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Abstract
This report documents a case of mixed motor and sensory neuropathy that resulted from ingestion of excessive amounts of pyridoxine. An 81-year-old woman was admitted to the hospital because of difficulty in walking and frequent falls. History revealed that she had been taking large doses of pyridoxine daily for several months as treatment for carpal tunnel syndrome. Diagnostic work-up failed to suggest a cause for her symptoms. Nerve conduction studies revealed slowing of motor conduction velocities, prolonged F wave latencies, and prolonged sensory latencies in both lower extremities. We believe the patient's complaints and the results of nerve conduction studies were secondary to pyridoxine neurotoxicity. Since the bases for this neurotoxicity are unknown, we suggest that treatment of carpal tunnel syndrome with oral pyridoxine be carefully monitored and that dosage limits not be exceeded.
... Elevated B6 levels may result from environmental factors or genetic defects. Vitamin B6 toxicity can induce sensory and motor neuropathies, causing numbness in the hands and feet, which are usually reversible upon discontinuation of supplementation [160]. Yet, substantial amounts of this cofactor are essential to saturate the numerous PLP-dependent enzymes and meet cellular demands. ...
Enzymes are crucial in metabolic processes, and their dysfunction can lead to severe metabolic disorders. Structural biology, particularly X-ray crystallography, has advanced our understanding of these diseases by providing 3D structures of pathological enzymes. However, traditional X-ray crystallography faces limitations, such as difficulties in obtaining suitable protein crystals and studying protein dynamics. X-ray free-electron lasers (XFELs) have revolutionized this field with their bright and brief X-ray pulses, providing high-resolution structures of radiation-sensitive and hard-to-crystallize proteins. XFELs also enable the study of protein dynamics through room temperature structures and time-resolved serial femtosecond crystallography, offering comprehensive insights into the molecular mechanisms of metabolic diseases. Understanding these dynamics is vital for developing effective therapies. This review highlights the contributions of protein dynamics studies using XFELs and synchrotrons to metabolic disorder research and their application in designing better therapies. It also discusses G protein-coupled receptors (GPCRs), which, though not enzymes, play key roles in regulating physiological systems and are implicated in many metabolic disorders.
... Discontinuation of pyridoxine usually improves symptoms, but residual abnormalities may persist. The mechanism of pyridoxine-induced toxicity remains unknown [7][8][9]. In our observation, the anamnesis, clinical and electrophysiological examinations confirmed the diagnosis of neuropathy, and the various complementary examinations made it possible to rule out another aetiology (diabetes, alcohol, hypothyroidism, renal failure, infections, etc.). ...
... Most studies that investigated supplemental vitamin B6 intakes that exceeded 500 mg/day were also not used in the evaluation and are listed in Appendix C (Schaumburg et al., 1982;Baer, 1984;Berger and Schaumburg, 1984;Vasile et al., 1984;Foca, 1985;Friedman et al., 1986;Waterston and Gilligan, 1987;Gdynia et al., 2008;No authors listed, 2009). This is the dose for which the SCF (2000) had already concluded that it represented a potentially toxic dose for humans associated with severe symptoms and which is also five times higher than the RP used by the SCF (2000) for setting the UL. ...
Following a request from the European Commission, the EFSA Panel on Nutrition, Novel Foods and Food Allergens (NDA) was asked to deliver a scientific opinion on the tolerable upper intake level (UL) for vitamin B6. Systematic reviews of the literature were conducted by a contractor. The relationship between excess vitamin B6 intakes and the development of peripheral neuropathy is well established and is the critical effect on which the UL is based. A lowest-observed-effect-level (LOAEL) could not be established based on human data. A reference point (RP) of 50 mg/day is identified by the Panel from a case-control study, supported by data from case reports and vigilance data. An uncertainty factor (UF) of 4 is applied to the RP to account for the inverse relationship between dose and time to onset of symptoms and the limited data available. The latter covers uncertainties as to the level of intake that would represent a LOAEL. This leads to a UL of 12.5 mg/day. From a subchronic study in Beagle dogs, a LOAEL of 50 mg/kg body weight (bw) per day can be identified. Using an UF of 300, and a default bw of 70 kg, a UL of 11.7 mg/day can be calculated. From the midpoint of the range of these two ULs and rounding down, a UL of 12 mg/day is established by the Panel for vitamin B6 for adults (including pregnant and lactating women). ULs for infants and children are derived from the UL for adults using allometric scaling: 2.2-2.5 mg/day (4-11 months), 3.2-4.5 mg/day (1-6 years), 6.1-10.7 mg/day (7-17 years). Based on available intake data, EU populations are unlikely to exceed ULs, except for regular users of food supplements containing high doses of vitamin B6.
