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The PCBm is not ideal as a comparator nerve for the neurophysiological diagnosis of CTS. The frequency of PCBm abnormality in CTS patients may be related to the concomitant damage in both of these nerves. Additionally, the present findings may help explain, at least in part, why patients with CTS often exhibit sensory involvement beyond the classical median nerve sensory borders.

Background and PurposeWe compared the motor-unit number estimation (MUNE) findings in patients who presented with signs and/or findings associated with carpal tunnel syndrome (CTS) and healthy controls, with the aim of determining if motor-unit loss occurs during the clinically silent period and if there is a correlation between clinical and MUNE findings in CTS patients.MethodsThe study investigated 60 hands of 35 patients with clinical CTS and 60 hands of 34 healthy controls. Routine median and ulnar nerve conduction studies and MUNE analysis according to the multipoint stimulation method were performed.ResultsThe most common electrophysiological abnormality was reduced conduction velocity in the median sensory nerve (100% of the hands). The MUNE value was significantly lower for the patient group than for the control group (p=0.0001). ROC analysis showed that a MUNE value of 121 was the optimal cutoff for differentiating between patients and controls, with a sensitivity of 63.3% and a specificity of 68.3%. MUNE values were lower in patients with complaints of numbness, pain, and weakness in the median nerve territory (p<0.05, for all comparisons), and lower in patients with hypoesthesia than in patients with normal neurological findings (p=0.023).ConclusionsThe MUNE technique is sensitive in detecting motor nerve involvement in CTS patients who present with sensorial findings, and it may be useful in detecting the loss of motor units during the early stages of CTS. Larger-scale prospective clinical trials assessing the effect of early intervention on the outcome of these patients would help in confirming the possible benefit of detecting subclinical motor-unit loss in CTS.

Diabetic polyneuropathy is the most common neurologic complication of diabetes mellitus. Underlying mechanisms of diabetic polyneuropathy are related to various metabolic and inflammatory pathways. Pentraxin 3 (PTX3) is an acute phase protein that is produced locally at the inflammatory sites by several cell types. Thioredoxin binding protein 2 (TBP2) is a thioredoxin regulator involved in intracellular energy pathways and cell growth. We measured the plasma levels of PTX3 and TBP2 in type 2 diabetic patients (n = 27) with pain complaints and compared their levels with those of healthy age-and sex-matched subjects (n = 24). Moreover, the diabetic patients were divided into two groups using the Leeds Assessment of Neuropathic Symptoms and Signs (LANSS) pain scale: patients with nociceptive pain that is caused by tissue damage and patients with neuropathic pain that is caused by nerve damage. Patients with LANSS scores of < 12 were considered to have nocicceptive pain (n = 15), while patients with LANSS scores of ≥ 12 were considered to have neuropathic pain (n = 12). We found that PTX3 levels were significantly higher in diabetic patients compared to controls (p = 0.03), but there was no significant difference in the TBP2 levels. Importantly, patients with nociceptive pain had significantly higher PTX3 levels compared to patients with neuropathic pain (p < 0.05). Thus, plasma PTX3 levels can be helpful for discrimination of nociceptive pain from neuropathic pain in diabetic patients. We propose that PTX3 may contribute to the onset of nociceptive pain.

BackgroundCongenital sphingosine-1-phosphate (S1P) lyase deficiency due to biallelic mutations in SGPL1 gene has recently been described in association with primary adrenal insufficiency and steroid-resistant nephrotic syndrome. S1P lyase, on the other hand, is therapeutically inhibited by fingolimod which is an oral drug for relapsing multiple sclerosis (MS). Effects of this treatment on adrenal function has not yet been evaluated. We aimed to test adrenal function of MS patients receiving long-term fingolimod treatment.MethodsNineteen patients (14 women) with MS receiving oral fingolimod (Gilenya®, Novartis) therapy were included. Median age was 34.2 years (range; 21.3–44.6 years). Median duration of fingolimod treatment was 32 months (range; 6–52 months) at a dose of 0.5 mg/day. Basal and ACTH-stimulated adrenal steroid measurements were evaluated simultaneously employing LC-MS/MS based steroid panel. Basal steroid concentrations were also compared to that of sex- and age-matched healthy subjects. Cortisol and 11-deoxycortisol, 11-deoxycorticosterone and dehydroepiandrosterone were used to assess glucocorticoid, mineralocorticoid and sex steroid producing pathways, respectively.ResultsBasal ACTH concentrations of the patients were 20.8 pg/mL (6.8–37.8 pg/mL) (normal range; 5–65 pg/mL). There was no significant difference in the basal concentrations of cortisol, 11-deoxycortisol, 11-deoxycorticosterone and dehydroepiandrosterone between patients and controls (p = 0.11, 0.058, 0.74, 0.15; respectively). All patients showed adequate cortisol response to 250 mcg IV ACTH stimulation (243 ng/mL, range; 197–362 ng/mL). There was no significant correlation between duration of fingolimod treatment and basal or ACTH-stimulated cortisol or change in cortisol concentrations during ACTH stimulation test (p = 0.57, 0.66 and 0.21, respectively).ConclusionModification and inhibition of S1P lyase activity by the long-term therapeutic use of fingolimod is not associated with adrenal insufficiency in adult patients with MS. This suggests that S1P lyase has potentially a critical role on adrenal development rather than the function of a fully mature adrenal gland.