Rehabilitation essential in the recovery of multifactorial subacute combined degeneration

Abstract

Subacute combined degeneration (SCD) is a rapidly progressive myelopathy with a constellation of neurologic deficits, including progressive sensory abnormalities in the vibratory and proprioceptive domains, ascending paresthesias, gait ataxia, hyper- or hypo-reflexia, and, less commonly, motor weakness and loss of bowel and bladder control [1,2]. SCD is a result of dorsal and lateral spinal cord demyelination [3]. This form of myelopathy is secondary to a cobalamin or vitamin B12 deficiency, dietary insufficiency, malabsorption and/or, less commonly, excretion. Pernicious anemia, also known as autoimmune gastritis, is a common cause of vitamin B12 deficiency. Nitrous oxide (N2O) exposure during recreational use or surgical intervention has also been reported to convert B12 to B12 analogues, which are then excreted in the urine, reducing B12 levels [3,4]. Up until now, much of the literature has presented the clinical manifestations of SCD primarily in the context of nitrous oxide (N2O) abuse and exposure. Conversely, we report on a patient with a triple-insult SCD of the spinal cord, one insult secondary to noncompliance with B12 replacement therapy for pernicious anemia, one insult secondary to alcohol abuse, and one insult secondary to prolonged recreational use of nitrous oxide.