Research
A 2008 literature review concluded that, "based on principles of evidence-based medicine and evaluations of methodology, there is only a possible association of celiac disease and peripheral neuropathy due to lower levels of evidence and conflicting evidence. There is not yet convincing evidence of causality. "A 2019 review concluded that "gluten neuropathy is a slowly progressive condition. About 25% of the patients will have evidence of enteropathy on biopsy (CD [celiac disease]) but the presence or absence of an enteropathy does not influence the positive effect of a strict gluten-free diet. "Stem-cell therapy is also being looked at as a possible means to repair peripheral nerve damage, however efficacy has not yet been demonstrated. See also
Scrambler therapy
Giant axonal neuropathy

References
Further reading
External links

Peripheral Neuropathy from the US NIH
Peripheral Neuropathy at the Mayo Clinic
General consensus has it with a half-life of approximately 100hr, however it has also been reported in one study to have a half life of 34-42 hr.The primary way the body terminates activity is by oxidation of radicals at C5, with other biotransformations contributing to a lesser extent. Butabarbital is metabolized almost entirely by the liver, products including polar alcohols, ketones, phenols, or carboxylic acids, before it is renally excreted in the urine.Half-Life: ~100 hr
Duration: 6-8 hr
Onset: 45-60 min
Enzymes induced: CYP1A2, CYP2C9/10, CYP3A4
Excretion: Urine

Mechanism of action
The mechanism of action by which barbiturates exert their effect is not yet completely understood, however they are believed to be involved in the enhancement of GABA inhibitory neurotransmitter activity in the CNS via GABAA receptors. Butabarbital, as a member of this drug class, acutely potentiates inhibitory GABAergic tone by binding with a specific site associated with a Cl− ionopore at the GABAA receptor. Butabarbitals binding causes the channel to remain open longer and thus prolongs post-synaptic inhibition by GABA. Less well characterized effects of barbiturates include direct inhibition of AMPA-type glutamate receptors, suppressing excitatory glutamatergic neurotransmission. References
External links
"Butabarbital". Drug Information Portal. U.S. National Library of Medicine.