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Screening and Pharmacological Management of Neuropathic Pain
Published in Suvardhan Kanchi, Rajasekhar Chokkareddy, Mashallah Rezakazemi, Smart Nanodevices for Point-of-Care Applications, 2022
Manu Sharma, Ranju Soni, Kakarla Raghava Reddy, Veera Sadhu, Raghavendra V. Kulkarni
Pain is an obnoxious sensory and emotional experience that significantly affects the general and psychological health of individuals along with their social and economic wellbeing [1]. Pain may arise due to some external stimulus, like thermal, mechanical, or chemical, approaching harmful intensity or damage to system conducting signals, i.e. neurons [2]. It is a complex sensory response that often occurs due to extreme or injurious stimuli [3]. Pain also serves as a warning to indicate damage or impending danger to nerves. It can be categorized into two types, namely neuropathic and nociceptive [4]. Numerous diseases like multiple sclerosis, spinal cord injury, stroke, and central lesion are responsible for neuronal injury or ailments in peripheral or central nervous systems and are the main cause of neuropathic pain [5,6]. On the other hand, detrimental stimuli like any chemical, mechanical, or thermal stimuli at sensory endings of tissue result in nociceptive pain. Pain affects millions of people around the world. It may be associated with various diseases like diabetes, heart disease, cancer, stroke, stress, burn, etc., or any external harmful stimulus [7]. Thus, it affects the wellbeing, performance, and socioeconomic status of the sufferer and creates a huge burden on the health system and state economies [8].
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.
Homo Sapiens (“Us”): Strengths and Weaknesses
Published in Michael Hehenberger, Zhi Xia, Our Animal Connection, 2019
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.
Ameliorative effect of vitamin E and selenium against bisphenol A-induced toxicity in spinal cord and submandibular salivary glands of adult male albino rats
Published in International Journal of Environmental Health Research, 2023
Dina W. Bashir, Yasmine H. Ahmed, Mohamed A. El-Sakhawy
It considered an endocrinedisrupting chemical, it is classified as a probable human carcinogen (Besaratinia and Pfeifer 2007). It is considered a xenoestrogen and triggers the estrogenic effect by binding to estrogen receptors (Kim et al. 2014). The effect of BPA has been studied on different organs in both humans and experimental animals (Borrell 2010). Bisphenol A may impair the functioning of internal organs and systems, including the nervous, gastrointestinal, cardiovascular, reproductive, and excretory systems (Wazir and Mokbel 2019). Studies conducted on animals and humans have reported that exposure to BPA during the gestational period affects brain development in the unborn child (Jones and Watson 2012). After BPA exposure, neurological problems, such as attention deficits and hyperactivity disorders may induce (Wolstenholme et al. 2011). Choi et al. (2007) reported that BPA accumulates easily in the brain, being a lipophilic substance. Within the central nervous system (CNS), it has a direct impact on nerve cell function by modifying the cellular pathways involved in pain and nociception.
Workshops of the eighth international brain–computer interface meeting: BCIs: the next frontier
Published in Brain-Computer Interfaces, 2022
Jane E. Huggins, Dean Krusienski, Mariska J. Vansteensel, Davide Valeriani, Antonia Thelen, Sergey Stavisky, James J.S. Norton, Anton Nijholt, Gernot Müller-Putz, Nataliya Kosmyna, Louis Korczowski, Christoph Kapeller, Christian Herff, Sebastian Halder, Christoph Guger, Moritz Grosse-Wentrup, Robert Gaunt, Aliceson Nicole Dusang, Pierre Clisson, Ricardo Chavarriaga, Charles W. Anderson, Brendan Allison, Tetiana Aksenova, Erik Aarnoutse
Pain is a common medical problem but difficult to objectify as a personal experience of a sensation. Using TCREs both to selectively stimulate pain fibers and to record pain-related evoked potentials (PREPs) is one method of objectifying pain sensation [31–37]. Custom-made concentric stimulating electrodes can selectively stimulate pain afferents where conventional electrical stimulation with mono- or bi-polar stimulating electrodes failed. TCREs delivered paired electrical stimulations to the dorsal non-dominant hand. PREPs were recorded at Cz referenced to ear. For control participants, average PREP N1-P2 amplitude was significantly diminished by electroacupuncture. In another experiment control participants showed the expected habituation of PREP N1-P2 amplitude over time, but those with chronic low back pain showed an increase in PREP amplitude, presumably a physiological marker of central sensitization, the increased responsiveness to sensory information such as nociception.
Increasing cannabis use and importance as an environmental contaminant mixture and associated risks to exposed biota: A review
Published in Critical Reviews in Environmental Science and Technology, 2022
Emily K. C. Kennedy, Genevieve A. Perono, Dion B. Nemez, Alison C. Holloway, Philippe J. Thomas, Robert Letcher, Chris Marvin, Jorg Stetefeld, Jake Stout, Oliver Peters, Vince Palace, Gregg Tomy
Cannabinoids can also induce their effects via mechanisms independent of CB1/CB2. The transient receptor potential (TRP) superfamily are nonselective cation channels that modulate cellular passage of calcium and sodium ions (Starkus et al., 2019). Several studies have reported that TRP channels, particularly TRPV1-4, TRPA1, and TRPM8, interact with cannabinoids (Reviewed in: (Pertwee et al., 2010)). TRPV1 is widely expressed in brain and sensory neurons (mainly in dorsal root and trigeminal ganglia) and is co-localized with CB1 receptors (Lowin & Straub, 2015), allowing for concerted modulation of cannabinoid signaling involved pathophysiological conditions such as pain, nociception, epilepsy, thermoregulation and itch (Heblinski et al., 2020; Morales et al., 2017). Phytocannabinoids, including CBD and endocannabinoids such as AEA, are known agonists of TRPV1 (Muller et al., 2018). Activation of TRPV1 permits membrane depolarization (via Na+ influx) in excitable neurons and increases intracellular concentrations of Ca2+ (via rise in influx or release from intracellular stores). This effect can facilitate pain reduction, modulating neurotransmitter release and desensitization of TRPV1 channels (Pertwee et al., 2010; Starkus et al., 2019).