Here's an excellent article about pain. I may end up quoting it all! Seriously. Read it!! http://www.medscape.org/viewarticle/481798
They wind it up by saying "Why does local injury resulting from trauma lead to chronic, intractable pain in some patients? Tissue injury leads to a constellation of changes in spinal excitability, which includes elevated spontaneous firing, increased response amplitude and duration, decreased threshold, enhanced discharge to repeated stimuli, and expanded receptive fields. The persistence of these changes, which are collectively termed central sensitization, appears to be fundamental to the prolonged enhancement of pain sensitivity that defines chronic pain. Various medications and local anesthetic neural blockade may limit the magnitude of this CNS windup..."
I'll try to spell it out a little further but keep it concise- I will be using their quotes frequently below:
Severe trauma, including surgical trauma, sets off a downhill spiral of events. "Severe trauma" involves an inflammatory response (lots of inflammation involved with endo)- "cytokines and chemokines, substances that are meant to mediate the process of healing and tissue regeneration. However, these agents are also irritants and change the properties of the primary sensory neurons surrounding the area of trauma.Thus, the major features triggering inflammatory pain include damage to the high-threshold nociceptors (peripheral sensitization), modifications and modulation of the neurons in the nervous system, and amplification of the excitability of neurons within the CNS."
With that inflammation you get the COX-2 enzymes involved and they increase prostaglandins which increases, you guessed it, sensitivity (aka pain!). So you've got neurotransmitters that either create excitement or calm it down. "The process of peripheral and central sensitization is maintained, at least theoretically and experimentally, through the excitatory neurotransmitter, glutamate, which is believed to be released when the N-methyl-D-aspartate (NMDA) receptor is activated." So your nerves get all excited and they are jacked up like a 2 year old on red bulls and sugar at Christmas. Recurrent pain keeps the nerves excited and they just can't calm down. Nerves not calming down. Now we're getting into central sensitization.
"Central sensitization describes changes that occur in the brain in response to repeated nerve stimulation. Following repeated stimulation, levels of neurotransmitters and brain electrical signals change as neurons develop a 'memory' for responding to those signals. Frequent stimulation results in a stronger brain memory, so that the brain will respond more rapidly and effectively when experiencing the same stimulation in the future.... the enhanced reflex excitability after peripheral tissue damage does not depend on continuing peripheral input; rather, hours after a peripheral injury, spinal dorsal horn neuron receptive fields continued to expand." Just like repeating something over and over again helps you to recall it quicker, your nerves can travel that path of pain quicker. Or like with exercise, they say you get 'muscle memory.' You get 'nerve memory.' Even without the original stimulus (the original thing that caused the nerves to fire off "pain!" in the first place). (Again the quotes are from http://www.medscape.org/viewarticle/481798)
"It has previously been reported in the literature that women with endometriosis frequently experience more comorbid conditions than the general population including interstitial cystitis, migraines, fibromyalgia, and chronic fatigue syndrome [1,2,3]. These overlapping pain syndromes and endometriosis share similar clinical presentations, which include multifocal pain coupled with somatic symptoms like:
- cognitive/memory problems
- psychological distress
"The aim of this study was to test the hypothesis that persistent nociceptive input from endometriotic tissues leads to central sensitization manifested by somatic hyperalgesia and increased referred pain areas to experimental saline-induced muscle pain in patients with endometriosis, compared to healthy control subjects....Manifestation of central sensitization in women with endometriosis is demonstrated by increased muscle nociceptor input in the form of increased post-saline pain intensity, pain areas at the FDI, and hypersensitivity to pressure stimulation. These findings provide new insights into the complex pain mechanisms associated with endometriosis." http://www.ncbi.nlm.nih.gov/pubmed/14622679
What the heck can I do about it?!?
If only I knew... There's not really a lot about it out there that I have found so far. There's some anecdotal but not that many studies I've located.
First thing is to catch it early. An ounce of prevention is worth a pound of cure. The earlier you catch it, hopefully the easier it'll be break those neural pathways. "Once central sensitization is established, larger doses of analgesics are required to suppress it. Preemptive analgesia, or treatment before pain progresses, may reduce the impact of all these stimuli on the CNS. Woolf demonstrated that the morphine dose needed to prevent central hyperexcitability, given before brief noxious electrical stimulation in rats, was one tenth the dose required to abolish activity after it had developed. This translates to clinical practice. In a clinical trial of 60 patients undergoing abdominal hysterectomy, those who received 10 mg of morphine intravenously at the time of induction of anesthesia required significantly less morphine for postoperative pain control. Furthermore, pain sensitivity around the wound (secondary hyperalgesia) was also reduced in the morphine pretreated group." http://www.medscape.org/viewarticle/481798
So if you're looking at this, chances are it's gone beyond "early." What else is available?
"Interest has been growing in the immune pathways involved in pain. At the heart of the research are the body's glial cells -- including microglia and astrocytes -- which disperse inflammatory cytokines when activated by certain biological triggers, such as opioids. These cytokines can send messages to neurons that counter analgesia...To hamper that inflammatory response, researchers have been targeting the toll-like-receptor-4 (TLR-4) on glial cells. Indeed, Younger said naltrexone can stifle the immune response and, ultimately, symptoms of fibromyalgia by blocking TLR-4 on microglia....
"Younger and colleagues found that patients reported an overall greater reduction in pain when they were on low-dose naltrexone than when they took placebo (48.5% versus 27.4%, P=0.006). In addition to the half of patients who reported feeling very much or much improved when on low-dose naltrexone, an additional quarter felt minimally improved, Younger said. He added that there was no impact on fatigue or sleep quality, and patients reported low-dose naltrexone to be as tolerable as placebo (89.2% versus 89.4% rated on a 100-point scale). Side effects reported more commonly with low-dose naltrexone were vivid dreams (37% versus 13% on placebo) and headache (16% versus 3%). Other drugs may have also improved pain via the immune pathway, including naloxone, fluorocitrate, minocycline, and dextromethorphan, Younger said. Generic versions of some of these drugs are available, which would make them significantly less expensive, he added." http://www.medpagetoday.com/MeetingCoverage/AAPM/31371
PS Someone had a good question about adhesions. I haven't found a direct link between adhesions and central sensitization, but I did find an article about nerve involvement in adhesions.
"Nerve fibers, identified histologically, ultrastructurally, and immunohistochemically, were present in all the peritoneal adhesions examined. The location of the adhesion, its size, and its estimated age did not influence the type of nerve fibers found. Further, fibers expressing the sensory neuronal markers calcitonin gene-related protein and substance P were present in all adhesions irrespective of reports of chronic abdominopelvic pain. The nerves comprised both myelinated and nonmyelinated axons and were often, but not invariably, associated with blood vessels." http://www.ncbi.nlm.nih.gov/pmc/articles/PMC1422013/