Category: Pain Management

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Anti-epileptic Drug May Reduce Migraine Aura

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A new study by researchers at Lund University in Sweden found that 85 percent of patients with aura-dominant migraine experienced a reduction in monthly aura days by at least half following treatment with the anti-epileptic drug lamotrigine. The findings need to be confirmed in a controlled study, but could eventually be significant for a patient group that currently lacks a specific treatment for the aura itself.

Around 1.5 million people in Sweden suffer from migraine. Migraine affects both individuals’ daily lives and society as a whole. The disease limits the ability to work and participate in social activities, and leads to significant costs through sick leave, reduced productivity and increased healthcare needs. Women are three times as likely to be affected as often as men, a difference that is largely due to hormonal factors.  

Up to a third of people with migraine experience aura – a temporary neurological symptom that can cause visual disturbances, loss of vision, sensory disturbances, balance problems, and speech and language difficulties, among other symptoms. For some patients, aura is the most debilitating symptom of the disease, but there is currently no established treatment that specifically targets it. 

“Around 50,000 people in Sweden suffer from aura-dominant migraine. Aura is thought to be linked to cortical spreading depolarisation (CSD), a slowly progressing wave of altered nerve cell activity in the cerebral cortex,” says Gürdal Sahin, a researcher at Lund University and a specialist in neurology at the Skåneuro private clinic. 

Migraine with aura is also associated with a slightly increased risk of ischaemic stroke, particularly when combined with other vascular risk factors. It is therefore important to reduce modifiable risk factors. 

“There are now several effective treatments for migraine, including new medicines that block the neurotransmitter CGRP, which plays a key role in migraine attacks. Botulinum toxin is also used as a preventative treatment for chronic migraine. However, as there is no established treatment that specifically targets the aura itself, migraines with and without aura are often treated in a similar way, even though the aura appears to be partly based on mechanisms other than the headache itself,” Gürdal Sahin continues. 

The medicine lamotrigine is approved for the treatment of epilepsy and bipolar disorder, but not for migraine. However, as both epilepsy and migraine aura involve temporary changes in nerve cell activity, the researchers wanted to investigate whether the drug could also prevent aura. Lamotrigine affects the electrical activity of nerve cells by acting on sodium and potassium channels, and also reduces the release of, amongst other things, the neurotransmitter glutamate. In this way, the medicine can reduce the excessive excitability of the nerve cells. In theory, these mechanisms could help to prevent the emergence and spread of CSD. 

“In our study, we examined 81 patients with frequent or particularly troublesome migraine aura and treated them with lamotrigine. Among the patients included the number of days with aura fell on average from 6.9 to 1.4 days per month, representing a reduction of around 80 per cent,” says Sena Uzun, a doctoral student at Lund University. 

While previous studies involving lamotrigine have shown mixed results, the results of this study were particularly promising for patients with aura-dominant migraine. In this group, 85 per cent of patients experienced at least a 50 per cent reduction in the number of days with aura. Another interesting observation was that a slower dose escalation was associated with fewer side effects, which may be relevant when the treatment is evaluated in future clinical trials. 

“As the study is retrospective and lacks a control group, the results need to be confirmed. We are now proceeding with a national, randomised, double-blind, placebo-controlled trial of lamotrigine. If the results can be confirmed, the drug could become a relatively inexpensive and well-established treatment option for a group of patients who currently have no treatment for the aura itself,” concludes Sena Uzun.

Original written by Åsa Hansdotter

Source: Lund University

Categories : Obstetrics & Gynaecology Pain ManagementTags :

New Method Makes IUD Insertion Less Painful for Women

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Blausen.com staff (2014). “Medical gallery of Blausen Medical 2014“. WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436. – Own work

A simple method involving local anaesthesia in the uterus can reduce pain during IUD insertion, according to a new study from the Karolinska Institutet, published in the journal JAMA. The method also increased the proportion of women who found the procedure tolerable. The results may encourage more women to choose an IUD as a method for contraception.

