MRI Abnormalities in Vitamin B12 Deficiency Myelopathy
abstracts & commentary
Sources: Katsaros VK, et al. MRI of spinal cord and brain lesions in subacute combined degeneration. Neuroradiol 1998;40:716-719; Locatelli ER, et al. MRI in vitamin B12 deficiency myelopathy. Can J Neurol Sci 1999;26:60-62.
Katsaros and colleagues describe a 60-year-old woman who presented with a gradual gait disturbance two months following a cholecystectomy, during which nitrous oxide was administered. She was unable to walk or stand without assistance, had a spastic ataxic paraparesis, with a right Babinski, and markedly reduced vibratory and position sense. There was a normal, slightly decreased Hgb and macrocytosis (13.1 g/dL, MCV 117.7), a low vitamin B12 "< 100 pg/mL," positive anti-parietal cell antibodies, and a normal cerebrospinal fluid exam. MRI analysis showed a continuous area of increased signal throughout the dorsal columns of the cervical spinal cord, with other scattered focal lesions in the brainstem and cerebellum. Following vitamin B12 therapy, the neurologic deficits improved such that she was walking independently by two months. The MRI abnormalities of the cervical cord only had resolved by four months.
Locatelli and colleagues report a 30-year-old woman with an 18-month history of progressive paraparesis, trunk and limb numbness, and urinary and bowel incontinence. MRI of the spinal cord showed increased signal from C3-C8, in the posterior columns more than lateral, with gadolinium enhancement. The patient had a macrocytic anemia (Hgb 7.9 g/dL, MCV 123) with a vitamin B12 of 60 pg/mL (nL 200-1610). Intrinsic factor antibodies were positive. She was treated for vitamin B12 deficiency and hypothyroidism, with modest clinical improvement, but with resolution of MRI findings after 42 days.
COMMENTARY
Patients presenting with paresthesias and ataxic paraparesis regularly undergo MRI scanning of the spinal cord and brain, which often may reveal areas of high signal in the central nervous system. As indicated by the the above reports, severe vitamin B12 deficiency resulting in subacute combined degeneration of the spinal cord must also be considered in the broad differential diagnosis, in addition to multiple sclerosis, collagen-vascular disease, sarcoidosis, or other intramedullary lesions such as neoplasm. With a clinically significant low B12 level, the patient may have a corresponding elevation in the serum/urinary methylmalonic acid or homocysteine level, positive antiparietal cell/anti-intrinsic factor antibodies, and/or a macrocytic anemia. However, the best method to make an accurate diagnosis of cobalamin/vitamin B12 deficiency is a source of much medical controversy (e.g., see Green R. Ann Int Med 1996;124:509-511; Green R, Kinsella LJ. Neurol 1995;45:1435-1440; Healton EB, et al. Medicine 1991;70:229-244).
Potentially confusing the diagnostic interpretation of the MRI abnormalities and clinical presentation is the possibility of concomitant neurologic or systemic disease. For example, some patients with clinically definite multiple sclerosis have been shown to have low vitamin B12 levels, possibly on an autoimmune basis (see Reynolds EH, et al. Arch Neurol 1992;49:649-652). Similarly, patients with alcoholic disease of the nervous system can have a contributing nutritional B12 and folate deficiency. In the patients described above, one had been treated with nitrous oxide, which can inactivate cobalamins, and the other had autoimmune hypothyroidism.
Delay in the diagnosis and treatment of subacute combined degeneration is more likely to result in a residual clinical deficit. Prompt B12 supplementation, 1000 mcg/d injection for one week followed by monthly injections, may limit the extent of neurologic disability.
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