Case Presentation: A 51-year-old male with a past medical history of diabetes, hypertension, and chronic kidney disease (CKD) presented to the hospital following a fall at home. The patient described a disease course that started six months prior with bilateral knee weakness and shooting pains that progressed to severe gait imbalance and inability to ambulate. Additionally, the patient had a notable decrease in sensation in his bilateral lower extremities below the level of the knees. He had no prior history of stroke, smoking, alcohol, or recreational drug use. He denied any recent illnesses, travel, tick bites, back pain or episodes of incontinence. Physical exam was significant for absent patellar and Achilles reflexes and 2/5 muscle weakness below the knees bilaterally, along with diminished proprioception and sensation to light touch. Laboratory workup was significant for CBC with anemia, CMP with CKD, ESR of 24 and vitamin B12 level of 241 with a positive intrinsic factor blocking antibody and elevated homocysteine level. Hemoglobin A1C was 8.2%, although it was 11.5% previously. Infectious disease workup was grossly normal. CSF studies revealed a protein of 165 but was otherwise normal. CT scan of the head, chest, abdomen was grossly normal. An MRI of the spine revealed no spinal canal compromise. EMG testing was significant for severe sensorimotor polyneuropathy with mixed axonal and demyelinating features.Patient was initially evaluated and treated for presumed chronic inflammatory demyelinating polyneuropathy (CIDP) with IVIG. However, it was felt the etiology of symptoms was likely to be multifactorial from diabetic polyneuropathy and vitamin B12 deficiency. Upon further review by the hospital medicine team, it was noted that the patient had a VDRL screening test that resulted negative. Given concern for underlying tabes dorsalis after further history taking, a treponema pallidium particle agglutination test was collected and resulted positive. The patient was then started on a two-week course of penicillin therapy in addition to high dose vitamin B12 injections and strict glycemic control, and on 1-week post-hospitalization follow-up, noted to ambulate 75 feet with a walker.

Discussion: Here we present a unique case of severe sensorimotor polyneuropathy with a mixed picture of infectious (tabes dorsalis), nutritional deficiency (B12), metabolic dysfunction (diabetes), and possible inflammatory (CIDP). Upon collecting a more thorough social history, it was discovered that the patient had been a service member in Southeast Asia in 1990 during which he had multiple encounters involving unprotected sex. However, he denied any symptoms, and therefore had no prior testing or treatment. It is important to note that treponemal antibodies often remain positive for years in contrast to non-treponemal titers that may decline during tertiary syphilis (1). In fact, in cases of suspected tertiary syphilis, VDRL testing is only 71% sensitive (2).

Conclusions: Tabes dorsalis is a consequence of neurosyphilis, and typically rare, but important to treat as it can lead to paralysis. Clinical suspicion with thorough history taking and appropriate diagnostic testing are the keys to timely and accurate diagnosis and subsequent treatment of neurosyphilis. As in our case, nontreponemal tests may be nonreactive and therefore, treponemal tests should be performed when there is suspicion for late forms of neurosyphilis.