... This case series of Dutch ADR reports has a pattern in clinical features and time to onset similar to those of published cases. Reported dosages in the literature vary from 24 mg [9] to extremely high dosages of multiple grams used daily [29][30][31]. In 37 of the reports to Lareb, the vitamin B 6 dosage in the products was equal to or higher than the maximum acceptable intake of 25 mg for adults [8] but generally lower than the mega doses described in the literature (see Table 3). ...
Introduction:
In the literature, vitamin B6 has been linked to the development of polyneuropathy. Most often, these complaints were seen when taking high doses of vitamin B6 for a long time. Evidence as to whether a lower dosage range of vitamin B6 (< 50 mg/day) can also induce neuropathy is scarce.
Objective:
We aim to comprehensively describe the cases of neuropathy associated with vitamin B6 received by the Netherlands Pharmacovigilance Centre Lareb and to assess the case series concerning the use of vitamin B6 and neuropathic complaints.
Methods:
We describe the number and nature of the reported cases, including suspect product, dosage, duration of use, and vitamin B6 serum levels. In addition, we describe the causality for the individual cases (Naranjo Probability Scale) and for the entire case series (Bradford Hill criteria).
Results:
In total, 90 reports on products containing vitamin B6 included at least one adverse drug reaction in the standardized Medical Dictionary for Regulatory Activities (MedDRA®) query (SMQ; broad) 'peripheral neuropathy'. The amount of vitamin B6 in the products varied between 1.4 and 100 mg per tablet. The serum vitamin B6 level was known in 36 cases (88-4338 nmol/l), and the mean serum vitamin B6 level was 907 nmol/l. However, no statistical correlation between dosage and vitamin B6 blood levels was found.
Discussion and conclusion:
Causality assessment of the case series of 90 reports to Lareb shows it is plausible for the vitamin B6 supplements to have caused complaints such as neuropathies. This is especially the case with higher dosages and prolonged use, but dosages < 50 mg/day also cannot be excluded.
... The levels of B 6 could also be raised as a result of an environmental insult or genetic defects. Toxicity of vitamin B 6 is known to cause sensory as well as motor neuropathies leading to numbness in hands and feet, that are usually reversible when supplementation is stopped [41]. ...
Vitamin B-6 is a generic term referring to pyridoxine. pyridoxamine, pyridoxal and their related phosphorylated forms. Pyridoxal 5'-phosphate is the catalytically active form of vitamin B-6, and acts as cofactor in more than 140 different enzyme reactions. In animals, pyridoxal 5'-phosphate is recycled from food and from degraded B-6-enzymes in a "salvage pathway", which essentially involves two ubiquitous enzymes: an ATP-dependent pyridoxal kinase and an FMN-dependent pyridoxine 5'-phosphate oxidase. Once it is made, pyridoxal 5'-phosphate is targeted to the dozens of different apo-B-6 enzymes that are being synthesized in the cell. The mechanism and regulation of the salvage pathway and the mechanism of addition of pyridoxal 5'-phosphate to the apo-B-6-enzymes are poorly understood and represent a very challenging research field. Pyridoxal kinase and pyridoxine 5'-phosphate oxidase play kinetic roles in regulating the level of pyridoxal 5'-phosphate formation. Deficiency of pyridoxal 5'-phosphate due to inborn defects of these enzymes seems to be involved in several neurological pathologies. In addition, inhibition of pyridoxal kinase activity by several pharmaceutical and natural compounds is known to lead to pyridoxal 5'-phosphate deficiency. Understanding the exact role of vitamin B-6 in these pathologies requires a better knowledge on the metabolism and homeostasis of the vitamin. This article summarizes the current knowledge on structural, kinetic and regulation features of the two enzymes involved in the PLP salvage pathway. We also discuss the proposal that newly formed PLP may be transferred from either enzyme to apo-B-6-enzymes by direct channeling, an efficient, exclusive, and protected means of delivery of the highly reactive PLP. This new perspective may lead to novel and interesting findings, as well as serve as a model system for the study of macromolecular channeling. This article is part of a Special Issue entitled: Pyridoxal Phosphate Enzymology.
