You Could Have Asked Me…

New findings published in Arthritis & Rheumatology, a journal of the American College of Rheumatology (ACR), suggest that brain abnormalities in response to non-painful sensory stimulation may cause the hypersensitivity (increased unpleasantness) that patients experience in response to (‘normally’ non-painful) daily visual, auditory and tactile stimulation.

According to the study, patients reported increased unpleasantness in response to multi-sensory stimulation in daily life activities. Furthermore, the fMRI images displayed reduced activation of both the primary and secondary visual and auditory areas of the brain, and increased activation to visual, auditory and tactile stimulation that patients reported to experience in daily life.

191. broken wing

Lead study author, Dr Marina López-Solà from the Institute of Cognitive Science, University of Colorado Boulder said, “Our study provides new evidence that fibromyalgia patients display altered central processing in response to multi-sensory stimulation, which are linked to core fibromyalgia symptoms and may be part of the disease pathology. The finding of reduced cortical activation in the visual and auditory brain areas that were associated with patient pain complaints may offer novel targets for neuro-stimulation treatments in fibromyalgia patients.”


Sleep Searching

As most of us are really, really feeling, non-restorative sleep is a core symptom of FM. What would you give to get a good night’s sleep?

While it seems logical to assume that pain leads to disturbed sleep, there is increasing evidence that dysfunctional sleep leads to hyperalgesia (an increased sensitivity to pain) and allodynia (the experience of pain from a non-painful stimulation of the skin).1 These symptoms are the classical features of FM.2

It cannot be coincidental that FM-like symptoms can be induced in healthy normal people by the deprivation of stage 4 (N3) sleep,3 leading to hyperalgesia, fatigue and bodily hypersensitivity.4  As such, it is reasonable to believe that the improvement of sleep patterns will be beneficial to us.

Sodium oxybate (SXB) is thought to reduce non-restorative sleep abnormalities. SXB is another name for GHB, a substance that is often illegally sold and abused. It is prescribed to prevent attacks of cataplexy (episodes of muscle weakness that begin suddenly and last for a short time) in patients who have narcolepsy (a sleep disorder that may cause extreme sleepiness, sudden uncontrollable urge to sleep during daily activities, and cataplexy). Sodium oxybate is in a class of medications called central nervous system depressants. It has been marketed under the name Xyrem, and is approved in the USA, Canada and Europe for the treatment of symptoms in narcolepsy. The way that SXB works to treat narcolepsy is not known.

Results from a recent international phase 3 trial,5 combined with findings from previous phase 2 and 3 studies, provide supportive evidence that SXB therapy offers important benefits across multiple symptoms in patients with FM.

573 patients with FM (according to the 1990 criteria) were enrolled at 108 centres in eight countries. Subjects were randomly assigned to placebo, 4.5g or 6g of SXB per night. Assessments were made in the areas including reduction in pain, function, sleep quality, effect of sleep on function, fatigue, tenderness, health-related quality of life and the patients’ impressions of change in overall wellbeing.

The proportion of patients who experienced more than or equal to 30% pain reduction was 42.0% for 4.5g SXB and 51.4% for 6g SXB. Quality of sleep improved by 20% for 4.5g SXB and 25% for 6g SXB. Sounds good, right?

Adverse effects included nausea, dizziness, vomiting, insomnia, anxiety, somnolence, fatigue, muscle spasms and peripheral oedema (the swelling of tissues, usually in the lower limbs, due to the accumulation of fluids) in less than 5% of patients. Nothing we haven’t experienced before, right?

So bring on the clinical trials…




  1. Lautenbacher S, Kundermann B, Krieg JC. Sleep deprivation and pain perception. Sleep Med Rev 2006;10:357–69; Kundermann B, Spernal J, Huber MT, et al. Sleep deprivation affects thermal pain thresholds but not somatosensory thresholds in healthy volunteers. Psychosom Med 2004;66:932–7; Roehrs T, Hyde M, Blaisdell B, et al. Sleep loss and REM sleep loss are hyperalgesic. Sleep 2006;29:145–51; and Moldofsky H. Rheumatic manifestations of sleep disorders. Curr Opin Rheumatol 2010;22:59–63.
  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 Rheum1990;33:160–72.
  3. Moldofsky H, Scarisbrick P, England R, et al. Musculosketal symptoms and non-REM sleep disturbance in patients with “fibrositis syndrome” and healthy subjects. Psychosom Med 1975;37:341–51.
  4. Roehrs T, Hyde M, Blaisdell B, et al. Sleep loss and REM sleep loss are hyperalgesic. Sleep 2006;29:145–51.
  5. Spaeth M, Bennett RM, Benson BA, Wang YG, Lai C and Choy EH. ‘Sodium Oxybate Therapy Provides Multidimensional Improvement in Fibromyalgia: Results of an International Phase 3 Trial.’