This application is a continuation-in-part of U.S. patent application Ser. No. 13/211,101 filed Aug. 16, 2011 and also claims the benefit of priority to U.S. Provisional Application No. 61/475,908, filed Apr. 15, 2011, each of which is incorporated herein by reference in its entirety.
FIELD OF THE INVENTION
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The field of the invention is chronic pain management, and more specifically to administration of specific low doses of human chorionic gonadotropin (HCG).
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An ongoing and pervasive problem in the medical community is treating patients with chronic pain syndromes. It is well recognized today that chronic pain is fundamentally different from acute pain, also referred to as nociceptive pain, which pain results from a mechanical, chemical, metabolic or inflammatory insult.
It has been recognized by some that since the mechanisms and pathways for chronic and acute pain are physiologically different, they require different approaches for treatment. Unfortunately, many in the medical community continue to treat patients suffering from chronic pain syndromes with agents designed to address acute nociceptive pain pathways. Such methods are often fraught with toxicity and dependence issues, and in the end are generally unsatisfactory in ending pain and/or improving quality of life. A new diagnostic paradigm and treatment protocol is therefore needed to address chronic pain.
Central sensitization is a newly recognized diagnostic entity that underlies a broad range of phenotypic syndromes, including various chronic pain and mood disorders. As used herein, central sensitization means an abnormal state of functioning of the neurons and circuitry of the central pain intensity, perception and modulation systems; due to synaptic, chemical, functional and/or structural changes, in which pain is no longer coupled, as acute nociceptive pain is, to particular peripheral stimuli. Instead, the central nervous system (CNS) initiates, maintains and contributes to the generation of pain hypersesensitivity and perception, absent a peripheral stimulus. As used herein, therefore chronic pain and central sensitization represent an overlapping constellation of diagnostic conditions and syndromes.
The present inventors consider the following to be a non-exhaustive listing of conditions associated with (causative or resulting from) central sensitization, each of which is thought to be applicable to humans or other vertebrates.
1. Autonomic neuropathies
2. Chronic back pain
3. Chronic joint pain associated metabolic neuropathy
4. Chronic joint pain associated with inflammation
6. Irritable bowel syndrome
8. Neuropathic pain
10. Post Herpetic neuralgia
11. Post surgical pain syndromes
12. Post Traumatic Stress Disorder Pain Syndrome
13. Rheumatoid, arthritic, psoriatic and other chronic arthropathies
14. Spinal nerve compression syndromes associated with neoplasia and/or disc herniation
15. Trigeminal neuralgia
16. Vulvodynia syndrome
Central sensitization is currently thought to be established via a well characterized constellation of cellular changes termed, neuroplasticity. Neuroplasticity consists of the physical remodeling of neuronal and microglial cytoarchitecture; such as changes in synaptic gap junctions, membrane excitability shifts due to ion channel modulation, and gene transcription. Neuroplasticity changes can be bi-directional. In other words, appropriately functioning cells can undergo remodeling that results in a dysfunctional operating state creating the ‘disease states’ of chronic pain and mood disorders. Conversely, these neuroplasticity mediated dysfunctional changes can be reversed with a return to ‘normal’ functioning, which can correspond clinically to a resolution of a ‘disease’ state.
Central sensitization involves, in part, shifts in gene transcription involved in nociception and pain modulation. Huber, et al has clearly shown this phenomenon occurring at specific HCG concentration levels in endometriotic tissue (1). Some of the specific genes identified in this study were genes encoding for G-protein coupled receptor (GPCR) function (2). See: