Hemodynamic Considerations in the Pathophysiology of Peripheral Neuropathy

Peripheral neuropathic pain presents one of the greatest on going challenges to both acute and chronic pain management yet our understanding of the origins and pathogenesis of this complex disease state are severely lacking. The purpose of this chapter is to review the current literature regarding neuropathic pain as impacted by hemodynamic alterations. Because of the varied origins of neuropathy, this cannot be discussed as a single entity but we can seek to identify a final common pathway. We will for this rea son examine each known pathogenetic category of neuropathy separately then discuss the effect of hemodynamic alterations through changes in blood pressure to determine any correlations between these alterations and specific effects upon neural structure and function. We have divided this chapter into sections which describe the more commonly known and encountered neuropathies. These are diabetes mellitus, neurotoxic medica- tions, alcohol-related neuropathy, Vitamin B 12 deficiency, end-stage renal disease, inflam - matory bowel disease, and rheumatoid arthritis. control the presence sensorimotor peripheral neuropathy. glycated lipid and the presence of and macro-vascular in 31 consecutive outpa II age 60.7 7.5 who had been within 10 years of the the of hypertension- defined as a blood pressure 140/90-was in sensorimotor peripheral diabetic neuropathy-positive patients. a step and regression analysis on the date that after for duration, glycated and lipids a hypertension sensorimotor diabetic peripheral neuropathy. strong the statistical measure of how close the the of In other methyl ester (L-NAME) which was infused throughout the protocol [124]. The study compared 2 groups using microdialysis fibers placed in the forearm skin of 10 young subjects (age 22 ± 2 years) and 10 older subjects (77 ± 5 years) with skin blood flow subsequently measured by laser-Doppler flowmeters. The protocol entailed the heating of both sites to 42°C for approximately 60 minutes with data expressed as a percentage of maximal vasodilation. The work revealed that local heating before L-NAME infusion resulted in a significantly reduced initial peak, 61 ± 2% CVC max, in younger subjects vs. 46 ± 4% CVC max in older subjects; and a reduced plateau CVC in younger subjects (93 ± 2% CVC max) as well as in older subjects (82 ± 5% CVC max). When the nitric oxide synthetase (NOS) inhibitor was infused following 40 minutes of heating CVC declined to the same value in the young and older adults. They concluded from the work that the overall contribution of nitric oxide to the plateau phase of the SkBF response to local heating was less in the older subjects. Further they concluded that age-related changes in both axon reflex-mediated and NO mediated vasodilation contributed to attenuated cutane ous vasodilator responses in the elderly [124]. In 2010, Fromy et al. focused upon mecha-nosensitivity and vasodilation or pressure-induced vasodilation (PIV) or the dilation of the cutaneous microvasculature when a non-nociceptive external pressure is locally applied to neuroprotective angiogenesis while inhibiting pathogenic angiogenesis and control-ling concomitant beneficial perfusion pressures may lead to optimal results as we seek to alleviate suffering from peripheral neuropathy.