International Conference on Fibromyalgia and Chronic Pain June 15-16, 2016 Philadelphia, Pennsylvania, USA

Biography:

Dr. Samreen Ahmed has completed her MBBS at the age of 24 years from Dow Medical College, Pakistan, and currently volunteering as a Research Assistant at University of Illinois at chicago. Dr. Ahmed has written 3 case reports as a first author that were published in the IJBCP
 

Abstract:

Fibromyalgia, a condition in which there is stiffness and pain in soft tissues, such as muscles and tendons, has an unknown etiology. However, arterial spasm caused by stress hence hampering the oxygen supply can precipitate the pain. The pain in fibromyalgia is accompanied with fatigue, anxiety, and insomnia. The areas most affected comprises of cervical, and thoracic areas, however any part of the body can be affected.  Females are more commonly affected. Fibromyalgia, often present in depression patients, lack any pathognomonic laboratory findings. The purpose of this review is to elaborate the effects of different interventions for fibromyalgia, particularly with psychiatric symptoms. A literature review of various articles is conducted on MEDLINE, PSYCH Info, and PUBMED to evaluate the role of different treatment options in fibromyalgia patients, accompanying psychiatric symptoms. Literature review revealed aspirin and acetaminophen may be useful in treating pain, whereas, NSAIDS may also give effective response in some cases. Although, first -line of treatment, shown by evidence is cognitive-behavioral therapy, and exercise. However, amitriptyline, is the proven solid pharmacologic intervention, for short durational pain periods. Interestingly, Transcranial Magnetic Stimulation, also has potential in being helpful for chronic neuropathic pain syndromes, based on current data. tDCS, in combination with aerobic exercise is helpful significantly for anxiety, and pain.  In patients suffering from Fibromyalgia with depression, SSRI can be considered for managing depression, however, there is no fair evidence that SSRI are superior to placebo in intervening fibromyalgia’s key symptoms like fatigue, and sleep disturbance. Based on some evidence, amitriptyline should be considered when choosing for the first- line therapy. Different treatment options, such as aspirin and acetaminophen can help with the pain. Although stress reduction techniques, and message can also be helpful.  We suggest accessing patients with fibromyalgia thoroughly to look for psychiatric symptoms so that they could be addressed accordingly. TMS, CBT, and tDCS have potential in treating pain although there is insignificant data, hence we recommend more research in this field. 

Biography:

Jana Sawynok has a PhD in Pharmacology, and has been particularly interested in developing novel analgesics (adenosine-based therapeutics, topical analgesics). Since 2000, she has been interested in Complementary and Alternative Medicine, with applications in chronic pain. She has published 180 papers in reputed journals, including 8 publications on qigong. She currently supervises (in collaboration with Mary Lynch, MD, FRCPC) medical students conducting pragmatic observational trials of qigong in the context of self-care at a tertiary pain care setting

Abstract:

Qigong, which has a long history in China, is currently considered as “meditative movement” or “movement-based embodied contemplative practice” and is being explored for its health benefits in diverse areas (e.g. fibromyalgia, chronic fatigue syndrome). In traditional theory, benefits result from the removal of blockages and promotion of the free flow of qi (vital energy) within the energy system. Contemporary theories involve regulation of central pathways, neuroendocrine modulation, and enhanced sympatho-vagal balance. Fibromyalgia is a chronic pain condition with multiple comorbidities (e.g. sleep and mood disturbances), in which impaired parasympathetic nervous system activity is prominent. The vagus nerve is a major component of the parasympathetic nervous system, and activity contributes to homeostatic cardiovascular regulation; it also can modulate pain, inflammation and immune function. Several observations support the notion that health benefits of qigong in fibromyalgia may be due to improved parasympathetic function. (1) Direct vagal nerve stimulation (using implanted electrodes) has been shown to improve symptoms of fibromyalgia. (2) Qigong practice has been shown to alter heart rate variability parameters in a manner consistent with enhanced parasympathetic function in healthy adults and in the elderly. (3) Other treatments useful for treating fibromyalgia (exercise, Tai Chi, hydrotherapy) have been demonstrated to improve parasympathetic activity. It is hypothesized: (a) that a prominent physiological transducer for the health benefits of qigong involves increased parasympathetic activity, and (b) that targeting a functional system that is perturbed has the potential to produce benefits in multiple health areas. This hypothesis is amenable to direct testing. 

Biography:

Abstract:

Until now, no study has investigated the neuropathic pain component in patients with a rotator cuff tear (RCT). The aim of the study was to identify the neuropathic pain component in patients with RCT and to determine the factors correlated with neuropathic pain in patients with RCT.

Methods: We prospectively studied 134 patients with full-thickness tears requiring arthroscopic rotator cuff repair. We use the Leeds Assessment of Neuropathic Symptoms and Signs pain scale self-report version (LANSS) pain scale and Douleur neuropathique 4 questions (DN4) to assess neuropathic pain. The visual analogue scale (VAS) at admission and a VAS for the most severe pain within 4 weeks before admission and mean pain level during the last 4 weeks were checked. The atrophy grades of the rotator cuff muscle were classified on magnetic resonance images according to the Goutallier classification. The size of the RCT was measured and classified into small (<1 cm), medium (1–3 cm), large (3–5 cm), and massive (>5 cm) during arthroscopic repair for RCT.

Results: The severest VAS pain within the last 4 weeks was 6.35 ± 1.37. Eight (6%) of the 134 patients were diagnosed with likely neuropathic pain by both instruments. A weak correlation was detected between male sex and neuropathic pain (r = 0.284, p = 0.001), between smoking and neuropathic pain (r = 0.513, p < 0.001), and between tear grade and neuropathic pain (r = 0.237, p = 0.006). No correlation was detected between neuropathic pain and age, symptom duration, dominant arm, VAS at admission, severest VAS within the last 4 weeks, mean VAS in the last 4 weeks, or the Goutallier classification.