The IUD is an effective and long-acting contraceptive, but fear of pain during insertion make many women choose not to have one inserted. Currently, IUDs are inserted without local anaesthesia or, in some cases, with local anaesthesia administered via an injection into the tissue around the cervix – an injection that could be experienced as painful.

In the new randomised study, researchers investigated whether a small amount of local anaesthetic, introduced into the uterus via a thin plastic catheter a couple of minutes before the procedure, could make the procedure less painful.

The study involved 370 women aged between 18 and 31 who had not previously given birth. The participants were randomly allocated to receive either the local anaesthetic mepivacaine or a saline solution prior to IUD insertion. Neither the participants nor the healthcare staff knew which treatment was being administered.

The results show that pain was reduced in the group receiving active treatment. On a scale from 0 to 100, the average pain score was 43.8 compared with 58.6 in the control group – a reduction of around 15 units. At the same time, the proportion of participants who found the pain tolerable rose from 91.4 to 98.3 per cent.

“We can see that the method not only reduces pain, but also means that more people find the procedure acceptable,” says Helena Kopp Kallner, professor at the Department of Clinical Sciences, Danderyd Hospital, Karolinska Institutet, and senior consultant at the Women’s Clinic at Danderyd Hospital, who is co-last author with Niklas Envall, a postdoctoral researcher at the same department.

The overall experience was also improved. More than half of the women in the treatment group found the procedure easier than expected, compared with around a third in the control group.

An important aspect of the study was that the administration of the anaesthetic itself should also be gentle. The results show that most participants found the administration to be only mildly painful.

“It is a simple method that does not require needles and is easy to use in everyday clinical practice,” says lead author Karin Elgemark, PhD student at the same department. 

The researchers point out that the study does not compare the method with other types of pain relief, which is a limitation. This means it is not possible to determine whether the method is more effective than alternative treatments. The results are also based on self-reported pain, which may be influenced by individual experiences.

“Our study shows that the method works when compared with no active treatment, but it also needs to be compared with other pain relief methods,” says Helena Kopp Kallner.

The study was carried out at eleven gynaecological clinics and youth health centres in Sweden. It was funded by the Swedish Research Council. Some of the researchers have reported receiving remuneration for lectures from companies that manufacture intrauterine devices (IUDs), but these organisations played no role in the conduct or analysis of the study.

Source: Karolinska Institutet

Categories : Pain Management Skeletal SystemTags :

Managing Stiffness in Deep Calf Muscles Using Ultrasound Stimulation

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Research shows ultrasound stimulation can reduce passive stiffness in the soleus, suggesting potential for non-invasive management of deep muscle stiffness

Ultrasound stimulation was applied to the calf for 10 minutes, and passive muscle stiffness was assessed using shear wave velocity. The study compared the superficial medial gastrocnemius (MG) and deeper soleus (SOL) muscles. Passive muscle stiffness decreased in the SOL after ultrasound stimulation, while no significant change was observed in the MG. Image credit: Mr Tomohiro Umeda from Doshisha University, Japan

Passive muscle stiffness is a risk factor for muscle strain injuries. Stretching, heat, and vibration have been evaluated on superficial muscles, but approaches for decreasing stiffness in deeper muscles remain unclear. In a recent study, researchers from Japan showed that 10 minutes of ultrasound stimulation can reduce stiffness in a deep calf muscle called the soleus, hinting at a promising non-invasive strategy for managing deep muscle stiffness, with potential future application in sports injury prevention.

Muscle strain injuries are a common problem in sports, and injuries to the triceps surae, the calf muscle group that includes the gastrocnemius and soleus, can significantly affect athletic performance and return to play. One factor that is thought to influence a muscle’s susceptibility to strain is passive muscle stiffness, which refers to the resistance of a relaxed muscle to being stretched. A recent genetic study has strengthened the idea that stiffer muscles are more prone to injury, suggesting that passive muscle stiffness is an important risk factor. Thus, finding safe and feasible ways to reduce this stiffness might help prevent associated injuries.

