Showing posts with label pain. Show all posts
Showing posts with label pain. Show all posts

Sunday, February 6, 2011

Higher Levels of Pain Intensity in Multiple Chemical Sensitvity -Says Study

"this is the first study to show facilitated pain processing in MCS and EC patients with the most abnormal responses in MCS"
The Clinical journal of pain, Vol. 27, No. 2. (February 2011), pp. 156-162. Key: citeulike:8774097


Read more: CiteULike: Increased capsaicin-induced secondary hyperalgesia in patients with multiple chemical sensitivity.:

Recommended: Chemical Sensitivity: A Guide to Coping With Hypersensitivity Syndrome, Sick Building Syndrome and Other Environmental Illnesses

Wednesday, June 30, 2010

Female Hormones May Contribute to Sexual Dimorphism in TMJ~!

Comment: I suspect this is going to has implications on other pain conditions as well, especially those under the environmental illness umbrella like CFS and fibromyalgia....

"hippocampal TRPV1 can modulate central pain processing and estradiol may contribute to the sexual dimorphism of TMD pain sensitivity through upregulation of TRPV1 expression in the hippocampus"


Link:CiteULike: 17-beta-Estradiol Enhanced Allodynia of Inflammatory Temporomandibular Joint through Upregulation of Hippocampal TRPV1 in Ovariectomized Rats:

Tuesday, May 25, 2010

Astroglial Amino Acid Shuttle Involved in Nociceptive Pain Sensitization!

"This study has demonstrated that the central sensitization induced in functionally identified nociceptive neurons in trigeminal subnucleus caudalis (the medullary dorsal horn) by application of an inflammatory irritant to the rat's tooth pulp can be significantly attenuated by continuous intrathecal superfusion of methionine sulfoximine, an inhibitor of the astroglial enzyme glutamine synthetase that is involved in the glutamate–glutamine shuttle......Further, the lack of any observed significant effects of MSO alone, in contrast to our findings that it significantly attenuates MO-induced central sensitization, suggests that its action on astroglial GS is not evident in basal conditions but is apparent in hyperexcitable states, consistent with findings by ourselves and others that glia may not affect basal nociceptive processing but rather participate in exaggerated pain states. It is also noteworthy that an excess of glutamine in the CNS is involved in ammonia neurotoxicity possibly through its detrimental effects on mitochondrial function."




CiteULike: Astroglial Glutamate Glutamine Shuttle Is Involved in Central Sensitization of Nociceptive Neurons in Rat Medullary Dorsal Horn: "Chiang, C.-Y., Wang, J., Xie, Y.-F., Zhang, S., Hu, J. W., Dostrovsky, J. O., and Sessle, B. J. (2007). Astroglial glutamate glutamine shuttle is involved in central sensitization of nociceptive neurons in rat medullary dorsal horn. J. Neurosci., 27(34):9068-9076."


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Mhalla, A., de Andrade, D. C. C., Baudic, S., Perrot, S., and Bouhassira, D. (2010). Alteration of cortical excitability in patients with fibromyalgia. Pain, 149(3):495-500.
http://www.citeulike.org/user/HEIRS/article/6962057
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Chen, P.-C., Vargas, M. R., Pani, A. K., Smeyne, R. J., Johnson, D. A., Kan, Y. W., and Johnson, J. A. (2009). Nrf2-mediated neuroprotection in the mptp mouse model of parkinson's disease: Critical role for the astrocyte. Proceedings of the National Academy of Sciences, 106(8):2933-2938. http://www.citeulike.org/user/HEIRS/article/6551224?show_msg=already_posted

More Support for Brain Changes in Fibromyalgia, Says Study!

"fibromyalgia is associated with deficits in intracortical modulation involving both GABAergic and glutamatergic mechanisms, possibly related to certain aspects of the pathophysiology of this chronic pain syndrome"

CiteULike: Alteration of cortical excitability in patients with fibromyalgia.:

Sunday, May 23, 2010

Il-6 Modulates CRF in the Hypothalamus in Response to Different Signals.

Module: 5/22/2010

Background: CRF can regulate signaling in response to different odors. In those cases, it can lead to an anxiolytic or elevation and other responses typical of the stress response including pain generation, immune regulation, itch, rash and other changes such as gastric function alterations. Of course, these are symptoms characteristic of chemical sensitivity and also some symptoms characteristic of other environmentally influenced conditions such as CFS and sickness syndrome.

A major regulator of sickness syndrome is Il-6 which can be functionally modulated through Il-10 and ultimately most probably HO-1 which has been shown in other studies to increase during exercise. Interestingly, one can identify similarities in cancer-related fatigue to some chronic symptoms of CFS and sickness syndrome including the exhausting fatigue and cachexia that is exhibited in the latter, in animals and humans. Preliminary studies suggest cytokine Il-6/Il-8 may modulate the severity of cancer-related fatigue and others show cancer-related fatigue is common with serotonin dysregulation. Coincidentally, in the trout corticotrophin activation by ammonia is associated with alterations in neurotransmitter levels including dopamine and serotonin. So here again, we see potential especially with periods of aberrant corticotrophin signalling, where symptoms of environmental illness such as anxiety, depression, weakeness and fatigue may present itself. These findings supports past studies that suggest that fatigue in CFS may be in part due to serotonin dysregulation and elevations in Il-6.(Ryan)

CiteULike: Transcriptional regulation of hypothalamic corticotropin-releasing factor gene.: "Glucocorticoid-dependent repression of cAMP-stimulated CRF promoter activity is mediated by both nGRE and SRE in hypothalamic cells. Interleukin (IL)-6 produced in the hypothalamus stimulates the CRF gene. Suppressor of cytokine signaling-3, which is induced by a cAMP stimulant and IL-6, is involved in the negative regulation of CRF gene expression in hypothalamic cells. Such complex mechanisms would contribute to stress responses and homeostasis in the hypothalamus."

