ROS: Mitochondrial Dysfunction in CRPS

Here's a clue as to how scientistic I am, versus, say, those gifted and serious scientific types whose research into the mysteries of CRPS I am always appropriating for this blog:

Every time I encounter work that stems from findings based on the goopy gleanings from amputated limbs... I spend a good hour freaking out. 

The Amputated-CRPS-Limb One-Hour Freak Out has three stages:

1.  Maintaining steady pressure on the joystick such that my wheelchair goes round and round and round.  Duration is dependent on degree of battery charge.

2.  Going from one navigable end of Marlinspike Hall to another at my top speed of 4.25 mph, leaving an audible bloody trail of alphabet and punctuation marks in bolded cursive typeface, often in the form of "Ewwwww!!!!" -- although "Bleckkkkk!!!!" is also common.

3.  Nearly silent weeping, face buried in Aunt Jewel's beautiful Plauen lace wedding hankie.

If the reference to amputation occurs in the course of a doctor's visit and references my own limbs, I don't have the luxury of The Manor's airy venues, of course, so I go shopping -- for heat, for hot things, for unnaturally red Serranos.

This time, we are considering separated limbs in order to assess mitochondrial dysfunction in skeletal muscle tissue, something that apparently cannot be done from ordinary surgical detritus or using biopsies from living, oxygenated flesh. 

Ewwwww!!!! Bleckkkkk!!!!

Skeletal muscle stained for both cytochrome oxidase (COX) and succinic dehydrogenase (SDH), two mitochondrial respiratory

chain enzymes. Fibers that stain only for SDH and are COX-negative appear blue. Original magnification X 50.

European Journal of Pain

Volume 15, Issue 7

Pages 708-715, August 2011.

Mitochondrial dysfunction in muscle tissue of complex regional pain syndrome type I patients

Edward C.T. Tan, Antoon J.M. Janssen, Peggy Roestenberg, Lambert P. van den Heuvel, R. Jan A. Goris, Richard J.T. Rodenburg

ABSTRACT:  Reactive oxygen species (ROS) * are known to be involved in the pathophysiology of complex regional pain syndrome type I (CRPS I). Since the mitochondrial respiratory chain is a major source of ROS, we hypothesized that mitochondria play a role in the pathophysiology of CRPS I. The hypothesis was tested by studying mitochondrial energy metabolism in muscle tissue from amputated limbs of CRPS I patients. We observed that mitochondria obtained from CRPS I muscle tissue displayed reduced mitochondrial ATP production and substrate oxidation rates in comparison to control muscle tissue. Moreover, we observed reactive oxygen species evoked damage to mitochondrial proteins and reduced MnSOD levels. It remains to be established if the mitochondrial dysfunction that is apparent at the end-stage of CRPS I is also present in earlier stages of the disease, or are secondary to CRPS I. The observation of a reduced mitochondrial energy production combined with reactive oxygen species induced damage in muscle tissue from CRPS I patients warrants further studies into the involvement of mitochondrial dysfunctioning in the pathophysiology of CRPS.

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WARNING:  As I was trying to read about some of the terms and concepts involved in discussions of ROS, ischemia, and the role of impaired oxygenation in the CRPS disease process, I encountered some strange, highly-glossed "articles" on several "pain clinic" sites, apparently part of the bait to reel in patients for treatments using Direct Intravenous Ozone Therapy (DIV).  Please be careful and exercise good judgment!  Think "embolism," for example...