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April 10, 2018; 90 (15 Supplement) April 25, 2018

Vitamin B6 Toxicity Revisited: A Case of Reversible Pyridoxine-associated Neuropathy and Disequilibrium. (P4.021)

Rohitha Moudgal, Shahla Hosseini, Patricia Colapietro, Oluwole Awosika
First published April 9, 2018,
Rohitha Moudgal
1University of Cincinnati College of Medicine Cincinnati OH United States
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Shahla Hosseini
2University of Cincinnati Department of Neurology and Rehabilitation Medicine Cincinnati OH United States
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Patricia Colapietro
2University of Cincinnati Department of Neurology and Rehabilitation Medicine Cincinnati OH United States
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Oluwole Awosika
2University of Cincinnati Department of Neurology and Rehabilitation Medicine Cincinnati OH United States
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Citation
Vitamin B6 Toxicity Revisited: A Case of Reversible Pyridoxine-associated Neuropathy and Disequilibrium. (P4.021)
Rohitha Moudgal, Shahla Hosseini, Patricia Colapietro, Oluwole Awosika
Neurology Apr 2018, 90 (15 Supplement) P4.021;

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Abstract

Objective: To present the salient features, and reversibility of pyridoxine (vitamin B6) induced peripheral neuropathy, in conjunction with its electrodiagnostic correlate.

Background: B-Complex vitamins are essential for functioning of the nervous system, and supplementation is generally well tolerated. Although rare, excess pyridoxine can lead to paradoxical neurotoxicity— resulting in irreversible sensory neuropathy. Herein, we report a case of reversible pyridoxine induced sensorimotor neuropathy and disequilibrium in an octogenarian.

Case: 87-year-old right-handed Caucasian female with a four-year history of supplementing with B-Complex vitamins for chronic gastrointestinal illness, presents with five months of progressively worsening fatigue, left lower extremity weakness, numbness, and ataxia. Neurologic examination was notable for pronounced atrophy of foot intrinsics (right >left) and hand interossei. Sensory examination was notable for length dependent multimodal sensory loss in a stocking-glove pattern, and diminished joint position sense. She had absent deep tendon reflexes in both upper and lower extremities, and a steppage gait on the left. Work-up: Serum pyridoxine were markedly elevated at 398.4 nmol/L (ref: 20.0 – 125.0). Additional work-up, including serum B12, hemoglobin A1c, thyroid panel, SPEP/UPEP were unremarkable. MRI of cervical-lumbar spine showed degenerative changes, and was otherwise unremarkable. Nerve conduction studies of the left lower extremity were notable for evidence of chronic, length-dependent, sensorimotor, axonal, peripheral polyneuropathy with extensive active denervation in distal muscles. No evidence of radiculopathy was appreciated on paraspinal testing.

Intervention: Pyridoxine supplementation was discontinued and the patient underwent intensive physiotherapy. In a two-month follow up visit, her balance was markedly improved on the Berg Balance Test and Timed Up and Go tests. Repeat serum pyridoxine level was 23.9 nmol/L.

Conclusions: In conclusion, sensorimotor neuropathy secondary to pyridoxine toxicity can be debilitating, but is potentially reversible with timely cessation of vitamin B6 supplementation and intensive physiotherapy.

Disclosure: Dr. Moudgal has nothing to disclose. Dr. Hosseini has nothing to disclose. Dr. Colapietro has nothing to disclose. Dr. Awosika has nothing to disclose.

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