The effect of taxifolin on oxidative sciatic nerve damage induced by cobalt chloride in rats: a biochemical and histopathological evaluation.

Cobalt is a trace element that increases lipid peroxidation and malondialdehyde levels and reduces the antioxidant defense mechanisms of nerve cells. High levels of cobalt exposure may cause peripheral neuropathy, but the mechanism behind this has not yet been elucidated. Taxifolin is a flavonoid whose antioxidant and anti­inflammatory properties are well­known. We aimed to investigate the effect of taxifolin on cobalt­induced oxidative sciatic nerve damage. Eighteen albino male Wistar rats were assigned to three groups: Control, Cobalt, and Taxifolin + Cobalt groups. Total oxidant and total antioxidant status and levels of malondialdehyde, total glutathione, and superoxide dismutase were measured to determine the effect of taxifolin on cobalt­induced sciatic nerve injury. The following statistically significant effect of taxifolin was observed: It prevented cobalt­induced oxidative sciatic nerve damage by reducing malondialdehyde levels and total oxidant status and increasing total antioxidant status, total glutathione levels, and superoxide dismutase levels. In a histopathological analysis, we observed similar findings in Control and Taxifolin + Cobalt groups. We determined that taxifolin is effective in preventing cobalt­induced oxidative damage in sciatic nerve injury.

Trigger Point Injection as a Rare Cause of Ischemic Stroke: A Case Report.

INTRODUCTION: Myofascial pain syndrome is a painful local or regional disease caused by myofascial trigger points. Trigger point injection (TPI) is a frequently used method for the treatment of myofascial pain. Major complications associated with TPI have rarely been reported in the literature. CASE REPORT: A 24-year-old woman, without medical history of any disease, was diagnosed with myofascial syndrome based on the presence of long-standing neck and right arm pain, and TPI with lidocaine was applied to the right trapezius region. During the procedure, blurred vision and loss of strength in the left arm occurred. Magnetic resonance and computed tomography imaging of the brain revealed findings that were consistent with an ischemic stroke in the right capsular interna and right occipital region. CONCLUSION: The reported patient is the first in the literature who suffered from ischemic stroke after TPI. The use of ultrasound for injections into the neck muscles could avoid serious complications.

The Effect of Anakinra on Acrylamide-induced Peripheral Neuropathy and Neuropathic Pain in Rats

Abstract Acrylamide is a neurotoxic compound. Moreover, anakinra is an interleukin-1 (IL-1) receptor antagonist used in rheumatoid arthritis treatment. This study investigated the effect of anakinra on acrylamide-related neuropathy and neuropathic pain. Acrylamide exposure caused a significant decrease in the pain threshold; an increase in malondialdehyde (MDA), tumor necrosis factor-alpha (TNF-α), and interleukin-1 beta (IL-1ß) levels; and a decrease in total glutathione (tGSH) values in the sciatic nerve. This indicates hyperalgesia presence, oxidative stress, and peripheral nerve tissue inflammation. Anakinra treatment significantly reduced the MDA, IL-1ß, and TNF-α levels, and increased the pain threshold and mean tGSH values. The analgesic effect of anakinra was 67.9% at the first hour, increasing to 74.9% and 76.7% at the second and third hours, respectively. The group receiving acrylamide exhibited histopathological changes (e.g., swollen and degenerated axons, hypertrophic and hyperplasic Schwann cells, and congested vessels). The use of anakinra significantly improved these morphological changes. Anakinra is concluded to reduce neuropathic pain and prevent neurotoxic effect of acrylamide on peripheral nerves due to its analgesic, antioxidant, and anti-inflammatory properties

Prevalence and Treatment of Neuropathic Pain in Kidney and Liver Transplant Recipients.

OBJECTIVES: Neurologic complications are common after kidney and liver transplant. Neurologic complications affect mortality and morbidity in transplant recipients, and neuropathic pain is an important symptom affecting a patient's quality of life. The aim of the present study was to provide readers with our experience regarding causes and treatment of neuropathic pain in patients undergoing kidney and liver transplant at our transplantation center. MATERIALS AND METHODS: The medical data of 553 kidney transplant recipients and 258 liver transplant recipients who received transplant procedures at the Baskent University Transplantation Center between 2008 and May 2016 were retrospectively reviewed. Fifty-one patients who were examined by an expert neurologist and diagnosed with neuropathic pain on the basis of clinical, neurologic examination, and laboratory findings were included for analyses. RESULTS: Among 811 transplant recipients, 51 patients (6.2%) were diagnosed with neuropathic pain. Of these, 22 were female and 38 were male patients, and 42 were kidney transplant recipients and 9 were liver transplant recipients. Causes of neuropathic pain included uremia, diabetes mellitus, ischemic peripheral arterial disease, inflammatory neuropathy, vasculitis, discopathy, postherpetic neuralgia, carpal tunnel syndrome, and multiple myeloma. Patients with symptoms too mild to affect daily life activities were treated conservatively. Plasmapheresis, gabapentin, pregabalin, alpha-lipoic acid, and duloxetine were administered as treatment modalities and medications. CONCLUSIONS: Neuropathic pain was lower in our transplant recipients than in the general population. Treatment medications were effective for transplant recipients at lower doses for the management of neuropathic pain impairing quality of life than doses for the general population.

Neurologic Complications After Cardiac Transplant.

OBJECTIVES: Cardiac transplant is the best available therapy for patients with end-stage heart failure. Neurologic complications occur at a rate of 30% to 70% in patients undergoing cardiac transplant, and they affect mortality and morbidity of these patients. Risk factors for neurologic complications include immunosuppressive medication toxicity, infections, brain lesions, and metabolic disorders. The aim of our study was to determine the incidence of neurologic complications in adult patients undergoing cardiac transplant. MATERIALS AND METHODS: We retrospectively evaluated the medical records of 70 patients who underwent cardiac transplant between 2004 and April 2016. We recorded the demographic data, neurologic symptoms, neurologic examination findings, laboratory test results, brain imaging study results, and treatments received of the patients. RESULTS: Of the 70 patients enrolled, 55 were male and 15 were female patients. The age range was 18 to 63 years, and the mean age was 42.4 years. Twelve patients had encephalopathy, 4 had neuropathic pain, 3 had tremor, 2 had ischemic cerebrovascular accident, 7 had posterior reversible encephalopathy syndrome, and 1 had drop foot. Encephalopathy usually developed secondary to other neurologic disorders. The incidence of neurologic complications in adult patients undergoing cardiac transplant was 30%. CONCLUSIONS: Neurologic complications are common after cardiac transplant. We observed an incidence of 30% for neurologic complications in our clinic, with encephalopathy being the most common complication. Encephalopathy most commonly developed secondary to posterior reversible encephalopathy syndrome.