peripheral neuropathy

Demyelinating peripheral neuropathy has been described in association with tumor necrosis factor (TNF) inhibitors. It is rarely developed after treatment discontinuation. We present the case of a child with juvenile idiopathic arthritis who developed peripheral neuropathy few months after TNF inhibitor withdrawal with clinical worsening of the neurological sequelae while undergoing treatment with abatacept.

Treatment options in multiple myeloma (MM) based on novel agents are often limited by dose-related neurotoxicity. Bortezomib, a highly active reversible proteasome inhibitor, frequently causes peripheral neuropathy (PN). Bortezomib-induced PN (BIPN) is characterized by a length-dependent, sensory, axonal polyneuropathy (PNP) with predominant small fiber-affection. Following dose reduction or drug discontinuation, BIPN resolves within 3-4 months in the majority of patients. The pathophysiological mechanisms of BIPN are unclear. Rare cases of a severe demyelinating or mixed BIPN with prominent motor involvement have been attributed to autoimmune or inflammatory reactions. A case report, including nerve pathology, is presented of a 59-year-old man with stage III IgG-κ MM who was treated with bortezomib on the occurrence of progressive disease. After the fourth cycle, he developed a painful distal symmetric sensory PNP followed by gait instability and muscle weakness increasing over 3 months despite early cessation of bortezomib.Neurological examination revealed a distal flaccid tetraparesis mainly of the lower limbs with sensory loss and severe ataxia, electrophysiological features of a mixed axonal-demyelinating PNP, and pathomorphological evidence of neuritis. Steroid treatment was initiated, and partial recovery of the neurological symptoms within 6 months was observed. While a neurotoxic effect may explain the initial distal sensory disturbances, the worsening of neurological dysfunction after bortezomib withdrawal and the clinical pattern with steroid-responsive muscle weakness predominantly of the legs are consistent with an immune-mediated mechanism. This is in line with the sural nerve biopsy findings. Toxic BIPN followed by an immune-mediated BIPN in the same patient has not been reported before.

Background: Diabetic peripheral neuropathy is a symmetrical length-dependent sensorimotor polyneuropathy due to chronic hyperglycemia. The World Health Organization (WHO) identified diabetes as a major global health concern. Diabetic neuropathy is characterized by motor dysfunctions (weakness and atrophy) especially at the distal muscles of lower limbs, and impaired dynamic muscular control in type 2 diabetes patients. Symptoms start in a distal-to proximal pattern in the feet, and ankle and proximally in the hip and knee for both flexors and extensors. Proximal muscle weakness affects postural stability. Dorsiflexor weakness causes increased hip, knee flexion and metatarsophalangeal extension in the initial swing whereas weakness in plantar flexors causes a greater amount of hip and knee flexion during the stance phase.Methodology: 34 subjects with Diabetic Peripheral Neuropathy who fulfilled all the inclusion criteria were recruited for the study. Ethical standards have been maintained and informed consent was taken. Subjects were randomly assigned by lottery method into two groups, intervention, and control with 17 in each. Since it is a single blinded study subjects were blinded about the interventions provided. Pre and post-test scores were taken before and after 4 weeks using Surface Electromyography (sEMG), Kinovea Software, Functional Gait Assessment (FGA) and Short Form -36 (SF-36).Results: The pre and post-score values of the kinematics of gait, Functional Gait Assessment, and Short Form - 36 were analyzed using a Paired t-test and Wilcoxon Signed Rank test within the group analysis, Mann- Whitney U test and Independent t-test for between the group analysis. Both groups displayed notable variations, whereas the intervention group exhibited more significant differences (p < 0.05). Thus, it can be inferred that lower extremity training significantly improves gait kinematics and quality of life in diabetic neuropathy.Conclusion: Lower extremity training is effective in improving the kinematics of gait and quality of life in diabetic neuropathy.

Chemotherapy-Induced Peripheral Neuropathy (CIPN) is a major limiting side effect of many common chemotherapeutics often leading patients to terminate their chemotherapy treatment regimen early. The development of CIPN differs by chemotherapeutic class, with platinum- and taxane-based treatments demonstrating the highest incidence rates. Despite its relatively high prevalence, there are currently no FDA-approved treatments for CIPN, and clinicians must rely on the off-label use of several analgesics and various non-pharmacological approaches to treat CIPN symptoms in patients. Novel insights on the development of CIPN have identified new drug targets leading to several Phase II clinical trials to be initiated. Here, we describe recent advances in drug development for CIPN.

Background: Cancer treatment frequently depends on the intricate and potent effects that are acknowledged for their potential to save lives. Chemotherapy can have adverse effects on both the central and peripheral nervous systems, posing significant challenges.Objective: •    To assess the causative agent, development, and timing of occurrence.•    To improve management of neurological complications.•    To discriminate the iatrogenic effects of cancer therapy and neurological progression.Method: A prospective observational study was conducted in a hospital setting, focusing on the neurotoxic effects of chemotherapy in cancer patients over a span of six months. The research involved participants from both the oncology in-patient and daycare departments. After obtaining informed consent, individuals in the study population were interviewed to gather information about any neurological symptoms they encountered following their chemotherapy sessions.Results and discussion: Within our study population, a predominant 67% comprised female patients, while male patients constituted 33%. Of the total participants, 66% reported experiencing neurological symptoms. Among these symptoms, the majority of patients encountered sensations such as tingling, numbness, and a burning sensation. Other reported symptoms included headaches, distal weakness, myalgia, seizures, and ataxia.Conclusion: In this current study, 66% of the study population encountered neurological side effects. Generally, the presence of comorbidities, vitamin deficiencies, and advanced age can significantly contribute to the development of peripheral neuropathy. Depending on the severity of neuropathy, recommendations for interventions include the prescription of vitamin supplements, calcium supplements, duloxetine, and pregabalin.