Pathophysiology of pain

The sodium-channel inhibitor Amiloride is used for the treatment of chronic bronchitis, and the most frequently used anesthetic drug, lidocain, inhibits voltagegated sodium-channel a subunits, which mediate the pathophysiology of pain. 

R. Gorlin, "Pathophysiology of Pain" in "Cardiovascular Drug Therapy, The Eleventh Hahnemman Symposium, A. N. Brest, J. H. Moyer (Ed), New York, Grune and Stratton, 1965, P. 266. 

The pathophysiology of pain involves a complex array of neural networks in the brain that are acted on by afferent stimuli to produce... 

Modified from Ghori M, Sinatra RS.Tbe pathophysiology of pain, in Sinatra RS, Viscusi G, de Leon-Casasda O, Ginsberg B., eds., Acute Pain Management. Cambridge University Press, 2008. 

Jensen T. Pathophysiology of pain from theory to clinical evidence. Eur J Pain Supp 2008 2 13-17. 

Schaible H. Pathophysiology of Pain. Heidelberg Langenbecks Archives of Surgery, 2004, pp. 237-243. 

Pain and Nociception. Table 1 Physiology and pathophysiology of the nociceptive system... 

White FA, Jung H et al (2007) Chemokines and the pathophysiology of neuropathic pain. Proc Natl Acad Sci USA 104(51) 20151-20158... 

Westmoreland SV, Rottman JB, Williams KC, Lackner AA, Sasseville VG (1998) Chemokine receptor expression on resident and inflammatory cells in the brain of macaques with simian immunodeficiency virus encephalitis. Am J Pathol 152 659-665 White FA, Jung H, Miller RJ (2007) Chemokines and the pathophysiology of neuropathic pain. Proc Natl Acad Sci U S A 104 20151-20158... 

In broad terms, pain can be divided into two categories, acute and chronic, which differ in their aetiology, mechanisms and pathophysiology. Acute pain and its associated responses are provoked by noxious stimulation and/or disease, or by abnormal function of muscle or viscerae which does not involve actual tissue damage. Although acute pain conditions may last for a length of time if not treated effectively, many cases of acute... 

The pathophysiologic mechanisms of TTH are not clearly understood. The pain is thought to originate in the myofascial tissues of the head, but central brain processing is believed to be an important modulator of pain perception.14... 

All the drugs used for migraine headache are aimed at symptom relief and not against the yet unrecognized cause. Two observations are however most striking first the impact on the concept of pain (for example see analgesics in the chapter on the treatment of pain) and secondly the fact that the pathophysiological principles are poorly defined. 

Heim C, Ehlert U, Rexhausen J, Hanker JP, Hellhammer DH (1998) Abuse-related post-traumatic stress disorder and alterations of the hypothalamic-pituitary-adrenal axis in women with chronic pelvic pain. Psychosom Med 60 309-318 Heim C, Ehlert U, Hellhammer DH (2000) The potential role of hypocortisolism in the pathophysiology of stress-related bodily disorders. Psychoneuroendocrinology 25 1 -35 Heim C, Newport DJ, BonsaU R, MiUer AH, Nemeroff CB (2001) Altered pituitary-adrenal axis responses to provocative challenge tests in adult survivors of childhood abuse. Am J Psychiatry 158 575-581... 

Nearly all cells express kinin receptors that mediate the activities of both bradykinin and kallidin. The activation of these G-protein coupled receptors causes relaxation of venular smooth muscle and hypotension, increased vascular permeability, contraction of smooth muscle of the gut and airway leading to increased airway resistance, stimulation of sensory neurons, alteration of ion secretion of epithelial cells, production of nitric oxide, release of cytokines from leukocytes, and the production of eicosanoids from various cell types [11,12]. Because of this broad spectrum of activity, kinins have been implicated as an important mediator in many pathophysiologies including pain, sepsis, asthma, rheumatoid arthritis, pancreatitis, and a wide variety of other inflammatory diseases. Moreover, a recent report demonstrated that bradykinin B2 receptors on the surface of human fibroblasts were upregulated three-fold beyond normal in patients with Alzheimer s disease, implicating bradykinin as a participant in the peripheral inflammatory processes associated with that disease [13]. 

The trials described so far have commonly shown a lack of usefulness of NKi receptor antagonists in the treatment of pain. But we do not know whether the failure of the selected compounds is a matter of pharmacodynamics (e.g. poor penetration of the blood brain barrier) or a genuine discrepancy between animal and human pain pathophysiology (Urban and Fox, 2000). Hence, animal tests should carefully be chosen whether they are predictive or not, and it would be helpful if a wider range of conditions could be examined (Hill, 2000a). Therefore, new preclinical analysis methods should be developed for a more effective judgement of likely clinical outcomes. 

Woolf, C.J. and Decosterd, I. Implications of recent advances in the understanding of pain pathophysiology for the assessment of pain in patients, Pain Suppl. 1999, 6, S141-S147. 

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