Experimental model of pyridoxine (B6) deficiency-induced neuropathy.

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.

Associations of tibia lead, DMSA-chelatable lead, and blood lead with measures of peripheral nervous system function in former organolead manufacturing workers.

BACKGROUND: The goals of the present study were to compare and contrast associations of blood lead, DMSA-chelatable lead, current tibia lead, and back-extrapolated "peak" tibia lead with four peripheral nervous system (PNS) sensory and motor function measures in older males with past exposure to organic and inorganic lead. METHODS: Data were collected from former organolead manufacturing workers with an average of 16 years since last occupational lead exposure. Current tibia lead levels were measured by (109)Cd x-ray fluorescence. Sensory pressure thresholds (index and pinky fingers) and pinch and grip strength were measured with the Pressure-Specified Sensory Device (PSSD). RESULTS: In adjusted analyses, none of the four lead biomarkers was associated with sensory pressure threshold of the index finger or pinch or grip strength. In contrast, all four biomarkers were associated (P < or = 0.10) with pressure threshold of the pinky finger. The final linear regression models accounted for a small proportion of the variance in the sensory (1-3%) and motor measures (10-21%). CONCLUSIONS: This study found no strong association between lead biomarkers and selected PNS sensory or motor function measures among former organolead manufacturing workers with no recent occupational exposure to lead. Previously reported CNS findings in this cohort suggest that the PNS may be less sensitive to the chronic toxic effects of lead in this dose range among adults. It is also possible that the PNS has a greater capacity for repair than does the CNS, or that the PNS measures were less sensitive for detection of lead-related health outcomes than were the CNS measures.

Pressure perception in the normal lower extremity and in the tarsal tunnel syndrome.

For quantitative sensory testing to be useful for the management of peripheral nerve problems, a normative database must be developed. The Pressure-Specified Sensory Device (PSSD), a handheld instrument whose hemispherical metal probe tips are connected via a force transducer to a computer, has been found reliable and valid for the upper extremity. In the present study, the PSSD was used to measure the cutaneous pressure threshold at four lower extremity sites in 34 normal adults and in 22 patients with tarsal tunnel syndrome (6 bilateral). Each of the 28 limbs that was symptomatic for tarsal tunnel syndrome had a cutaneous pressure threshold greater than the 99% confidence limit of the age-matched controls (< or = 45 years, > 45 years of age). Screening for tarsal tunnel syndrome can be done utilizing the measurement of the two-point static-touch thresholds for pressure and distance.

Computer-assisted measurement in diabetic patients with and without foot ulceration.

Computer-assisted measurement of sensibility was done at four anatomical sites of the foot of patients with diabetes with (19) and without (40) foot ulceration. Cutaneous pressure threshold measurements of patients with diabetes were compared with measurements on 30 patients without diabetes who had nonulcerated feet. Both groups had mean one-point static and moving touch, and two-point discrimination thresholds significantly different from the general population. Computer-assisted sensibility testing demonstrated significantly higher pressure thresholds for one-point static and moving touch and two-point discrimination in the ulcerated compared with the nonulcerated foot of patients with diabetes. This measurement technique is valid for documenting diminished sensation in the foot.

Correlation of measurements of pressure perception using the pressure-specified sensory device with electrodiagnostic testing.

Quantitative sensory testing of pressure threshold has been recommended for diagnosis and monitoring of peripheral nerve problems, yet there has been no validation of the results of such testing with electrodiagnostic testing (EDT), the "gold standard." The Pressure-Specified Sensory Device (PSSD) was used to measure the pressure threshold in 72 clinical nerve entrapment syndromes (23 carpal, 23 cubital, and 16 tarsal tunnel syndromes, and 10 common peroneal nerve entrapment at the fibular head), each of which also had EDT. There was diagnostic agreement between both EDT and PSSD in 54 of the 72 nerve entrapments (75%). The sensitivity of the PSSD was 100% for each of the four nerve entrapments. In those patients in whom there was a disagreement, the PSSD was abnormal when the EDT was normal. In conclusion, quantitative sensory testing with the PSSD has a high sensitivity, but a low specificity, when compared with EDT for diagnosis of peripheral nerve entrapment.

Identification of elastic fibres in the peripheral nerve.

Traditional histological staining techniques, as well as elastin-specific antibodies and electron microscopy, have been used to assess the distribution of elastin within the peripheral nerve. The location of the elastin identified by the VerHoeff-VanGiesen or Weigert stains has been shown to coincide with the unambiguous identification of elastin by immunospecific stains and electron microscopy. Elastin is located in all three connective layers of the peripheral nerve. Thick elastic fibres, consisting of amorphous elastin protein and microfibrils, are located consistently in the perineurium and, to a lesser extent, in the epineurium. The endoneurium contains small collections of elastic fibres widely distributed between the axons. Compared with collagen, the overall content of elastin, however, is small, suggesting that the visco-elastic properties of peripheral nerve may be due primarily to collagen.