Category Archives: Pelvic Pain

26Oct/14
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Pelvic pain in men

Pain is a whole person experience

Pain is a whole person experience

Many men experience chronic pelvic pain that significantly affects their lives. When we talk of pelvic pain, we often think about women and their suffering, however, this problem is one that besets both sexes and hence we must encourage all who endure such pain to seek help. As with any persisting pain state, pelvic pain impacts upon the way we think, the way we act and the decisions we make, thereby intruding on quality of life.

There are many reasons why men can suffer pelvic pain. To identify all the causes is not the purpose of this blog, but rather to highlight the problem and provide an insight into how the body becomes stuck in a protective mode. This is the experiential dimension, the story that is told and the narrative that provides all the clues. For the pelvic pain itself is downstream, and with chronic pain we must also go upstream to look at the context within which the pain is happening.

Most people who come to see me do not have pathology or ‘damage’ that justifies the pain response that they suffer. Some have nothing of note at all as shown by scans and other tests. Understanding that you can be in pain without an injury is an important step towards changing pain — for those new to this notion, consider phantom limb pain for a moment. Often there is a start point that involves inflammation, which shifts the body into protect mode. Protect mode involves many body systems, conscious and unconscious behaviours (the latter being habits and conditioned responses). When the body is protecting itself, the area needing attention and defending will hurt, but we also move differently and think differently — if you have a painful ankle, you may think twice about ‘popping’ out to the shop for a paper.

In many cases, these protective responses die down as healing progresses. However, this does not always happen, and with statistics suggesting that 20% of the population suffer chronic pain, many continue to experience protection despite the tissues healing — pain, tension, a different sense of the body (there are many other feelings and sensations described to me, and I encourage this narrative so that I can fully appreciate the story). My thinking about this on-going protection is that the body senses all is not as well as it should be. In other words, the individual is not fully fit, the tissues (muscles, joints etc) are not entirely healthy, behaviours are not orientated towards health, and lifestyle factors in which pain is embedded have not been addressed satisfactorily. This is a huge topic to address at another time, but suffice to say, as much as pain is multi-factoral, so is recovery, which is why a programme to change pain must address the biology of pain and all the influences upon this biology (they are also biology!).

Back to the pelvis, an area full of muscles, nerves, blood vessels, ligaments and other soft tissues. From the pelvis ‘hang’ the legs, and on top sits the trunk. And let’s not forget the genitals, and both their importance and necessary sensitivity. The deep tension and pain that one feels in this region is truly visceral, radiating out into the groin and abdomen, accompanied by an awful tension and pulling in the muscles and testicles. Once the pelvis is grabbing your attention, it can be hard to distract yourself without learning how to change body tension.

Tim Parks - Teach us to sit stillIn this very personal tale of pelvic pain, Tim Parks describes his own journey via the book he wrote, “Teach us to sit still”. It’s a wonderful read for so many reasons, and I frequently encourage patients to tuck in. For me though, the bottom line is that Tim has validated a problem that needs addressing in a comprehensive manner, because so often there is no serious pathology despite the significance of the suffering. Getting to grips with this is part of moving forward and should be embraced. We do not need pathology to hurt. There are other reasons, one of which includes, as Tim says, sitting on your pelvis for 20 years and being stressed — this is by far enough to cause nasty pelvic pain!

What do you do when you are stressed? Tense muscles. This has an energy cost and impacts on the way oxygen is delivered to those very muscles. Consider exercising a muscle over and over. It hurts. It is exactly the same in the pelvis that you may be parked (no pun intended Tim!) on for extended periods of time. “I don’t get stressed” you may say. First of all, I don’t believe you (sorry!), because we all stress out at times and secondly, most of the time we are unaware of what our body is doing in response to our thoughts, environment and what we are doing; that is until it is too late — ooh, my ____ hurts because I haven’t moved for ____ hours (fill in the gaps).

So, what can we do. What do we need to do. Here are a few things that I believe are fundamental to changing what your body is doing:

  • Understand your pain and condition — that’s your clinician’s job, to help you.
  • Create awareness of how your body is responding rather than being on autopilot and then fire-fighting when it gets too much.
  • Think about what the body needs — oxygen to the tissues, especially nerves that become very grumpy when the supply drops (numb bum from being sat too long) — and make sure you do enough to nourish the muscles: move and breathe!
  • Go upstream of the pelvic pain, and look long and hard at your lifestyle and environments — e.g. How are you doing things? Where are you doing things? What habits can you release and change?

Chronic pain is a huge and costly global problem. The main reason why this is true is because of misunderstandings and the low expectations of successfully overcoming the condition (patients and clinicians) because the focus is upon treating ‘structures’ deemed to cause pain. Pain is not a structure, hence why this approach fails. The science of pain has moved forward hugely over the past 10 years and continues to deliver a new understanding. This new understanding challenges existing thinking, and it needs to. Pioneers of pain are hard at work and are finding ways to reduce suffering, and we can. It starts with a change of thinking based on new knowledge. Your knowledge that is translated into effective action.

If you are suffering pelvic pain, get in touch and start your programme to overcome your pain — call us now 07518 445493 — Specialist clinic in London and Surrey for chronic pain & persisting pain

 

13Aug/13
Endometriosis & melatonin | Women and pain series

Endometriosis & Melatonin | Women and Pain Series

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.

Pain. 2013 Jun;154(6):874-81. doi: 10.1016/j.pain.2013.02.025. Epub 2013 Mar 5.

