Alcoholic peripheral neuropathy involves degeneration of the peripheral motor neurons, typically in the lower extremities, accompanied by painful sensations and impairments in gait as a direct result of alcohol's toxicity on the nervous system. Symptoms can range from mild to severe, and many factors, such as use history, comorbidities, lifestyle, and family history, determine the disease course and success of treatment. Laboratory values include deficiencies in many key nutrients for neuron health, including vitamin B1 (thiamine), vitamin B12, and folic acid. Here, we discuss a case of a 31-year-old female patient who presented with symptoms of severe peripheral neuropathy, including paresthesias, pain, burning, and gait impairment, as a result of years of alcohol use. Following a diagnosis of peripheral neuropathy, complete alcohol cessation and symptom management are indicated as treatment. The patient's regimen includes a multifactorial, supportive approach with neuropathic, opioid, and anti-inflammatory medications in addition to physical therapy and lifestyle changes to keep a stable baseline.

Background and objective Peripheral neuropathy (PN) is a common and debilitating complication of chronic kidney disease (CKD), particularly in patients undergoing hemodialysis (CKD stage 5 on dialysis, CKD5D). This study aimed to determine the prevalence of PN among CKD5D patients at a tertiary care center in Nepal and to characterize its clinical and electrophysiological features. Methodology A single-center, observational, cross-sectional study was conducted at Tribhuvan University Teaching Hospital (TUTH) from November 2020 to October 2021. Adult patients (≥18 years) with CKD5D undergoing maintenance hemodialysis were included. Patients with a prior renal transplant or known neurological disorders were excluded. Peripheral PN was assessed by using the Michigan Neuropathy Screening Instrument (MNSI) questionnaire and physical examination, and confirmed by nerve conduction studies (NCS). Data were analyzed using SPSS® Statistics version 25 (IBM Corp., Armonk, NY), and ethical approval was obtained from the Institutional Review Board. Results Among the 116 enrolled patients, 80 were male (68.9%), with a mean age of 44.9 ± 15.47 years. The etiology of CKD was undetermined in 76 patients (65.5%), followed by diabetic kidney disease in 32 patients (27.6%). The mean duration of hemodialysis was 14 months, and 91 patients (78.4%) received eight hours of dialysis per week. PN was detected in 106 patients (91.4%), including all 35 diabetic participants (100%) and 71 out of 81 non-diabetic patients (87.7%). Based on the MNSI questionnaire, 14 patients (12.1%) reported neuropathic symptoms, while 60 (51.7%) had signs of PN on physical examination. Distal sensorimotor axonal neuropathy was the predominant pattern observed. The most frequently affected nerves were the common peroneal nerve (motor) and the sural nerve (sensory). Notably, lower serum albumin levels were significantly associated with the presence of PN (p=0.017). Conclusions PN is highly prevalent in CKD5D patients in Nepal, including among non-diabetics. Routine screening using clinical tools such as the MNSI, complemented by electrodiagnostic testing, may facilitate early detection and guide management strategies.

Peripheral neuropathy (PN) is a prevalent and debilitating complication of obesity, prediabetes, and type 2 diabetes, which remains poorly understood and lacks disease-modifying therapies. Fortunately, diet and/or exercise have emerged as effective treatment strategies for PN. Here, we examined the impact of caloric restriction (CR) and high-intensity interval training (HIIT) interventions, alone or combined (HIIT-CR), on metabolic and PN outcomes in high-fat diet (HFD) mice. HFD feeding alone resulted in obesity, impaired glucose tolerance, and PN. Peripheral nerves isolated from these mice also developed insulin resistance (IR). CR and HIIT-CR, but not HIIT alone, improved HFD-induced metabolic dysfunction. However, all interventions improved PN to similar extents. When examining the underlying neuroprotective mechanisms in whole nerves, we found that CR and HIIT-CR activate the fuel-sensing enzyme AMPK. We then performed complimentary in vitro work in Schwann cells, the glia of peripheral nerves. Treating primary Schwann cells with the saturated fatty acid palmitate to mimic prediabetic conditions caused IR, which was reversed by the AMPK activator, AICAR. Together, these results enhance our understanding of PN pathogenesis, the differential mechanisms by which diet and exercise may improve PN, and Schwann cell-specific contributions to nerve insulin signaling and PN progression.

All modern vaccines share the risk of neurological adverse effects. Only a few cases of Parsonage-Turner syndrome (PTS), an uncommon peripheral nerve condition associated with coronavirus disease 2019 (COVID-19) immunization, have been reported to date. We describe a case of COVID-19 vaccine-induced PTS and provide a brief literature review. A 78-year-old male non-smoker with a medical history of coronary artery disease presented with non-exertional, constant chest pain for one hour and new onset of bilateral hand weakness for three days. He had no neurological disease or allergies and denied any recent trauma or infection. Three weeks before the onset of the symptoms, the patient received a second dose of the BNT162b2 COVID-19 vaccine, which was administered 21 days after the first dose. Physical examination was significant for weakness in right-hand grip and wrist flexion. There were no other motor deficits, upper motor neuron signs, bulbar weakness, or sensory deficits. Diagnostic workup for the underlying diabetes mellitus, infections, or other autoimmune diseases was negative. Imaging workup revealed no demyelination, fracture deformity, traumatic subluxation, or compressive myelopathy. Nerve conduction studies, including needle electromyography, showed decreased motor unit recruitment in the bilateral first dorsal interosseous and right deltoid, biceps, and triceps muscles confirming PTS. The patient was treated with 40 mg/day of oral prednisone and occupational therapy to maintain range of motion and activities of daily living. PTS is also known as neuralgic amyotrophy, brachial plexus neuritis, brachial plexopathy, and shoulder-girdle syndrome. It is characterized by asymmetrical, chronic, resistant upper extremity neuropathic pain and neurological defects such as paralysis and paresthesia. There are two different types of PTS: non-hereditary and inherited. The etiology and pathophysiology of PTS are not fully understood. Various aspects such as genetic, environmental, and immunological predisposition may play a role in developing the syndrome. Infections, vaccines, and injuries are typical causes of non-hereditary forms. After the COVID-19 epidemic and the commencement of a global immunization effort, similar instances happened. Presently there is no available test that unequivocally confirms or excludes PTS itself. Electrodiagnostic study and imaging modalities help to rule out other differential diagnoses. Also, there is no specific treatment available; however, it may resolve independently of treatment with supportive care.

Following the implementation of gastric bypass for weight management, copper deficiency has become an increasingly recognized cause of myeloneuropathy. This condition typically presents with primarily sensory deficits leading to ataxia, similar to subacute combined degeneration from Vitamin B12 deficiency. We describe the case of a 72-year-old female patient who initially presented for insidious loss of sensation in her hands and feet, along with intermittent urinary retention. MRI findings included T2 hyperintensities of the dorsal cervicothoracic spinal cord. After identification of low serum copper, intravenous supplementation was started, with immediate improvement in symptoms by the time of discharge. Clinicians should recognize copper deficiency as a potential cause of progressive sensory neuropathy, particularly in patients with a history of gastric bypass.