Several strategies, including stretching, heat, and vibration, can significantly reduce passive muscle stiffness. However, research on these approaches has focused on muscles located close to the skin. The soleus, one of the main muscles of the triceps surae, sits deep underneath the medial and lateral gastrocnemius, which makes it a difficult target. Ultrasound stimulation is used in sports and rehabilitation and produces both heating and mechanical effects in biological tissue. As lower-frequency ultrasound can penetrate relatively deep into tissue, it raises the question: Could ultrasound actually reduce the stiffness of a deep muscle like the soleus?

To this end, a research team including Ph.D. student Tomohiro Umeda, Professor Tatsuya Hojo, and Professor Taku Wakahara from the Graduate School of Health and Sports Science at Doshisha University, Japan, examined the effects of ultrasound stimulation on calf muscle stiffness in 20 healthy adults. Their work was published in the Journal of Biomechanics.

A randomly selected leg of each participant received 10 minutes of continuous ultrasound stimulation at a frequency of 1 megahertz (MHz) and an intensity of 2.0 W/cm², while the other leg served as an untreated control. The researchers then used shear wave elastography, an imaging technique that measures how quickly mechanical waves travel through tissue, to assess muscle stiffness before and immediately after the ultrasound stimulation. Faster shear waves generally indicate stiffer tissue, so a decrease in shear wave velocity (SWV) was interpreted as a decrease in passive muscle stiffness.

The results showed a clear difference between the soleus and the medial gastrocnemius. SWV, an indicator of passive muscle stiffness, decreased significantly in the soleus after the ultrasound stimulation, while no significant change was observed in the untreated leg. In contrast, no significant change in SWV was observed in the more superficial medial gastrocnemius. Interestingly, participants who initially had stiffer soleus muscles tended to show greater reductions in stiffness following ultrasound stimulation. “Our findings suggest that ultrasound stimulation may have the potential to non-invasively decrease passive stiffness in deep muscles such as the soleus,” remarks Mr Umeda, “In the future, this approach may contribute to the development of conditioning and rehabilitation strategies for the prevention of sports-related muscle injuries.”

The different responses of the soleus and medial gastrocnemius may be related partly to their anatomical locations. The soleus is located about 2.44cm below the skin, whereas the gastrocnemius is much closer to the surface at just about 0.53cm. Moreover, differences in the muscles’ tissue composition may also contribute to their different responses, although the underlying mechanisms remain unclear. “Future research could clarify the optimal ultrasound parameters for different muscles and identify which individuals respond most effectively to ultrasound stimulation. Such knowledge could lead to more individualised conditioning and rehabilitation strategies for athletes,” concludes Mr Umeda.

Overall, the results highlight the potential of ultrasound stimulation as a non-invasive approach for managing stiffness in deep muscles that can be difficult to target with other methods. Further research will be needed to determine whether this approach can be incorporated into individualised conditioning and rehabilitation strategies and ultimately contribute to the prevention of sports-related muscle injuries.

Source: Doshisha University

Categories : Antibiotics Pain ManagementTags :

Are Antibiotics an Effective Treatment for Chronic Low Back Pain?

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There has been considerable interest in prescribing antibiotics for chronic low back pain from disc herniation, stemming from the hypothesis that low-grade bacterial infections within spinal discs may contribute to persistent symptoms, particularly in cases involving Modic changes, which are bone marrow abnormalities visible on MRI.

A new randomised clinical trial investigated whether the antibiotic amoxicillin-clavulanate could effectively reduce chronic low back pain in patients with disc herniation. Researchers conducted a double-blind, placebo-controlled study involving 170 participants over a 12-month period to assess improvements in pain intensity and disability.

The trial found that taking amoxicillin-clavulanate for 90 days provided no significant reduction in pain or disability compared to a placebo. These findings suggest that the routine prescription of antibiotics for back issues is ineffective and potentially harmful due to the risk of side effects and the global threat of antimicrobial resistance.