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.

Source

Laboratory of Pain & Neuromodulation at Hospital de Clínicas de Porto Alegre (HCPA)/Universidade Federal do Rio Grande do Sul (UFRGS), Porto Alegre, Brazil.

Abstract

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

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J Pain Symptom Manage. 2012 Nov 27. 

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.

Source

Postgraduate Program in Medical Sciences, Faculty of Medicine, Federal University of Rio Grande do Sul, Porto Alegre, Brazil.

Abstract

CONTEXT:

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.

OBJECTIVES:

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.

METHODS:

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.

RESULTS:

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.

CONCLUSION:

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.

10Jul/13

Women and Pain Clinic @ 132 Harley Street

The Women and Pain clinic is dedicated to providing contemporary treatment, training and coaching for females who suffer persisting pain.

Common examples of on-going painful problems include:

  • pelvic pain: including pain from endometriosis, bladder problems, muscular spasm & guarding of the pelvis and abdominal area
  • back pain
  • joint pain (often multiple)
  • abdominal pain (irritable bowel syndrome or similar sensitivities)
  • migraine & headache
  • jaw pain & dysfunction
  • fibromyalgia

It is not uncommon for there to be several painful areas that are seemingly unrelated. However, with the advancing understanding of the neurobiology of pain, we know that there is a common thread that ties these problems together. This is termed central sensitisation and refers to adaptations within the nervous system that both amplify pain and reduce our natural ability to dampen sensitivity. The body areas that hurt can expand and involve a range of body systems, hence why the pain can manifest in different regions and organs. The pain is an expression of this underlying sensitivity that needs to be targeted at a nervous system-immune system-endocrine system level as well as addressing the health of the body tissues. We use a contemporary and neuroscience-based programme of treatment, training and coaching to tackle the problem of pain, focusing upon the inter-related dimensions of pain: physical-cognitive-emotional.

Working closely with leading gynaecologists and gastroenterologists in Harley Street, you will have a detailed assessment that includes diagnostics as indicated, a full explanation of the nature of the pain and symptoms (pain education) and a comprehensive treatment programme designed for you. 

How do we treat these problems?

A pathological or structural basis for pain only explains part of the problem or in some cases not at all. It is the adaptations within body systems that create the pain experience to which we respond in thought and action. Whilst acute pain serves a vital survival purpose, drawing our attention to a body region that needs protecting for healing, a persisting pain becomes increasingly about the neuroimmune system and endocrine system responses. Pain certainly emerges from the body yet there is an underpinning correlate of activity within a vast network of brain cells that actually drives the experience. This network monitors the activity in the body systems and responds according to need. The response can be protective when the brain perceives the body to be in potential danger and includes pain, changes in movement and a range of other actions. In the early stages of a condition this is useful and adaptive, however if these responses continue beyond a useful time they themselves must be targeted alongside body nourishing strategies.

How can we target these systems? In an integrated manner, these systems can be re-trained with a range of sensorimotor techniques, specific exercises designed to restore a normal sense of the body and movement, strategies to deal with stress and anxiety that both affect the body systems, techniques for the progression of day to day living (work, home, sports), and general activity and exercise with confidence. Interlaced with these strategies, pain education (reduce the threat by developing your understanding of pain and the body’s ability to change), mindfulness-based stress reduction, focused attention training, resilience, coping and motivational skills, are used to optimise outcomes that are based upon improving your quality of life, sense of wellness and performance.

For further information, to book an appointment or to refer a patient please call us on 07932 689081

05Nov/12
Endometriosis & melatonin | Women and pain series

Women and pain | Part 1

‘As many as 50 million American women live with one or more neglected and poorly understood chronic pain conditions’ 

Generally I see more female patients than male. This observation supports the view that chronic pain is more prevalent in women than in men for some conditions – see the International Association for the Study of Pain fact sheet here. There are some ideas as to why this may be, including the role of the sex hormones and psychosocial factors such as emotion, coping strategies and roles in life. Additionally, experimental studies have shown that women have lower pain thresholds (this is a physiological reading) and tolerance to a range of pain stimuli when compared to men although this does not clarify that women actually feel more pain – see here. Pain is a subjective experience of course, and modulated by many factors.

A campaign for women’s pain | Chronic pain in women (2010) report

It is not uncommon for a female patient to tell me about her back pain and continue the narrative towards other body areas that hurt and cause problems. This may include pelvic pain, migraine, headache, irritable bowel syndrome, chronic knee pain, widespread sensitivity and gynaecological problems (including dysmenorrhoea, endometriosis and difficulty conceiving). These seemingly varied conditions are typically looked after by a range of medical and surgical disciplines: gynaecology, neurology, rheumatology, gastroenterology and orthopaedics. More recent science and thinking has started to join the dots on these problems, offering new insight into the underpinning mechanisms and more importantly approaches that can affect all the conditions in a positive way. This is certainly my thinking on this hugely significant matter.

Reconceptualising pain

Undoubtedly pain is complex. This is particularly the case when pain persists, disrupting and impacting upon life. Reconceptualising pain according to modern neuroscience is making a real difference to how we think and treat pain – see this video. Briefly, thinking of pain as an output from the brain as a result of a complex interaction of circumstance, biology, thought, emotion and memory begins to give an insight into the workings of the brain and body. Pain is individual, it is in the ‘now’ but so coloured by the past and what it may mean to the individual. The context or situation in which the pain arises is so very important. We talk about pain from the brain but of course we really feel it in our physical bodies, but the location is where the brain is projecting the sensation – see this video.

