The research shows that B6 deficiency symptoms are not the same of B6 toxicity symptoms. The idea that deficiency causes neuropathy got into the literature based on a handful of isolated case studies that were not likely related to B6 deficiency. Read below for more information on this.
Excerpt from: Vitamin B-6-Induced Neuropathy: Exploring the Mechanisms of Pyridoxine Toxicity
“There are a few isolated case reports, but these were likely related to other underlying health conditions. Previously, it was suggested that demyelinating peripheral neuropathy in elderly patients on chronic peritoneal dialysis may have been caused by a vitamin B-6 deficiency. However, peripheral neuropathy in patients on dialysis has also been attributed to uremic intoxication, hormonal imbalances, disruptions in ion concentration gradients, and/or other vitamin deficiencies. In rhesus monkeys, the animal model most relevant to humans, a vitamin B-6 deficiency did not induce neuropathy. Most of the evidence in favor of an association between vitamin B-6 deficiency and neuropathy in humans is related to pharmaceutical interventions.”
Excerpt from: Revisiting the Evidence for Neuropathy Caused by Pyridoxine Deficiency and Excess
“Literature on neuropathy attributed to primary pyridoxine deficiency is scant. Although pyridoxine deficiency anemia was well known by the 1950s, the only patient with pyridoxine-responsive anemia and neuropathy was reported in 1963. This single reported patient had a significant preceding weight loss and was from a low-income social background. She may have had other coexisting nutritional deficiencies, which were not investigated. There are no other case reports attributing neuropathy primarily to pyridoxine deficiency. Other reported patients with pyridoxine deficiency neuropathy had either coexisting nutritional deficiencies and medical conditions predisposing to neuropathy or were taking medications interfering with pyridoxine.”
Excerpt from: The Role of Vitamin B6 in Peripheral Neuropathy: A Systematic Review
Low vitamin B6 levels can be seen in patients suffering from peripheral neuropathy of various etiologies. However, this finding is due either to overall poor nutritional status (which means low levels of other vitamins, deficiencies in which can cause PN, such as B12) or to an adverse effect of treatments that these patients received for conditions that can lead to neuropathy, such as diabetes or chronic renal failure. Therefore, to date, there is no firm evidence that low B6 levels have a direct causal relationship with PN. Measuring levels of B6 in patients with CIAP who receive no nutritional supplements could shed light on this association and should be undertaken as a research project in the future.
Many studies have suggested a subjective improvement of neuropathy symptoms in patients suffering from PN of various etiologies after receiving B6 supplementation. In none of those studies, however, has B6 been administered as a monotherapy but as part of a combination treatment, usually with other vitamins. Therefore, the potential therapeutic role of B6 cannot be confirmed to date.