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Home » Types of Pain » Rheumatologic and Myofascial Pain
8 Articles in Volume 6, Issue #6
Choosing and Using a Low Level Laser in Pain Management
Clinical Bioethics
Cranial Electrotherapy Stimulation in the Treatment of Fibromyalgia
Fibromyalgia: New Hope and New Pharmaceuticals
Identifica tion and Management of Cardiac -Adrenal-Pain Syndrome
Interventional Therapy
Superior Pharyngeal Constrictor Muscle Pain
Treating Neuropathic Pain in Multiple Sclerosis (MS)
While few therapies have proven effective in the past, recent pharmacologic advances provide new hope for this difficult-to-treat disorder.
By Andrew J. Holman, MD
Fibromyalgia may produce pain ranging from mild to severe and is now among the major reasons for referral to a pain center. Until now, few therapies have proven effective but several new agents provide pain relief in most cases. This update reviews both the old and new pharmacologic agents used to treat fibromyalgia.
Despite the introduction of the term fibrositis in 1904 by Gower,1 progress in understanding FMS has been slow. However, recent innovative strategies and broader investigation of its cause, beyond a myopic focus on psychiatric or musculoskeletal research, have finally led to a new expectation of improved treatment outcome.
Firm confidence in a diagnosis is essential before formulating and implementing an effective treatment strategy in any medical condition. For many clinicians, the diagnosis of FMS remains confusing despite validated criteria published by the American College of Rheumatology in 1990 (See Table 1).2 While specific tenderness, or tender points, have been promoted as diagnostic evidence of this disorder, honest debate and, at times, unruly skepticism, is evident even among rheumatologists. While helpful as inclusion criteria for research studies, fibromyalgia tender-point intensity can still vary from day to day in clinical practice, leading to diagnostic uncertainty. Nevertheless, clinicians can readily recognize and attempt to treat the common presentation of chronic, unexplained, widespread pain, tenderness, and fatigue of fibromyalgia.
Table 1. The 1990 American College of Rheumatology Criteria for the Classification of Fibromyalgia2
History of Widespread Pain. Definition:
Pain is considered widespread when all of the following are present:
Pain in the left side of the body
Pain in the right side of the body
Pain above the waist
Pain below the waist
In addition, axial skeletal pain (cervical spine or anterior chest or thoracic spine or low back) must be present. In this definition, shoulder and buttock pan is considered as pain for each involved side. Low back pain is considered lower segment pain.
Pain in 11 of 18 Tender Point Sites on Digital Palpation. Definition:
Pain on digital palpation, must be present in at least 11 of the following 18 tender point sites:
Occiput: bilateral, at the suboccipital muscle insertion
Low cervical: bilateral, at the anterior aspects of the intertransverse spaces at C5-C7
Trapezius: bilateral, at the midpoint of the upper border
Supraspinatus: bilateral, at origins, above the scapula spine near the medial border
Second rib: bilateral, at the second costochondral junctions, just lateral to the junctions on upper surfaces
Lateral epicondyle: bilateral, 2 cm distal to the epicondyles
Gluteal: bilateral, in the upper outer quadrants of buttocks in anterior fold of muscle
Greater trochanteric: bilateral, posterior to the trochanteric prominence
Knee: bilateral, at the medial fat pad proximal to the joint
Digital palpation should be performed with an approximate force of 4 kg. for tender point to be considered positive the subject must state that the palpation was painful. Tender is not to be considered painful.
Clinical Characteristics
Fibromyalgia syndrome (FMS) is a specific musculoskeletal condition affecting 10 million Americans validated by specific criteria published by the American College of Rheumatology in 1990.
Diagnosis is based on demonstration of widespread pain for at least 3 months and specific tenderness to gently palpation symmetrically at tender points.
FMS tender points are located at the occiput, trapezius, medial clavicle, lateral epicondyle, sacroiliac, greater trochanteric and medial knee regions.
FMS is not a diagnosis of exclusion and important comorbid pain can complicate the presentation and require independent diagnosis and treatment.
FMS symptoms have been reproduced after auditory fragmentation of stage III/IV sleep for 4 nights.
Similar experiments in athletes and disruption of rapid eye movement (REM) sleep did not lead to FMS symptoms.
Pain and tenderness have been attributed to amplified central pain processing, but the specific mechanism has not yet been identified.
Abnormal regulation of autonomic control is a prominent feature of FMS and may explain the strong association of irritable bowel syndrome, irritable bladder, palpations and vasomotor instability with FMS.
Inadequate hippocampal attenuation of autonomic arousal fragmenting sleep appears to be a fundamental feature of FMS.
Dopaminergic control of hippocampal function suggests a novel treatment approach to FMS.
There is no consensus regarding pathogenesis, but an abnormality of centrally mediated pain processing has gained greater acceptance.3 Functional magnetic resonance imaging (fMRI)4 and pain-testing studies5 have significantly strengthened this concept of centrally amplified pain perception. Observations of abnormal sleep-stage architecture6 and induction of FMS symptoms with specific disruption of deep, non-rapid eye movement (nREM), stage IV sleep,7 have encouraged consideration of how sleep affects a variety of CNS functions influencing pain, fatigue and cognitive behavior. Sophisticated measurements of autoimmune regulation with validated tools, including heart rate variability and tilt-table testing, have increased the awareness that patients with FMS fail to maintain normal sympathetic homeostasis.8-14 In turn, perturbed sleep, psychiatric arousal (e.g., post-traumatic stress disorder, bipolar disorder and anxiety disorder), peripheral vasomotor tone, cardiac rhythm, and bowel motility focus future research directly on new autonomic mechanisms that may lead to an improved understanding of FMS.
Almost 85% of FMS cases occur in women, but men are often undiagnosed. In fact, the divergent presentation of FMS in men compared with women has been well reported.15 Pain and muscular spasm are generally more diffuse and vague in men. It appears that the hallmark diagnostic finding in FMS, 11 of 18 specific tender points, becomes apparent to the clinician and male patients much later in its clinical course. Response rates (RRs) to a variety of pharmacologic options are also less robust in men. The cause of these gender differences in presentation and response is uncertain, but may relate to behavioral differences, comorbidities, or hormonal variations, including clinically amenable testosterone deficiency in men receiving chronic opioids.
The variability and unpredictability of treatment response has fueled clinician skepticism regarding FMS as a specific disorder, and gender differences also enhance this debate. Some explain this paradox by considering FMS as a family of disorders and suggest defining FMS subsets to improve treatment outcomes for specific medications.16 Unfortunately, the importance of comorbidities accompanying FMS and interfering with the treatment response has been given little consideration. Due to the general vagueness of fatigue and widespread pain as symptoms, most clinicians find teasing apart comorbidities particularly difficult in patients with FMS. Nevertheless, defining all accompanying causes of pain when treating FMS, such as arthritis, myelopathy, bursitis, tendonitis, and migraine to name a few, is as important as identifying all risk factors for cardiovascular disease.
Pain and tenderness should be widespread in all four limbs and the axial spine. FMS is not a diagnosis of exclusion One must be confident of the diagnosis and even more aware of comorbidities before considering treatment or evaluating a treatment response. Effective treatment of other causes of pain such as stress, insomnia, and autoimmune dysfunction are equally important to the overall outcome as the choice of treatment for FMS.
Traditional Treatment
Treatment of FMS has been effectively reviewed over the past few years, but some authors tend to favor more traditional approaches.17 Until the "magic bullet" is discovered, a balanced and comprehensive approach appears reasonable since these modalities have sometimes provided a benefit. Even among nonbelievers, most clinicians encourage exercise for patients with FMS. In 1988, a randomized trial of exercise demonstrated improvement in FMS pain threshold compared with flexibility training after 20 weeks.18 Aerobic exercise,19 muscle strengthening, pool exercises20 and spa therapy21 have been found to be helpful. Many studies supportive of exercise vary in methodology and have significant limitations, including inadequate blinding and small sample size.
However, a thorough review by Goldenberg and colleagues concluded that all patients with FMS should begin a cardiovascular program.22
Analysis of these exercise studies reveals important limitations, including appropriate matching of specific therapies with heterogeneous patients and consistent adherence to exercise regimens.23 In addition, while statistical significance was routinely achieved, the magnitude of the benefit (25-30% improvement) would not be considered robust. Most clinicians note that many of their patients with FMS fail to respond to exercise and many decline, or are unable to participate in such structured programs implemented at an experienced research facility. Regrettably, outcomes from many exercise trials simply do not translate into clinical practice.
The notion of exercise as an effective therapeutic option for FMS may have arisen from the observation that aerobic fitness may be preventative. In 1975, Moldofsky induced widespread pain suggestive of FMS by disrupting stage IV sleep with an auditory arousal for four nights in healthy college students.6 Similar results did not occur when he repeated the experiment in fit military recruits or after disruption of REM sleep stages.7 It is not clear how fitness preserves the benefits of stage IV sleep, but incorporation of aerobic exercise into an FMS treatment strategy remains popular.
Evidence that other nonpharmacologic remedies are effective is debatable, yet accepted by many clinicians. Soft-tissue injection with saline, local anesthetics and/or corticosteroids have been offered to patients with FMS, but placebo-controlled trials are unavailable. Acupuncture may reduce pain and analgesic requirements but, of three controlled studies,24-26 only one demonstrated a significant treatment benefit compared with placebo. Massage,27 ultrasound,28 and mineral baths29 demonstrate a benefit for pain compared with placebo, but sustained meaningful improvement is unusual. Cognitive behavioral therapy has become a logical and helpful therapeutic approach for FMS,30 but many patients lack access to skilled therapists.
