Vitamin B12 deficiency neuropathy: A clinical and electrophysiological study

Vitamin B12 deficiency is a metabolic disorder with many causes. The neurological features of vitamin B12 deficiency are heterogeneous [2]. Peripheral neuropathy often described [3], but its frequency and its type is controversial [1]. The present study was conducted to describe electro-clinical pre...

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Bibliographic Details
Published in:Neurophysiologie clinique Vol. 48; no. 3; p. 130
Main Authors: Bouattour, Nadia, Sakka, Salma, Farhat, Nouha, Kacem, Hanen Haj, Hdiji, Olfa, Dammak, Mariem, Mhiri, Chokri
Format: Journal Article
Language:English
Published: Paris Elsevier Masson SAS 01-06-2018
Elsevier Science Ltd
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Summary:Vitamin B12 deficiency is a metabolic disorder with many causes. The neurological features of vitamin B12 deficiency are heterogeneous [2]. Peripheral neuropathy often described [3], but its frequency and its type is controversial [1]. The present study was conducted to describe electro-clinical presentations of peripheral neuropathy in patients with vitamin B12 deficiency. A Retrospective review of 32 subjects with neurological abnormalities due to vitamin B12 deficiency, were subjected to a detailed motor and sensory nerve conduction studies of median, ulnar, external popliteal sciatic, internal popliteal sciatic and sural nerves. Patients that have another reason for neuropathy or another disease that can effect nerve conduction studies were excluded. The median age of the patients was 51 (±16.57) years old, (range 18–84 years old), sex ratio (M/F) was 1.66 (20/12). Clinical features of neuropathy: paraesthesia, hyporeflexia, ataxia and limb weakness were present in 20 (62.5%) patients. Electromyography showed abnormal nerve conduction in 25 (78.12%) patients and it was normal in 7 (21.88%) patients. On nerve conduction study: 16 (50%) had axonal impairment, 3 (9.3%) had demyelinating neuropathy and 6 (18.75%) had mixed features. Eleven patients (34.37%) presented a pure sensory impairment and 14 (43.75%) presented mixed pattern sensory and motor impairment. All cases underwent treatment with intramuscular hydroxocobalamin treatment (daily injection of 1000μg cyanocobalamin for 4 weeks, followed by injections of 1000μg each month) with marked clinical and haematological improvement. We conclude that nearly 80% patients with neurologic manifestations of vitamin B12 deficiency had evidence of peripheral neuropathy which is mainly axonal with some demyelinating features. Sensory and motor nerve conduction were affected. Evolution is generally good if the treatment was initiated early.
ISSN:0987-7053
1769-7131
DOI:10.1016/j.neucli.2018.05.007