Case Presentation: A 45-year old male was escorted to our tertiary medical center from a prison for evaluation of 40 lb weight loss, paraplegia and recently developed urinary and fecal incontinence. The patient had been on a 7-month long hunger-strike, during which he only consumed one meal per day. In addition to incontinence, he reported a progressive course of paresthesia, numbness and weakness in the legs. He became wheelchair bound four months into the strike. Neurological exam revealed a malnourished and disoriented male with 1/5 strength in the lower extremities, decreased muscle tone, bilateral lower leg swelling, and wasting of intrinsic foot muscles. The patient also had bilateral symmetrical loss of vibratory, tactile senses and proprioception in both legs, and areflexia in all extremities. CBC demonstrated moderate anemia with high MCV (107 fL), low serum vitamin B12 (82 pg/ml), and elevated homocysteine (272.8 µmol/L) and methylmalonic acid (83,248 nmol/L). Serum and RBC folate levels were normal. Spinal cord MRI and myelogram were unremarkable. Anti-parietal cell and anti-intrinsic factor antibodies were elevated. NCS/EMG demonstrated severe, symmetrical, distal polyneuropathy of the lower limbs. Venous duplex ultrasound examination showed bilateral lower extremity DVT. The patient was diagnosed with subacute combined degeneration and pernicious anemia. Cyanocobalamin injections were initiated. Within a month of treatment, strength in the lower extremities increased to 4/5; but his urinary incontinence persisted. Over the following nine months, the patient reached full hematological recovery; however, he remained weakened and Foley-dependent.

Discussion: This case illustrates how delays in diagnosing vitamin B12 deficiency can result in a personal tragedy. Presentation can occur without typical CBC changes and poses a formidable diagnostic challenge due to poor correlation between B12 levels and symptoms. Vitamin B12 deficiency promotes a hypercoagulable state, likely due to increased homocysteine which can lead to DVT and, potentially, pulmonary emboli. Neuropsychiatric symptoms often dominate over other symptoms, and appropriate treatment does not guarantee complete neurological recovery. Treatment extent, dosing and monitoring are poorly supported with evidence-based medicine. If vitamin B12 intake ceases, deficiency typically does not develop for at least one to two years, sometimes longer. Deficiency will develop faster in patients with pernicious anemia which promotes the depletion of vitamin B12 stores via decreased absorption and impaired enterohepatic circulation.

Conclusions: Vitamin B12 deficiency is still exceedingly common and likely underdiagnosed. The spectrum of manifestations varying from pancytopenia to neuropsychiatric symptoms is well defined, but the natural course of the deficiency is poorly understood in part due to its highly variable presentation. A high index of suspicion and prompt treatment are necessary to avoid irreversible sequelae.