In 2004, Goldenberg and colleagues provided an evidence-based review of FMS management.22
Their assessment of FMS studies based on study size, design, and reproducibility is clearly the most thorough review of traditional treatment options for FMS to date. The greatest improvement in pain as an outcome variable compared with placebo was also reported by Goldenberg in 1996 in a study of fluoxetine (20mg each morning) combined with amitriptyline (25mg at bedtime).31 In this four-arm, 6-week, double-blind, crossover study, fluoxetine alone and amitriptyline alone improved pain and global function, but not fatigue or tender-point score. Combined, in the fourth arm, improvement in pain and fibromyalgia impact questionnaire (FIQ) scores improved maximally (34%). Other studies with amitriptyline alone have confirmed a statistically significant decrease in FMS pain of approximately 30%.32 Uncontrolled reports of serotonin (5-hydroxytryptamine (5-HT)) reuptake inhibitors, including sertraline,33 also suggest modest efficacy.
The second most frequently studied drug class for the treatment of FMS are the muscle relaxants, including cyclobenzaprine. Dosed at 10-30mg at bedtime, a meta-analysis of randomized studies demonstrated a benefit similar to amitriptyline.34 Even doses as low as 1-4mg at bedtime have demonstrated some analgesic efficacy and improved sleep stage architecture.35 Decreased levels of cerebrospinal fluid (CSF) neuroamines and substance P were reported by Russell with tizanidine 4-24mg each day.36 Carisoprodol dosed at 1200mg/day decreased FMS pain compared with placebo in one study,37 but this result has not been confirmed. Other muscle relaxants are routinely used by clinicians without literature support.
Other classes of medication available to treat FMS have not demonstrated efficacy compared with placebo, including ibuprofen (2400mg/day for 3 weeks).38 naproxen (1000mg/day for 6 weeks)39 or prednisone (15mg/day for 2 weeks).40 Temazepam (15-30mg at bedtime for 12 weeks) demonstrated a modest statistical benefit,41 but alprazolam (0.5-3.0mg at bedtime) was not superior to placebo.42 Finally, a randomized 13-week trial of tramadol in combination with acetaminophen in 315 subjects demonstrated significant analgesic efficacy without any serious adverse effects.43
A controlled trial of zolpidem (Ambien®, Sanofi-Synthelabo) may provide an important illustrative example. As a sedative hypnotic, zolpidem induces stage II rather than stage IV sleep. Subjects noted improved sleep duration and decreased sleep latency, but did not note improved FMS pain or fatigue compared with subjects receiving placebo.44 Perhaps, if the medication effectively restored depleted stage IV sleep, an improvement in FMS symptoms may have been found.
Finally, although controlled trials are unavailable, the safety of clonazepam and lorazepam in 160 patients over 12 months was encouraging.45 Patients did not escalate their bedtime dose (2.0mg) or note significant adverse events, including withdrawal seizures. Contrary to other benzodiazepines, lorazepam and clonazepam effectively reduce restless legs syndrome (RLS) symptoms,46 a common source of arousal fragmenting sleep quality in patients with FMS.
New Pharmacologic Treatment Options
Research in fibromyalgia has grown exponentially and new, meaningful treatment options are now at hand. Every clinician brave enough to accept patients with FMS recognizes many obstacles that interfere with successful treatment. However, embracing a team approach, identification of important comorbidities, and consideration of novel medications are improving outcomes. In addition, large pharmaceutical companies are engaged in a race to discover an effective treatment. A list of promising new therapies for FMS include the following:
Pregabalin (Lyrica™, Pfizer)
Milnacipran (Dalcipran®, Cypress Bioscience)
Duloxetine (Cymbalta®, Eli Lilly)
Sodium oxybate (Xyrem®, Orphan Medical/Jazz Pharmaceuticals) and the dopamine agonists
Ropinirole (Requip®, G1axoSmithKline)
Pramipexole (Mirapex®, Boehringer- Ingelheim)
In one of the largest controlled trial for FMS to date with 528 patients, pregabalin demonstrated significant improvement in pain score, sleep quality, fatigue and global measures of change.47 Pregabalin—a precursor of gabapentin (Neurontin®, Pfizer)—has analgesic, anxiolytic, and antiepileptic effects in animals. It is a ligand for a2-S subtype 1 and 2 receptors that adheres to voltage-gated calcium channels without affecting g-aminobutyric acid (GABA) receptors.48 Its activity is limited to neurons and it does not affect vascular calcium channels. Reduction of calcium influx at the neuron reduces release of substance P, glutamate and norepinepherine (NE),49 which is thought to mediate its analgesic and anxiolytic actions.
Subjects were assigned (1:1:1:1) to placebo or one of three pregabalin doses (150, 300 or 450mg/day) for eight weeks. Demographics for each group were similar, including 90% women, 95% Caucasian, with an FMS duration of eight years and mean pain score of 7 (range: 1 [no pain] - 11 [worst pain]). Patients discontinued prior medications and 77% completed the trial. All active arms improved within approximately two weeks and demonstrated sustained improvement through to week eight. Treatment with pregabalin was associated with statistically significant dose-dependent improvement. However, improvement in pain score was modest, even in the 450mg arm (-0.93, 1-11 scale), and the p-value (p=0.0009) reflected the large size of the study. Adverse events were common but mild and transient, including dose-dependent dizziness (49% in the 450mg arm vs. 11% for placebo). Somnolence (28%), dry mouth (13%), peripheral edema (11%), and weight gain (7%) were also more common with pregabalin than placebo.
"Every clinician brave enough to accept patients with FMS recognizes many obstacles that interfere with successful treatment. However, embracing a team approach, identification of important comorbidities, and consideration of novel medications are improving outcomes."
Pregabalin represents an extension of the neuropathic/anticonvulsant therapeutic approach to FMS. While psychiatric medications have been the mainstay of FMS pharmacopeia, many pain centers have addressed pain, and FMS specifically, as a neuropathic pain.50 Narcotic analgesic efficacy for FMS has been mixed,51 but anticonvulsant medications have become very popular based on anecdotal evidence. In fact, off-label use of gabapentin has been so widespread in North America that the U.S. Food and Drug Administration (FDA) fined its original manufacturer, Warner-Lambert (Parke-Davis Division, New Jersey), for promoting unapproved uses (www.FDA.gov). To date, there are no FDA-approved medications indicated for the treatment of FMS, and evaluation of innovative off-label FMS therapies has become more difficult in the United States following this reprimand.
The dual 5-HT and NE reuptake inhibitors (SNRIs) have received widespread attention as the next breakthrough for patients with FMS. While a controlled study of venlafaxine (Effexor®, Wyeth) was inconclusive,52 two case reports suggested a significant benefit at higher dosage.53,54 Milnacipran, a popular antidepressant in Japan, is a novel SNRI that favors reuptake inhibition of NE over 5-HT. Reduction of pain in a variety of animal models may be related to the roles of NE and 5-HT in pain-modulating systems via the descending inhibitory pathways in the brain and spinal cord.55 Tricyclic antidepressants mediate pain through 5-HT and NE neurotransmission and reduce FMS pain. This potential mechanism of pain amplification supports the consideration of SNRIs, which may be better tolerated than tricyclics, for the treatment of FMS.
In a 12-week, double-blind, placebo controlled Phase II trial, 125 patients with FMS were randomized (3:3:2) to receive milnacipran once or twice daily (up to 200mg/day) or placebo.56 RR was defined as the percentage of subjects who achieved a 50% or greater pain reduction by visual analog scale on an electronic diary. For this outcome milestone, the intention-to-treat (ITT) analysis RR for twice daily dosing was 37%, 22% for once daily, and 14% for placebo. Only the twice-daily dose response was statistically superior to placebo (p=0.04), but both twice and once daily outcomes on a secondary efficacy measure, the patient global impression of change (PGIC), were superior to placebo (p=0.003). Multiple components of the FIQ and the short-form McGill pain questionnaire (SF-MPQ) also showed statistically significant superiority over placebo for both the once- and twice-daily dosing arms.
Adverse events were unremarkable. A Phase III trial has been completed, but details have not yet been reported. However, data discovered by investors and briefly discussed by Cypress Bioscience suggest that their study barely failed to achieve a statistically positive outcome despite enrolling over 800 subjects (P=0.06). This news lead to a sudden 40% drop in the share price of Cypress Bioscience in September 2005, but its partner, Forest Pharmaceutics, has decided to continue development with redesigned studies and different primary outcomes. Milnacipran is not yet available in the USA, but this focus on SNRIs and the role of 5-HT and NE in pain modulation, and for FMS specifically, represents a hopeful and increasingly popular approach.
Two large controlled trials of duloxetine have been recently reported in patients with FMS, demonstrating interesting results. Duloxetine is a SNRI approved by the FDA in 2005 for the treatment of major depressive disorder and neuropathic pain associated with diabetic peripheral neuropathy. Its inhibition of 5-HT and NE reuptake is relatively balanced without interacting with opioid, muscarinic, histamine-1, a-adrenergic, dop-amine, 5-HT1A, 5-HT1B, 5-HT1D, 5-HT2A and 5-HT3C receptors. Once again, in animal models, this SNRI reduced pain behavior and did so with greater potency than venlafaxine, amitriptyline or desipramine.
These two trials illustrate important issues in FMS research. The first trial, reported in 2003, randomized (1:1) 207 subjects to duloxetine 60mg twice daily for 12 weeks or placebo.57 Demographic variables were equally distributed in the two arms and included 87% women (85% Caucasian), with 38% having major depression. The coprimary outcomes were FIQ total score (0-80) and FIQ pain subscore (0 [no pain]-10 [severe pain]).