Vitamin B6 is frequently utilized as a therapeutic agent for nausea and vomiting of pregnancy (NVP). Research indicates that excessive intake of vitamin B6 can have implications on neurological function, underscoring the importance of cautious consideration when administering vitamin B6 treatment during early pregnancy. This systematic review investigates the effects of high doses of vitamin B6 on pregnant women experiencing NVP. We searched the PubMed® MEDLINE® database for articles using the following terms: “pregnancy” or “nausea and vomiting during pregnancy” and “vitamin B6.” Women with nausea and vomiting symptoms during pregnancy use more than the tolerable amount of vitamin B6. A total of 136 articles were identified from the PubMed® MEDLINE® database. The etiology and treatment of NVP are briefly outlined, followed by a summary and analysis of 19 relevant literature sources. Among these sources, 12 reports detailed the adverse effects of excessive vitamin B6 intake in women; 164/1226 individuals experienced neurological symptoms such as burning, tingling, paresthesia, ataxia, or perioral numbness. Additionally, out of 245 women, four experienced miscarriages and one had an intrauterine demise. The overconsumption of vitamin B6 has the potential to impact nerve function, particularly during the critical first trimester of embryonic development. It might result in adverse outcomes such as miscarriage, intrauterine fetal demise, and congenital abnormalities.
Pyridoxal-5'-phosphate (PLP), the active form of vitamin B6, is required for numerous enzymatic reactions. Vitamin B6 deficiency or exceptionally high levels of PLP have negative implications, making measurements of PLP imperative for diagnoses and monitoring in many clinical scenarios. Traditional assays are enzymatic, ELISA based, or employ HPLC with various detection modalities; all of these are prone to interferences and crossreactivity with other compounds. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) has been increasingly used to overcome these issues, but the high polarity of PLP raises chromatographic challenges. Using ion pairing reagents in the mobile phases is a possible solution, but these reagents often have deleterious effects on instrumentation. An alternative strategy is the addition of an ion pairing reagent after extraction, but prior to injection. To prove this, we used 1-octanesulfonic acid (OSA) without changing the LC method or column. With this technique, we observed a 2-4 fold increase in signal-to-noise ratio. Intraday and interday precision of replicate measurements also improved drastically compared to analyses without OSA, while also yielding a dramatic improvement in column life compared to our previous approach and to this point no deleterious effects on instrument hardware commonly associated with traditional ion pairing reagent techniques have been observed.
To support EFSA in the preparatory work for the assessment of Tolerable Upper Intake Levels (UL) for vitamin B6, a tailored ‘high level’ protocol was developed, based on a template protocol and taking into account the specificities of vitamin B6. This protocol outlined the methods, the relevant endpoints and priority adverse health effects in relation to high intakes of vitamin B6. Systematic reviews (SR) were conducted following a tailored literature search, data extraction, evidence appraisal (i.e. risk of bias (RoB) assessment) and evidence synthesis. Narrative reviews (NR) were conducted to gather contextual evidence relevant to the interpretation of the main body of evidence. In the SR on the dose‐response relationship between vitamin B6 and peripheral neuropathy, 3793 records were identified and reduced to 32 individual records after screening for eligibility. The evidence appraisal revealed an overall moderate to high RoB of the individual studies and an overall rating of the total body of evidence as very low due mainly due to the type of data from case studies/case reports and limited number of other data. The available evidence confirmed a high degree of inter‐individual variability to sensitivity to a high exposure of vitamin B6 in relation to development of peripheral neuropathic outcomes but did not allow to determine a No Observed Adverse Effect Level or Lowest Observed Adverse Effect Level. In the SR on developmental toxicity, 4941 records were identified and reduced to 23 individual records including human and animal studies after screening for eligibility. The available data demonstrated a high degree of heterogeneity with respect to exposure and adverse health outcomes and overall, showed no positive or causal relationship between vitamin B6 intake and adverse developmental effects, including congenital defects. The NRs showed a paucity of data on high intake of vitamin B6 vitamers and their metabolism.
