Subacute combined degeneration (SCD) of the spinal cord is a complication of vitamin B12 deficiency, which is reversible if diagnosed and treated early. There is dysfunction of the dorsal column,
lateral corticospinal tract and sometimes lateral spinothalamic tracts of the spinal cord (2). B12 deficiency is frequently associated with pernicious anemia, malabsorption syndromes, or a decreased
intake of B12. Inadequate intake of B12 is rare in western countries, and its deficiency has been reported in vegetarians, as occurred in our patient, alcoholics or as a complication of administering
nitrous oxide anesthesia (1). The initial symptoms are usually paresthesia in the hands and feet. This condition may progress to sensory loss, gait ataxia and distal weakness, particularly in the
legs. The diagnosis of B12 deficiency is based on a low serum B12 level. Pathologic studies of the spinal cord show multifocal demyelinated and vacuolated lesions in the posterior, lateral, and
sometimes anterior columns of the thoracic and cervical spinal cord, whereas involvement of the medulla may occasionally be seen (2). The mechanism of myelopathy has not been elucidated; it has been
postulated that B12 interferes with methylation reactions of myelin phospholipids, so that a lack of B12 results in unstable myelin (2). Treatment of SCD includes lifelong administration of B12 (1).
Descriptions of SCD are scarcely found in the radiological literature. On MR imaging, SCD is seen as an intramedullary lesion with an increased signal on T2-weighted images which involve mailnly the
dorsal columns as shown in our patient (2–4). Enhancement of the lesion after gadolinium administration and mild expansion of the spinal cord may also be seen (2,3,5). SCD should be considered
in the differential diagnosis of an intramedullary lesion that includes demyelinating disorders, infectious causes such as ADEM and HIV vacuolar myelopathy, inflammatory processes such as
sarcoidosis, ischemia, and neoplasms. The location of the SCD in the posterior columns may narrow down the differential diagnosis although it is a nonspecific finding; posterior columns are typically
affected in demyelinating disease, but the size of the lesions do not exceed two vertebral bodies and are usually multiple, whereas in SCD, the abnormal signal extends in length over several
continuous vertebral bodies. Sarcoidosis frequently involves the pial surface of the spinal cord with an intramedullary extension, whereas the lesions are more scattered and nodular. In ADEM, the
patient typically has a history of antigenic challenge days or weeks prior to the onset of symptoms. Neoplastic or inflammatory processes cause a more prominent enhancement or cord expansion or both;
however, the differential diagnosis may be impossible to make on the basis of imaging findings alone. Vacuolar myelopathy pertaining to AIDS may resemble SCD both pathologically and on MR imaging and
the differential diagnosis is based on the history (2,4). The diagnosis of SCD is confirmed by the resolution of clinical symptoms and radiologic findings after parenteral administration of B12.
Resolution of symptoms is inversely proportional to their duration and severity, and therefore, it is necessary to make an early diagnosis (1). MR imaging may contribute in making a prompt diagnosis
and in evaluation of the efficacy of the treatment.