Compared with placebo, duloxetine reduced total FIQ significantly (-5.53, 95% confidence interval [95% CI]: -10.43,-0.63 [p=0.027]), but did not reduce the FIQ pain subscore (p=0.13). Many other secondary measures of pain were found to be statistically improved, including the brief pain inventory (BPI), PGIC, number of tender points, FIQ stiffness subscore, and several quality of life measures. A subanalysis revealed that men with FMS failed to respond to duloxetine, and that comorbid depression did not influence FMS treatment response. Reported adverse events were typical of SNRI therapy and included insomnia, dry mouth, and constipation more frequently than placebo. Duloxetine intolerance was mild-to-moderate and did not lead to significant withdrawal from the study.
The study was repeated with the exclusion of men, the primary outcome was changed, and the sample enlarged to favor a statistically significant treatment response.58 The FIQ became a secondary outcome measure and the BPI became the primary outcome. In this new 12-week study, 354 women with FMS were randomized (1:1:1) to receive duloxetine 60mg daily, 60mg twice daily or placebo. Pain decreased significantly in subjects treated with duloxetine (daily and twice daily) compared with placebo (p<0.001), as assessed by the BPI. RR was defined as a 30% (rather than 50%) reduction in pain and was achieved by 55% in the daily arm, 54% in the twice-daily arm, and by 33% in the placebo arm. The size of the study ensured that these differences were statistically significant. The authors' conclusion, that duloxetine is an efficacious and safe treatment for FMS, is not unreasonable. However, scrutiny of the two study designs, including exclusion of nonresponders (men) and changing to a more favorable outcome variable emphasizes the importance of careful review of study design.
Sodium Oxybate
A third treatment approach for FMS focuses directly on sleep physiology and is based on the importance of a-wave fragmentation of stage IV sleep more than on SNRI- or anticonvulsant-mediated modulation of pain neurotransmission. Diminished slow-wave sleep has been identified as an important feature in FMS and different types of a-wave intrusion of stage IV sleep have been identified.59,60 Sodium oxybate is a commercially available form of g-hydroxybuyrate (GHB), a naturally occurring CNS metabolite primarily found in the hippocampus and basal ganglia. It is the only compound known to increase growth hormone secretion and deep, slow-wave stage IV sleep and is FDA approved for the treatment of cataplexy in patients with narcolepsy.
A double-blind, crossover trial of sodium oxybate in 24 patients was conducted over 1 month intervals with a 2-week washout period.61 A total of 18 subjects completed the trial of sodium oxybate (6.0mg at bedtime) compared with placebo and were monitored by polysomnogram (PSG), tender-point index and subjective measurements of improvement in daily diaries. A variety of pain and fatigue scores improved by 29-33% in the active arm compared with 6-10% in the placebo arm (p<0.005). Tender-point score decreased by 8.4 points with sodium oxybate compared with an increase of 0.4 points in the placebo arm (p=0.008). PSG measures of inappropriate CNS arousal, including a-wave intrusion, sleep latency and 'REM decreased with treatment, while stage III and IV slow-wave sleep increased compared with placebo (p<0.005).
This study provided preliminary yet compelling evidence that FMS pain and fatigue improve with increased slow-wave sleep and decreased a-wave intrusion. A larger, multicenter, controlled study was reported at the 2005 annual meeting of the American College of Rheumatology. In this 8-week, placebo controlled Phase II trial, subjects were randomized (1:1:1) to placebo, 4.5 gm or 6.0 gm of sodium oxybate. Their primary outcome was a triple composite, including simultaneous 20% improvement in FIQ, 20% improvement in 10 cm VAS pain score and 'much better' or 'very much better' on Patient Global Impression of Change (PGIC). More subjects in the active arms achieved this level of treatment response than those in the placebo arm (placebo 17% , 4.5 gm 35% [p=0.005], 6.0 gm 27%, [p=0.05]).62
The therapeutic role of restoring stage IV deep sleep to address FMS symptoms provides another important approach quite different from treating FMS with analgesics, anticonvulsants, or SNRIs. Based on Moldofsky's landmark sleep deprivation studies6,7 and these sodium oxybate results, a renewed emphasis on the restoration of normal sleep-stage architecture has gained more attention as a primary, rather than secondary, therapeutic goal.
Ropinirole
Most FMS reviews do not mention dopamine agonists (e.g., ropinirole and pramipexole), as initial reports were anecdotal until late 2004. These medications were FDA-approved for the treatment of Parkinson's disease in 1997 and the reasoning behind their use is far afield of traditional approaches to FMS. Ropinirole is a dopamine receptor agonist with specificity for the dopamine 2 and 3 subreceptors (D2, D3). It is metabolized in the liver by the cytochrome P450 (CYP)C1A isoenzyme and has negligible affinity for muscarinic, acetylcholine, adrenergic, opioid, or 5-HT receptors.
In 2003, the first use of ropinirole for the treatment of FMS was reported in an open-label assessment of 17 patients who noted a 64% decrease in tender-point pain score over 4 months at a mean dose of 6.0mg at bedtime.63 While the approved maximum dose for RLS is 4.0mg at bedtime, the typical dose for Parkinson's disease is 1-8mg orally three times daily. In 2004, in a controlled trial of 30 patients with FMS,64 20 patients were randomized to ropinirole and 10 were assigned to the placebo arm. Ropinirole was gradually increased over 14 weeks to 8mg at bedtime. Although 45% of patients receiving ropinirole achieved a 50% or greater reduction in 10 cm visual analog pain score compared with 30% of placebo patients, the results of this small, pilot study were not statistically significant (p=0.31). All other measures of efficacy (tenderness, fatigue and function) also showed a trend towards the efficacy of ropinirole compared with placebo.
The most common adverse events were typical intolerances seen with dopaminergic therapy, including mild-to-moderate nausea. Interestingly, sudden, uncontrolled daytime sleepiness (sleep attacks) as well as orthostatic hypotension, experienced by patients with Parkinson's disease treated with daily dopamine agonists, were not seen in this FMS trial.
Table 2. Comparison of Treatments/Medications for Fibromyalgia
Exercise, usually aerobic and carefully graded, consistently reduces FMS symptoms for some patients, but fails to address FMS pathogenesis.
Controlled trials with acupuncture, massage, ultrasound, mineral baths and cognitive behavioral therapy demonstrates 30% reduced pain.
Fluoxetine (20mg), amitriptyline (25mg), sertraline (50mg), cyclobenzaprine (1-30mg), tizanidine (4-24mg), carisoprodol (1200mg) and temazepam (15-30mg), demonstrated a modest clinical benefit in controlled trials.
Ibuprofen (2400mg), naproxen (1000mg), prednisone (15mg) and alprazolam (0.5-3.0mg) failed to benefit FMS patients in controlled trials. Zolpidem (5-15mg) improved sleep, but not FMS pain.
Neuropathic Approach
Pregabalin, a precursor of gabapentin, is a ligand for a2-d subtype 1 and 2 receptors affecting CNS voltage-gated.
In 528 patients, pregabalin (450mg) significantly reduced FMS pain over 8 weeks.
A total of 29% of patients receiving pregabalin achieved more than 50% decreased pain compared with 11% receiving placebo.
Psychiatric Approach
Milnacipran and duloxetine are mixed 5-hydroxytryptamine (5-HT) and norepinepherine reuptake inhibitors (SNRI) indicated for the treatment of depression.
In a Phase II trial, 37% of patients with FMS receiving milnacipran noted a greater than 50% pain reduction compared with 14% receiving placebo. Adverse events were unremarkable.
In two large trials, duloxetine did not reduce pain in men, but effectively reduced many FMS symptoms, including pain, in women. In the first trial, including men, 28% receiving duloxetine noted greater than 50% decreased pain compared with 17% receiving placebo.
Stage IV Sleep Induction Approach
Sodium oxybate induces stage IV sleep and is a commercial form of d-hydroxybutyrate (GHB), a naturally occurring CNS metabolite. It is indicated for the treatment of narcolepsy in patients with cataplexy.
In a pilot controlled trial in 24 patients, sodium oxybate significantly increased stage IV sleep duration, decreased arousals fragmenting sleep and reduced FMS pain and fatigue by 29-33%.
Dopamine Agonist Approach
Ropinirole and pramipexole are selective dopamine D3 receptor agonists developed for the treatment of Parkinson's disease and commonly used for the treatment of restless legs syndrome. Both show promise for treatment of FMS with pramipexole demonstrating the highest pain response to date.
Recently, a controlled FMS trial with a new extended-release ropinirole formulation dosed at bedtime was completed in Europe. While subjects were expected to receive 16-24mg of extended-release ropinirole at the discretion of their investigator, the mean treatment dose was only 8.2mg qd. This dose correlates with approximately 3mg of immediate release ropinirole. This inadequate dosing scheme may have contributed to it failure to demonstrate a statistically significant treatment effect.65
Nevertheless, the rationale for using a dopamine agonist begins with a greater appreciation of the higher incidence of RLS in patients with FMS (31%) compared with normal controls (3%).66 In May 2005, ropinirole became the first medication approved for the treatment of RLS by the FDA.
This RLS arousal inhibits deep sleep and ties in with the Moldofsky findings. While sedating medications are commonly offered to promote deep sleep by overwhelming arousal in FMS, the dopamine agonist was intended to reduce arousal fragmenting normal sleep.
Interestingly, dopamine agonists are not sedating and their mechanism of action in FMS is under investigation. Abnormal sympathetic arousal has been documented in FMS, and these patients maintain poor autonomic homeostasis. Excessive fight-or-flight responses as well as specific arousals such as intense chronic pain, frustration, post-traumatic stress disorder, and anxiety have been well documented in FMS. Any of these arousals can chronically disrupt deep, restorative sleep.
D3 receptors are primarily found in the limbic system, including the hippocampus, but not in the sympathetic arousal centers in the brainstem. The hippocampus attenuates and balances sympathetic arousal.67 Inadequate dopaminergic control of autonomic drive from the hippocampus has been suggested as a fundamental issue in FMS pathogenesis.68 In fact, preliminary magnetic resonance imaging (MRI) volumetric assessment has demonstrated hippocampal atrophy in patients with FMS compared with normal controls.69,70 Consequently, a medication capable of decreasing RLS and restoring normal hippocampal dampening of brainstem autonomic arousal would be a logical therapeutic option for FMS.