Neuroscience has shown us that the danger signals from the body tissues are significantly modulated by the brain before the end output is experienced. Factors that influence the messages include attention, expectation and the circustance in which the individual finds herself. We have powerful mechanisms that can both facilitate and inhibit the flow of these signals and these reside within the brain and brain stem. For this reason we must consider the person’s situation, their expectations, hopes, goals, past experiences and current difficulties, and how these can affect their current pain.

Stress & emotion

Any hugely emotive issue within someone’s life can impact enormously upon pain and sensitivity. This can be the stress of a situation including caring for a relative, losing someone close, work related issues and divorce. The problem of conception certainly features in a number of cases that I see, causing stress and turmoil for both partners but clearly in different ways. Fertility receives a great deal of attention in the media and there are a many clinics offering treatment and therapies, in effect raising awareness and attention levels towards the problem. The pain caused by difficulties having children can manifest physically through the stress that is created by the situation. Thoughts, feeling and emotions are nerve impulses in the brain like any other and will trigger physical responses including tension. Stress physiology affects all body systems, for example the gastrointestinal system (e.g./ irritable bowel), nervous system (e.g. headaches, back pain) and the immune system (e.g. repeated infections).

Lifestyle

Lifestyle factors play a significant role in persisting pain. Modern technology and habits that we form easily may not be helpful when we have a sensitive nervous system. For example, sedentary work, the light from computer screens, pressures at work, limited exercise, poor diet, binge drinking and smoking to name but a few. All are toxic in some way as can be our own thinking about ourselves. When we have a thought, and we have thousands each day, and we pay attention, becoming absorbed in the process, the brain reacts as if we are actually in that situation. Consequently we have physical and emotional responses that can be repeated over and over when we dwell on the same thinking. This is rumination and is likely due to ‘hyper-connectivity’ between certain brain areas – see here. We can challenge this in several ways including by changing our thinking and using mindfulness, both of which will alter brain activity and dampen these responses. It does take practice but the benefits are attainable for everyone.

In summary, the underlying factors that must be addressed are individual and both physical and psychological. Pain is complex and personal, potentially affecting many different areas of life. How we live our lives, what we think and how we feel are all highly relevant in the problem of pain as borne out of sensible thinking and the neuroscience of pain. Understanding the pain, learning strategies to reduce the impact, receiving treatment that targets the underlying mechanisms, making healthy changes to lifestyle and developing good habits alongside the contemporary brain based therapies can make a huge difference and provide a route forwards.

For information on our ‘join the dots’ treatment programmes for chronic pain, contact us here or call 07932 689081

 

29Oct/12
The brain changes in pain

The brain changes

The nervous system is plastic meaning that it changes and moulds according to the stimuli presented. Norman Doidge wrote about the ‘brain that changes itself’ and we have seen over the past 10 years or so an increasing number of studies that show this in a range of conditions, some painful and others not. Our ability to change and adapt have been a vital characteristics for our survival and to learn new skills. The same principles apply when we think about rehabilitation and treatment of painful conditions. We need to tap into these properties and stimulate the brain and other body systems (e.g. immune system, neuroendocrine) so that we are creators of health manifesting physically through normal movement, function and optimal performance.

Here are some examples of studies that have shown brain changes using functional MRI. You will note the variety that includes rheumatoid arthritis, osteoarthritis, pain, chronic pelvic pain, schizophrenia and fibromyalgia. This has serious implications for treatment in that we need brain focused therapies as well as those that target the tissues and end-organs. This includes the absolute need to explain pain and symptoms from a neuroscience perspective.

Arthritis Rheum. 2012 Feb;64(2):371-9. doi: 10.1002/art.33326.

Structural changes of the brain in rheumatoid arthritis.

Wartolowska K, Hough MG, Jenkinson M, Andersson J, Wordsworth BP, Tracey I.

Abstract

OBJECTIVE: To investigate whether structural changes are present in the cortical and subcortical gray matter of the brains of patients with rheumatoid arthritis (RA).

METHODS: We used two surface-based style morphometry analysis programs and a voxel-based style analysis program to compare high-resolution structural magnetic resonance imaging data obtained for 31 RA patients and 25 age- and sex-matched healthy control subjects.

RESULTS: We observed an increase in gray matter content in the basal ganglia of RA patients, mainly in the nucleus accumbens and caudate nucleus. There were no differences in the cortical gray matter. Moreover, patients had a smaller intracranial volume.

CONCLUSION: Our results suggest that RA is associated with changes in the subcortical gray matter rather than with cortical gray matter atrophy. Since the basal ganglia play an important role in motor control as well as in pain processing and in modulating behavior in response to aversive stimuli, we suggest that these changes may result from altered motor control or prolonged pain processing. The differences in brain volume may reflect either generalized atrophy or differences in brain development.

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Am J Psychiatry. 2002 Feb;159(2):244-50.

Volume changes in gray matter in patients with schizophrenia.

Hulshoff Pol HE, Schnack HG, Bertens MG, van Haren NE, van der Tweel I, Staal WG, Baaré WF, Kahn RS.

Abstract

OBJECTIVE: Schizophrenia is generally characterized by a progressive decline in functioning. Although structural brain abnormalities, particularly decrements in gray matter volume, are considered important to the pathology of schizophrenia, it is not resolved whether the brain abnormalities become more prominent over time.

