jetjock1 -
I've had a modified form it off and on the same spot since shortly after I was diagnosed with a positive response to a LSB. On the inside of my left ankle. Which is of note only because while I suffered a bilateral injury to my tendons and have RSD in both feet, there is no corresponding bruising on my right foot. Also the first time I showed it to a "pain specialist" he had no idea what to make of it!
That said, mine don't bleed through, all I have is the apparent "bruise." My understanding of the process may be a little different than yours, however. Based on what I have read, the walls of all blood vessels other than capillaries are filled with nerves (they are said to be "innervated") that are in general controlled by the sympathetic nervous system. In CRPS/RSD there are two principal dysfunctions of the vascular system, and while in theory they happen sequentially, I've got them at the same time in different parts of my body: neurogenic vasodilatation and neurogenic constriction. In the former, vascular tone is lost, initially resulting in the loss of mater from the vessel through "extravasation" (essentially, osmosis) - which is called edema - and then finally, as the wall of the vessel loses all tone, spaces appear that are large enough for the hemoglobin to escape, and we have a bruise or an outright hematidrosis if it makes it's way through the skin.
On the other hand, with neurogenic vasoconstriction, the flood flow is reduced or lost altogether. In my case that's most obviously manifest by my inability to be fitting with any iv larger than a 22 gauge: this is something that was first picked up in me about 20 months into the RSD, whereas while I also had the bruising from close to the start, it wasn't accompanied with dramatic edema for another six years. (Another example of no two cases of RSD being the same.)
Where the theories get tricky is in explaining the signaling mechanisms to the nerves. And for that I can only lay out what I understand to be the two leading contemporary schools of thought.
Anne Louis Oaklander, MD, PhD, sees this, and virtually every other aspect of CRPS as part and parcel of small-fiber neuropathy, which is doubtless going on, but there is some question as to whether the two are casually related or simply act as co-variants of a common underlying cause. See, e.g., Oaklander AL, Fields HL, Is reflex sympathetic dystrophy/complex regional pain syndrome type I a small-fiber neuropathy? Ann Neurol. 2009 Jun;65(6):629-38:
Department of Neurology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA. aoaklander@partners.org
Abstract
Neurologist S. Weir Mitchell first described "causalgia" following wartime nerve injury, with its persistent distal limb burning pain, swelling, and abnormal skin color, temperature, and sweating. Similar post-traumatic symptoms were later identified in patients without overt nerve injuries after trauma. This was labeled reflex sympathetic dystrophy (RSD; now complex regional pain syndrome type I [CRPS-I]). The pathophysiology of symptoms is unknown and treatment options are limited. We propose that persistent RSD/CRPS-I is a post-traumatic neuralgia associated with distal degeneration of small-diameter peripheral axons. Small-fiber lesions are easily missed on examination and are undetected by standard electrophysiological testing. Most CRPS features-spreading pain and skin hypersensitivity, vasomotor instability, osteopenia, edema, and abnormal sweating-are explicable by small-fiber dysfunction. Small fibers sense pain and temperature but also regulate tissue function through neuroeffector actions. Indeed, small-fiber-predominant polyneuropathies cause CRPS-like abnormalities, and pathological studies of nerves from chronic CRPS-I patients confirm small-fiber-predominant pathology. Small distal nerve injuries in rodents reproduce many CRPS features, further supporting this hypothesis. CRPS symptoms likely reflect combined effects of axonal degeneration and plasticity, inappropriate firing and neurosecretion by residual axons, and denervation supersensitivity. The resulting tissue edema, hypoxia, and secondary central nervous system changes can exacerbate symptoms and perpetuate pathology. Restoring the interest of neurologists in RSD/CRPS should improve patient care and broaden our knowledge of small-fiber functions. [Emphasis added.]
PMID: 19557864 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/19557864
In principle contrast is the inflammation theme expounded upon by, among others, Frank Birklein and Martin Schmelz in Neuropeptides, Neurogenic Inflammation and Complex Regional Pain Syndrome (CRPS), Neurosci Letters. 2008; 437:199-202, FREE FULL TEXT at
http://www.rsds.org/2/library/articl...in_Schmelz.pdf
Abstract
This review explains symptoms and nature of neuropeptide signaling and its importance for clinical symptoms of CRPS. Neurogenic inflammation regularly accompanies excitation of primary afferent nociceptors. It has two major components-plasma extravasation and vasodilatation.The most important mediators are the calcitonin gene-related peptide (CGRP) and substance P(SP). After peripheral trauma immune reaction (e.g. cytokines) and the attempts of the tissue to regenerate (e.g. growth factors) sensitize nociceptors and amplify neurogenic inflammation. This cascade of events has been demonstrated in rat models of CRPS. Clinical findings in these animals strongly resemble clinical findings in CRPS, and can be prevented byanticytokine and anti-neuropeptide treatment. In CRPS patients, there is meanwhile also plenty of evidence that neurogenic inflammation contributes to clinical presentation. Increased cytokine production was demonstrated, as well as facilitated neurogenic inflammation. Very recently even "non-inflammatory" signs of CRPS (hyperhidrosis, cold skin) have been linked to neuropeptide signaling. Surprisingly, there was even moderately increased neurogenic inflammation in unaffected body regions. This favors the possibilitythat CRPS patients share genetic similarities. The future search for genetic commonalities will help us to further unravel the "mystery" CRPS.
PMID: 18423863 [PubMed - indexed for MEDLINE]
http://www.ncbi.nlm.nih.gov/pubmed/18423863
And as set forth in the text:
. . . it has become clear that action potentials from activated nociceptors invade end branches of primary afferent neurons by retrograde conduction ("axon reflex") and release neuropeptides from their terminals [62]. The acute effects of primary afferent fiber induced neuropeptide release are vasodilation and protein extravasation, which has been therefore termed "neurogenic inflammation". Pivotal neuropeptides in the induction of neurogenic inflammation are calcitonin gene-related peptide (CGRP) for vasodilation and substance P (SP) for the induction of protein extravasation-at least in rodents [27]. As a result of previous studies, mechano-insensitive, but heat-and chemo-sensitive C-nociceptors have been found to be responsible for the neurogenic vasodilation in pig [38] and human skin [57] . . . . [at 199]
Notes
[27] P. Holzer, Neurogenic vasodilatation and plasma leakage in the skin, Gen. Pharmacal. 30 (1998) 5-11.
[38] B. Lynn, S. Schutterle, EK. Pierau, The vasodilator component of neurogenic inflammation is caused by a special subclass of heat-sensitive nociceptors in the skin of the pig, J. Physiol. (Lond.) 494 (1996) 587-593.
[57] M. Schmelz, K. Michael, e. Weidner, R. Schmidt, H,E, Torebjiirk, H.O. Handwerker, Which nerve fibers mediate the axon reflex flare in human skin? Neuroreport 11 (2000) 645-648.
[62] J. Szolcsanyi, Capsaicin-sensitive sensory nerve terminals with local and systemic efferent functions: facts and scopes of an unorthodox neuroregulatory mechanism, Prog. Brain Res. 113 (1996) 343-359
That said, this may all just be the tip of the iceberg. For a cogent and readable treatment of what appears to cover perhaps 80% of the science today, see, Maihofner C, Seifert F, Markovic K, Complex Regional Pain Syndromes: New Pathophysiological Concepts and Therapies,
Eur J Neurol. E-pub 18 Feb 2010, FREE FULL TEXT at
http://www.rsds.org/2/library/articl...eurol_2010.pdf
I hope this is useful.
Mike