Pramipexole
Although pramipexole is indicated only for the treatment of Parkinson's disease by the FDA, it also effectively reduces RLS.71 Its profile is similar to that of ropinirole, except that it is renally metabolized and has mild affinity for central adrenergic a2 receptors (the target of tizanidine and clonidine) in addition to D2 and D3 receptors.
Following two positive open-label reports,72,73 a controlled trial of pramipexole for FMS in 60 subjects (57 women, 3 men) was recently presented.74 Over 14 weeks, subjects were randomized (2:1) to a weekly fixed dose escalation of pramipexole from 0.25 to 4.5mg at bedtime or placebo. Significant reductions in visual analog pain, fatigue, total FIQ score, and global function at week 14 were found. The mean pain score decreased by 36% in the active arm compared with 9% for placebo by ITT analysis (p=0.008). A pain reduction of 50% or greater was seen in 42% of patients receiving pramipexole compared with 14% receiving placebo. All other secondary outcome measures trended better for the active arm, including tender-point index, Beck anxiety score, and Hamilton depression scale, without achieving statistical significance.
The most common adverse event was nausea, occurring in 79% of the active arm and 71% of the placebo arm. Nausea did not lead to discontinuation of pramipexole and was addressed by concomitant use of proton pump inhibitors. A mean weight gain of 3 lbs was seen in the placebo arm, while 40% of patients in the active arm noted 5-25 lb. weight loss at week 14 (p=0.001). Transient increased anxiety (14%) and vomiting (16%) were seen in the active arm but were not reported in the placebo arm. One episode of transient amnesia (<24h) required hospitalization for evaluation, but the patient fully recovered and completed the trial (double-blinded) six weeks later.
This study was very atypical for a FMS study. Subjects were allowed to maintain stable doses of other medications and psychiatric and pain comorbidities were allowed. A total of 53 of the 59 patients who completed the trial maintained stable doses of other medications, including 50% requiring daily narcotic analgesics. For any addition of a new medication during the study, the final untainted assessment was used as the final outcome. In addition, 30% of subjects were disabled, of whom one returned to work during the study (active arm).
Most FMS clinical trials only include patients without comorbidities who are willing to wash out all other medications and risk receiving a placebo for many months. This bias may affect interpretation of results and question the relevance of study conclusions for the clinician caring for patients with comorbidities and more severe FMS. It is unlikely that future pregabalin, milnacipran, sodium oxybate or ropinirole FMS trials will assess a similarly disabled and narcotic dependent FMS cohort, but perhaps a more traditional trial with pramipexole as monotherapy will be completed. Then, results from these different trials may be compared more fairly.
Potential new therapies for FMS from divergent approaches are developing at an unprecedented pace. A comparison of different treatments/medications is shown in Table 2. Scientific principles of FMS are becoming clearer as basic scientists study neuropharmacology and clinicians observe unexpected benefits and confirm them in randomized trials. Application of traditional, conservative treatments remain an option, but greater response rates have emerged with the use of medications capable of manipulating 5-HT, NE, and dopamine. As with any review of randomized trials, only longer and larger studies can confirm or refute these early findings. However, with these new developments, clinician can begin to have more confidence in their ability to improve the lives of patients with fibromyalgia.
Note: papers of special note have been highlighted as either of interest (*) or of considerable interest (**) to readers.
1. Gowers WR: Lumbago—its lessons and analogues. Br. Med. J. 1904. 1;117-121.
2. Wolfe F, Smythe HA, Yunus MB, et al. The American College of Rheumatology 1990 criteria for the classification of fibromyalgia: report of the multicenter criteria committee. Arthritis Rheum. 1990. 33(2);160-172 .
3. Bennett RM. Emerging concepts in the neurobiology of chronic pain; evidence of abnormal sensory processing in fibromyalgia. Mayo Clin. Proc. 1999. 74(4), 385-398.
* Fundamentally important paper on pain processing in fibromyalgia syndrome (FMS).
4. Gracely RH, Petzke F, Wolf JM, and Clauw DJ. Functional magnetic resonance imaging evidence of
augmented pain processing in fibromyalgia. Arthritis Rheum. 2002. 46(6), 1333-1343.
* Innovative support for abnormal central pain processing in FMS.
5. Price DD and Staud R. Neurobiology of fibromyalgia syndrome. J. Rheumatol Suppl. 2005. 75, 22-28.
* Important review of peripheral and CNS mechanisms in FMS.
6. Moldofsky H, Scarisbrick P, England R, and Smythe H. Musculoskeletal symptoms and non-REM
sleep disturbance in patients with 'fibrositis syndrome' and healthy subjects. Psychosom.
Med. 1975. 37;341-351.
* An important paper describing pathogenesis.
7. Moldofsky H and Scarisbrick P. Induction of neurasthenic musculoskeletal pain syndrome by selective sleep stage deprivation. Psychosom. Med. 1976. 38;35-44.
* Important paper demonstrating the importance of sleep stage architecture in FMS.
8. Petzke F and Clauw DJ. Sympathetic nervous system function in fibromyalgia. Curr. Rheumatol. Rep. 2000. 2(2);116-123.
* Important overview of the role of the autonomic nervous system in FMS.
9, Cohen H, Neumann L, Shore M, Amir M, Cassuto Y, and Buskila D. Abnormal sympathovagal balance in men with fibromyalgia. J Rheumatol. 2001. 28(3), 581-589.
10. Rosner I, Rozenbaum M, Naschitz JE, Sabo E, and Yeshurum D. Dysautonomia in chronic fatigue syndrome vs. fibromyalgia. Irr Med. Assoc. J. 2000. 2(Suppl.);23-24.
11. Martinez-Lavin M and Hermosillo AG. Autonomic nervous system dysfunction may explain the multisystem features of fibromyalgia. Semin. Arthritis Rheum. 2000. 29(4);197-199.
12. Raj SR, Brouillard D, Simpson CS, Hopman WM, and Abdollah H. Dysautonomia among patients with fibromyalgia; a noninvasive assessment. J Rheumatol. 2000. 27;2660-2665.
13. Martinez-Lavin M, Hermosillo AG, Rosas M, and Soto M. Circadian studies of autonomic nervous balance in patients with fibromyalgia: a heart variability analysis. Arthritis Rheum. 1998. 41(11);1966-1971.
14. Vaeroy H, Qiao ZG, Morkrid L, and Forre 0. Altered sympathetic nervous system response in patients with fibromyalgia (fibrositis syndrome). f. Rheumatol. 1989. 16(l 1);1460-1465.
15. Yunus MB: Gender differences in fibromyalgia and other related syndromes. J. Gend, Specif, Med. 2002. 5(2);42-47.
16. Turk DC. The potential of treatment matching for subgroups of patients with chronic pain: lumping versus splitting. Clin. J. Pain. 2005. 21(1);44-55.
17. Clauw DJ and Crofford LJ. Chronic widespread pain and fibromyalgia: what we know, and what we need to know. Best Pract..Res. Clin. Rheumatol. 2003. 17(4);685-701.
18. McCain GA, Bell DA, Mai FM, et al. A controlled study of the effects of a supervised cardiovascular fitness training program on the manifestations of primary fibromyalgia. Arthritis Rheum. 1988. 31;1135-1141.
19. Gowans SE, DeHueck A, Voss S, and Richardson M. A randomized controlled trial of exercise and education for individuals with fibromyalgia. Arthritis Care Res. 1999. 12;120-128.
20. Jentoft ES, Kvalvik AG, and Mengshoel AM: Effects of pool-based and land-based aerobic exercise on women with fibromyalgia/widespread pain muscle pain. 2001. Arthritis Rheum. 45;42-47.
21. Donmez A, Karaguille MZ, Tercan N, et al. SPA therapy in fibromyalgia; a randomized controlled clinic study. Rheumatol Int. 2005. (E-pub ahead of print).
22. Goldenberg DL, Burckhardt C, Crofford L: Management of fibromyalgia syndrome: JAMA 2004. 292(19); 2388-2395.
** Comprehensive review of FMS treatment through 2004 with emphasis on evidencebased conclusions.
23. Mannerkorpi K. Exercise in fibromyalgia. Cur. Opin. Rheumatol. 2005. l7(2);190-194.
24. Deluze C, Bosia L, Zirbs A, Chantraine A, and Vischer TL. Electroacupuncture in fibromyalgia; results of a controlled trial. Br. Med. J. 1992. 305;1249-1252.
25. Harris RE, Tian X, Cupps TR, et al.: The treatment of fibromyalgia with acupuncture. Arthritis Rheum. 2003. 48;S692 (Abstract).
26. Assefi NP, Sherman K, Jacobsen C, et al. A randomized clinical trial of acupuncture compared with sham acupuncture in fibromyalgia. Ann. Intern. Med. 2005. 143(l);124.
27. Brattberg G: Connective tissue massage in the treatment of fibromyalgia. Eur J Pain. 1999. 3; 235-244.
28. Almeida TF, Roizenblatt S, Benedito-Silva AA, and Tufik S. The effect of combined therapy (ultrasound and interferential current) on pain and sleep in fibromyalgia. Pain. 2003. 104;665-672.
29. Buskila D, Abu-Shakra M, Neumann L, et al.: Balneotherapy for fibromyalgia at the Dead Sea. Rheumatal. 2001. Int. 20;105-108.
30. Redondo JR, Justo CM, Moraleda FV, et al.: Long-term efficacy of therapy in patients with fibromyalgia: a physical exercise-based program and a cognitive-behavioral, approach. Arthritis Rheum. 2004. 51(2);184-192.