METHOD: Magnetic resonance brain images from 159 patients with schizophrenia and 158 healthy comparison subjects between 16 and 70 years of age were compared. Using linear regression analysis, the authors analyzed the relationship between the volumes of the total brain, gray and white matter, cerebellum, and lateral and third ventricles with patient age.

RESULTS: Total brain (-2.2%), cerebral gray matter (-3.3%), prefrontal gray matter (-4.4%), and prefrontal white matter (-3.5%) volumes were smaller, and lateral (27%) and third (30%) ventricle and peripheral CSF (11%) volumes were larger in schizophrenia patients. A significant group-by-age interaction for gray matter volume was found, as shown by a steeper regression slope between age and gray matter volume in patients (-3.43 ml/year) than in healthy comparison subjects (-2.74 ml/year).

CONCLUSIONS: The smaller brains of the patients with schizophrenia can be explained by decreases in gray matter volume. Moreover, the finding that the smaller gray matter volume was more pronounced in older patients with schizophrenia may suggest progressive loss of cerebral gray matter in schizophrenia patients.

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Psychosom Med. 2009 Jun;71(5):566-73. Epub 2009 May 4.

Decreased gray matter volumes in the cingulo-frontal cortex and the amygdala in patients with fibromyalgia.

Burgmer M, Gaubitz M, Konrad C, Wrenger M, Hilgart S, Heuft G, Pfleiderer B.

Abstract

OBJECTIVE: Studies in fibromyalgia syndrome with functional neuroimaging support the hypothesis of central pain augmentation. To determine whether structural changes in areas of the pain system are additional preconditions for the central sensitization in fibromyalgia we performed voxel based morphometry in patients with fibromyalgia and healthy controls.

METHODS: We performed 3 Tesla magnetic resonance imaging of the brain in 14 patients with fibromyalgia and 14 healthy controls. Regional differences of the segmented and normalized gray matter volumes in brain areas of the pain system between both groups were determined. In those areas in which patients structurally differed from healthy controls, the correlation of disease-related factors with gray matter volumes was analyzed.

RESULTS: Patients presented a decrease in gray matter volume in the prefrontal cortex, the amygdala, and the anterior cingulate cortex (ACC). The duration of pain or functional pain disability did not correlate with gray matter volumes. A trend of inverse correlation of gray matter volume reduction in the ACC with the duration of pain medication intake has been detected.

CONCLUSIONS: Our results suggest that structural changes in the pain system are associated with fibromyalgia. As disease factors do not correlate with reduced gray matter volume in areas of the cingulo-frontal cortex and the amygdala in patients, one possible interpretation is that volume reductions might be a precondition for central sensitization in fibromyalgia.

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Brain. 2008 Dec;131(Pt 12):3222-31. Epub 2008 Sep 26.

Working memory performance is correlated with local brain morphology in the medial frontal and anterior cingulate cortex in fibromyalgia patients: structural correlates of pain-cognition interaction.

Luerding R, Weigand T, Bogdahn U, Schmidt-Wilcke T.

Abstract

Fibromyalgia (FM) is a disorder of unknown aetiology, characterized by chronic widespread pain, stiffness and sleep disturbances. In addition, patients frequently complain of memory and attention deficits. Accumulating evidence suggests that FM is associated with CNS dysfunction and with an altered brain morphology. However, few studies have specifically investigated neuropsychological issues in patients suffering from FM. We therefore sought to determine whether neuropsychological deficits found in FM patients may be correlated with changes in local brain morphology specifically in the frontal, temporal or cingulate cortices. Twenty FM patients underwent extensive testing for potential neuropsychological deficits, which demonstrated significantly reduced working memory and impaired non-verbal long-term memory (limited to free recall condition) in comparison with normative data from age- and education-matched control groups. Voxel-based morphometry (VBM) was used to evaluate for potential correlations between test results and local brain morphology. Performance on non-verbal working memory was positively correlated with grey matter values in the left dorsolateral prefrontal cortex, whereas performance on verbal working memory (digit backward) was positively correlated with grey matter values in the supplementary motor cortex. On the other hand, pain scores were negatively correlated with grey matter values in the medial frontal gyrus. White matter analyses revealed comparable correlations for verbal working memory and pain scores in the medial frontal and prefrontal cortex and in the anterior cingulate cortex. Our data suggest that, in addition to chronic pain, FM patients suffer from neurocognitive deficits that correlate with local brain morphology in the frontal lobe and anterior cingulate gyrus, which may be interpreted to indicate structural correlates of pain-cognition interaction.

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Pain. 2012 May;153(5):1006-14. Epub 2012 Mar 2.

Changes in regional gray matter volume in women with chronic pelvic pain: a voxel-based morphometry study.

As-Sanie S, Harris RE, Napadow V, Kim J, Neshewat G, Kairys A, Williams D, Clauw DJ, Schmidt-Wilcke T.

