Background: Glaucoma is a multi-factorial optic neuropathy characterized by a loss of retinal ganglion cells with subsequent loss of the retinal nerve fibers ultimately resulting in visual impairment. The macula region has a high density of retinal ganglion cells thereby being a likely region to detect early cell loss .Since glaucoma affects mainly the inner layers of the retina, Ganglion Cell Complex (GCC) mapping can help to detect glaucomatous damage early as compared to the total retinal thickness. Purpose: To map GCC thickness and average Macular Retinal (MR) thickness with high-speed Fourier-Domain Optical Coherence Tomography (FD-OCT) and correlate it with the Retinal Nerve fiber layer (RNFL) thickness in preperimetric glaucoma. Design: Observational cross-sectional study. Methods: Forty four eyes diagnosed as preperimetric glaucoma were studied. GCC, MR thickness and RNFL thickness was mapped using the RTVue FD-OCT system. The GCC thickness map, the deviation map and the significance map were obtained in all cases. Average GCC thickness and MR thickness were correlated with the RNFL thickness. Results: Average GCC of patients was 85.99±6.9 µm. There was GCC loss in 35 (87.5%) eyes which correlated well with areas of RNFL loss (r=0.408, p<0.001). Nine (22.5%) eyes were seen to have decreased MR thickness. GCC loss correlated well with the loss of average RNFL thickness and MR thickness. Further GCC loss was also seen in 23 (74.19 %) eyes with a normal MR thickness. Conclusion: GCC analysis may prove to be a robust diagnostic parameter and is complementary to RNFL analysis in preperimetric glaucoma.

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.

The case report presents a neuromyelitis optica in a 19 years old male. Brain and spinal cord MRI showed bilateral optic neuropathy, multiphasic demyelinating process involving the cervical and thoracic spinal cord. Cerebrospinal fluid showed negative NMO Ig G. We will describe the radiological aspect of neuromyelitis optica with a review of the literature.

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.

Neuropathy is when nerve damage interferes with the functioning of the peripheral nervous system (PNS). When the cause can’t be determined, it’s called idiopathic neuropathy(Idiopathic neuropathy, now designated as chronic idiopathic axonal polyneuropathy (CIAP).There are three kinds of nerves within the PNS. Sensory nerves relay messages from the sense organs to the brain. This allows sensations of temperature and touch. Motor nerves transmit signals from the brain to the muscles. This helps the brain control the muscles. Autonomic nerves control body functions like heart rate, breathing, and digestion.Damage to nerve cells can affect how the PNS communicates with the rest of the body. Symptoms can include numbness, pain, and balance issues.It’s called acute neuropathy when symptoms develop suddenly. Alternately, it’s called chronic neuropathy when symptoms start slowly and increase over time. Diagnosis involves physical examination and review of medical history. Diagnostic testing may include blood tests, nerve testing, and imaging tests.There is no cure for idiopathic neuropathy. Treatments including medication, physical therapy, and lifestyle modifications can help you function and feel better.We report a case of idiopathic polyneuropathy presented with frequent acute pulmonary edema for a year.

Among the conditioning factors of Diabetic Foot (DF), neuropathy is considered the main factor, arteriopathy the aggravating factor, and foot deformities the triggering factor. The preventive interventions for DF and its complications are distributed by levels of care. At the higher level, hospital care focuses on reducing DF amputations. At the lower level, Primary Care (PC) and Podiatry, focused on preventing DF. PC is considered the ideal place to identify the conditioning factors of DF. In this area, prevention follows the recommendations of the International Working Group on Diabetic Foot (IWGDF) by screening neuropathy focused on the sensitive or insensitive foot. The American Diabetes Association (ADA) a recommends person-centered assessment of neuropathy by clinical examination of symptoms and signs testing sensory, motor, and autonomic neuropathy. This controversy lead us to investigate which methodology (screening or clinical examination) could be more accurate in identifying the conditioning factors of DF in a group of people recruited in the TERMOPIEDI study. Neuropathy was assessed following the definition of diabetic neuropathy, the Young MJ diagnostic criteria, and the Toronto Council diagnostic category. These results allowed us to know the applicability of this procedure in PC within nursing competencies, detecting a greater number of patients with neuropathy compared to the screening method. People with neuropathy presented higher plantar temperature, concluding that neuropathy interferes with foot thermoregulation.

Objective: To evaluate the effects on quality of life and body composition of a Ketogenic Diet (KD) in a woman with Charcot-Marie-Tooth (CMT) disease. Methods: Physical (PCS) and mental (MCS) health conditions were evaluated with the SF-36 questionnaire; dual-energy x-ray absorptiometry was used to determine body composition; parameters were determined at baseline and after 12 weeks of KD.Results: At baseline PCS and MCS were 20.6 and 20.7 respectively with 37.9% fat mass. After 12 weeks SF-36 values significantly improved: PCS 55 and MCS 66.1 with 33.9% fat mass. Conclusion: KD improved the patient’s quality of life and decreased fat mass. Further studies will be needed to better elucidate the beneficial effects of KD among people with CMT.

Chronic foot and heel pain is a clinical dilemma that Pain Physicians often encounter in their daily practice. In the younger active patients, this is often attributed to plantar fasciitis but other rarer etiologies should also be considered. In patients who present with pain over the medial calcaneus, entrapment neuropathy of the inferior calcaneal nerve, the first branch of the lateral plantar nerve (FBLPN), also known as “Baxter’s nerve” must be considered [1,2]. Initially described in 1984 by Baxter and Thigpen, it is often overlooked as a cause of medial heel pain, particularly in athletes, where it may coexist with plantar fasciitis [3]. The nerve has a tortuous course in the foot and can be entrapped as it passes through the fascia of the abductor hallucis, travels in close proximity to a plantar spur or the medial calcaneal tuberosity, or gets enmeshed in scar tissue from prior surgery [1,3].

This case suggests that POEMS syndrome does present with a constellation of signs and symptoms that may lead a clinician to a multitude of other possible diagnoses. Diagnosis is often difficult and delayed. A good history and physical examination as well as a careful review of all workups are paramount in establishing this particular diagnosis. The major criteria of diagnostic for the syndrome are polyradiculoneuropathy, clonal plasma disorder, sclerotic bone lesions, the presence of Castleman disease, and elevated vascular endothelial growth factor. Minor features include organomegaly, extravascular volume overload, endocrinopathy, characteristic skin changes, papilledema, and thrombocytosis. The diagnosis is made with three of the major criteria, two of which must include polyradiculoneuropathy and clonal plasma cell disorder, and at least one of the minor criteria. In this article, we discuss the differential diagnosis and outline the clinical evaluation indicated.

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.