Introduction: Elevated plasma level of homocysteine (eHcy) has been observed to be related to various neurological conditions including peripheral neuropathy (PN). However, studies on eHcy as an independent risk factor for the development of PN are sparse. To explore the association of eHcy with PN, we conducted a clinical observational study.Methods: Retrospective chart review was performed over 5 years on patients with peripheral neuropathy or with primary headaches as controls. Patients with simultaneously measured homocysteine, methylmalonic acid, Vitamin B12 and folate were recorded. Patients without homocysteine measurement or with any identifiable etiologies, other than eHcy, for neuropathy were excluded. Demographic, clinical and laboratory data were analyzed.Results: A total of 202 subjects who met the inclusion and exclusion criteria were collected, including 161 with PN and 41 with headaches. Higher levels of homocysteine were observed in PN patients (15.5 ± 12.2 µmol/L, 95% CI: 0.6369-8.2631, p = 0.02) than in the headache controls (10.6 ± 3.4 µmol/L). Additionally, the frequency of eHcy was also significantly higher in PN (51.6%, OR: 4.39, 95% CI: 1.91-10.09, p = 0.0002) than in headache controls (19.5%). Discussion:The current study confirmed the previous observation that increased prevalence of eHcy is seen in patients with PN and validated the hypothesis that eHcy may potentially be an independent risk factor contributing to the etiology of PN.

Introduction: Laboratory studies to uncover the underlying etiology for patients with neuropathy are essential in practice. To address if there is an increased frequency of abnormal routine laboratory finding in patients with acral paresthesia, we performed a retrospective clinical observational study. Methods: Charts of patients with acral paresthesia with or without numbness were retrospectively reviewed. They all had neurologically either normal examinations or only mildly distal sensory abnormalities. Their clinical data and routine laboratory findings were collected and analyzed. Results: Two hundred and two patients (mean age: 56.3 ± 13.7 years, male/ female = 88/114) were studied. Significantly increased frequencies of abnormal findings, such as elevated values of HbA1c (p < 0.002), body mass index (p < 0.003) and decreased vitamin D levels (p < 0.0001), were noted. Discussion: Our study suggests that, in addition to diabetes mellitus, vitamin D deficiency and obesity may frequently be seen in patients with acral paresthesia. Highlights • Patients with acral paresthesia are frequently seen in clinic for neuromuscular consultation. • Laboratory studies to uncover the underlying etiologies for patients with acral paresthesia is critical. • Abnormal HbA1c, vitamin D-25OH and BMI are most commonly seen with acral paresthesia. • Diabetes, vitamin D deficiency and obesity may potentially serve as a biomarker for acral paresthesia.

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Aim: Elevated plasma level of homocysteine (eHcy) is a recognized risk factor for dementia. However, whether the central conduction is affected in patients with an isolated eHcy is unknown. In this study, we addressed whether central conduction is altered in adults with eHcy. Methods: Evoked potential studies including somatosensory (SSEP), visual (VEP) and brainstem auditory evoked potentials (BAEP), were performed to evaluate central conduction in patients with isolated eHcy. Results: Nine SSEP, 7 VEP, and 6 BAEP were studied in 9 patients with eHcy (age: 63.3 ± 7.5 years old, mean ± standard deviation, male/female: 4/5). SSEP with median nerve stimulation was delayed in peak latency of N9 (5/9/55.6%, abnormal/total subjects/percentage), N13 (7/9/77.8%), N20 (6/9/66.7%), and/or interpeak latency of N9-N13 (5/9/55.6%), N13-N20 (5/9/55.6%), and N9-N20 (4/9/44.4%). There was one delayed P100 latency (1/7/14.3%) in 7 VEP. BAEP was within normal limits in all the 6 subjects tested. Conclusion: Our pilot study provided neurophysiologic evidence of central conduction slowness in patients with eHcy, which may be due to a large diameter fiber dysfunction within the somatosensory, but not the visual and auditory, white matter pathway. The central conduction slowing in eHcy may be relevant to the pathophysiologic background for slowing the central processing.

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