Neuropathies associated with nutritional deficiencies are routinely encountered by the practicing neurologist. Though these neuropathies assume different patterns, most are length‐dependent, sensory axonopathies. Cobalamin deficiency neuropathy is the exception, often presenting with a non‐length‐dependent sensory neuropathy. Patients with cobalamin and copper deficiency neuropathy characteristically have concomitant myelopathy, whereas vitamin E deficiency is uniquely associated with a spinocerebellar syndrome. In contrast to those nutrients for which deficiencies produce neuropathies, pyridoxine toxicity results in a non‐length‐dependent sensory neuronopathy. Deficiencies occur in the context of malnutrition, malabsorption, increased nutrient loss (such as with dialysis), autoimmune conditions such as pernicious anemia, and with certain drugs that inhibit nutrient absorption. When promptly identified, therapeutic nutrient supplementation may result in stabilization or improvement of these neuropathies. This article is protected by copyright. All rights reserved.
Introduction:
Vitamin B6 is contained in a number of over-the-counter drugs and vitamin supplements. It may cause severe neurological troubles in case of overdosage.
Case report:
We report the case of a 92-year-old women with gait disorders. A diagnosis of peripheral neuropathy with both motor and sensitive deficits was established and investigated. Blood level of vitamin B6 was measured to investigate a potential deficiency. Unexpectedly, the results showed hypervitaminosis B6, which appears to be due to self-administration of an over-the-counter drug containing vitamin B6. Discontinuation of this drug was associated with decrease in vitamin B6 level as well as gait improvement. We also discuss the toxicity of vitamin B6.
Conclusion:
Hypervitaminosis B6 remains a possible cause of peripheral neuropathy and it may be caused by self-administration of over-the-counter vitamin-containing drugs.
Nutritional deficiencies occur when the body’s supply of nutrients is exceeded by its demand. The first signs of vitamin or mineral deficiencies may manifest in the oral cavity due to the unique environment and rapid cell turnover. The aim of this chapter is to outline the oral signs and symptoms occurring with vitamin deficiencies, which the astute clinician may identify. These manifestations are reviewed and treatments suggested. The significance of hematinic deficiencies in burning mouth syndrome management is also discussed.
Pyridoxine 5′-phosphate oxidase (PNPO) is a key enzyme for the biosynthesis of pyridoxal 5′-phosphate. Pyridoxal 5′-phosphate is the catalytically active form of vitamin B6, and acts as a cofactor involved in a high diversity of biochemical reactions. The expression and regulation of PNPO are implicated in numerous physiological and pathological processes. The genomic organization of human PNPO has been reported previously whereas the promoter functional identification is not there yet. In this study, we identified the proximal promoter region of human PNPO gene and analyzed its function. Bioinformatics analysis showed that the transcription start site is at 153 bp upstream of the translation initiation site ATG. Progressive truncation analysis of the 5′-flanking region of PNPO gene demonstrated that two important regulatory regions are located at −996/−852 and −412/+85 bp relative to the transcription start site. From the regulatory regions one USF site, two E2F1 site and multiple Sp1 sites were found. Deletion and mutation experiments indicated that these cis-regulatory elements contribute to the basic promoter activity on different degrees. Downregulation of the transcription factors further indicated that E2F1 plays a dominant role in the transcriptional regulation of PNPO through the binding site at −867/−857, which was confirmed by ChIP assay. Our present study should facilitate further studies on the mechanism regulating the expression of this important gene.
Nutritional deficiencies occur when bodily metabolic requirements are not matched by intake and absorption. Reasons for this discrepancy are numerous, but often social, economic, medical, and even psychiatric factors may play a role. Vitamins and minerals are required for appropriate rapid cell turnover of the oral mucosa. The oral cavity is a unique anatomic environment that may manifest early signs of nutritional disorders as well as other indicators of systemic disease. Knowledge of these oral manifestations and associated findings will allow a practitioner to consider a nutritional disorder when evaluating oral changes, and in turn, initiate appropriate therapy. A systematic approach to examination of the mouth and perioral skin is suggested. A detailed medical and social history complements the physical exam in identifying patients at risk for nutritional disorders and heightening the clinical suspicion to warrant additional nutritional screening. The rising prevalence of anorexia and bulimia, as well as fad diets, add to the population of patients at risk for vitamin and mineral deficiencies that a clinician must now consider.
