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Homo Sapiens (“Us”): Strengths and Weaknesses
Published in Michael Hehenberger, Zhi Xia, Huanming Yang, Our Animal Connection, 2020
Michael Hehenberger, Zhi Xia, Huanming Yang
Nociception (derived from the Latin verb nocere, which means “to harm”) distinguishes the physiological process related to pain from the “subjective” experience of pain. In nociception, intense chemical, mechanical, or thermal stimulation of sensory nerve cells called nociceptors produces a “noxious” signal that travels along nerve fibers via the spinal cord to the brain. Nociceptors are nerve endings that detect such stimuli. They can be found in the skin, on internal body surfaces and in some internal organs. The concentration of nociceptors varies throughout the body. The categorization of nociceptors is based on the axons that travel from the receptors to the spinal cord or brain. Nociceptors require a minimum intensity of stimulation before they trigger a signal. Once this threshold is reached, a signal is passed along the axon of the neuron into the spinal cord.
Clinical Effects of Pollution
Published in William J. Rea, Kalpana D. Patel, Reversibility of Chronic Disease and Hypersensitivity, Volume 5, 2017
William J. Rea, Kalpana D. Patel
These well-recognized terms should not be confused with the recently used description of CP or central sensitization.102–104 In reality, all perceived pain is centralized. Pain arises from activation of nociceptors, and the sensory receptors in skin, muscle, joints, and the viscera (exceptions being CP syndromes), which then activate second-order neurons in the CNS (spinal cord or brain stem). These, in turn, convey the “nociceptive information” to several sites in the brain, including eventually the cortex, where the conscious appreciation of the activated nociceptor is realized as pain. Therefore, most chronic pain states are driven by activation of nociceptors (or injured nerves) in peripheral tissue. The evidence in support of this derived from experiments in humans with fibromyalgia, irritable bowel syndrome, neuropathic pain, and bladder pain syndrome, in which peripheral blockage of input by local anesthetics disrupts the chronic pain for the duration of local anesthetic action.105,106
Chapter 3 Physics of the Senses
Published in B H Brown, R H Smallwood, D C Barber, P V Lawford, D R Hose, Medical Physics and Biomedical Engineering, 2017
The primary function of nociceptors is to signal pain when the intensity of stimulation exceeds a particular threshold. Although most receptors initiate a pain response if the intensity is too great, some receptors are specifically designed to start to signal at the pain threshold. For example, some thermal nociceptors transmit only at steady temperatures exceeding 42 ◦C and some transmit only at temperatures below 10 ◦C. There are rapid pain receptors, transmitting through myelinated fibres, that let us know very quickly that something is wrong. The conduction velocity of these nerve fibres is up to 30 m s−1. There are also persistent pain receptors, mostly non-myelinated, that react more slowly but maintain the sensation of pain. These receptors and the associated fibres are amongst the smallest and slowest nerve fibres in the body, with conduction velocities down to 2 m s−1 and below.
Improved skin-permeated diclofenac-loaded lyotropic liquid crystal nanoparticles: QbD-driven industrial feasible process and assessment of skin deposition
Published in Liquid Crystals, 2021
Tejashree Waghule, Shalini Patil, Vamshi Krishna Rapalli, Vishal Girdhar, Srividya Gorantla, Sunil Kumar Dubey, Ranendra Narayan Saha, Gautam Singhvi
DDE is a low molecular weight compound (369.3 g/mol) which is amphiphilic. It has high protein binding thus more affinity towards albumin which gets accumulated in high concentrations in the surrounding region of the inflamed tissue and joints. DDE exhibits pKa of 4.0, thus remain un-ionised at acidic pH around inflamed tissues, cross the membrane barriers efficiently and accumulate in the neutral intracellular space where COX-2 enzymes are present. Due to these reasons, DDE is considered as a suitable candidate for topical delivery in pain management [3,4]. Topical NSAIDs act on the peripheral pain receptors (nociceptors) which are present in abundant quantities in the articular tissues with relatively less central effects. The topical treatment of pain requires improved concentration of drug in the synovial tissue and muscles as compared to the plasma concentrations. Thus, for the topical DDE to show effect, the drug first has to overcome the outermost stratum corneum barrier of the skin, then diffuse/permeate into the deeper skin layers (epidermis, dermis, muscle/synovial tissue) and reach the site of action in therapeutic concentrations to inhibit the COX-2 enzyme. The movement of drugs through the skin follows Fick’s law of diffusion through the intracellular pathway. Drug transport follows the passive diffusion process followed by partitioning into tissues. Although improved permeation can cause some drug to enter into the systemic circulation (present in the dermis), the plasma levels fall 0.2–8% as compared to after oral administration. Thus, the systemic exposure can be reduced significantly [3,5].
Burst and high frequency stimulation: underlying mechanism of action
Published in Expert Review of Medical Devices, 2018
Shaheen Ahmed, Thomas Yearwood, Dirk De Ridder, Sven Vanneste
Pain is described as a wide range of unpleasant sensory and emotional experiences associated with actual or potential damage [1]. Pain is subdivided into two types: nociceptive and neuropathic pain. Nociceptive pain is physiological in that it is caused by the stimulation of sensory fibers through the activation of nociceptors. Neuropathic pain is the result of damaged, dysfunctional, or injured sensory nerve fibers and is therefore, in principle, pathological [2]. This latter type of pain can be felt as a sharp prickle, a burning sensation, or a dull muscular ache and can range intensity from mildly uncomfortable to completely disabling [3]. Moreover, analgesic medication often has an insufficient effect on neuropathic pain [4]. Spinal cord stimulation (SCS) provides a valuable option when neuropathic pain is intractable with medication [5]. The first clinical trial of SCS was tested in 1967 by Shealy et al. to treat cancer pain by stimulating the dorsal columns [6]. The US FDA approved SCS in 1989 to relieve chronic discomfort from neuropathic pain in the arms and legs. Besides treating neuropathic pain, SCS has been effective in patients with neurogenic lower urinary tract dysfunction resulting from spinal cord injury [7].