High-Frequency Spinal Cord Stimulation at 10 kHz for the Treatment of Complex Regional Pain Syndrome: A Case Series of Patients With or Without Previous Spinal Cord Stimulator Implantation.

BACKGROUND: High-frequency spinal cord stimulation at 10 kHz (HF10-SCS) has been demonstrated to provide enhanced and durable pain relief in patients with chronic back and radiating leg pain. Patients with pain related to complex regional pain syndrome (CRPS) in the chronic stages are commonly challenging to treat and often receive traditional spinal cord stimulation (SCS). Very little information is currently available about the therapeutic outcomes following application of high-frequency stimulation in this cohort of patients. METHODS: The purpose of the retrospective case series was to report on the initial experience of HF10-SCS in 13 patients with CRPS, some of whom had been exposed to low-frequency SCS. A temporary trial of HF10-SCS was carried out for 1 week, and those achieving a minimum of 50% pain intensity reduction underwent implantation. Successful responders were those who achieved a 50% decrease in pain intensity on subsequent follow-up. RESULTS: Thirteen patients were trialed, 12 of whom went on to receive a permanent implant. Of the patients receiving permanent implants, the responder rate (50% pain relief) was 67% (95% confidence interval [CI] 0.34 to 0.90), with an average follow-up period of 12.1 ± 4.6 months. Of the 5 patients who had sympathetically independent pain, 3 were responders, and of the 7 patients who had sympathetically mediated pain, 5 were responders. There were no adverse events. CONCLUSION: This small case series suggests that HF10-SCS may be a viable option for patients with CRPS who have chronic intractable pain, including those who had suboptimal results from traditional SCS.

Role of Alternative Therapies for Chronic Pain Syndromes.

There is increasing interest in the use of complimentary and alternative medicine (CAM) for the treatment of chronic pain. This review examines alternative and complimentary therapies, which can be incorporated as part of a biopsychosocial approach in the treatment of chronic pain syndromes. In the present investigation, literature from articles indexed on PubMed was evaluated including topics of alternative therapies, complimentary therapies, pain psychology, biofeedback therapy, physical exercise therapies, acupuncture, natural and herbal supplements, whole-body cryotherapy, and smartphone technologies in the treatment of chronic pain syndromes. This review highlights the key role of psychology in the treatment of chronic pain. Cognitive behavior therapy appears to be the most impactful while biofeedback therapy has also been shown to be effective for chronic pain. Exercise therapy has been shown to be effective in short-, intermediate-, and long-term pain states. When compared to that in sham controls, acupuncture has shown some benefit for neck pain immediately after the procedure and in the short term and improvement has also been demonstrated in the treatment of headaches. The role of smartphones and whole-body cryotherapy are new modalities and further studies are needed. Recent literature suggests that several alternate therapies could play a role in the treatment of chronic pain, supporting the biopsychosocial model in the treatment of pain states.

Dietary fructose inhibits intestinal calcium absorption and induces vitamin D insufficiency in CKD.

Renal disease leads to perturbations in calcium and phosphate homeostasis and vitamin D metabolism. Dietary fructose aggravates chronic kidney disease (CKD), but whether it also worsens CKD-induced derangements in calcium and phosphate homeostasis is unknown. Here, we fed rats diets containing 60% glucose or fructose for 1 mo beginning 6 wk after 5/6 nephrectomy or sham operation. Nephrectomized rats had markedly greater kidney weight, blood urea nitrogen, and serum levels of creatinine, phosphate, and calcium-phosphate product; dietary fructose significantly exacerbated all of these outcomes. Expression and activity of intestinal phosphate transporter, which did not change after nephrectomy or dietary fructose, did not correlate with hyperphosphatemia in 5/6-nephrectomized rats. Intestinal transport of calcium, however, decreased with dietary fructose, probably because of fructose-mediated downregulation of calbindin 9k. Serum calcium levels, however, were unaffected by nephrectomy and diet. Finally, only 5/6-nephrectomized rats that received dietary fructose demonstrated marked reductions in 25-hydroxyvitamin D(3) and 1,25-dihydroxyvitamin D(3) levels, despite upregulation of 1alpha-hydroxylase. In summary, excess dietary fructose inhibits intestinal calcium absorption, induces marked vitamin D insufficiency in CKD, and exacerbates other classical symptoms of the disease. Future studies should evaluate the relevance of monitoring fructose consumption in patients with CKD.