Explore chapters and articles related to this topic
Neurological Disease
Published in John S. Axford, Chris A. O'Callaghan, Medicine for Finals and Beyond, 2023
Peripheral neuropathy is a dysfunction of lower motor neurones or sensory neurones or both. Hereditary motor and sensory neuropathy (HMSN) has at least 76 recognized genetic causes, which may be autosomal dominant or recessive, or X-linked. Some are due to genes integral to normal nerve function while others may be secondary to metabolic disturbance.
Peripheral Neuropathy
Published in Charles Theisler, Adjuvant Medical Care, 2023
Peripheral neuropathy refers to compressed, damaged, or diseased nerves outside the brain and spinal cord that are malfunctioning. Often, it results in numbness, tingling, burning, or stinging pain, especially in the hands or feet. Peripheral neuropathy is tied to significant morbidity and decreases in quality of life.
Diabetic Neuropathy
Published in Jahangir Moini, Matthew Adams, Anthony LoGalbo, Complications of Diabetes Mellitus, 2022
Jahangir Moini, Matthew Adams, Anthony LoGalbo
Prevention of large fiber peripheral neuropathy involves managing underlying conditions and limiting risk factors. Alcohol use, as well as use of tobacco products, should be stopped or reduced. Patients should avoid exposures to toxins, limit activities that could cause physical trauma or injury, have good sleep hygiene, engage in healthy and safe exercise regimens, eat a balanced diet rich in vitamins and minerals, and take vitamin B 12 supplements if eating a vegetarian or vegan diet.
Mechanisms behind diffuse idiopathic peripheral neuropathy in humans – a systematic review
Published in Scandinavian Journal of Gastroenterology, 2023
Hanna Tufvesson, Viktor Hamrefors, Bodil Ohlsson
Many patients have signs and symptoms of peripheral neuropathy without any obvious etiology. In these idiopathic cases, it may be difficult and time-consuming to rule out the causes of neuropathy. Most mechanism studies are performed in animals and need to be confirmed in humans, due to different physiology and anatomical distribution of structures between different species [12,13]. Few reviews about mechanisms behind enteric neuropathy and GI dysmotility or general peripheral neuropathy have been published. The aim of the present systematic review was therefore to identify mechanisms behind diffuse idiopathic peripheral neuropathy involving internal organ systems in humans, and to identify the background to that some patients develop mainly large fiber neuropathy and others mainly SFN.
Clinical significance of SIRT3 and inflammatory factors in multiple myeloma patients with bortezomib-induced peripheral neuropathy: a cohort study
Published in Scandinavian Journal of Clinical and Laboratory Investigation, 2021
Huiqi Yang, Can Liu, Fen Yuan, Fang Li
Normally distributed continuous data were presented by mean ± SD and non-normally distributed data were expressed as median (range). The distribution of the data was analyzed by Kolmogorov–Smirnov method. Comparison between two groups was conducted by Student’s t test for normally distributed data and Mann–Whitney U test was conducted for non-normally distributed data. One-way analysis of variance (ANOVA) followed by Tukey’s post hoc test was used for normally distributed data for comparison among three or more groups. Chi-squared analysis was used to analyze the rates. The correlation among SIRT3 and inflammatory factors was analyzed by Pearson rank correlation analysis. ROC curve was used for diagnostic analysis. Logistic regression was conducted for risk factors of peripheral neuropathy. p < 0.05 was regarded as statistically different. All data were calculated using SPSS software, version 20.0 (IBM, Armonk, NY, USA) and Graphpad Prism 6.0 (GraphPad Software, Inc.).
Enfortumab Vedotin, a fully human monoclonal antibody against Nectin 4 conjugated to monomethyl auristatin E for metastatic urothelial Carcinoma
Published in Expert Opinion on Investigational Drugs, 2019
Bradley A McGregor, Guru Sonpavde
In the phase 2 trial, TRAEs resulted in discontinuation in 12% of patients. Most common related TRAEs were fatigue (50%), alopecia (49%), and decreased appetite (44%). TRAE ≥3 occurring in over 5% of patients included rash (12%), neutropenia (8%), anemia (7%), hyperglycemia (6%), and fatigue (6%.) Peripheral neuropathy, rash, and hyperglycemia were pre-identified as TRAEs of special interest. Treatment-related peripheral neuropathy occurred in ~50% of patients, the majority (94%) were ≤ grade 2 with sensory neuropathy more common than motor neuropathy. Most patients (76%) with peripheral neuropathy had either resolution or only Grade 1 symptoms at last follow-up. Any treatment-related rash occurred in 48% of patients, most of which were low grade (75% ≤Grade 2;) and onset was usually within the first treatment cycle. The rash was manageable with topical emollients and corticosteroids and of all patients who experienced rash, 93% had resolution or improvement at last follow-up. Treatment-related hyperglycemia occurred in few patients and was manageable (11%.). Of those with hyperglycemia at baseline (N = 19) 68% did not develop worsening hyperglycemia. Of those who did develop hyperglycemia, 71% had resolution or improvement at the time of last follow-up and there was one grade 4 toxicity that resolved without the need for long-term therapy. Only one patient required cessation of therapy due to hyperglycemia. There were no treatment-related deaths during the 30-day safety-reporting period [24].