disorders such as tubercular arachnoiditis, sarcoidosis, demyelinating, and hereditary neuropathies. There is overlap in imaging features of inflammatory and neoplastic processes affecting LS roots. The rapidity of progression, presence of pain, and associated bowel/bladder involvement may suggest neoplastic etiology. PET-CT and histopathology help to confirm etiology. It is important to highlight that carcinomatous infiltration of cauda equina can be the presenting feature of underlying neoplasm. Based on imaging and histopathological features, diagnosis of leptomeningeal carcinomatosis can be pursued even if the primary source of neoplasm remains undetected.[1,2,3,4]
There are no conflicts of interest.