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Neurological Sciences 2011-Feb

Serial nerve conduction studies in vitamin B12 deficiency-associated polyneuropathy.

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Chi-Ren Huang
Wen-Neng Chang
Nai-Wen Tsai
Cheng-Hsien Lu

關鍵詞

抽象

This report is on a 22-year-old male vegetarian with acute polyneuropathy secondary to vitamin B(12) deficiency. He presented with weakness and numbness of the distal limbs and absent deep tendon reflex in all four extremities. Nerve conduction study (NCS) showed an axonal type sensori-motor polyneuropathy. Serum biochemical studies revealed vitamin B(12) level of 119 pg/mL (reference range 185-710 pg/mL), with elevated creatine kinase (CK) (719 U/L) and homocysteine (Hcy) (24.04 μmol/L) levels. Anti-parietal cell antibody test was positive. The patient received both oral and intramuscular injection of vitamin B(12). The amplitude of the median and ulnar motor NCS increased 2.5 months later, while muscle power of the ankle plantar flexion and dorsiflexion recovered after 3.5 and 5.5 months, respectively. Follow-up NCS after 14.5 months showed response in sural NCS, but not the peroneal NCS. Follow-up also showed decreased serum Hcy and CK to 9.6 μmol/L and 198 U/L, respectively, and increasing amplitude of response. Recovery sequence involved muscle power of the proximal muscles, hands, plantar flexion, and dorsiflexion of the feet, and followed by sensory conduction.

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