Abstract

Chronic pelvic pain (CPP) is a highly prevalent pain condition, estimated to affect 15%-20% of women in the United States. Endometriosis is often associated with CPP, however, other factors, such as preexisting or concomitant changes of the central pain system, might contribute to the development of chronic pain. We applied voxel-based morphometry to determine whether women with CPP with and without endometriosis display changes in brain morphology in regions known to be involved in pain processing. Four subgroups of women participated: 17 with endometriosis and CPP, 15 with endometriosis without CPP, 6 with CPP without endometriosis, and 23 healthy controls. All patients with endometriosis and/or CPP were surgically confirmed. Relative to controls, women with endometriosis-associated CPP displayed decreased gray matter volume in brain regions involved in pain perception, including the left thalamus, left cingulate gyrus, right putamen, and right insula. Women with CPP without endometriosis also showed decreases in gray matter volume in the left thalamus. Such decreases were not observed in patients with endometriosis who had no CPP. We conclude that CPP is associated with changes in regional gray matter volume within the central pain system. Although endometriosis may be an important risk factor for the development of CPP, acting as a cyclic source of peripheral nociceptive input, our data support the notion that changes in the central pain system also play an important role in the development of chronic pain, regardless of the presence of endometriosis.

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Arthritis Rheum. 2010 Oct;62(10):2930-40.

Thalamic atrophy associated with painful osteoarthritis of the hip is reversible after arthroplasty: a longitudinal voxel-based morphometric study.

Gwilym SE, Filippini N, Douaud G, Carr AJ, Tracey I.

Abstract

OBJECTIVE: Voxel-based morphometry (VBM) is a method of assessing brain gray matter volume that has previously been applied to various chronic pain conditions. From this previous work, it appears that chronic pain is associated with altered brain morphology. The present study was undertaken to assess these potential alterations in patients with painful hip osteoarthritis (OA).

METHODS: We studied 16 patients with unilateral right-sided hip pain, before and 9 months after hip arthroplasty. This enabled comparison of gray matter volume in patients with chronic musculoskeletal pain versus healthy controls, as well as identification of any changes in volume following alleviation of pain (after surgery). Assessment involved self-completion questionnaires to assess pain, function, and psychosocial variables, and magnetic resonance imaging scanning of the brain for VBM analysis.

RESULTS: Significant differences in brain gray matter volume between healthy controls and patients with painful hip arthritis were seen. Specifically, areas of the thalamus in patients with chronic OA pain exhibited decreased gray matter volume. Furthermore, when these preoperative changes were compared with the brain morphology of the patients 9 months after surgery, the areas of reduced thalamic gray matter volume were found to have “reversed” to levels seen in healthy controls.

CONCLUSION: Our findings confirm that gray matter volume decreases within the left thalamus in the presence of chronic pain and disability in patients with hip OA. The results also show that these thalamic volume changes reverse after hip arthroplasty and are associated with decreased pain and increased function. These findings have potential implications with regard to optimizing the timing of orthopedic interventions such as arthroplasty

20Jul/12

Pudendal Neuralgia & Pudendal Neuropathy

Pudendal Neuralgia & Pudendal Neuropathy

From Hopkins Medicine

Also termed pudendal nerve entrapment, this problem afflicts both men and women having immense effects upon quality of life. The pudendal nerve is a sensory, autonomic, and motor nerve that carries signals to and from the genitals, anal area, and urethra. There are three branches of the nerve on each side of the body: rectal, perineal and clitoral/penile. Pudendal neuropathy occurs when the nerve or one of its branches is damaged, inflamed, or becomes entrapped.

The symptoms can be on one side or bilateral, starting acutely or developing over time. They include:

  • Pain in the areas innervated by the pudendal nerve or one of its branches
  • Burning
  • Reduced or loss of sensation
  • Electric shock-like pain, stabbing pain, knife-like or aching pain
  • The sense of a lump or foreign body – increased sense of size of the affected area
  • Altered sense of temperature
  • Constipation with pain on straining with bowel movements
  • Urination causes a burning pain
  • Painful intercourse
  • Sexual dysfunction

Once diagnosed, treatment often involves a combination of medication, procedures such as a pudendal nerve block, and physical therapy to address the pelvic floor muscles.

A contemporary approach to pain

Similar to other persisting pain states, to think about the suffering individual as much as the condition is fundamental. The wide ranging affects of the pain, associated symptoms and subsequent limitations have to be carefully considered within the treatment programme. The underpinning neurobiology is the basis for the problem but the responses of the body and brain and the individual are key determinants upon the impact. Initially developing a good understanding of the pain and the problem through high quality education creates a strong platform for effective coping and engagement in the rehabilitation and training programme.

The neuroimmune system is designed to adapt and change. This is how we learn. On the basis of the plasticity characteristic of neurons and how they fire together, we believe that change is possible with the right strategies based upon the right understanding within a realistic time-frame. See here

When we are in pain we move differently. The brain and body changes the way that the muscles are used including increased tension to protect the affected area. This is called guarding. The fact that the muscles are overworking creates its own issues including soreness, tightness, difficulty moving and often pain. Trigger points can develop that refer pain into other areas. Tackling changes in the motor system, especially those in response to nerve injury, needs an approach that considers the top-end, the brain (motor cortices and the areas of the brain that communicate with the motor centres, e.g. visual areas, emotional areas). It is important to understand that the associated thoughts about pain and the situation affect the way in which we move. If our belief is that the pain is a sign of damage and danger, we are going to be more protective and hence feed back into guarded posturing and movement. This is how understanding pain and the influences upon pain can really help. Changing our thinking through deeper understanding uses the frontal cortex to change our perception of pain. This is because the frontal cortex is part of the matrix of brain cells (neurons) that underpins the experience of pain. Directly targeting the areas of the brain involved in pain is a logical and now scientifically demonstrated way of dealing with pain.