31. Goldenberg D, Mayskiy M, Mossey C, Ruthazer R, and Schmid C. A randomized, double-blind crossover trial of fluoxetine and amitriptyline for the treatment of fibromyalgia. Arthritis Rheum. 1996. 39(11);1852-1859.
* Important crossover study demonstrating significant therapeutic benefit with fluoxetine and amitryptyline.
32. Carette S, Oakson G, Guimont C, and Steriade M. Sleep electroencephalography and the clinical response to amitriptyline in patients with fibromyalgia. Arthritis Rheum. 1995. 38(9);1211-1217.
33. Gonzalez-Viejo MA, Avellanet M, and Hernandez-Morcuende MI. A comparative study of fibromyalgia treatment: ultrasonography and physiotherapy versus sertraline treatment. Ann. Readapt. Med. Phy. 2005. (E-pub ahead of print).
34. Tofferi JK, Jackson JL, and 0'Malley PG. Treatment of fibromyalgia with cyclobenzaprine: a meta-analysis. Arthritis Rheum. 2004. 51;9-13.
35. Moldofsky H. A double-blind, randomized, parallel study of the safety, efficacy and tolerability of very-low-dosage cyclobenzaprine compared to placebo in subjects with fibromyalgia. Arthritis Rheum. 2002. 46;S614 (Abstract).
36. Russell IJ, Michalek JE, Xiao Y, Haynes W, Vertiz R, and Lawrence RA. Therapy with a central alpha-2- agonist (tizanidine) decreases cerebral spinal substance R and may reduce serum hyaluronic acid as it improves clinical symptoms of the fibromyalgia syndrome. Arthritis Rheum. 2002. 46;S614 (Abstract).
37. Vaeroy H, Abrahamsen A, Forre 0, and Kasse E. Treatment of fibromyalgia (fibrositis syndrome): a parallel double-blind trial with carisoprodol, paracetamol and caffeine (somadril comp) versus placebo. Clin. Rheumatol. 1989. 8(2);245-250.
38. Yunus MB, Masi AT, and Aldag JC: Short-term effects of ibuprofen in primary fibromyalgia syndrome: a double-blind, placebo-controlled trial. J. Rheumatol. 1989. 16(4);527-532.
39. Goldenberg DL, Felson DT, and Dinerman H. A randomized, controlled trial of amitriptyline and naproxen in the treatment of patients with fibromyalgia. Arthritis Rheum. 1986. 29(11);1371-1377.
40. Clark S, Tindall E, and Bennett RM. A double-blind crossover trial of prednisone versus placebo in the treatment of fibrositis. J. Rheumatol. 1985.12(5);980-983.
41. Hench PK, Cohen R, and Mitler MM. Fibromyalgia: effects of amitriptyline, temazepam and placebo on pain and sleep. Arthritis Rheum. 1989. 32; S47 (Abstract).
42. Russell IJ, Fletcher EM, Michalek JE, McBroom PC, and Hester GG. Treatment of primary fibrositis/fibromyalgia syndrome with ibuprofen and alprazolam. A double-blind, placebo-con trolled study. Arthritis Rheum. 1991. 340; 552-560.
43. Bennett RM, Kamin M, Karim R, and Rosenthal N. Tramadol and acetaminophen combination tablets in the treatment of fibromyalgia pain; a double-blind, randomized, placebo-controlled study. Am. J. Med. 2003. 114(7);537-545.
* Important paper for clinicians treating patients with FMS.
44. Moldofsky H, Lue FA, Mously C, Roth-Schechter B, and Reynolds WJ. The effect of zolpidem in patients with fibromyalgia: a dose ranging, double-blind, placebocontrolled, modified crossover study. J. Rheumatol. 1996. 23;529-533.
45. Holman AJ. Safety and efficacy of lorazepam for fibromyalgia after one year. Arthritis Rheum. 1999. 42(9);S152 (Abstract).
46. Jankovic J. Section Five: The Extrapyramidal Disorders. In: Cecil's Textbook of Medicine, 19th Edition. Wyngaarden J, Smith L, Bennett J (Eds), WB Saunders Co. Philadelphia, PA.1992. p 2137.
47. Crofford LJ, Rowbotham MC, Mease PJ, et al.; Pregabalin for the treatment of fibromyalgia syndrome: results of a randomized, double-blind, placebocontrolled trial. Arthritis Rheum. 2005. 52(4);1264-1273.
* Fundamentally important paper introducing a new treatment concept.
48. Taylor CP. Gabapentin: Mechanisms of Action. In: Anti-epileptic Drugs, 4th Edition. Levy RH, Mattson RH, Meldrum HS (Eds), Raven Press. New York, NY. 1995. pp 829-841.
49. Fink K, Dooley DJ, Meder WP et al.: Inhibition of neuronal Ca (2t) influx by gabapentin and pregabalin in the human neocortex. Neuropharmacology 2002. 42;229-236.
50. Offenbaecher M and Ackenheil M. Current trends in neuropathic pain treatments with special reference to fibromyalgia. CNS Spectr. 2005. 10(4); 285-297.
51. Moulin DE. Systemic drug treatment for chronic musculoskeletal pain. Clin. J. Pain 2001. 17 (Suppl. 4);S86-S93.
52. Zijsltra TR, Barendregt PJ, and van der Laar MA. Venlafaxine in fibromyalgia: results of a randomized placebo-controlled, double blind trial. Arthritis Rheum. 2002. 46, S 105 (Abstract).
53. Dwight MM, Arnold LM, 0'Brien H, et al. An open clinical trial of venlafaxine treatment of fibromyalgia. Psychosomatics 1998. 39;14-17.
54. Sayar K, Aksu G, Ak I, and Tosum M. Venlafaxine treatment of fibromyalgia. Ann. Pharmacother. 2003. 37;1561-1565.
55. Kranzler JD, Gendreau JF, and Rao SG. The psychopharmacology of fibromyalgia: a drug development perspective. Psychopharmacol Bull. 2002. 36(1);165-213.
** Excellent and thorough review of the merits of addressing serotonin and norepinepherine in FMS drug development.
56. Vitton 0, Gendreau M, Gendreau J, Kranzler J, and Rao SG. A double-blind, placebocontrolled trial of milnacipran in the treatment of fibromyalgia. Hum. Psychopharmacol Clin. 2004. Exp. 19; S27-S35.
57. Arnold LM, Lu Y, Crofford LJ, et al: A double-blind multicenter trial comparing duloxetine to placebo in the treatment of fibromyalgia with and without major depressive disorder. Arthritis Rheum. 2004. 50(9);2974-2984.
58. Wernicke JF, Rosen AS, Lu Y et al.: Duloxetine in the treatment of fibromyalgia. Arthritis Rheum. 2004. 50(Suppl. 9), S 1867 (Abstract).
59. MacFarlane JG, Shahal B, Mously C, and Moldofsky H: Periodic K-alpha sleep EEG activity and periodic limb movements during sleep: comparisons of clinical features and sleep parameters. Sleep. 1996. 19(3);200-204.
60. Roizenblatt S, Moldofsky H, Benedito-Silva AA, and Tufik S. Alpha sleep characteristics in fibromyalgia. Arthritis Rheum. 2001. 44(1);222-230.
61. Scharf MB, Baumann M, and Berkowitz DV: The effects of sodium oxybate on clinical symptoms and sleep patterns in patients with fibromyalgia. J. Rheumatol. 2003. 30;1070-1074.
62. Russell IJ, Bennett RM, and Michalek JE. Sodium oxybate relieves pain and improves sleep in Fibromyalgia syndrome [FMS]: a randomized, double-blind, placebo-controlled, multi-centered trial [abstract]. Arthritis Rheum. 2005. 52(12):4110.
63. Holman AJ. Ropinirole, a dopamine agonist, for refractory fibromyalgia: preliminary bbservations. J. Clin. Rheum. 2003. 9(4);277-279.
64. Holman AJ. Treatment of fibromyalgia with the dopamine agonist ropinirole: a 14-week double-blind, pilot, randomized controlled trial with 14-week blinded extension. Arthritis Rheum. 2004. 50(9);S698 (Abstract).
65. Data on file GlaxoSmithKline.
66. Yunus M, and Aldag J: Restless legs syndrome and leg cramps in fibromyalgia syndrome: a controlled study. Br. Med. J. 1996. 312;1339.
* Important paper describing restless legs syndrome in FMS.
67. Lopez JF, Akil H, Watson SJ: Neural circuits mediating stress. Biol. Psychiatry 1999. 46(11);1461-1471.
68. Wood PB. Fibromyalgia syndrome: a central role for the hippocampus - a theoretical construct. J Musculoskeletal Pain. 2004. 12(1);19-26.
** Critically important paper for those interested in FMS pathogenesis.
69. Wood PB, Hill AL, Featherstone L, and Patterson JP. Hippocampal metabolite abnormalities in fibromyalgia and their symptom correlates. J Musculoskeletal Pain. 2004. 12, S73 (Abstract).
70. Glabus MF, Hill AL, Featherstone L, and Wood P. Brain structural abnormalities and their symptom correlates in fibromyalgia syndrome. Neuroimage. 2004, CD-ROM. Proceedings of the 10th International Conference on Functional Mapping of the Human Brain, Poster TU 342 (Abstract).
71. Lin SC, Kaplan J, Burger CD, and Fredrickson PA. Effect of pramipexole in treatment of resistant restless legs syndrome. Mayo Clin. Proc. 1998. 73(6); 497-500.
72. Holman AJ. Pramipexole and fibromyalgia: promise and precaution. J.Rheumatol. 2003. 30(12);2733.
73. Holman AJ, Neiman RA, and Ettlinger RE. Preliminary efficacy of the dopamine against, pramipexole for fibromyalgia: the first, open label, multicenter experience. J Musculoskeletal Pain. 2004. 12(1);69-74.