Related: Hummel, M., Cummons, T., Lu, P., Mark, L., Harrison, J. E., Kennedy, J. D., and Whiteside, G. T. (2010). Pain is a salient ßtressor" that is mediated by corticotropin- releasing factor-1 receptors. Neuropharmacology.
http://www.citeulike.org/user/HEIRS/article/7177466
Coric, V., Feldman, H. H., Oren, D. A., Shekhar, A., Pultz, J., Dockens, R. C., Wu, X., Gentile, K. A., Huang, S.-P. P., Emison, E., Delmonte, T., D'Souza, B. B., Zimbroff, D. L., Grebb, J. A., Goddard, A. W., and Stock, E. G. (2010). Multicenter, randomized, double-blind, active comparator and placebo-controlled trial of a corticotropin-releasing factor receptor-1 antagonist in generalized anxiety disorder. Depression and anxiety, 27(5):417-425.
http://www.citeulike.org/user/HEIRS/article/7193107
Theoharides, T. C., Singh, Boucher, W., Pang, X., Letourneau, R., Webster, E., and Chrousos, G. (1998). Corticotropin-releasing hormone induces skin mast cell degranulation and increased vascular permeability, a possible explanation for its proinflammatory effects. Endocrinology, 139(1):403-413.
http://www.citeulike.org/user/HEIRS/article/7207688
Mustian, K. M., Fisher, S., Adams, J., Janelsins, M., Palesh, O., Darling, T., Peppone, L., Heckler, C., Williams, J., and Morrow, G. (2009). Cytokine-mediated changes associated with improvements in cancer-related fatigue induced by exercise: Results from a randomized pilot study of cancer patients receiving radiotherapy. Journal of Clinical Oncology, 27(15s).
http://www.citeulike.org/user/HEIRS/article/7207720
Ryan, J. L., Carroll, J. K., Ryan, E. P., Mustian, K. M., Fiscell, K., and Morrow, G. R. (2007). Mechanisms of cancer-related fatigue. The Oncologist, 12(1 supp):22-34.
http://www.citeulike.org/user/HEIRS/article/7207823

Wednesday, December 9, 2009

Associations between polymorphisms in dopamine neurotransmitter pathway genes and pain response in healthy humans

Summary: "The results of this study together with the known function of the investigated candidate gene polymorphisms, suggest that low dopaminergic activity can be associated with high pain sensitivity and vice versa."


Treister, R., Pud, D., Ebstein, R. P., Laiba, E., Gershon, E., Haddad, M., and Eisenberg, E. (2009). Associations between polymorphisms in dopamine neurotransmitter pathway genes and pain response in healthy humans. Pain, 147(1-3):187-193. http://www.citeulike.org/group/6034/article/5884847

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Friday, October 23, 2009

Fibromyalgia pain severity not linked to psychological symptoms

"A new study finds that the pain of fibromyalgia is linked to reduced activity in the areas of the brain that inhibit sensation and dispells the myth that the illness and severity of pain reported is linked to psychological causes." According to researcher, "we've made careful measurements and have found no correlation at all between pain sensitivity in fibromyalgia patients and the degree of anxiety or depression they show." Click here to read more.

Friday, October 16, 2009

Study: What Makes Patients With Fibromyalgia Feel Better?

Title: What makes patients with fibromyalgia feel better? correlations between patient global impression of improvement and changes in clinical symptoms and function: A pooled analysis of 4 randomized placebo-controlled trials of duloxetine.

Summary: Factors that may make a patient with fibromyalgia feel better determined by the results of this study include reductions in pain, reduced fatigue, physical functioning, better mood and improved quality of life.


Citation: Hudson, J. I., Arnold, L. M., Bradley, L. A., Choy, E. H. S., Mease, P. J., Wang, F., Ahl, J., and Wohlreich, M. M. (2009). What makes patients with fibromyalgia feel better? correlations between patient global impression of improvement and changes in clinical symptoms and function: A pooled analysis of 4 randomized placebo-controlled trials of duloxetine. The Journal of Rheumatology, 36(10). http://www.citeulike.org/user/HEIRS/article/5952226

Thursday, October 1, 2009

Elevated insular glutamate in fibromyalgia is associated with experimental pain.

Title: Elevated insular glutamate in fibromyalgia is associated with experimental pain.

Summary: The author concluded "enhanced glutamatergic neurotransmission resulting from higher concentrations of Glu within the posterior insula may play a role in the pathophysiology of FM and other central pain augmentation syndromes."



Harris, R. E., Sundgren, P. C., Craig, A. D., Kirshenbaum, E., Sen, A., Napadow, V., and Clauw, D. J. (2009). Elevated insular glutamate in fibromyalgia is associated with experimental pain. Arthritis & Rheumatism, 60(10):3146-3152.