scholarly journals Headache of Analgesic Abuse as a Cause of New Pain Pathways Development

Author(s):  
Silvia Ussai ◽  
Alessandro Rizzardo
Keyword(s):  
2010 ◽  
Vol 6 (3) ◽  
pp. 208-215
Author(s):  
Nidhi Sofat ◽  
Philip Hamann ◽  
Thomas R. Barrick ◽  
Franklyn A. Howe

Author(s):  
Sascha R. A. Alles ◽  
Anne-Marie Malfait ◽  
Richard J. Miller

Pain is not a simple phenomenon and, beyond its conscious perception, involves circuitry that allows the brain to provide an affective context for nociception, which can influence mood and memory. In the past decade, neurobiological techniques have been developed that allow investigators to elucidate the importance of particular groups of neurons in different aspects of the pain response, something that may have important translational implications for the development of novel therapies. Chemo- and optogenetics represent two of the most important technical advances of recent times for gaining understanding of physiological circuitry underlying complex behaviors. The use of these techniques for teasing out the role of neurons and glia in nociceptive pathways is a rapidly growing area of research. The major findings of studies focused on understanding circuitry involved in different aspects of nociception and pain are highlighted in this article. In addition, attention is drawn to the possibility of modification of chemo- and optogenetic techniques for use as potential therapies for treatment of chronic pain disorders in human patients.


Author(s):  
Maria Fitzgerald ◽  
Michael W. Salter

The influence of development and sex on pain perception has long been recognized but only recently has it become clear that this is due to specific differences in underlying pain neurobiology. This chapter summarizes the evidence for mechanistic differences in male and female pain biology and for functional changes in pain pathways through infancy, adolescence, and adulthood. It describes how both developmental age and sex determine peripheral nociception, spinal and brainstem processing, brain networks, and neuroimmune pathways in pain. Finally, the chapter discusses emerging evidence for interactions between sex and development and the importance of sex in the short- and long-term effects of early life pain.


2017 ◽  
Author(s):  
Lucia Daiana Voiculescu

Antiepileptics and antidepressants are two categories of drugs frequently used as adjuvant analgesics. They interfere with the pain pathways at different levels through complex and not always well-defined molecular mechanisms. Although only a few have been licensed for use in the treatment of certain types of pain, anticonvulsants and antidepressants are widely prescribed off-label for pain associated with a variety of conditions. Most solid data come from experience with their use for postherpetic neuralgia, pain associated with diabetic neuropathy, and fibromyalgia. Anticonvulsants and antidepressant drugs are frequently used as first-line therapy in the treatment of pain, especially neuropathic type. Key words: antidepressant drugs, antiepileptic drugs, carbamazepine, gabapentinoids, neuropathic pain, off-label use, serotonin-norepinephrine reuptake inhibitors, serotonin syndrome, tricyclic antidepressants, use in specific populations


Author(s):  
Edgar T. Walters

Chronic pain lasting months or longer is very common, poorly treated, and sometimes devastating. Nociceptors are sensory neurons that usually are silent unless activated by tissue damage or inflammation. In humans their peripheral activation evokes conscious pain, and their spontaneous activity is highly correlated with spontaneous pain. Persistently hyperactive nociceptors mediate increased responses to normally painful stimuli (hyperalgesia) in chronic conditions and promote the sensitization of central pain pathways that allows low-threshold mechanoreceptors to elicit painful responses to innocuous stimuli (allodynia). Investigations of rodent models of neuropathic pain and hyperalgesic priming have revealed many alterations in nociceptors and associated cells that are implicated in the development and maintenance of chronic pain. These include chronic nociceptor hyperexcitability and spontaneous activity, sprouting, synaptic plasticity, changes in intracellular signaling, and modified responses to opioids, along with alterations in the expression and translation of thousands of genes in nociceptors and closely linked cells.


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