China
Africa
Explore chapters and articles related to this topic
Clinical and Experimental Evaluation of Sympatho-Vagal Interaction: Power Spectral Analysis of Heart Rate and Arterial Pressure Variabilities
Published in Irving H. Zucker, Joseph P. Gilmore, Reflex Control of the Circulation, 2020
Alberto Malliani, Massimo Pagani, Federico Lombardi, Sergio Cerutti
This approach has also proven very useful in assessing the existence of peripheral neuropathies such as the one occurring in diabetic patients. In a recent study (Pagani et al., 1988b), we found that patients with uncomplicated diabetes, as compared to controls, were characterized by a reduced R-R variance at rest, as already reported (Kitney et al., 1982; Lishner et al., 1987), and by an altered response to tilt of spectral indices of sympathetic activation and vagal withdrawal.
Skin
Published in Pritam S. Sahota, James A. Popp, Jerry F. Hardisty, Chirukandath Gopinath, Page R. Bouchard, Toxicologic Pathology, 2018
Zbigniew W. Wojcinski, Lydia Andrews-Jones, Daher Ibrahim Aibo, Rie Kikkawa, Robert Dunstan
Unmyelinated nerve endings penetrate the epidermis and convey sensory information from the skin to the central nervous system. These intraepidermal nerve fibers (IENFs) have receptors, which sense pain (nociceptors), itch (pruriceptors), or heat (thermoceptors), and aid in sensing non-painful touch through interactions with mechanoreceptors. Peripheral neuropathies (sensory neuropathies) are characterized by loss of the smallest and most peripheral nerve fibers first, and can cause significant debility to affected patients. The etiologies of peripheral neuropathies are numerous and include metabolic conditions such as diabetes, infectious agents such as herpes and human or simian immunodefiency virus (HIV, SIV), and some drugs such as some chemotherapeutic agents, and antiretroviral therapeutics used to treat HIV. IENF density is a way to serially quantify these sensory nerves, both in patients, and laboratory animals. Punch biopsies of 3 mm size are collected from a predetermined site, and fixed to enable 50 um thick sections, that are then stained with a panaxonal marker such as anti-PGP9.5 (protein gene product 9.5). Computer software is available to count the IENF. A guideline to performing these IENF density counts in human patients was published by a joint task force of the EFNS and PNS (Lauria et al. 2010). Methods for the use of IENF counts to study peripheral neuropathy in non-human primates (Mangus et al. 2016) or rodents (Siau et al. 2006 among others) have been published.
Nerve and Retinal Changes in Experimental Diabetes
Published in John H. McNeill, Experimental Models of Diabetes, 2018
Functional changes of peripheral neuropathies have been extensively demonstrated in rodent diabetes. In the study of peripheral neuropathy, slowing of motor nerve conduction velocity is the major functional alteration. A wide range of pharmaceutical agents, such as insulin, AR inhibitors, myoinositol, Ca2+ channel blocker, hyperbaric oxygen, and ganglioside, were found to prevent slowing of nerve conduction velocity, autonomic disturbance, and axoplasmic transport in rats with chemical or spontaneous diabetes.40–43,49,55,62–127 Several additional treatment modalities such as essential fatty add, prostaglandin El analog, ACTH analog, α-glucosidase inhibitor, methylcobolamine, and acetylcamitine, were found to prevent loss of nerve conduction velocity.62–127 These data suggest that although hyperglycemia is a key initiating event, it may subsequently lead to several biochemical abnormalities, all of which may contribute in part to loss of nerve conduction velocity. Several of these factors possibly act through reduced neurofilament synthesis, transport, and subsequent axonal atrophy.7 Impaired low- and high-molecular-weight neurofilament mRNA expression has been demonstrated in the dorsal root ganglion cells of STZ diabetic rats.128,129
Effects of training with a neuro-mechano stimulator rehabilitation bicycle on functional recovery and paired-reflex depression of the soleus in individuals with incomplete paralysis: a proof-of-principle study
Published in International Journal of Neuroscience, 2019
Niyousha Mortaza, Zahra Moussavi, Katinka Stecina, Jennifer E. Salter, Steven R. Passmore, Phillip F. Gardiner, Cheryl M. Glazebrook
Ten participants were allocated for the NMSR training from the local rehabilitation hospital between June 2015 and December 2016. All participants provided written informed consent approved by the Biomedical Research Ethics Board of the University of Manitoba prior to participation (Figure 2). The inclusion criteria for the study were individuals with level C or D spinal cord injury, according to the American Spinal Injury Association score (ASIA) [30], who were (i) at least 12 months post-injury; (ii) were discharged from all rehabilitation to ensure stability of the patient’s neurological condition; (iii) had the ability to walk 10 meters or more with or without assistance; (iv) had range of motion in the lower limb joint sufficient to allow the cycling exercise; (v) had the ability to maintain current anti-spasticity medication dosages throughout training/test sessions. Exclusion criteria were: (i) peripheral neuropathies that affected the lower limbs; (ii) impaired mental capacity; (iii) any medical condition that was contraindication to cycling training including significant diagnosed osteoporosis, excessive spasticity in the legs as measured by a score of more than 3 on the Modified Ashworth Scale or any spasticity that limits the possibility of cycling exercise or walking, obstructive and/or restrictive pulmonary disease, severe spinal and lower limb deformities, decubitus ulcer in the area in contact with the NMSR’s bed and pedals.
Glial-derived neurotrophic factor is essential for blood-nerve barrier functional recovery in an experimental murine model of traumatic peripheral neuropathy
Published in Tissue Barriers, 2018
Chaoling Dong, E. Scott Helton, Ping Zhou, Xuan Ouyang, Xavier d‘Anglemont de Tassigny, Alberto Pascual, José López-Barneo, Eroboghene E. Ubogu
The total annual cost of diabetic peripheral neuropathy and its complications in the United States of America (U.S.A.) alone was estimated to be ∼$66.2 billion in 2012, with significantly increased total direct costs in patients with peripheral neuropathy compared to patients without neuropathy.1,2 A common consequence of peripheral neuropathies is chronic neuropathic pain, a condition that is estimated to affect about 1–10% of the general population worldwide.3-7 Diabetic patients with severe peripheral neuropathy had ∼5-fold higher direct medical costs in the U.S.A. compared to unaffected diabetics.2 Peripheral neuropathy and its consequential chronic neuropathic pain cause significant reduction in productivity and burden on health care resources worldwide.6,8-10 Current medical management of peripheral neuropathies and neuropathic pain aims to identify and specifically treat its cause. However, most treatments are non-specific and are partly efficacious.11,12
HDAC6 as a potential therapeutic target for peripheral nerve disorders
Published in Expert Opinion on Therapeutic Targets, 2018
Robert Prior, Lawrence Van Helleputte, Yvonne Eileen Klingl, Ludo Van Den Bosch
Despite the clinically similar phenotype of patients with peripheral neuropathies, these diseases are very heterogeneous in their etiology as well as in their pathophysiology. Common among all peripheral neuropathies is the lack of disease-modifying pharmacological interventions. So far, no therapy is available in the clinic to effectively cure or reverse these disorders and accessible treatments only show modest improvements. Therefore, a better understanding of disease-modifying targets is essential. With potential benefits on multiple levels of the neurodegenerative cascade, combined with positive effects on concomitant disorders underlying the neuropathy (e.g. cancer, immunological or metabolic disorders), we believe one such targetable modifier could be HDAC6.