Conclusion: The prevalence of neuropathic pain in patients with a RCT requiring arthroscopic repair was 6% according to the LANSS pain scale and the DN4. Neuropathic pain in patients with a full-thickness RCT was more relevant in males with large tears and those who smoked. It is important to consider the existence of neuropathic pain when treating a patient with RCT pain. 

 

Biography:

Fukuhara K has completed PhD at Yamaguchi University and is employed at Nipro co. R & D. She is the expert of Neurochemical and protein analysis.
 

Abstract:

Chronic pain is often complicated with pain-emotion that significantly affects the quality of life. Recent studies have revealed that a lack of brain-derived neurotrophic factor (BDNF) in anterior cingulate cortex (ACC) lead to pain-emotion. It is reasonable that BDNF can play an important role in limbic system. In facts, spinally transplanted cells containing BDNF reduced chronic pain. In addition, recent reports revealed that 4-methylcatechol (4-MC), inducer of BDNF, reduced chronic pain with depression. The magnetic stimulation (MS) to skin is used for treatment of neuropathic pain but no reliable mechanisms. Thus, we aimed to characterize the 4-MC on the CREB/ BDNF mRNA comparing with MS.  S-D rats were subjected to chronic constriction injury (CCI). Then rats were received i.c.v. inj 4-MC or MS for 7 days after the CCI. 4-MC reduced decrease in paw withdrawal latency associated with increase of immobility time( forced swim test). These analgesic and anti-depressant effects were reversed by K252a. Both 4-MC and MS reduced decreases in pCREB/BDNF mRNA in ACC, and that was reversed by K252a.  We demonstrated that a lack of BDNF/CREB in ACC mediates pain-emotion. In addition, 4-MC and MS normalize derangements of CREB/BDNF synthesis, suggesting the possible induction of BDNF. These data suggest an important role of BDNF in pain–emotion. 

Biography:

Furuta T has completed MS at Yamaguchi University and is employed at Major Research Institute He is the expert of Neurobehabiour and protein analysis.

Abstract:

Depression-like behavior is often complicated by chronic pain. A lack of 5-HT and/or BDNF can result in pain-depression. In fact, antidepressants imipramine (IMI) increases 5-HT along with BDNF mRNA. Moreover, magnetic stimulation (MS) can evoke 5-HT release of spinal cord. However, the induction of BDNF with MS has not been established. We aimed to investigate depression with chronic pain modulates BDNF synthesis and to evaluate the effect of MS with induction of BDNF comparing from IMI. A chronic constriction injury (CCI) was constructed in S-D rats. MS was consequently exposed to skin located injury site. In other rats, IMI was administered after CCI. Hyperalgesia was assessed by paw withdrawal latency (PWL) using plantar test. The depression was used forced swim test. Anterior cingulate cortex (ACC) and rostal ventromedial medulla (RVM) samples for 5-HT and BDNF (ELISA) contents and also BDNF mRNA expression (RT-PCR) were removed. CCI rats showed a significant reduction in PWL of the injured leg to thermal stimuli with time. Both MS and IMI-treated rats reduced hyperalgesia and an increased immobility time that were reversed by anti-BDNF antibody and 5,7-DHT. Analgesia effects of MS were antagonized by naloxone. MS was also reduced decrease in BDNF mRNA.This study clearly shows that a lack of 5-HT coupled with BDNF in the descending inhibitory system leads pain-emotion. MS ameliorates this symptom by activating 5-HTergic neurons by spinal microdialysis associated with induction of BDNF. Moreover, these effects were similar actions to those of antidepressant, IMI, which suggests that MS activates 5-HTergic neurons concurrent with an interaction of BDNF.

Biography:

Furuta T has completed MS at Yamaguchi University and is employed at Major Research Institute He is the expert of Neurobehabiour and protein analysis.

Abstract:

Depression-like behavior is often complicated by chronic pain. A lack of 5-HT and/or BDNF can result in pain-depression. In fact, antidepressants imipramine (IMI) increases 5-HT along with BDNF mRNA. Moreover, magnetic stimulation (MS) can evoke 5-HT release of spinal cord. However, the induction of BDNF with MS has not been established. We aimed to investigate depression with chronic pain modulates BDNF synthesis and to evaluate the effect of MS with induction of BDNF comparing from IMI. A chronic constriction injury (CCI) was constructed in S-D rats. MS was consequently exposed to skin located injury site. In other rats, IMI was administered after CCI. Hyperalgesia was assessed by paw withdrawal latency (PWL) using plantar test. The depression was used forced swim test. Anterior cingulate cortex (ACC) and rostal ventromedial medulla (RVM) samples for 5-HT and BDNF (ELISA) contents and also BDNF mRNA expression (RT-PCR) were removed. CCI rats showed a significant reduction in PWL of the injured leg to thermal stimuli with time. Both MS and IMI-treated rats reduced hyperalgesia and an increased immobility time that were reversed by anti-BDNF antibody and 5,7-DHT. Analgesia effects of MS were antagonized by naloxone. MS was also reduced decrease in BDNF mRNA.This study clearly shows that a lack of 5-HT coupled with BDNF in the descending inhibitory system leads pain-emotion. MS ameliorates this symptom by activating 5-HTergic neurons by spinal microdialysis associated with induction of BDNF. Moreover, these effects were similar actions to those of antidepressant, IMI, which suggests that MS activates 5-HTergic neurons concurrent with an interaction of BDNF.