Hi. This topic, sometimes referred to as "brain rot," comes up with some regularity. (So my apologies to those who've heard some of this before.) And we've all been told by our doctors that it's all the meds we're on, as though going to cognative-behavioral boot camp is going to make this all better. But the comments of KS would appear to put that to the lie, as does the stufy from the "Pain and Pleasure Labratory" of A. Vania Apkarian, Ph.D. at Northwestern - perhaps the leading academic lab for the study of the neuroscience of pain in the United States - which is at the end of the post.
But to begin with the meds, Baclofen for one can be hard on short term memory. I knew that from prior experience while I was still trying to practive law and have it up after a day and a half. Over the last few years, I've been back in it, having blown through Zanaflex and been advised that it's the most effective drug out their for CNS induced spasms, in constrast to - say - Flexeril, which is designed for cramping secondary to local muscle tears and the like. Opioids can, of course, have their effects as well.
I'm on a lot of meds though, and niether Zanaflex nor Oxycontin
should be contributing to the profound loss of organization ("executory function") I've experienced over the last year: where my consumption of meds has been stabile for years: but I'm told that "rare reactions" are possible. And while I got an overblown diagnosis of small vessel brain ischemia from a radiologist in August, and had an apparent TIA in September, a complete neurovascular workup at UCLA by a stroke specialist just came back clean, including any constriction of the arterioles, the small diameter blood vessels in microcirculation that extend and branch out from arteries and lead to capillaries:
Arterioles have thin muscular walls (usually only one to two layers of smooth muscle) and are the primary site of vascular resistance. Arterioles receive autonomic nervous system innervation and respond to various circulating hormones in order to regulate their diameter.
http://en.wikipedia.org/wiki/Arteriole
Schwartzman et al found that in a study of 656 patients had CRPS duration of greater than 1 year, found, among other things that:
More than half of the patients in this study reported cognitive and memory difficulties. Deficits in information processing48 and short-term memory49 have been reported in patients afflicted with chronic pain. Chronic pain has also been shown to impair working memory50 and decision-making.51 The disruption of cognitive performance in chronic pain patients could result from a number of factors such as pain medications,50 stress,52 the engagement of the prefrontal cortex by chronic pain,51 and the fact that pain may act as a distractor resulting in impairedworking memory.50
Notes
48. Grigsby J, Rosenberg NL, Busenbark D. Chronic pain is associated with deficits in information processing. Percept Mot Skills. 1995;81:403–410.
49. Ling J, Campbell C, Heffernan TM, et al. Short-term prospective memory deficits in chronic back pain patients. Psychosom Med. 2007;69:144–148.
50. D_i_c_k BD, Rashiq S. Disruption of attention and working memory traces in individuals with chronic pain. Anesth Analg. 2007;104:1223–1229.
51. Apkarian AV, Sosa Y, Krauss BR, et al. Chronic pain patients are impaired on an emotional decision-making task. Pain. 2004;108:129–136.
52. Patil PG, Apfelbaum JL, Zacny JP. Effects of a cold-water stressor on psychomotor and cognitive functioning in humans. Physiol Behav. 1995;58:1281–1286.
Schwartzman RJ, Erwin KL, Alexander GM, The Natural History of Complex Regional Pain Syndrome,
Clin J Pain. 2009;25:273-280, 278, FREE FULL TEXT AT
http://www.rsds.org/2/library/articl...lexanderGM.pdf
My hunch had been that it was a side effect of the sympathetic neurogenicvasoconstriction (and vasodilation in areas of edema, wahere water leeched out of the untoned blood vessels). See, e.g., J. Schattschneider, K. Hartung, M. Stengel, et al, Endothelial dysfunction in cold type complex regional pain syndrome, Neurology 2006;67;673-675, 674-65:
Microcirculation is regulated by neural and endothelial factors. Disturbances in thermoregulatory control of skin blood flow followed by a decrease in skin temperature due to enhanced vasoconstriction have been demonstrated in chronic stages of CRPS.7 It is assumed that in cold type CRPS patients, peripheral vasoconstriction results in tissue hypoxia and tissue acidosis. 2,3 The production of free radicals within the ischemic limb may be responsible for the endothelial dysfunction observed in the present study and the histopathologic changes observed by others.8 This process may induce a vicious cycle of impaired perfusion, hypoxia, and acidosis followed by the production of even more free radicals. [Italics in original.]*
Notes
2. Birklein F, Weber M, Ernst M, Riedl B, Neundorfer B, Handwerker HO.
Experimental tissue acidosis leads to increased pain in complex regional
pain syndrome (CRPS). Pain 2000;87:227–234.
3. Koban M, Leis S, Schultze-Mosgau S, Birklein F. Tissue hypoxia in
complex regional pain syndrome. Pain 2003;104:149–157.
7. Wasner G, Schattschneider J, Heckmann K, Maier C, Baron R. Vascular
abnormalities in reflex sympathetic dystrophy (CRPS I): mechanisms
and diagnostic value. Brain 2001;124:587–599.
8. van der Laan L, ter Laak HJ, Gabreels-Festen A, Gabreels F, Goris RJ.
Complex regional pain syndrome type I (RSD): pathology of skeletal
muscle and peripheral nerve. Neurology 1998;51:20–25.
However, when I was tested at UCLA with transcranial Doppler under a CO2 challenge, my "Pulsiltility Index" was within nomal limits, e.g., there was no evidence that the arterioles in the brain failed to dilate properly when presented with a loss of O2. And while my neuologist has advised me that the transcranial Doppler is not as reliable as the "Gold Standard" test of CT angiogram, I have to discuss the "risk/reward" scenario with my internist, where I've had my share of nuclear medicine studies over the last few years.
Finally, there remains the area of gray matter loss secondary to chronic pain in general, and CRPS in particular. See, e.g., Geha PY, Baliki MN, Harden RN, Bauer WR, Parrish TB, Apkarian AV, The Brain in Chronic CRPS Pain:
Abnormal Gray-White Matter Interactions in Emotional and Autonomic Regions,
Neuron 2008;60:570-581, 577-578, FREE FULL TEXT AT
http://www.rsds.org/2/library/articl...aliki_etal.pdf
Conclusions
We provide several lines of evidence indicating that the patient with CRPS has multiple pathological changes of the brain. We observe global disorganization of the relationship between gray and white matter in these subjects. Regional gray matter atrophy seems limited to brain regions that can be related to these patients’ deficits in emotional decision-making and abnormal sympathetic outflow. Regional white matter anisotropy was observed in a bundle in the hemisphere contralateral to the gray matter atrophy, where long distance connections and branching patterns were reduced. The interrelationship between gray matter atrophy and white matter connectivity provided evidence for both decreased long distance connectivity and regional increases and decreases in connectivity and branching patterns. These results suggest that the abnormal anatomy of the CRPS brain may underlie many of the autonomic, cognitive, and pain abnormalities seen in this pernicious syndrome.
While the article is technical and taxing in spots, most of the terms that are used are dedined in it, and those that aren't can be accessed using the Medline Medical Dictionary at the top of the NT page. If you are not aleady familiar with area of this work, I suggest that you look it over now. It may well be the answer to the question this thread has posed. And as such, it makes potential cures like ketamine (which I can't have due to pre-existing glaucoma) and maybe even RUL ECT (illegal for the treatment of chronic pain in California since a 1976 voter initiative campaign) look a heck of a lot less radical, all things considered.
Mike
* If anyone wants a copy of this one (for personal, non-commercial use) just drop me a PM with your email address.