74. Holman AJ and Myers RR. A randomized, double-blind, placebo-controlled trial of pramipexole, a dopamine agonist, in patients with fibromyalgia receiving concomitant medications. Arthritis Rheum. 2005. 52(8);2495-2505.
Last updated on: May 16, 2011


text:
Jeanine Taylor
Located in Sanford's historic Hotchkiss Building.
Exterior facade installed by the late Mr. Imagination.
QUESTIONS or REQUESTS?
info@jtfolkart.com
Or use the contact form and we will be in touch.
The Historic Hotchkiss Building
The Hotchkiss building that Jeanine Taylor Folk Art moved into in 2005 was a far cry from its original form. Rebuilt after the Great Fire in 1887, the historic Hotchkiss building has become an easily recognizable landmark in Downtown Sanford. Built in the style of Romanesque Revival, local legend has it that rubble from the initial structure was salvaged and used in the re-construction of the iconic pediment on the corner of the building. Manuel Jacobson's Department Store was the building's most notable past inhabitant.

redpajama_set_name: RedPajamaCommonCrawl


Ace, 1983. Cover by Jodi Penalva. Out of print. All the stories in this collection have been reprinted in Spicy Adventures (REH Foundation Press, 2011), and restored to Howard's original typescripts where possible.


text:
Infinity Wars => Cards and Factions => General Game Discussion => Flame Dawn => Topic started by: JSlayerXero on August 02, 2014, 12:56:18 AM
Title: Aberion's Banner
Post by: JSlayerXero on August 02, 2014, 12:56:18 AM
During this thread: http://forum.lightmare.com.au/index.php?topic=61967.0 I found that Aberion's Banner only gives +5/+5 when attacking and stops after the attack is over... Except it's worded until the end of the turn. I can understand that the attacker dies once the Banner wears off if it took far too much damage, but the banner might as well just be a +5 period if it's going to reset every turn. The only practical use I can think of to making it increase health is to shrug off infect. Again though, it's worded wrong.
Do you think they should change the wording to reflect the effect, change the effect to reflecting the wording, or do something completely different, since Aberion's thing is being invincible while attacking?
Title: Re: Aberion's Banner
Post by: Swiftwynd on August 02, 2014, 04:34:17 AM
Another fun wording inconsistency is Shrine to the Heavens.
It state directly that "you win the game" but it only really insures that the opponent loses all morale,without doing anything to prevent a tie. It either needs to be reworded to morale loss or changed to fully restore the users health and morale by an insane amount to prevent the tie.
Post by: Thechynd on August 02, 2014, 11:31:50 AM
Agree that the description on Aberion's Banner is misleading and the +5 health winds up irrelevant 99% of the time. They should just not have it give health at all if that's how they want it to work. Also you can't really have Shrine to the Heavens prevent a tie completely unless you decide that in the case of both players achieving it on the same turn the winner depends on initiative.
Post by: Abyss on August 02, 2014, 11:32:23 PM
Aberion's Banner would also buff something with Unstoppable, which is likely the intended interaction for it giving + Health. After all, there's at least one Unstoppable character in faction.
Post by: Nehkrimah on August 03, 2014, 02:09:18 AM
the banner's health also works with multistrike to help keep it alive for the additional attacks
Except, unless they changed it, it's pointed out in the thread I linked to that it only works for the attack, and not like Bloodthrist. After the attack is over, that character loses the +5 Health on top of Toughness. This means that the health is only useful if stop something from being infected when it dies. So if my 1 HP character gets +5 and rams into a guy with 1 attack, he dies after the attack ends because my character has its health dropped down to 0. While I would've thought it would be useful for Unstoppable and Multistrike, unless changed at some point, both of you understood how it works incorrectly, as did I. I don't own the card, I can only go off of what I was told. If you guys know it works like that, I'll freely admit I have no idea what I'm talking about.
Post by: Abyss on August 03, 2014, 08:26:00 AM
Ah, so you're saying it stops work after the first attack resolves, rather than after 'the attack step' or whatever it's called. And then presumably reactivating for additional attacks, but wouldn't be enough to save the character.
Truth is, I haven't tried it, but now I want to give it a go.
Post by: DrayGon777 on August 04, 2014, 04:59:57 AM
I might be wrong. It may buff up multiple times. I can't say I've tried it personally. It's something worth checking out. It was just my understanding that it went away after the attack, but it's been a while since I used the card.
Post by: Nehkrimah on August 04, 2014, 12:36:42 PM
Just given it a test, the buff applies once, and lasts until the end of the attack phase.
It does work with Multistrike and Unstoppable to help keep the creature alive until end of attack phase.
Post by: JSlayerXero on August 04, 2014, 12:52:53 PM
*insert I have no idea what I was talking about* Well then... A shame there's still not too many uses for it that I can think of though. I mean, yes, it's useful with multistrike and unstoppable, but unless it does work like temporary hit points, then the character will die from going beyond its regular HP toughness once the attack phase ends. So, deflecting Infect and killing slightly more characters before dying... *shrugs*
Post by: stardustdragon258 on October 09, 2014, 12:09:59 AM
I like bromic's banner more, it is more flame-dawn-like giving everything in the assault zone +2/+0.
Aberions banner's effect is actually really weird on a flame dawn card...
Post by: Deadguy on October 09, 2014, 01:56:29 AM
Quote from: stardustdragon258 on October 09, 2014, 12:09:59 AM
Yeah, attacking alone isn't really very flame dawn-ey. More of a Warpath thing.


2016 Officers Wanda Wright, Secretary; Michael Moore, Vice President; John Wright, Outgoing President; Lois Weiss, President; and Debra Halling, Treasurer.
Current officers for SCTAL are: Lois Weiss, President; Michael Moore, Vice-President; Debra Halling, Treasurer; and Dianne Appelt, Secretary.
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text:
Diane Lee Wilson, Author, DK Publishing, Author DK Publishing (Dorling Kindersley) $16.95 (244p) ISBN 978-0-7894-6802-4
I Rode a Horse of Milk White Jade
Raven Speak
Fans of Wilson's gripping debut novel, I Rode a Horse of Milk White Jade, may be disappointed in her latest horse tale, set in 640 B.C. Assyria. As the novel opens, 13-year-old Soulai broods over his negligence in allowing a lion to claim one of the goats in his family's herd; he was too busy sculpting clay horses to notice the predator. That same day, the burning lamp he had used to admire his sculptures causes a fire that destroys his family's home, as well as some expensive pieces that his father, a harness maker, was working on. His father sees no choice but to offer Soulai in payment to Jahdunlin, whose harnesses were destroyed; Jahdunlin in turn sells Soulai to the Assyrian prince Habasle to work as a stable hand. Unfortunately, neither Soulai nor Habasle is a character readers will sympathize with; Soulai is careless, Habasle cruel, and the journey through the lengthy novel grows tiresome. The setting here is not as tactile as 14th-century Mongolia was in Wilson's previous novel; even Ti, the central horse character, is weak-willed and unlikable. The author seems to set up a prince/pauper situation with repeated references to the likeness of slave owner and slave, yet nothing ever comes of it. The change of heart in Soulai, Habasle and Ti (and other minor characters, such as the royal stable master, Soulai's supervisor) comes too belatedly and unconvincingly to hold most readers' attention. Ages 9-up. (Oct.)


text:
Q: Adding custom jquery to meanjs yeoman generator I would like to know if there is a way to include custom jquery to the meanjs yeoman generator.   The public folder has serval sub-folders and files in it that seem to be there only for including angular and css files. I am not sure where a custom jquery file should go and how it should be wired up to the rest of the app.

A: If you add the script into the folder public/lib/ then if you go to the config/env/all.js and open that file there will be an assets section in there you will then need to add public/lib/name of jquery file.js to that array of javascript files. It should look something like the below
assets: {
    lib: {
        css: [
            'public/lib/bootstrap/dist/css/bootstrap.css',
            'public/lib/bootstrap/dist/css/bootstrap-theme.css',
        ],
        js: [
            'public/lib/angular/angular.js',
            'public/lib/angular-resource/angular-resource.js',
            'public/lib/angular-cookies/angular-cookies.js',
            'public/lib/angular-animate/angular-animate.js',
            'public/lib/angular-touch/angular-touch.js',
            'public/lib/angular-sanitize/angular-sanitize.js',
            'public/lib/angular-ui-router/release/angular-ui-router.js',
            'public/lib/angular-ui-utils/ui-utils.js',
            'public/lib/angular-bootstrap/ui-bootstrap-tpls.js',
            // Add yours here
        ]
    }
 }

I hope this helps.

redpajama_set_name: RedPajamaStackExchange


text:
Lindsey Buckingham Talks Fleetwood Mac Tour, New EP
'Stevie and I have probably more of a connection now than we have in years'
By ANDY GREENE
It's been exactly a decade since Fleetwood Mac released a full album, but that hasn't stopped a new generation of fans from discovering the band. "We're doing the best business we've done in 20 years," guitarist Lindsey Buckingham tells Rolling Stone a few hours before the Tulsa, Oklahoma stop on the band's latest tour. "There seems to be a cyclical re-igniting of interests, and there's certainly a lot more young people out there than three years ago."
Months before they started tour rehearsal, the band cut a four-song EP titled Extended Play with producer Mitchell Froom. "When we finally decided this was going to be the year we were going to tour again, I thought it would be great to cut some new stuff," says Buckingham. "I knew we wouldn't have time to cut a new album. Stevie [Nicks] was still caught up in her solo thing, but I got John [McVie] and Mick [Fleetwood] over from Hawaii. They played their asses off. It was a great experience."
