Multifocal Motor Neuropathy Associated with Infliximab.

BACKGROUND: The anti-tumour necrosis factor [TNF] monoclonal antibody, infliximab, is commonly prescribed in both ulcerative colitis and Crohn's disease. Neurological side effects such as optic neuritis are well recognised, although not as frequently seen as hypersensitivity and serious infections. CASE: We present a case of peripheral neuropathy in a young man on infliximab therapy for ulcerative colitis. This presented as an asymmetrical and slowly progressive weakness in his right upper limb, severely impacting on function. Investigations confirmed a diagnosis of multifocal motor neuropathy [MMN]. This has been previously described in patients receiving infliximab for rheumatological conditions. The exact mechanism is unclear, but the neuropathy responds well to intravenous immunoglobulin. In our case, infliximab was discontinued. The patient was treated with immunoglobin for 5 days and recovered rapidly. Mercaptopurine was instituted as maintanence therapy, with good effect. CONCLUSION: Gastroenterologists prescribing infliximab should be cognisant of both peripheral and central neurological complications, ensuring prompt withdrawal of the offending agent and appropriate alternative treatment.

Platelet-rich plasma limits the nerve injury caused by 10% dextrose in the rabbit median nerve.

INTRODUCTION: We evaluated the effect of platelet-rich plasma (PRP) injection in a rabbit model of dextrose-induced median nerve injury. METHODS: New Zealand white rabbits (n = 15) were divided randomly into 3 groups. Three different regimens (group 1: 0.1 ml saline; group 2: 10% dextrose with PRP; group 3: 10% dextrose with saline) were injected within the carpal tunnel. Electrophysiological and histological findings were evaluated 12 weeks after the injection. RESULTS: The mean median motor latency in group 3 was significantly longer than that in groups 1 and 2. The cross-sectional area of the median nerve and subsynovial connective tissue thickness in group 3 were significantly larger than those in groups 1 and 2. CONCLUSIONS: PRP injection may be effective in controlling median nerve injury, as demonstrated by improvement in electrophysiological and histological findings 12 weeks after dextrose injection.

δ-Aminolevulinic acid dehydratase genotype predicts toxic effects of lead on workers' peripheral nervous system.

There is a wide variation in sensitivity to lead (Pb) exposure, which may be due to genetic susceptibility towards Pb. We investigated whether a polymorphism (rs1800435) in the δ-aminolevulinic acid dehydratase (ALAD) gene affected the toxicokinetics and toxicodynamics of Pb. Among 461 Chinese Pb-exposed storage battery and 175 unexposed workers, allele frequencies for the ALAD1 and ALAD2 alleles were 0.968 and 0.032, respectively. The Pb-exposed workers had a higher fraction of the ALAD1-2/2-2 genotype than unexposed workers (7.8% vs. 2.3%, p=0.01). The Pb levels in blood (B-Pb) and urine (U-Pb) were higher in Pb-exposed workers carrying the ALAD2 allele compared to homozygotes for ALAD1 (median B-Pb: 606 vs. 499 µg/L; U-Pb: 233 vs. 164 µg/g creatinine), while there was no statistically significant difference in the unexposed controls (median: 24 vs. 37 µg/L, and 3.9 vs. 6.4µg/g creatinine, respectively). High B-Pb and U-Pb were associated with statistically significantly lower sensory and motor conduction velocities in the median, ulnar and peroneal nerves. At the same B-Pb and U-Pb, ALAD1 homozygotes had lower conduction velocities than the ALAD2 carriers. There were similar trends for toxic effects on haem synthesis (zinc protoporphyrin and haemoglobin in blood) and renal function (albumin and N-acetyl-d-ß-acetylglucosaminidase in urine), but without statistical significance. There was no difference in Pb toxicokinetics and toxicodynamics associated with VDR BsmI polymorphism. Our results show that the ALAD genotype modifies the relationship between Pb and its toxic effects on the peripheral nervous system. This must be considered in the assessment of risks at Pb exposure.

[Neuropathy of the median nerve caused by intraneural haematoma after carpal tunnel release in an anticoagulated patient]. / Neuropathie des Nervus medianus durch intraneurale Blutung bei einem antikoagulierten Patienten nach Karpaltunnelspaltung.

We report about the sudden onset of a median nerve neuropathy in an anticoagulated patient eight weeks after uneventful carpal tunnel release. Several differential diagnosis have to be considered: compression syndrome as well as iatrogenic damage of the median nerve due to the preliminary procedure or even concomitant disease can generate symptoms of peripheral neuropathy. We diagnosed an intraneural haematoma through surgical exploration. This rare complication of oral anticoagulation therapy occurred spontaneously and was treated successfully by interfascicular neurolysis.

Carpal tunnel syndrome. A new feature in the natural history of TOS?

OBJECTIVE: To ascertain whether carpal tunnel syndrome (CTS) in patients affected with toxic oil syndrome (TOS) is associated with conditions and diseases considered risk factors for CTS in the general population and/or with certain clinical manifestations of TOS. METHODS: We conducted a case-control study to compare 89 TOS patients residing in Madrid diagnosed with CTS from 1981 through July 2001 (cases) against 638 TOS patients not affected with CTS (controls). Risk factors for CTS and clinical manifestations of TOS were analyzed. RESULTS: Multivariate logistic regression analysis yielded the following odds ratios (95% confidence interval): 3.32 (1.47-7.50) for TOS-related neuropathy; 2.85 (1.14-7.13) for TOS-related thromboembolic events; 2.63 (1.36-5.06) for female gender; 0.43 (0.24-0.80) for TOS-related scleroderma; 0.26 (0.12 0.59) for smoking; and, in women, 2.53 (1.06-5.70) for fibrositis and 1.84 (1.04-3.20) for miscarriages. CONCLUSION: Our study findings support the hypothesis that CTS in TOS patients is more linked to certain clinical manifestations of TOS, mainly neuropathy, than to conditions and diseases considered risk factors for CTS in the general population.

Nerve conduction changes in patients with mitochondrial diseases treated with dichloroacetate.

Serial measurements of nerve conduction velocities and amplitudes were performed in 27 patients with congenital lactic acidemia over 1 year of sodium dichloroacetate (DCA) administration. Patients were treated with oral thiamine (100 mg) and DCA (initial dose of 50 mg/kg) daily. Nerve conduction velocity and response amplitude were measured in the median, radial, tibial, and sural nerves at 0, 3, 6, and 12 months, and plasma DCA pharmacokinetics were measured at 3 and 12 months. Baseline electrophysiologic parameters in this population were generally below normal but as a group were within 2 standard deviations of normal means. Although symptoms of neuropathy were reported by only three patients or their families, nerve conduction declined in 12 patients with normal baseline studies, and worsening of nerve conduction occurred in the two who had abnormalities at baseline. Peripheral neuropathy appears to be a common side effect during chronic DCA treatment, even with coadministration of oral thiamine. Nerve conduction should be monitored during DCA treatment.