Exceptions
High parenteral doses of vitamin B6 are used to treat isoniazid overdose with no adverse effects found, although a preservative in parenteral vitamin B6 may cause transient worsening of metabolic acidosis. High doses of vitamin B6 are used to treat gyromitra mushroom (false morel) poisoning, hydrazine exposure and homocystinuria Doses of 50 mg to 100 mg per day may also be used to treat pyridoxine deficient seizures and when patients are taking other medications that reduce vitamin B6. Daily doses of 10 mg to 50 mg are recommended for patients undergoing hemodialysis.Outside of rare medical conditions, placebo-controlled studies have generally failed to show benefits of high doses of vitamin B6. Reviews of supplementing with vitamin B6 have not found it to be effective at reducing swelling, reducing stress, producing energy, preventing neurotoxicity, or treating asthma. A

Diagnosis
The clinical hallmark of megavitamin-B6 syndrome is ataxia due to sensory polyneuropathy. Blood tests are performed to rule out other causes and to confirm an elevated level of vitamin B6 with an absence of hypophosphatasia. Examination does not typically show signs of a motor deficit, dysfunction of the autonomic nervous system or impairment of the central nervous system, although in severe cases motor and autonomic imparement can occur. When examined, patients typically have diminished reflexes (hyporeflexia), such as a diminished response when performing an ankle jerk reflex test. Nerve conduction studies typically show normal motor conduction but decrease in large sensory wave amplitude in the arms and legs. Needle electromyography studies generally reveal no signs of denervation.
Megavitamin-B6 syndrome has been reported in doses as low as 24 mg/day.Symptoms may also be dependent on the form of vitamin B6 taken in supplements. It has been proposed that vitamin B6 in supplements should be in pyridoxal or pyridoxal phosphate form rather than pyridoxine as these are thought to reduce the likelihood of toxicity. A tissue culture study, however, showed that all B6 vitamers that could be converted into active coenzymes (pyridoxal, pyridoxine and pyridoxamine) were neurotoxic at similar concentrations. It has been shown, in vivo, that supplementing with pyridoxal or pyridoxal phosphate increases pyridoxine concentrations in humans, meaning there are metabolic pathways from each vitamer of B6 to the all other forms. Consuming high amounts of vitamin B6 from food has not been reported to cause adverse effects.Early diagnosis and cessation of vitamin B6 supplementation can reduce the morbidity of the syndrome. Cause
While vitamin B6 is water-soluble, it has a half-life of 25–33 days and accumulates in the body where it is stored in muscle, plasma, the liver, red blood cells and bound to proteins in tissues. Potential mechanisms
The common supplemental form of vitamin B6, pyridoxine, is similar to pyridine which can be neurotoxic. Pyridoxine has limited transport across the blood–brain barrier explaining why the central nervous system is spared. Cell bodies of motor fibers are located within the spinal cord that is also restricted by the blood-brain barrier explaining why motor impairment is rare.