This manuscript reports three independent accidental cases of vitamin (Vit) B6 toxicosis in gyrfalcons ( Falco rusticolus ) and peregrine falcons ( Falco peregrinus ) and a toxicology study that was conducted to characterize the clinical responses of gyrfalcons and gyrfalcon × peregrine falcons to a range of single intramuscular (IM) and oral (PO) doses of Vit B6. Both lethal and nonlethal doses were determined. Twelve female gyrfalcons died following IM injection of 1 ml of a vitamin B preparation. Within 30 min of injection, the birds passed pistachio green-colored urates and progressed to vomiting, anorexia, cessation of normal activity, ptosis, collapse, and death, occurring 24-36 hr post injections. Three individuals vomited frothy, partially digested blood and had clonic spasms and convulsions. Postmortem and histopathology revealed multifocal severe hepatic necrosis, splenic lymphoid tissue depletion and hemorrhages with arterial necrosis, and acute renal tubular necrosis. Following administration of a different, oral, mineral-vitamin supplement, a total of 21 peregrine falcons in two separate European facilities died suddenly. Histology of the liver showed diffuse congestion and multifocal coagulative necrosis with mild infiltration of heterophils. The particular nutritional supplement, used by both breeders, was analyzed and found to contain 5-9.7% Vit B6. Other randomly selected lots of the product contained 0.007-0.27% Vit B6. According to the product label, Vit B6 should have been present at 0.004%. To confirm the hypothesis that Vit B6 was responsible for the deaths of the falcons in Abu Dhabi, Vit B6 (British Pharmacopoeia [BP] grade) in powder form was diluted in water for injection and administered IM to four groups of falcons. Groups of four gyrfalcon × peregrine hybrid falcons or gyrfalcons (or both) were given a single IM dose of 5, 10, 15, or 20 mg/kg of Vit B6 or received an oral dose of 25, 50, or 75 mg of Vit B6. Only birds in the lowest-dose groups survived. The maximum nonlethal single doses of Vit B6 in falcons were 5 mg/kg i.m. and 25 mg/kg p.o.
Mit Datum vom 4.6.1986 wurden wir von der Firma Cascan beauftragt, ein auf einer Literaturrecherche basierendes Gutachten über mögliche Nebenwirkungen von Vitamin B1, B6 und B12 zu erstellen. Berücksichtigt werden sollten folgende Dosierungsbereiche: Vitamin B1 45 bis 600 mg, Vitamin B6 30 bis 1200 mg und Vitamin B12 60 bis 1500 μg.
Pyridoxine deficiency and excess have been implicated as a cause for peripheral neuropathy. As a result, unrelated neuropathies are often treated with pyridoxine based on questionable evidence. However, neurological practitioners frequently discourage patients from taking pyridoxine in excess of 50 mg/d given concerns around the development of a toxic sensory neuronopathy. There is no systematic review to support either of the 2 practices. To address this gap in knowledge, we reviewed the available literature on neuropathy attributed to pyridoxine deficiency and excess. Based on the current limited data, it can be concluded that very low doses of daily pyridoxine are required to prevent peripheral neuropathy. There is inadequate evidence to support routine pyridoxine supplementation in patients with disorders of peripheral nervous system. Supplementation with pyridoxine at doses greater than 50 mg/d for extended duration may be harmful and should be discouraged.
Animal models are pivotal for understanding the mechanism of neuropathic pain and development of effective therapy for its optimal management. A battery of neuropathic pain models has been developed to simulate the clinical pain conditions with diverse etiology. The present review exhaustively discusses the methodology, behavioral alterations, limitations, and advantages of about 40 different animal models of neuropathic pain along with their modifications. Development of these models has contributed immensely in understanding the chronic pain and underlying peripheral as well as central pathogenic mechanisms. Furthermore, research has resulted in the development of new therapeutic agents for neuropathic pain management, and the preclinical data obtained using these animal models have been successively translated to effective pain management in clinical setup also. As each animal model has been created with specific methodology and results tend to vary largely with the slight changes related to methodology, therefore, it is essential that data from different models should be reported and interpreted in the context of the specific pain model.