Certainly local treatment of the the superficial muscles about the lumbar spine and pelvis can be useful to ease tension. In fact, anything that relaxes the individual will help to ease tension. For example, watching a favourite film, laughing with a friend, listening to music or taking a bath. Going beyond the tissues is vital though in dealing with nerve related pain (neuropathy) because of the adaptations that occur in the neuroimmune system. In recent years the use of Graded Motor Imagery for pain and movement problems has provided us with a way of working with the higher centres (‘top-down’) alongside approaches that nourish and mobilise the tissues gradually and safely. Together with development of understanding and often mindfulness, this combined approach offers a tangible and effective way of bringing about change to reduce the impact factor, distress level, increase function and improve quality of life.

For further information upon our approach to pain please contact us here or call 07518 445493

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Research

Pain Med. 2012 Apr;13(4):596-603. doi: 10.1111/j.1526-4637.2012.01343.x. Epub 2012 Mar 5.

Response to pudendal nerve block in women with pudendal neuralgia.

School of Women and Children, University of New South Wales, Sydney, Australia. [email protected]

OBJECTIVE:

To examine the evolution of pain and the duration of numbness after neural blockade of the pudendal nerve in women with pudendal neuralgia and correlate with clinical and historical data.

DESIGN:

Prospective, single arm, open label study.

SETTING:

University hospital and outpatient clinic.

SUBJECTS:

Eighty-two adult female patients were recruited from November 8, 2008 to February 14, 2010. Patients were selected based on the presence of spontaneous or provoked pain in the distribution of the pudendal nerve.

INTERVENTIONS:

Subjects underwent a standardized pudendal nerve block.

OUTCOME MEASURES:

Visual analog pain scores and the presence of numbness were recorded before and for 64 hours after the pudendal nerve block. A complete clinical history and examination were documented.

RESULTS:

Sixty-six patients completed the study. About 86.9% had a reduction in one or more pain symptom, while 44.3% found that more than one of their pain symptoms did not return. About 69.7% of patients reported numbness lasting up to 16 hours or longer. Previous gynecological surgery was recorded in 75.8%, previous traumatic obstetric events in 47.0% of cases. Prolonged history of pain correlated with a reduced chance of positive outcome of the pudendal nerve block.

CONCLUSION:

In patients with pudendal neuralgia, the pudendal nerve block has a variable response, but may have a beneficial effect in a subset of women. Surgical and obstetrical trauma are common historical antecedents

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World J Gastroenterol. 2011 Oct 28;17(40):4447-55.

Chronic proctalgia and chronic pelvic pain syndromes: new etiologic insights and treatment options.

This systematic review addresses the pathophysiology, diagnostic evaluation, and treatment of several chronic pain syndromes affecting the pelvic organs: chronic proctalgia, coccygodynia, pudendal neuralgia, and chronic pelvic pain. Chronic or recurrent pain in the anal canal, rectum, or other pelvic organs occurs in 7% to 24% of the population and is associated with impaired quality of life and high health care costs. However, these pain syndromes are poorly understood, with little research evidence available to guide their diagnosis and treatment. This situation appears to be changing: a recently published large randomized, controlled trial by our group comparing biofeedback, electrogalvanic stimulation, and massage for the treatment of chronic proctalgia has shown success rates of 85% for biofeedback when patients are selected based on physical examination evidence of tenderness in response to traction on the levator ani muscle–a physical sign suggestive of striated muscle tension. Excessive tension (spasm) in the striated muscles of the pelvic floor appears to be common to most of the pelvic pain syndromes. This suggests the possibility that similar approaches to diagnostic assessment and treatment may improve outcomes in other pelvic pain disorders

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Neurourol Urodyn. 2008;27(4):306-10.

Diagnostic criteria for pudendal neuralgia by pudendal nerve entrapment (Nantes criteria).

Service d’Urologie, CHU Hôtel-Dieu, Nantes, France.

AIMS:

The diagnosis of pudendal neuralgia by pudendal nerve entrapment syndrome is essentially clinical. There are no pathognomonic criteria, but various clinical features can be suggestive of the diagnosis. We defined criteria that can help to the diagnosis.

MATERIALS AND METHODS:

A working party has validated a set of simple diagnostic criteria (Nantes criteria).

RESULTS:

The five essentials diagnostic criteria are: (1) Pain in the anatomical territory of the pudendal nerve. (2) Worsened by sitting. (3) The patient is not woken at night by the pain. (4) No objective sensory loss on clinical examination. (5) Positive anesthetic pudendal nerve block. Other clinical criteria can provide additional arguments in favor of the diagnosis of pudendal neuralgia. Exclusion criteria are also proposed: purely coccygeal, gluteal, or hypogastric pain, exclusively paroxysmal pain, exclusive pruritus, presence of imaging abnormalities able to explain the symptoms.

CONCLUSION:

The diagnosis of pudendal neuralgia by pudendal nerve entrapment syndrome is essentially clinical. There are no specific clinical signs or complementary test results of this disease. However, a combination of criteria can be suggestive of the diagnosis

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Neurourol Urodyn. 2007;26(6):820-7.

Pudendal entrapment as an etiology of chronic perineal pain: Diagnosis and treatment.

Fort Bend Neurology, Sugar Land, Texas 77479, USA. [email protected]

AIMS:

This study was conducted to evaluate pudendal entrapment as an etiology of chronic pain, a diagnostic protocol for pudendal entrapment, and clinical response to surgical decompression.

