Introduction
Magnetic resonance imaging (MRI) of the cervical spine is a commonly performed study for evaluation of cervical pain, radiculopathy, and myelopathy. Recognition of less common non-neoplastic disease processes is essential in order to diagnose and properly treat these entities.
Cobalamin or vitamin B12 is an organometallic compound not produced by the human body but is incorporated, instead, into the diet via meat and dairy products. It is bound in the duodenum to intrinsic factor (IF). This cobalamin-IF complex is resistant to proteolysis and is absorbed into the blood stream as it makes its journey to the distal small bowel.[1] This route of B12 intake is adequate for everyone except for strict vegetarians and their breastfed children. Pernicious anemia is the most common cause of cobalamin deficiency in temperate climates. Other conditions leading to cobalamin deficiency include malabsorption states, ileal resection, massive bacterial colonization of the intestines, and tropical sprue.[1]
Cobalamin deficiency affects not only the blood (megaloblastic anemia) and gastrointestinal tract, but also the nervous system, where it can result in subacute combined degeneration (SCD). The peripheral nerves, spinal cord, and cerebrum may also be involved.[1] In the spinal cord, involvement of the dorsal columns, lateral corticospinal tracts, and, occasionally, the lateral spinothalamic tracts leads to signs and symptoms, such as hand and feet paresthesia, numbness, sensory loss, gait ataxia, and mainly distal lower extremity weakness. If untreated, ataxic paraplegia may develop.[1,2]
Histologically, multifocal demyelination and vacuolization may be found in the posterior, lateral, and, occasionally, anterior columns.[3] Axonal degeneration and, ultimately, axonal death is characteristic.[1] The progression of demyelination is often from dorsal columns to lateral columns, with subsequent Wallerian degeneration. Cervical and thoracic cord lesions are typical, and the medulla may also be affected.[3]
MR imaging of SCD includes expansion of the affected cervical and thoracic cord segments with T2 prolongation, mainly of the dorsal columns and, occasionally, slight enhancement after gadolinium administration[4,5] (Figure 1). Lateral column involvement on MR imaging is usually not apparent, even though signs and symptoms may be attributable to these tracts.[6] Within the brain, multiple confluent areas of white matter T2 prolongation are seen. The differential diagnoses of an intramedullary lesion exhibiting non-specific characteristics similar to SCD include infectious (herpes virus, HIV vacuolar myelopathy), inflammatory (sarcoid), demyelinating (multiple sclerosis), ischemic, and, to a lesser degree, neoplastic processes (astrocytomas and ependymomas).[7] The main findings indicating the diagnosis of SCD are the clinical picture and the dorsal signal abnormality.
Subacute combined degeneration-vitamin B12 deficiency. (A) Sagittal T2-weighted image with signal abnormality in posterior columns (arrows). (B) Sagittal T1- weighted image shows no significant intramedullary signal abnormality. (C) Axial gradient-echo sequence confirms posterior column signal abnormality (arrow).
Subacute combined degeneration-vitamin B12 deficiency. (A) Sagittal T2-weighted image with signal abnormality in posterior columns (arrows). (B) Sagittal T1- weighted image shows no significant intramedullary signal abnormality. (C) Axial gradient-echo sequence confirms posterior column signal abnormality (arrow).
Subacute combined degeneration-vitamin B12 deficiency. (A) Sagittal T2-weighted image with signal abnormality in posterior columns (arrows). (B) Sagittal T1- weighted image shows no significant intramedullary signal abnormality. (C) Axial gradient-echo sequence confirms posterior column signal abnormality (arrow).
Treatment for cobalamin deficiency is intramuscular cyanocobalamin administration and management of any underlying disorder. Although patients show excellent response to treatment with regard to the hematologic manifestations, neurological symptoms may remain refractory.[1] Early treatment initiation may lead to clinical improvement in myelopathic symptoms with an accompanying decrease in dorsal spinal cord T2 prolongation.[7] Early diagnosis is critical, as clinical improvement of SCD is inversely proportional to its duration and severity.[2,4]
Appl Radiol. 2003;32(11) © 2003 Anderson Publishing, Ltd.
Cite this: MRI of the Cervical Spine: Unusual Non-Neoplastic Disease - Medscape - Nov 01, 2003.
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