Chronic pelvic pain is a troubling condition for many women. The reason for pelvic pain varies but certainly includes endometriosis where the lesions impact upon nerve health and function (see here) with consequential sensitisation. The purported mechanisms of pain include inflammatory pain and neuropathic pain with subsequent central sensitisation that underpins the persistance and variance often described.
Pain is an output, a response to the brain’s perception of what is happening in the body. The sensation of pain emerges from that part of the body deemed in need of protection. The pain itself is modulated by a range of factors including stress, fatigue, anxiety and the environment. The actual feeling of pain is the end result of the brain’s analysis of what is going on ‘now’ on the basis of what it already knows and has learned. Hence, prior experience can flavour the pain. Changes in the spinal cord and higher centres can amplify danger signals, modulate normal signals (begin as normal and communicate with nociceptors, therefore the brain receives a danger signal despite the initiating impulse being one of touch; i.e./ allodynia) and are responsible for the varying patterns of pain such as when a treatment helps on one occasion yet seemingly worsens the pain on a subsequent occasion.
Alongside the painful experience there are other body and brain responses to the perceived threat. Altered control of movement that includes guarding and protective posturing that leads to patterns of on-going chronic tension. In the case of pelvic pain this emerges around the pelvic girdle, in the abdomen and in the spinal muscles and often across the body. It is not unusual to find that there are many tender and tight areas when the body has been protected for some time, demonstrating a more widespread pattern. Often there is sensitivity expressed via other body systems , for example the gastrointestinal system in IBS, headaches, migraine and recurring bladder infections to name but a few. General health can often be impacted upon, with levels of activity diminishing alongside a fear of moving and socialising (a gradual withdrawal from being out with friends and family). This typically leads to a downward spiral affecting mood, self-esteem and manifesting with anxiety in many situations. It is really a ‘hyper-protective’ state physically and mentally where many cues become threatening and hence we protect, sometimes consciously by making choices and frequently automatically or habitually. Breaking this pattern however, is entirely possible.
We are fundamentally designed to change, evolve and grow. When we set the right conditions physically and mentally (and it has to be both), then we can move forward and change our outlook and experience. I know that an individual is going to progress when they start changing their language, metaphor use and at the same time their appearance changes via posture, facial expression and general demeanour. The spark returns.
The optimal approach requires that we consider all the dimensions of pain: physical, cognitive and emotional. This must be integrated and a programme created to meet the unique needs of the person. Concomitant with a range of strategies and training techniques to retrain normal movement, tension patterns, ease pain, tackle stress and anxiety etc, medication can play a role. The efficacy of pain medication is varied and often there are side-effects to consider. A recent study looked at the use of melatonin for endometriosis-associated pain with some very interesting results.
The commentary of Timothy Ness in Pain 154 (2013) 775 summarises the study below: ‘The article by Schwertner et al..demonstrated efficacy of the hormone, melatonin, in the treatment of endometriosis-associated pain…..one of the few medications which have proven useful in the treatment of endometriosis-associated pelvic pain but it is also notable as an example of the back-and-forth translational process associated with preclinical models of pain/analgesia and the clinical demonstration of treatment efficacy.’ And, ‘In this particular example the information flow went in both directions from humans to non-humans and then back again’. He refers to the fact that the data produced in rats was also found in humans. Many studies use rodents as subjects with obvious limitations in terms of extrapolating data for humans.
Efficacy of melatonin in the treatment of endometriosis: a phase II, randomized, double-blind, placebo-controlled trial.
Schwertner A, Conceição Dos Santos CC, Costa GD, Deitos A, de Souza A, de Souza IC, Torres IL, da Cunha Filho JS, Caumo W.
Laboratory of Pain & Neuromodulation at Hospital de Clínicas de Porto Alegre (HCPA)/Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, Brazil.
Endometriosis-associated chronic pelvic pain (EACPP) presents with an intense inflammatory reaction. Melatonin has emerged as an important analgesic, antioxidant, and antiinflammatory agent. This trial investigates the effects of melatonin compared with a placebo on EACPP, brain-derived neurotrophic factor (BDNF) level, and sleep quality. Forty females, aged 18 to 45 years, were randomized into the placebo (n = 20) or melatonin (10 mg) (n = 20) treatment groups for a period of 8 weeks. There was a significant interaction (time vs group) regarding the main outcomes of the pain scores as indexed by the visual analogue scale on daily pain, dysmenorrhea, dysuria, and dyschezia (analysis of variance, P < 0.01 for all analyses). Post hoc analysis showed that compared with placebo, the treatment reduced daily pain scores by 39.80% (95% confidence interval [CI] 12.88-43.01%) and dysmenorrhea by 38.01% (95% CI 15.96-49.15%). Melatonin improved sleep quality, reduced the risk of using an analgesic by 80%, and reduced BNDF levels independently of its effect on pain. This study provides additional evidence regarding the analgesic effects of melatonin on EACPP and melatonin’s ability to improve sleep quality. Additionally, the study revealed that melatonin modulates the secretion of BDNF and pain through distinct mechanisms.
For further information about our proactive treatment, training and coaching programmes for chronic pain and injury, or to book an appointment please call us on 07932 689081 | Women in Pain Clinic in Harley Street
Analgesic and Sedative Effects of Melatonin in Temporomandibular Disorders: A Double-Blind, Randomized, Parallel-Group, Placebo-Controlled Study.
Vidor LP, Torres IL, de Souza IC, Fregni F, Caumo W.
Postgraduate Program in Medical Sciences, Faculty of Medicine, Federal University of Rio Grande do Sul, Porto Alegre, Brazil.
The association between myofascial temporomandibular disorder (TMD) and nonrestorative sleep supports the investigation of therapies that can modulate the sleep/wake cycle. In this context, melatonin becomes an attractive treatment option for myofascial TMD pain.
To investigate the effects of melatonin on pain (primary aim) and sleep (secondary aim) as compared with placebo in a double-blind, randomized, parallel-group trial.
Thirty-two females, aged 20-40 years, with myofascial TMD pain were randomized into placebo or melatonin (5mg) treatment groups for a period of four weeks.
There was a significant interaction (time vs. group) for the main outcomes of pain scores as indexed by the visual analogue scale and pressure pain threshold (analysis of variance; P<0.05 for these analyses). Post hoc analysis showed that the treatment reduced pain scores by -44% (95% CI -57%, -26%) compared with placebo, and it also increased the pressure pain threshold by 39% (95% CI 14%, 54%). The use of analgesic doses significantly decreased with time (P<0.01). The daily analgesic doses decreased by -66% (95% CI -94%, -41%) when comparing the two groups. Additionally, melatonin improved sleep quality, but its effect on pain was independent of the effect on sleep quality.
This study provides additional evidence supporting the analgesic effects of melatonin on pain scores and analgesic consumption in patients with mild-to-moderate chronic myofascial TMD pain. Furthermore, melatonin improves sleep quality but its effect on pain appears to be independent of changes in sleep quality.