Vitamin B6 Toxicity Neuropathy

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Is a well-known cause of primary sensory, length-dependent, axonal polyneuropathy. To date, there is no objective evidence of autonomic dysfunction reported in the literature. This case highlights the need for consideration of small fiber nerve damage by obtaining autonomic testing in cases of pyridoxine toxicit.


The use of PN-containing supplements has gained lots of attention over the past years as they have been related to the development of peripheral neuropathy. In light of this, the number of reported cases of adverse health effects due to the use of vitamin B-6 have increased. Therefore, the present review is focused on investigating the mechanistic link between PN supplementation and sensory peripheral neuropathy.
The mechanism behind PDXK-induced neuropathy is unknown; however, there is reason to believe that it may be related to γ-aminobutyric acid (GABA) neurotransmission. Compounds that inhibit PDXK lead to convulsions and reductions in GABA biosynthesis.

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To present the salient features, and reversibility of pyridoxine (vitamin B6) induced peripheral neuropathy, in conjunction with its electrodiagnostic correlate.
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.
Mri of cervical-lumbar spine showed degenerative changes, and was otherwise unremarkable. Intervention: Pyridoxine supplementation was discontinued and the patient underwent intensive physiotherapy. 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. Colapietro has nothing to disclose. Dr. Awosika has nothing to disclos.

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We describe a case of peripheral neuropathy due to an excess of vitamin B6 from NOS energy drinks. Background: Pyridoxine, or vitamin B6, is a water soluble vitamin that serves as a coenzyme in biological reactions. The mechanism of pyridoxine induced peripheral neuropathy is necrosis of the dorsal root ganglion and is duration and dose dependent.
Exam revealed normal mentation, orientation, cranial nerves, motor strength and tone. He had decreased bulk of biceps and decreased sensation to multiple modalities. Upon cessation and physical therapy, symptoms have improve.

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