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维生素B12缺乏神经综合征:一项临床、MRI及电诊断研究

Vitamin B12 deficiency neurological syndromes: a clinical, MRI and electrodiagnostic study.

作者信息

Misra U K, Kalita J, Das A

机构信息

Department of Neurology, Sanjay Gandhi PGIMS, Lucknow.

出版信息

Electromyogr Clin Neurophysiol. 2003 Jan-Feb;43(1):57-64.

PMID:12613142
Abstract

BACKGROUND

Vegetarianism is an important cause of vitamin B12 deficiency, especially in countries like India. We managed 17 patients with neurological syndrome due to vitamin B12 deficiency in a tertiary care referral teaching hospital which caters to relatively affluent population.

AIM

To evaluate neurophysiological and MRI changes in patients presenting with vitamin B12 deficiency neurological syndrome and interpret these is the light of reported autopsy findings.

SETTING

Tertiary care referral teaching hospital.

METHODS

Patients with vitamin B12 deficiency neurological syndrome diagnosed by low serum vitamin B12 and/or megaloblastic bone marrow were subjected to clinical evaluation and spinal MRI. The neurophysiological tests included nerve conduction studies, tibial somatosensory evoked potential (SEP), motor evoked potential (MEP) and visual evoked potential (VEP) studies. The recovery was defined on the basis of 6 months Barthel Index score into complete, partial or poor.

RESULTS

There were 17 patients with vitamin B12 deficiency neurological syndrome, 3 were females and 12 lactovegetarian. The clinical syndrome was that of myelopathy in 8, myeloneuropathy in 5, dementia myelopathy in 3 and neuropathy in 1 patient. All the patients had impaired joint position and vibration sensation in the lower limbs and 4 had in upper limbs as well. Lower limbs were spastic in 13 and upper limbs in 2 patients. Spinal MRI revealed T2 hyperintensity in cervicodorsal region in 6 and cord atrophy in 3 patients. Sural nerve conduction was abnormal in 8 and peroneal conduction in 5 patients. In one patient all sensory nerve conductions were unrecordable but motor conductions were normal. Tibial SEP was abnormal in 12 out of 15 and lower limb MEP in 8 out of 12 patients. P100 latency of VEP was prolonged in 7 out of 13 patients. Right to left asymmetry was present in tibial SEP in 4 and VEP in 2 patients. At 6 months followup 2 patients improved completely, 7 partially and 3 had poor recovery. Clinical recovery correlated with MEP but not with SEP or MRI changes.

CONCLUSION

The evoked potential and MRI changes in vitamin B12 deficiency neurological syndrome are consistent with focal demyelination of white matter in spinal cord and optic nerve. Myelopathic presentation is commoner and SEP is more frequently abnormal. The outcome at 6 months correlated with MEP changes.

摘要

背景

素食主义是维生素B12缺乏的一个重要原因,在印度等国家尤其如此。我们在一家为相对富裕人群服务的三级转诊教学医院诊治了17例因维生素B12缺乏导致神经综合征的患者。

目的

评估维生素B12缺乏神经综合征患者的神经生理学和MRI变化,并根据已报道的尸检结果对这些变化进行解读。

地点

三级转诊教学医院。

方法

对血清维生素B12水平低和/或骨髓呈巨幼样变诊断为维生素B12缺乏神经综合征的患者进行临床评估和脊髓MRI检查。神经生理学检查包括神经传导研究、胫后体感诱发电位(SEP)、运动诱发电位(MEP)和视觉诱发电位(VEP)研究。根据6个月的巴氏指数评分将恢复情况定义为完全恢复、部分恢复或恢复不佳。

结果

17例维生素B12缺乏神经综合征患者中,女性3例,纯素食者12例。临床综合征表现为脊髓病8例,脊髓神经病5例,痴呆脊髓病3例,神经病1例。所有患者下肢关节位置觉和振动觉均受损,4例患者上肢也有受损。13例患者下肢痉挛,2例患者上肢痉挛。脊髓MRI显示6例患者颈胸段T2高信号,3例患者脊髓萎缩。8例患者腓肠神经传导异常,5例患者腓总神经传导异常。1例患者所有感觉神经传导均无法记录,但运动传导正常。15例患者中有12例胫后SEP异常,12例患者中有8例下肢MEP异常。13例患者中有7例VEP的P100潜伏期延长。4例患者胫后SEP和2例患者VEP存在右向左不对称。随访6个月时,2例患者完全恢复,7例部分恢复,3例恢复不佳。临床恢复与MEP相关,但与SEP或MRI变化无关。

结论

维生素B12缺乏神经综合征的诱发电位和MRI变化与脊髓和视神经白质的局灶性脱髓鞘一致。脊髓病表现较为常见,SEP异常更为频繁。6个月时的预后与MEP变化相关。

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