Stevie Nicks arrived at the sessions towards the end, and Buckingham presented her with "Sad Angel." "I wrote that song for Stevie," he says. "She always had to fight for everything. She was coming off a solo album and was in the process of reintegrating herself mentally in the band, and we're all warriors with a sword in one sort or another. She and I have known each other since high school. So I just wrote, 'Sad Angel have you come to fight the war/We fall to earth together, the crowd calling out for more.'"
Read the full interview at Rolling Stone
Like many of the group's greatest songs, "Sad Angel" reflects on Lindsey and Stevie's complex relationship. "All these years later, we are still writing songs that are dialogues for each other," he says. "That was part of the appeal of Rumours, and of the group in general . . . Of all the things we cut, 'Sad Angel' was, for lack of a better term, the most Fleetwood Mac-y. It was really kind of the best stuff that we have done in a while."
They also recorded "Without You," a song that's roughly 40 years old. "Stevie and I had a little disagreement over when it was written," Buckingham says. "It definitely predates our involvement in Fleetwood Mac. I believe it was written when we were in the process of culling material for a possible second Buckingham-Nicks album, before we were dropped by Polydor. She claims it was written earlier, but I'm not so sure. But it's a very sweet song that really harkens back to a time when we were far more innocent. She's writing to me and it's about our relationship, when we'd only been together for a very short time."
Stevie Nicks says that she rediscovered the song on YouTube. "I'm not really sure how it resurfaced," says Buckingham. "She brought it in one day and she brought it by my house. John and Mick didn't really work on that. There's kind of an appropriateness in doing something that predates Fleetwood Mac, because at this stage in time Stevie and I have more of a connection than we've had for a while. That's a nice thing."
"Sad Angel" and "Without You" are performed every night on Fleetwood Mac's ongoing world tour, but the vast majority of the set is devoted to songs from the group's deep catalog. "Creating a set list is like making a running order for an album," says Buckingham. "Certain things get pitted against one another that make more sense. One song sets another one off, or it might diminish it. You're just constantly looking for the next thing that's gonna make sense in a particular place."
The show begins with "Second Hand News," the kick-off track to band's 1976 landmark album Rumours. "It seemed like the obvious choice as the opener," says Buckingam. "There are certain touchstones that you always do. When you've been around for a while, you realize there's a body of work you're going to rely on every time. You're not going to reinvent the wheel every time you go out, because that would disappoint the audience."
After "Second Hand News," the group keeps the Rumours theme going with "The Chain" and "Dreams." "You get that out of the way," says Buckingham. "Then we do 'Sad Angel' and then we're segueing into various twists and turns from there."
A frenetic "Rhiannon" segues into four straight Tusk songs: "Not That Funny," "Sara," "Sisters of the Moon" and "Tusk." "After the success of Rumours, we were in this zone with this certain scale of success," Buckingham says. "By that point the success detaches from the music, and the success becomes about the success. The phenomenon becomes about the phenomenon. Warner Bros. would have very much liked to have seen a Rumours II. There was a need on my part – and the band as well, but I was certainly the instigator – to kind of subvert that notion."
Tusk was a huge bestseller, but the songs were less commercial, failing to live up to the enormous sales of Rumours. "We didn't want to be painted into a corner," Buckingham says. "If you want to be an artist in the long run, it isn't necessarily a good axiom to repeat formulas over and over until they're used up."
The rest of the show focuses on enormous hits like "Gypsy," "Go Your Own Way" and "Gold Dust Woman," but "Don't Stop" is the sole number written by former Mac keyboardist/vocalist Christine McVie. "On the last tour we did 'Don't Stop' and 'Say You Love Me,'" says Buckingham. "But it's hard to sustain her presence. There's no real reason to do it. She had some great songs, but it becomes a little schizoid to go out there and try to recreate her thing."
Christine McVie did participate in Fleetwood Mac's 1997 comeback album The Dance, but she left after the tour. "She was just in need of a radical life change," says Buckingham. "She pretty much burned all her bridges in Los Angeles. She sold her house, ended her relationship, quit the band and moved back to England. It was a fairly sweeping set of changes, and something she needed to do for her reasons, though I'm not particularly clear on what those were."
The group took a break after McVie quit, but regrouped in 2002 to begin work on Say You Will. "We all miss her, and we miss the equation that fivesome made," Buckingham says. "It's a different equation with the four. But for me, it actually opened up an opportunity to be a little more myself onstage. When you divide the material more or less down the middle, it gives me more of a chance to be the guy, and to be the kind of presence and energy I am onstage."
The adjustment has been more difficult for Stevie Nicks. "She misses the female camaraderie," says Buckingham. "So it's been a double-edged sword for her. But as the band evolved as a four-piece, it became less relevant to put songs of hers in there. We haven't felt a need to do that, even though she had some hits. It's just . . . it is what it is. The band is a different band now. On the other hand, 'Don't Stop' is just one of those anthems with a strong message. That's why Bill Clinton latched onto it. It's a very effective encore song for us."
The show wraps with "Say Goodbye," the only song of the night drawn from the group's 2003 LP Say You Will. "As I said, Stevie and I have probably more of a connection now than we have in years," says Buckingham. "You can feel it. It's tangible on stage. In many ways, that song is the embodiment of that. When you look at 'Without You,' it's Stevie writing a song about me when everything was before us and all those illusions were intact. 'Say Goodbye' was written 10 years ago, when most of our experience together was behind us. Part of those illusions had fallen away."
Much of their story may be behind them, but Lindsey and Stevie are still taking the stage together night after night and collaborating on new material. "It was difficult for years to get complete closure," Buckingham says. "There was never any time to not be together. It was kind of like picking the scab off an open wound again and again. That's part of the legacy of the band. But 'Say Goodbye' is a very sweet song, and it's about her: 'Once you said goodbye to me/Now I say goodbye to you.' It took a long time. All those illusions have fallen away, but that doesn't mean that there isn't resolve and hope and belief in the future in a different context. That's really what the song is about, and we end the set with just the two of us singing that song."
Posted by Nickslive at Tuesday, May 07, 2013
Labels: Fleetwood Mac 2013, Fleetwood Mac 2013 Extended Play, Lindsey Buckingham
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Medtech Innovator (MTI) is one of the leading medtech competition and virtual accelerators that consistently delivers phenomenally compelling companies and technologies. Last year's winner was MobileODT, a low cost colposcopy solution using smartphone technology for use in the developing world. Be sure to check out our interview with the CEO of the company.
If you have a medtech startup, this year's winner could be you! Today is the last day to apply to pitch to the MTI panel of judges. Over 300 companies from all over the world have been flying to these pitch sessions to try their hand at qualifying for the competition. At stake are $250k of cash prizes, expert mentorship, high-level networking, and glory.


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Engineering Manager, Identity Platform (Mountain View, CA or US Remote)
Last updated 6 minutes ago
Remote -
Atlassian is continuing to hire with all interviewing and on-boarding done virtually due to COVID-19. All new and existing Atlassians will continue to work from home until it's safe to return to our offices. When our offices re-open, every Atlassian will have the choice to work from an office or from home.
Atlassian is a leading provider of collaboration, development, and issue tracking software for teams around the world. With over 100,000 global customers (including 85 of the Fortune 100) and millions of users on our cloud platform, we are advancing the power of collaboration with products including Jira Software, Jira Service Desk, Confluence, Bitbucket, and more. Motivated by clear values, an AMAZING culture, and consistent revenue growth, we're on a journey to unleash the potential of every team. We'd like you to be a part of this journey.
The Identity Platform division is looking for a passionate engineering manager to lead the runtime-authentication team in our Mountain View, California office. Identity is an innovative and dynamic organization, and in this role you'll lead a team of talented developers in designing, building, and operating micro-services and capabilities that handle billions of API requests daily to authenticate and authorize millions of users and applications. As an engineering leader, you will drive technical excellence in your team as you contribute to evolving key Identity platform services and capabilities to meet the highest standards of reliability, performance and scale. Your greatest responsibility will be looking after the individuals reporting to you – coaching and supporting them in their professional development, unlocking their potential, and challenging them to step outside their comfort zone to grow and excel.
What you'll do...
Collaborate with developers, architects, and product managers across several engineering teams to build new and enhance existing Atlassian Identity Platform services and capabilities
Contribute to the technical and business strategy of the team, including making technical recommendations and functional solutions.
Guide your teams in understanding the right metrics to track and improve.
Provide developers with support: holding regular one on ones, giving context on priorities, collaborating with other teams, unblocking projects, resolving conflicts on the team.
No previous experience in the Identity domain is required. Candidates would benefit from previous experience with building and operating highly scalable micro-services and applications in AWS, and leading high-performing teams.
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We'd love for you to have significant experience as an engineer building large scale distributed systems, experience in leading a team, and experience in growing individual engineers. On your first day, we'll expect you to have:
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2+ years experience in engineering management following Agile development processes.
Experience developing and operating web applications in AWS, Microsoft Azure, Google Cloud or similar public cloud providers.
Prior experience working with large scale distributed systems.
Excellent prioritization and self organizing skills to individually detect and deliver the most important things first.
Outstanding verbal and written communication skills. Proven track record to explain your proposals well enough that others understand their value, are motivated to implement them, and become champions of them for you.
Experience setting a very high bar for excellence across your engineering team, and putting systems in place to measure against that bar.
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Strong skills mentoring, growing, and retaining talent.
Ability to work well in a team, have a positive attitude, patience, and humility.
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Previous experience with authentication and authorization domain, technologies, and protocols.
Previous exposure to web application security (authentication, authorization, session management, access controls, etc.) and privacy standards (SOC2, GDPR, etc.).
Experience in Continuous Delivery and the DevOps attitude.
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More about our benefits
Whether you work in an office or a distributed team, Atlassian is highly collaborative and yes, fun! To support you at work (and play) we offer some fantastic perks: ample time off to relax and recharge, flexible working options, five paid volunteer days a year for your favourite cause, an annual allowance to support your learning & growth, unique ShipIt days, a company paid trip after five years and lots more.
