To describe a suspected case of acute inflammatory demyelinating polyneuropathy (AIDP) found to be nitrous oxide-induced subacute combined degeneration (SCD) with atypical features.

Vitamin B12 deficiency classically causes SCD, with nonenhancing lesions involving the dorsal columns and corticospinal tracts. Twenty-five percent of patients with B12 deficiency will have a peripheral neuropathy, of which about 75% are axonal. CSF studies are usually normal. Nitrous oxide inhalation can cause an acute B12 deficiency.

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A 65-year-old male with treated urothelial carcinoma presented with two weeks of paresthesias in the legs and hands. He also had difficulty using tools for his work but no weakness.  His exam was significant for trace-to-absent reflexes, diminished pinprick and temperature in the legs and forearms, diminished vibration to the knees, and relatively spared proprioception. 

EMG/NCS demonstrated acute demyelinating sensorimotor polyneuropathy, and lumbar puncture demonstrated elevated protein to 104, so the patient was started on IVIg for possible AIDP. However, CSF studies were also significant for mild lymphocytic pleocytosis. The patient had sustained multiple tick bites but Lyme disease testing was negative, as were West Nile Virus testing, cytology, and flow cytometry. 

Due to lack of progression of symptoms, subjective abdominal sensory level, and pleocytosis, MRI cervical spine with and without contrast was obtained, and showed a nonenhancing T2-hyperintensity from C2-C6. 

Our case demonstrates a number of classic findings of subacute combined degeneration in nitrous-oxide induced B12 deficiency, such as nonenhancing T2 hyperintensities of the dorsal columns, but also a few atypical findings, including lymphocytic pleocytosis and demyelinating rather than axonal polyneuropathy.