METHODS:

A case series of 58 consecutive patients with a diagnosis of pudendal entrapment, based on clinical factors, neurophysiologic studies, and response to pudendal nerve infiltrations, is described. All patients were refractory to other treatment modalities. Patients were assessed before and after surgical decompression: degree of pain was assessed by visual analog scale (VAS) score, percent global overall improvement, and improved function and quality of life before surgery and 12 months or longer after surgery.

RESULTS:

The primary presenting feature was progressive, chronic, intractable neuropathic pain in the perineum (ano-rectal and/or urogenital) that worsened with sitting. Other symptoms included urinary hesitancy, frequency, urgency, constipation/painful bowel movements, and sexual dysfunction. After surgical decompression, 35 (60%) patients were classified as responders, based on one of the following three criteria: a greater than 50% reduction in VAS score, a greater than 50% improvement in global assessment of pain, or a greater than 50% improvement in function and quality of life.

CONCLUSIONS:

Pudendal entrapment can be a cause of chronic, disabling perineal pain in both men and women. Since symptomatic patients seek medical care from many different medical specialists, a reliable diagnostic protocol should be established. For patients refractory to conventional interventions, surgical decompression of the pudendal nerve can improve pain-related symptoms and disability. With ongoing work on this subject, which is a difficult disorder to accurately diagnose and treat, a better awareness of pudendal entrapment across specialties will emerge

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J Minim Invasive Gynecol. 2010 Mar-Apr;17(2):148-53. Epub 2010 Jan 12.

Pudendal neuralgia.

Department of Obstetrics and Gynecology, St. Joseph’s Hospital and Medical Center, Phoenix, Arizona 85013, USA. [email protected]

Pudendal neuralgia is a painful, neuropathic condition involving the dermatome of the pudendal nerve. This condition is not widely known and often unrecognized by many practitioners. The International Pudendal Neuropathy Association (tipna.org) estimates the incidence of this condition to be 1/100,000; however, most practitioners treating patients with this condition feel the actual rate of incidence may be significantly higher. Currently, there is fair paucity of medical literature and scientific evidence in the diagnosis and treatment of pudendal neuralgia. Diagnosis of this condition is based on the utilization of Nantes Criteria, in conjunction with clinical history and physical findings. CT-scan guided nerve blocks are also employed, by this author, to provide additional information. Subsequent treatment of pudendal neuralgia is medical and well as surgical, with Physical Therapy a key component to all aspects of treatment. The goal of this paper is to present evidence based information, as well as personal clinical experience, in treating approximately 200 patients with pudendal neuralgia.

Useful links

http://www.pudendalhope.info/ (please note that on the home page is a video demonstrating a surgical procedure. If you are particulalry sensitised it maybe advisable to avoid watching the film currently although with graded exposure this could become a goal. Seek the advice of your health professional)

http://www.instituteforwomeninpain.com/

 

 

21Jan/12

Central sensitisation is more common than you may think

Clifford Woolf recently said this about central sensitisation:

Nociceptor inputs can trigger a prolonged but reversible increase in the excitability and synaptic efficacy of neurons in central nociceptive pathways, the phenomenon of central sensitization. Central sensitization manifests as pain hypersensitivity, particularly dynamic tactile allodynia, secondary punctate or pressure hyperalgesia, aftersensations, and enhanced temporal summation. It can be readily and rapidly elicited in human volunteers by diverse experimental noxious conditioning stimuli to skin, muscles or viscera, and in addition to producing pain hypersensitivity, results in secondary changes in brain activity that can be detected by electrophysiological or imaging techniques. Studies in clinical cohorts reveal changes in pain sensitivity that have been interpreted as revealing an important contribution of central sensitization to the pain phenotype in patients with fibromyalgia, osteoarthritis, musculoskeletal disorders with generalized pain hypersensitivity, headache, temporomandibular joint disorders, dental pain, neuropathic pain, visceral pain hypersensitivity disorders and post-surgical pain. The comorbidity of those pain hypersensitivity syndromes that present in the absence of inflammation or a neural lesion, their similar pattern of clinical presentation and response to centrally acting analgesics, may reflect a commonality of central sensitization to their pathophysiology. An important question that still needs to be determined is whether there are individuals with a higher inherited propensity for developing central sensitization than others, and if so, whether this conveys an increased risk in both developing conditions with pain hypersensitivity, and their chronification. Diagnostic criteria to establish the presence of central sensitization in patients will greatly assist the phenotyping of patients for choosing treatments that produce analgesia by normalizing hyperexcitable central neural activity. We have certainly come a long way since the first discovery of activity-dependent synaptic plasticity in the spinal cord and the revelation that it occurs and produces pain hypersensitivity in patients. Nevertheless, discovering the genetic and environmental contributors to and objective biomarkers of central sensitization will be highly beneficial, as will additional treatment options to prevent or reduce this prevalent and promiscuous form of pain plasticity.