More about Atlassian
Creating software that empowers everyone from small startups to the who's who of tech is why we're here. We build tools like Jira, Confluence, Bitbucket, and Trello to help teams across the world become more nimble, creative, and aligned—collaboration is the heart of every product we dream of at Atlassian. From Amsterdam and Austin, to Sydney and San Francisco, we're looking for people who want to write the future and who believe that we can accomplish so much more together than apart. At Atlassian, we're committed to an environment where everyone has the autonomy and freedom to thrive, as well as the support of like-minded colleagues who are motivated by a common goal to: Unleash the potential of every team.
We believe that the unique contributions of all Atlassians is the driver of our success. To make sure that our products and culture continue to incorporate everyone's perspectives and experience we never discriminate on the basis of race, religion, national origin, gender identity or expression, sexual orientation, age, or marital, veteran, or disability status.
All your information will be kept confidential according to EEO guidelines.
Learn more about Atlassian's culture, interviewing flow, and hiring process by checking out our Candidate Resource Hub.
Company size 1,001-5,000


DMV-based five-piece Sunbathers just released an electric new track called "Sugar." It's an appropriate title for a song that goes down so sweet, largely in part due to falsetto harmonies, twinges of 8-bit like electronic moments and cinematic, pounding drums. "Sugar" is off of an upcoming followup to last year's self-titled debut EP.
"Sugar" represents the clearest definition of our sound to date. Diving deeper into experimentation with both our diverse range of influences and newfound production abilities led us to a song we feel captures our current essence as a band. With more experience under our belts, our approach became much more precise – sometimes almost painstakingly so – fine-tuning drum tones, synth sounds, and vocal melodies. We afforded ourselves more time to pay attention to those minute details we may have rushed over in the past, allowing for a more intentional songwriting process. The resulting song is one we are proud to stand behind as a statement of who we are as a band, as well as where we intend to go.


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An interview with Geoff Kabush - October 30, 2004
An Earth-shattering Kabush
Geoff Kabush is no newcomer to the mountain bike racing scene but his patient and steady approach to getting to the top has made this past season his best yet. Winning the NORBA final and overall series was the pinnacle of the year for the much-loved Canadian rider whose passion for the sport will see him racing his bike for many more years to come. Cyclingnews' Kristy Scrymgeour caught up with Kabush in between his autograph sessions at sponsors booths at Interbike.
Kabush with the SRAM girls at Interbike
Photo: © Cyclingnews
Geoff Kabush
Lives: Vancouver Island, Canada
Turned professional: 1996
Teams: Maxxis Professional MTB team
2004 - Maxxis
NORBA XC series champion
World Champion in XC Teams relay
2nd - Sea Otter
Five NORBA wins
15th - World XC Championships, France
2003 - Kona Clarks Factory Team
2nd - Canadian National CX Championships
Canadian National XC Champion
Five NORBA podiums
16th - World Championships
10th - Commonwealth Games
2001 - Kona Ford Focus
1st - Canada Cup Finals
Four NORBA podiums
2000 - Kona Factory Team
9th - Olympic Games Sydney
2nd - Canada Cup Series
Espoir National Champion
9th - Espoir World Championships
1st - Canada Cup Series
First year as senior elite
Walking around the booths of Interbike this year was like going to a celebration of Canadian mountain biker Geoff Kabush. The orange and black images of the Maxxis rider were everywhere and at many a booth you could catch him for an interview, a chat and perhaps even a beer. Although Kabush modestly laughed saying it was "pretty crazy and a bit over the top," he also admitted that it was "pretty exciting," - and rightly so. After making his big break back in 2000 by making the Canadian Olympic team for Sydney, Kabush has been gradually going from strength to strength and comes away from 2004 after his best season yet.
"I'd rather have a clean sport than one with more money in it."
"Every race this year except for a few I felt awesome, so I really had a great year," he said. The difference between this year and other years? "I've always been going to school and this was the first winter that I was able to totally focus on training. It really made a difference," explained Kabush. "I'm also older and smarter and endurance sports take a long time to build up to a good level. All the work over the years is finally paying off," he added.
Kabush at Waco 2004
Photo: © Mike Gladu/www.velodrome.com
Kabush raced his first year as a senior pro in 1996, each year building up the racing program and doing a little bit more. The year 2000 he calls his breakout with making the Olympic team being a motivator for years to come. But this year on the new Maxxis team Kabush says has been another inspiring year. "Joining a new team has been really motivational," he says. "The whole team and the sponsors have been really excited about it and we've had a lot of fun. Usually being on the road for so many months of the year burns me out but this year we had a great time on the road and I didn't really mind the traveling. At one stage I was away from home for 2 1/2 months at one time, but I just stayed relaxed. The team had a lot of fun this year and that has helped."
Kabush has many victories this year including five wins in NORBA events, a World Championship in the team relay in France and his win in the NORBA final in Durango, which confirmed his overall lead of the series among other. Out of all his successful days the boy from BC in Canada said that Durango was the most exciting. "I knew that it was possible to win the series but I also knew that one mistake and it was all over," he explained. "It was a big relief to win and it was nice to win the race and the overall series because it's nice to show that the top rider won the series overall."
Kabush at Nova Desert Classic 2004
Photo: © Jon Devich/www.epicimages.us
Since he started in the sport, Kabush has been training with a coach from Vancouver Island where he lives and trains. He also credits the island as the place that got him hooked on mountain biking. "Growing up in BC was what really got me into riding. I lived on Vancouver Island, which has great trails and a lot of people really get into it," he said. "I started out in a local club and got pretty hooked. I played a lot of sport at school but the mountain biking lifestyle was what I really got into. It's so much more fun to ride trails than run around a track."
Kabush's coach is Juerg Feldman. "He's originally from Switzerland where he was really involved in speed skating and biathlons," explained Kabush. "It was only when he moved to Canada that he got involved in mountain biking. He has a good background in physiology and we do a lot of scientific training and lactate testing etc and working with a PowerTap. Since the end of '95 has been a slow building process. I'm always learning new things and adding those into the program. He's a great coach. He sets our program and he really teaches us how to implement it well. I've worked with him for so long now that I really understand why we are doing things in a particular way."
Another motivator in Geoff's success this year has been Maxxis team manager Eric Wallace. "He knows that I need to do and he organizes everything. It's exciting. He's always got something going on," said Kabush.
Kabush at Tour de Tunnel 2004
Photo: �: Hyun Lee
Kabush is staying with Maxxis and is currently talking with the team about what his goals will be next year. "The NORBA will be a big focus," he said. "We'll have a lot more people back racing in the US next year not being an Olympic year. I still believe, especially after this year that I have the chance to do well at the World Cup level as well. I know on the right day I can be up there with the top guys."
An exciting development is that next year the Maxxis team is growing and according to manager Eric Wallace, a couple of very talented up-and-coming riders will be joining the team. For Kabush this is great. "It will be fun to have another guy up there for some team tactics," he said.
When asked whether he has plans of eventually switching over to the road as so many mountain bikers have done, Kabush is not sure. "I enjoy mountain biking and I think it will always be my first priority," he said. "I do like racing the road and I was bummed this year that I didn't fit in a road race but I'm sure I'll do a few more next year."
Career wise Kabush says things are looking up for mountain biking. "I certainly wish I was racing back in the glory days, but I love riding and racing," he explained. "Certainly the sponsorship isn't what it used to be, but changes are happening and people are still excited about racing and that's what matters."
On the topic of things looking up, Kabush also talked about the new hope that drugs in sport are being cleaned up. "I'd rather have a clean sport than one with more money in it," he exclaimed. "I used to think they were a long way behind in the battle to clean things up but actually they're doing a good job now at making it a lot harder for people to cheat."
Kabush mounted his own campaign in the war against drugs in sport this year. "All of us started wearing 'Dopers suck' shirts when we were in Aspen," he explained. "We want to let all the young kids coming up know that I'm winning races and I'm not taking drugs. It doesn't help when guys who aren't winning speak up because people just think it's sour grapes, but when guys who are winning speak out against drugs I think it can make a difference. There really is hope for the sport."
In Sea Otter this year, Kabush placed second overall in the hotly contested race that was won by Filip Meirhaeghe who later tested positive for EPO at a World Cup in Canada. "I know at Sea Otter I felt like I could have beaten Filip, so that gives me hope."
For now Kabush is not having an off-season at all. Instead he had a short break and started directly with the cyclocross season. "I had a little break after worlds but I'm still pretty motivated and really into the cross season. I'll take some time off after it's over."
Other Talking Cycling Interviews


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Sports: Adventure Racing, Cycling, Mountain Biking, trail running
Clinton Mackintosh is a world class Adventure Racer competing locally and internationally in the Adventure Racing World Series (ARWS). Clinton is the team captain for the highly successful Cyanosis Adventure Racing team with multiple wins locally and most recently in Paraguay becoming the first SA team to win a World Series event outside of SA….
Clinton Mackintosh is a world class Adventure Racer competing locally and internationally in the Adventure Racing World Series (ARWS). Clinton is the team captain for the highly successful Cyanosis Adventure Racing team with multiple wins locally and most recently in Paraguay becoming the first SA team to win a World Series event outside of SA. Adventure Racing is the ultimate race of human endurance. Teams of four athletes race non-stop, day and night through courses up to 800km in length. Each race is a unique journey including legs of mountain biking, trail running, kayaking and rope work. Teams must navigate using map and compass through remote wilderness checkpoints. They battle not only other teams but extreme fatigue, sleep deprivation and unpredictable weather. Clinton has been a member of the Cyanosis team for the past 13 years and continues to push his limits physically and mentally.
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