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Vitamin B12 deficiency in spinal cord injury: a retrospective study. | LitMetric

Vitamin B12 deficiency in spinal cord injury: a retrospective study.

J Spinal Cord Med

Spinal Cord Injury Service, Veterans Affairs Puget Sound Health Care System, Seattle, Washington 98108, USA.

Published: August 2003

AI Article Synopsis

  • Vitamin B12 deficiency is underrecognized in spinal cord injury patients, with 16 out of 34 showing probable deficiency over a 10-year study period.
  • Most had subnormal or low-normal levels without classic symptoms like paresthesias due to existing sensory impairments from their injuries.
  • Replacement therapy resulted in various clinical improvements, including reversal of anemia, improved gait, and enhanced mood and memory for several patients.

Article Abstract

Background/objective: Vitamin B12 (or cobalamin) deficiency is well known in geriatric patients, but not in those with spinal cord injury (SCI). This retrospective study describes vitamin B12 deficiency in SCI.

Methods: This study utilized a retrospective chart review of patients with SCI who had received serum vitamin B12 testing over the last 10 years.

Results: Probable vitamin B12 deficiency was noted in 16 patients with SCI. Twelve patients had subnormal serum vitamin B12 levels (< 220 pg/mL), whereas 4 patients had low-normal vitamin B12 levels (< 300 pg/mL) with neurologic and/or psychiatric symptoms that improved following vitamin B12 replacement. Classic findings of paresthesias and numbness often were not evident; such findings likely were masked by the pre-existing sensory impairment caused by SCI. Of the 16 SCI patients, 7 were ambulatory; 4 of the 7 presented with deterioration of gait. In addition, 3 of the 16 SCI patients presented with depression and fatigue, 2 had worsening pain, 2 had worsening upper limb weakness, and 2 had memory decline. Of the 12 patients with subnormal serum vitamin B12 levels, 6 were asymptomatic. Classic laboratory findings of low serum vitamin B12, macrocytic red blood cell indices, and megaloblastic anemia were not always present. Anemia was identified in 7 of the 16 patients and macrocytic red blood cells were found in 3 of the 16 patients. Only 1 of the 16 SCI patients had a clear pathophysiologic mechanism to explain the vitamin B12 deficiency (ie, partial gastrectomy); none of the patients were vegetarian. Twelve of the SCI patients appeared to experience clinical benefits from cyanocobalamin replacement (some patients experienced more than 1 benefit), including reversal of anemia (5 patients), improved gait (4 patients), improved mood (3 patients), improved memory (2 patients), reduced pain (2 patients), strength gain (1 patient), and reduced numbness (1 patient).

Conclusion: It is recommended that physicians consider vitamin B12 deficiency in their patients with SCI, particularly in those with neurologic and/or psychiatric symptoms. These symptoms often are reversible if treatment is initiated early.

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Source
http://dx.doi.org/10.1080/10790268.2003.11753669DOI Listing

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