And Latremolier

Central sensitization represents an enhancement in the function of neurons and circuits in nociceptive pathways caused by increases in membrane excitability and synaptic efficacy as well as to reduced inhibition and is a manifestation of the remarkable plasticity of the somatosensory nervous system in response to activity, inflammation, and neural injury. The net effect of central sensitization is to recruit previously subthreshold synaptic inputs to nociceptive neurons, generating an increased or augmented action potential output: a state of facilitation, potentiation, augmentation, or amplification. Central sensitization is responsible for many of the temporal, spatial, and threshold changes in pain sensibility in acute and chronic clinical pain settings and exemplifies the fundamental contribution of the central nervous system to the generation of pain hypersensitivity. Because central sensitization results from changes in the properties of neurons in the central nervous system, the pain is no longer coupled, as acute nociceptive pain is, to the presence, intensity, or duration of noxious peripheral stimuli. Instead, central sensitization produces pain hypersensitivity by changing the sensory response elicited by normal inputs, including those that usually evoke innocuous sensations. PERSPECTIVE: In this article, we review the major triggers that initiate and maintain central sensitization in healthy individuals in response to nociceptor input and in patients with inflammatory and neuropathic pain, emphasizing the fundamental contribution and multiple mechanisms of synaptic plasticity caused by changes in the density, nature, and properties of ionotropic and metabotropic glutamate receptors.

In essence we are talking about changes within the central nervous system that underpin the widespread, unpredictable and varied nature of persisting pain.

When I am listening to a patient, observing their movements and performing a ‘multi-system’ examination, I am in part looking for the pain mechanisms at play, including central sensitisation. Several of my questions are: ‘what is going on here to create this experience for the person in front of me?’, ‘why are the nervous and other systems responding in such a way?’ and ‘what is influencing the behaviour of those systems?’. I really need to know what it is that is prolonging this protection and is it really worthwhile for the individual.

Suspecting that there is a component of central sensitisation at play in many cases of chronic pain that I see, it is pleasing to see a group looking at this closely and finding evidence to support this thinking:

J Bone Joint Surg Br. 2011 Apr;93(4):498-502.

Evidence that central sensitisation is present in patients with shoulder impingement syndrome and influences the outcome after surgery.

Gwilym SE, Oag HC, Tracey I, Carr AJ.

Source

Department of Orthopaedics, Rheumatology and Musculoskeletal Sciences, Nuffield Orthopaedic Centre, Windmill Road, Headington, Oxford OX3 7LD, UK. [email protected]

Abstract

Impingement syndrome in the shoulder has generally been considered to be a clinical condition of mechanical origin. However, anomalies exist between the pathology in the subacromial space and the degree of pain experienced. These may be explained by variations in the processing of nociceptive inputs between different patients. We investigated the evidence for augmented pain transmission (central sensitisation) in patients with impingement, and the relationship between pre-operative central sensitisation and the outcomes following arthroscopic subacromial decompression. We recruited 17 patients with unilateral impingement of the shoulder and 17 age- and gender-matched controls, all of whom underwent quantitative sensory testing to detect thresholds for mechanical stimuli, distinctions between sharp and blunt punctate stimuli, and heat pain. Additionally Oxford shoulder scores to assess pain and function, and PainDETECT questionnaires to identify ‘neuropathic’ and referred symptoms were completed. Patients completed these questionnaires pre-operatively and three months post-operatively. A significant proportion of patients awaiting subacromial decompression had referred pain radiating down the arm and had significant hyperalgesia to punctate stimulus of the skin compared with controls (unpaired t-test, p < 0.0001). These are felt to represent peripheral manifestations of augmented central pain processing (central sensitisation). The presence of either hyperalgesia or referred pain pre-operatively resulted in a significantly worse outcome from decompression three months after surgery (unpaired t-test, p = 0.04 and p = 0.005, respectively). These observations confirm the presence of central sensitisation in a proportion of patients with shoulder pain associated with impingement. Also, if patients had relatively high levels of central sensitisation pre-operatively, as indicated by higher levels of punctate hyperalgesia and/or referred pain, the outcome three months after subacromial decompression was significantly worse.

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Treat the brain, treat the pain

Arthritis Rheum. 2009 Sep 15;61(9):1226-34.

Psychophysical and functional imaging evidence supporting the presence of central sensitization in a cohort of osteoarthritis patients.

Gwilym SE, Keltner JR, Warnaby CE, Carr AJ, Chizh B, Chessell I, Tracey I.

Source

University of Oxford, Oxford, UK. [email protected]

Abstract

OBJECTIVE:

The groin pain experienced by patients with hip osteoarthritis (OA) is often accompanied by areas of referred pain and changes in skin sensitivity. We aimed to identify the supraspinal influences that underlie these clinical manifestations that we consider indicative of possible central sensitization.

METHODS:

Twenty patients with hip OA awaiting joint replacement and displaying signs of referred pain were recruited into the study, together with age-matched controls. All subjects completed pain psychology questionnaires and underwent quantitative sensory testing (QST) in their area of referred pain. Twelve of 20 patients and their age- and sex-matched controls underwent functional magnetic resonance imaging (MRI) while the areas of referred pain were stimulated using cold stimuli (12 degrees C) and punctate stimuli (256 mN). The remaining 8 of 20 patients underwent punctate stimulation only.

RESULTS:

Patients were found to have significantly lower threshold perception to punctate stimuli and were hyperalgesic to the noxious punctate stimulus in their areas of referred pain. Functional brain imaging illustrated significantly greater activation in the brainstem of OA patients in response to punctate stimulation of their referred pain areas compared with healthy controls, and the magnitude of this activation positively correlated with the extent of neuropathic-like elements to the patient’s pain, as indicated by the PainDETECT score.

DISCUSSION:

Using psychophysical (QST) and brain imaging methods (functional MRI), we have identified increased activity with the periaqueductal grey matter associated with stimulation of the skin in referred pain areas of patients with hip OA. This offers a central target for analgesia aimed at improving the treatment of this largely peripheral disease.