scholarly journals Pregabalin Treatment of Peripheral Nerve Damage in a Murine Diabetic Peripheral Neuropathy Model

2018 ◽  
Vol 14 (3) ◽  
pp. 294-299
Author(s):  
J Li
2019 ◽  
Vol 7 (14) ◽  
pp. 2267-2270 ◽  
Author(s):  
Daniela Ristikj-Stomnaroska ◽  
Valentina Risteska-Nejashmikj ◽  
Marija Papazova

BACKGROUND: Diabetic peripheral neuropathy (DPN) means the presence of symptoms and/or signs of peripheral nerve damage that occur to people with diabetes, excluding all other causes of neuropathy. Chronic hyperglycaemia leads to increased secretion of tumour necrotic factor-alpha (TNF-α), with the development of micro and macroangiopathy, damage to nerve fibres and local demyelination. AIM: To determine the role of inflammation in the peripheral nerve damage process concerning people suffering from type II diabetes mellitus. MATERIAL AND METHODS: The study included a total of 80 subjects, men and women, divided into two groups: an examined group (n = 50) consisting of subjects with DPN at the age from 30 to 80 years and a control group (n = 30) of healthy subjects aged from 18 to 45. In the investigated group, a neurological examination was performed using the Diabetic Neuropathy Symptoms (DNS) Score and Electroneurography. All the subjects had the blood plasma concentration of TNF-α by ELISA technique. RESULTS: The average value of TNF-α in the test group was 8.24 ± 2.899 pg/ml, while the control group was 4.36 ± 2.622 pg/ml (p < 0.0001). The average value of TNF-α was correlated with the achieved DNS score in the investigated group (p = 0.005). Concerning the linear association of the concentration of TNF-α with the peripheral nerve velocity in the investigated group, no statistical significance was detected. CONCLUSION: Inflammation can play a role in the pathogenesis of diabetic autonomic neuropathy and cranial neuritis.


2021 ◽  
Author(s):  
Patricia Penna ◽  
Robson Vital ◽  
IZABELA PITTA ◽  
Mariana Hacker ◽  
Ana Salles ◽  
...  

Abstract Lepromatous leprosy (LL) patients have evidence of extensive peripheral nerve damage as soon as a diagnosis is made, but most of them have few or no symptoms related to peripheral neuropathy. Usually, they do not have the cardinal signal of leprosy neuritis. However, disability caused by peripheral nerve injuries has consequences throughout the entire life of these patients and the pathophysiological mechanisms of nerve damage are still poorly understood. The objective of this study was to evaluate the outcome of peripheral neuropathy in a group of LL patients in an attempt to understand the mechanisms of nerve damage. We evaluated medical records of 14 LL patients that had undergone a neurological evaluation at the beginning of Leprosy treatment then worsened at least 4 years after the end of treatment and underwent nerve biopsy. The symptoms at the beginning of treatment were compared with those at the time of the biopsy. Pain was a symptom in only one patient at the beginning and was a complaint in 9 patients by the time of biopsy. Neurological examination showed that the majority of patients already had alterations in medium and large caliber fibers at the beginning of the treatment, and pain increased by the time of biopsy, while neurological symptoms and signs deteriorated independently of the use of prednisone or thalidomide. Nerve Conduction Studies demonstrated that sensory nerves were the most affected. LL patients can develop a silent progressive degenerative peripheral neuropathy, which continues to develop despite high dose long term corticoid therapy.


Author(s):  
Michael Donaghy

Some causes of focal peripheral nerve damage are self-evident, such as involvement at sites of trauma, tissue necrosis, infiltration by tumour, or damage by radiotherapy. Focal compressive and entrapment neuropathies are particularly valuable to identify in civilian practice, since recovery may follow relief of the compression. Leprosy is a common global cause of focal neuropathy, which involves prominent loss of pain sensation with secondary acromutilation, and requires early antibiotic treatment. Mononeuritis multiplex due to vasculitis requires prompt diagnosis and immunosuppressive treatment to limit the severity and extent of peripheral nerve damage. Various other medical conditions, both inherited and acquired, can present with focal neuropathy rather than polyneuropathy, the most common of which are diabetes mellitus and hereditary liability to pressure palsies. A purely motor focal presentation should raise the question of multifocal motor neuropathy with conduction block, which usually responds well to high-dose intravenous immunoglobulin infusions.


2019 ◽  
Vol 2 (5) ◽  
pp. e194798 ◽  
Author(s):  
Johann M. E. Jende ◽  
Jan B. Groener ◽  
Christian Rother ◽  
Zoltan Kender ◽  
Artur Hahn ◽  
...  

2009 ◽  
Vol 106 (33) ◽  
pp. 14114-14119 ◽  
Author(s):  
G. Pelled ◽  
D. A. Bergstrom ◽  
P. L. Tierney ◽  
R. S. Conroy ◽  
K.-H. Chuang ◽  
...  

2017 ◽  
Vol 32 (3) ◽  
pp. 495-501 ◽  
Author(s):  
Igor Rafael Correia Rocha ◽  
Adriano Polican Ciena ◽  
Alyne Santana Rosa ◽  
Daniel Oliveira Martins ◽  
Marucia Chacur

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