Polyneuropathy related to decreased levels of Vitamin B6 are well known. In contrast, the association between elevated levels of pyridoxine and neuropathy is not well described. This study is a retrospective review of patients in our neuromuscular clinic that were found to have elevated B6 levels. Twenty-six patients were found to have elevated serum B6 levels. The mean B6 level was 68.8 ng/ml. Twenty patients (76.9%) reported daily vitamin use. Twenty-one patients (80.8%) reported only sensory complaints. The most common symptoms reported were numbness (96%), burning pain (49.9%), tingling (57.7%), balance difficulties (30.7%), and weakness (7.8%). Nine (out of 26) had an abnormal EMG/NCS. Eight patients had an abnormal quantitative sensory study. We conclude that elevated pyridoxine levels should be considered in the differential diagnosis of any sensory or sensorimotor polyneuropathy.
In this study, we examined prospectively the effect of pyridoxine on idiopathic carpal tunnel syndrome. Thirty-two patients with the disease were randomized to receive treatment or placebo. No differences in outcome were found in electrophysiologic signs, clinical signs, or significant symptoms. Our findings do not support the use of pyridoxine for treating carpal tunnel syndrome.
The literature at this time does not give convincing evidence for use of pyridoxine as the sole treatment when confronted with a patient with idiopathic CTS. It may be of value as an adjunct in conservative therapy through altered perception of pain and increased pain threshold. For patients not responsive to conservative therapy, surgical decompression of the carpal canal is the treatment of choice.
Case reports and small case series suggest that vitamin B6 deficiency is an important etiologic factor in carpal tunnel syndrome (CTS). This hypothesis has never examined in a randomly selected study population, particularly among active workers. We examined 125 randomly selected active workers from two industrial plants. Each worker completed a self-administered symptom questionnaire and underwent electrodiagnostic testing of the median and ulnar sensory nerves. Laboratory biochemical analyses of vitamin B6 status were also performed using the erythrocyte glutamic pyruvic transaminase assay, and quantification of plasma pyridoxal-5'-phosphate. Measurements of vitamin B6 status were unrelated to self-reported symptoms potentially consistent with CTS, electrophysiologically determined median or ulnar nerve function, and CTS defined on the basis of self-reported symptoms and electrophysiologic measurements. These results suggest that CTS among active industrial workers is unrelated to vitamin B6 status. Furthermore, in our opinion, empiric prescription of vitamin B6 to patients with CTS is unwarranted and potentially hazardous.
A pyridoxine (B6) dietary deficiency was studied in female adult Sprague-Dawley rats by hind-limb walking-track analysis. Serum levels of pyridoxine and three metabolites were quantified by high-pressure liquid chromatography with fluorescence measurement. Morphometric analysis of the sciatic and posterior tibial nerves (from within the tarsal tunnel) was performed after 1 year on a diet deficient in vitamin B6. The B6-deficient rats developed abnormal walking-track patterns by 8 months, and these track parameters were different from age- and sex-matched normal diet control rats at the p < 0.05 level. Adding B6 at 10 parts per million to the diet then partially corrected these parameters, whereas the addition of 30 parts per million B6 corrected the abnormal pattern completely. Serum pyridoxal concentration correlated with the functional parameters, dropping from a mean of 115 mg per liter to 39.5 mg per liter (p < 0.05), and correcting with the B6 additive. Morphometric analysis demonstrated that the B6-deficient nerve from the tarsal tunnel had a decreased nerve fiber density (p < 0.001), with a normal total myelinated nerve fiber number, and an increased axon-to-myelin ratio (p < 0.003). It is concluded that a diet totally deficient in vitamin B6 results in a peripheral neuropathy.
Excess ingestion of pyridoxine (vitamin B6) causes a severe sensory neuropathy in humans. The mechanism of action has not been fully elucidated, and studies of pyridoxine neuropathy in experimental animals have yielded disparate results. Pyridoxine intoxication appears to produce a neuropathy characterized by necrosis of dorsal root ganglion (DRG) sensory neurons and degeneration of peripheral and central sensory projections, with large diameter neurons being particularly affected. The major determinants affecting the severity of the pyridoxine neuropathy appear to be duration and dose of pyridoxine administration, differential neuronal vulnerability, and species susceptibility. The present study used design-based stereological techniques in conjunction with electrophysiological measures to quantify the morphological and physiological changes that occur in the DRG and the distal myelinated axons of the sciatic nerve following pyridoxine intoxication. This combined stereological and electrophysiological method demonstrates a general approach that could be used for assessing the correlation between pathophysiological and functional parameters in animal models of toxic neuropathy.
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