Abstract
Background Subacute combined degeneration of the spinal cord is caused by vitamin B 12 deficiency and is a kind of degenerative disease owing the characteristics of nervous system diseases. In addition, different patients have variously clinical manifestations and various prognoses after vitamin B 12 therapy. Objective To investigate and analyze diagnosis, clinical manifestations and prognosis of subacute combined degeneration of the spinal cord. Design Case analysis. Setting Department of Neurology, the Third Hospital of Peking University. Participants A total of 21 subacute combined degeneration of the spinal cord patients including 14 males and 7 females aged from 33 to 82 years were selected from Department of Neurology, the Third Hospital of Peking University from January 1999 to December 2005. Duration from onset to final diagnosis lasted for 1.5–108 months. All patients had typically clinical manifestations; meanwhile, level of serum vitamin B 12 was decreased and/or vitamin B 12 therapy was effective. All patients provided the confirmed consent. Methods Clinical data of 21 subacute combined degeneration of the spinal cord patients were retrospectively analyzed, while general data and clinical characteristics were recorded at the same time. Levels of blood routine, serum vitamin B 12 and homocysteine were measured at the phase of hospitalization. Normal value of serum vitamin B 12 was 187–1 059 ng/L and normal value of serum homocysteine was 5–15 μmol/L. All patients received neuroelectrophysiological examination and 15 patients received MRI examinations of spinal cord. After final diagnosis, patients were given vitamin B 12 therapy. And follow-up was performed to investigate the prognosis. Main outcome measures ▪ Levels of blood routine, serum vitamin B 12 and homocysteine; ▪ results of neuroelectrophysiological examination; ▪ results of MRI examination of spinal cord; ▪ prognosis. Results Clinical data of 21 patients and follow-up data of 20 patients were involved in the final analysis and 1 patient was lost because of living in the other province. ▪ Clinical manifestations: All 21 patients had typically clinical manifestations. The original symptoms included numbness of lower and/or upper limbs (5 cases), unstable gait (3 cases), limb asthenia (4 cases), limb numbness combined with light asthenia (5 cases), limb numbness combined with unskillful activity (3 cases), and limb numbness combined with unstable gait (1 case). ▪ Experimental results: Eight subacute combined degeneration of the spinal cord patients accompanied with mild-severe anemia and mean corpuscular volume of 13 patients were increased. Among 13 subacute combined degeneration of the spinal cord patients not administrating vitamin B 12 before hospitalization, the levels of serum vitamin B 12 of 2 patients were not measured but those of other patients were decreased. After vitamin B 12 therapy, the levels of serum vitamin B 12 of 8 patients were normal or increased. In addition, the levels of serum homocysteine of 6 patients were not measured but those of 7 patients were increased. While, the levels of homocysteine of 5 following-up patients were normal. The levels of serum vitamin B 12 of 8 patients who received with vitamin B 12 therapy before hospitalization were normal or increased. Among them, the levels of homocysteine were not measured in 4 patients, those of 3 patients were increased, and that of 1 patient was normal. ▪ Results of neuroelectrophysiological examination: Among all patients, 95% (20/21) patients had abnormal sensory-evoked potential, 89% (8/9) patients had abnormal motor evoked potential, 67% (10/15) patients had abnormal nerve conduction, 13% (2/15) patients had neurogenic muscle injury showed by electromyography (EMG), 70% (7/10) patients had abnormal brain-stem auditory evoked potential, and 40% (4/10) patients had abnormal visual evoked potential. ▪ Results of MRI examination of spinal cord: MRI examination demonstrated that 40% (6/15) patients had spinal cord lesion, but spinal cord lesion disappeared in 2 patients during follow up. In addition, clinical manifestations of patients were improved after standard vitamin B 12 therapy. Conclusion Nervous system lesion caused by vitamin B 12 deficiency is not only involved in spinal cord, also in peripheral nerve, optic nerve, auditory pathway, etc. Diagnosis of the lesion depends on clinical characteristics and level of serum vitamin B 12. Especially, neuroelectrophysiological examination, measurement of homocysteine and MRI examination of spinal cord are beneficial for diagnosis and evaluation of therapeutic effects.
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