1. Differential diagnosis of complex regional pain syndrome, Type I (RSD)
Of 38 patients referred to Mensana Clinic with the diagnosis of complex regional pain syndrome, Type I (CRPS Type I, formerly called RSD), 27/38 (71%) of the patients were found not to have clinical and diagnostic studies to support this diagnosis. Before referral to Mensana Clinic, 16/38 patients never received a sympathetic block (42%), which is considered one of the essential diagnostic tests needed to confirm the presence of CRPS I. After diagnostic evaluation at Mensana Clinic, only 1/38 (3%) of the patients actually had CRPS I exclusively, while 10/38 (26%) had a mixture of both CRPS Type I and nerve entrapment syndromes, thoracic outlet syndrome, disrupted disc, and/or radiculopathies. The largest category of missed diagnoses was nerve entrapment syndromes, which were verified at Mensana Clinic in 37/38 (96%) of the patients, followed by thoracic outlet syndrome found in 16/38 (42%). A simple diagnostic framework is reported, to assist in the differential diagnosis of CRPS I and nerve entrapment syndromes.
Hendler N. Differential diagnosis of complex regional pain syndrome, Type I (RSD). Pan Arab Journal Neurosurgery 2002; 6:1-9.
2. Fibromyalgia: An Afferent Processing Disorder Leading to a Complex Pain Generalized Syndrome
Fibromyalgia is a medical condition that appears to involve disordered afferent processing and which might be associated with multiple symptoms, the hallmarks being chronic widespread pain (in any bodily region including visceral organs), fatigue, sleep disturbances, and cognitive alterations. Many individuals also experience psychological distress and impaired function, including sexual dysfunction. This 30-page article with references includes: Fibromyalgia diagnosis and assessment, multi-component treatment, history, evolution, overlapping conditions, epidemiology, impact on quality of life, pathophysiology, and neuroimaging.
Smith HS, Harris R, Clauw D. Fibromyalgia: an afferent processing disorder leading to a complex pain generalized syndrome. Pain Physician 2011;14:217-245
3. Neuroimaging Biomarkers for Pain Sean Mackey, M.D., Ph.D. (pp. 67-84)
Presentation at FDA Chronic Pain Scientific Workshop, May 30, 2012, NIH Campus
...So if we shift gears -- we've talked a little bit about some of the individual differences and how the brain can play a role in that. But what about plasticity? What happens when pain goes bad and it fundamentally alters the central nervous system?
So one of the first studies that was done was by Vania Apkarian out of his group, in which he looked at patients with chronic low back pain. And this is not a brain activity study, but a structural study in which you use a standard T1 MRI to look at the changes in grey matter, comparing a group of patients with chronic low back pain and a group who are healthy controls. And what you find is that, by and large, we're all losing about a half percent of our grey matter per year after about the age of 30. Folks, that's the bad news. I keep trying to tell the people in my lab I'm learning how to use what I have left over more effectively. I don't think they're buying it.
But if you've got chronic low back pain, the numbers are about 5 and a half percent or so of premature grey matter loss, which works out to about a decade of grey matter loss as a consequence of just having chronic pain. And the majority of those losses were found to be in these prefrontal cortical regions, regions of the brain involved with executive functioning, with working memory; it's keeping pieces of information in mind and manipulating it. And so maybe many of the patients that we see with cognitive dysfunction, we always attribute it to a mood disorder or the medications. Maybe it's due to the chronic pain itself.
So we can look at structure as a way of identifying plasticity within the brain, but are there other ways of doing this? And the answer is yes.
4. Special Report: Strategies to Stay Motivated for Exercising in the New Year
...It is probably not a surprise to you that people with chronic pain are significantly less active than healthy peers, even though they probably know the benefits of exercise. The challenge therefore, is how do we motivate ourselves to be physically active when for example, we are afraid that exercise is just going to make our pain worse and/or cause fatigue. (Motivational patient article with guidelines for stretching, exercise log, and exercise behavioral contract)
Jones, JC. Special Report: Strategies to Stay Motivated for Exercising in the New Year. Fibromyalgia and Chronic Pain LIFE 2012; 3:8-13
5. Growth hormone treatment for sustained pan reduction and improvement in quality of life in severe fibromyalgia. Cuatrecasas, G, et al
Through the years, functional defects in growth hormone (GH) secretion and its efficacy as a complementary treatment have been suggested for fibromyalgia by a variety of world renowned fibromyalgia researchers. A recently published study in the July 2012 issue of Pain details a Spanish research group’s investigation of the efficacy and safety of low-dose GH as an add-on therapy in patients with both severe FM and low insulin-like growth factor 1 levels. As part of this study a total of 120 patients were enrolled in a multicenter, placebo-controlled study for 18 months. The participants were randomly assigned to receive either o.oo6mg/kg/day of GH subcutaneously (group A, n=60) or placebo) group B, n=60) for 6 months (blind phase of the study). The placebo arm of the study was switched to GH treatment from month 6 to month 12 (open phase), and a follow-up period after GH discontinuation was preformed until month 18. A standard treatment regimen for fibromyalgia (including selective serotonin re-uptake inhibitors, opioids, and amitriptyline) was maintained throughout the study. Different measurement tools and objective testing methods including: number and intensity of tender points, Fibromyalgia Impact Questionnaire (FIQ) with its subscales and EuroQol 5 dimensions test (EQ5D) with visual analogue scale (VAS ) were assessed at different time points. At the end of the study, 53% of group A patients obtained fewer than 11 positive tender points, vs 33% of group B patients (p<.05). 39.1% vs 22.4% reached more than 50% improvement in VAS (P<.05). Group A patients showed significantly improved FIQ scores (P+01) compared with group B. Although GH discontinuation worsened all scores in both groups during follow-up, impairment in pain perception was less pronounced in the GH-treated group (p-.05). The results of this largest and longest placebo-controlled trial performed in MF (NCT00933686),demonstrated that the addition of GH to the standard treatment for fibromyalgia is effective in reducing pain, showing sustained action over time.
Pain (2012 Jul) 153 (7) :1382-9
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