Clinical experts advise against this approach, noting that current evidence does not support using these drugs even when traditional treatments have failed. Consequently, the study reinforces the need for evidence-based management and cautions against relying on unproven pharmaceutical interventions for complex spinal conditions.

Listen to the podcast for a deep dive into the results!

Categories : Pain ManagementTags :

Cancer Protein Points to a New Way to Reduce Chronic Nerve Pain

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Researchers at The University of Texas MD Anderson Cancer Center found new evidence that BRAF, a protein commonly involved in cancer, plays a key role in developing, amplifying and maintaining chronic pain caused by nerve damage. Using BRAF inhibitors reduced pain sensitivity in preclinical models, suggesting the therapeutic potential of this approach for treating chronic nerve pain.

The study, published in Science Signaling, was co-led by Shao-Rui Chen, MD, professor of Anesthesiology and Perioperative Medicine, and Hui-Lin Pan, MD, PhD, endowed chair of Anesthesiology and Perioperative Medicine.

“Our findings identify the cancer-promoting protein BRAF as a key driver of pathological pain signaling following nerve injury,” Pan said. “Because BRAF inhibitors are already approved for cancer treatment, this discovery raises the possibility of rapidly repurposing existing therapies to reduce the level of pain signals entering the spinal cord and improve patient quality of life.”

How does nerve injury cause chronic pain?

Chronic nerve pain, or neuropathic pain, can come from injury, disease or even life-saving cancer treatments. This pain can be intense and persistent, and it responds poorly to conventional pain medications, negatively affecting patient quality of life.

Protein channels in the brain and spinal cord, known as NMDA receptors, help nerve cells communicate. After nerve injury, these NMDA receptors can become hyperactive, amplifying pain signals. To identify potential mechanisms, the researchers explored the role of BRAF on NMDA receptor activity.

What did the researchers find in this study?

Using preclinical models of nerve injury, the researchers discovered that BRAF moved from peripheral sensory nerve cells to their terminals inside the spinal cord, where it activated molecular signals to increase NMDA receptor activity. They also found a correlation between BRAF signaling proteins and NMDA receptors in human spinal cord samples.

These initial results suggested that targeting BRAF could help reduce activity in the NMDA receptors to reduce pain.

Does targeting BRAF reduce pain?

In the preclinical models, the BRAF inhibitor vemurafenib and the MEK inhibitor selumetinib reduced sensitivity to touch, pressure and heat but did not change normal response in models without nerve injury.

Deleting the Braf gene also resulted in less persistent pain sensitivity. Conversely, activating BRAF directly caused pain sensitivity in models that did not have nerve injury, highlighting the key role of BRAF in starting and maintaining neuropathic pain.

What does this mean for patients who have nerve injury and chronic pain?

These results are preclinical, and researchers will need to further examine the appropriate dosing, delivery methods and possible side effects of BRAF inhibitors prior to clinical trials in humans. The researchers also hope to understand how nerve injury triggers the translocation of BRAF from the nerves to the spinal cord.

However, these results suggest that BRAF signalling is associated with NMDA receptor activation in the spinal cord and that currently available BRAF inhibitors have therapeutic potential to treat neuropathic pain.

Source: The University of Texas MD Anderson Cancer Center

Categories : Pain ManagementTags :

Can Humans Regulate Acute Inflammation Through Attention?

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We usually think of bodily sensations as information the brain receives. What if the way we attend to those sensations can feed back and change the biological response itself?

Attention is already known to shape how bodily sensations are perceived. Focusing away from pain or itch, for example, can make these sensations feel less intense. A new study from the lab of Dr Liron Rozenkrantz at Bar-Ilan University’s Azrieli Faculty of Medicine, published in Nature Human Behaviour, shows that attention can also influence the body’s inflammatory response.

When people voluntarily focused their attention on sensations arising from a small area of inflammation in their arm, the inflammatory response was smaller and showed faster recovery dynamics than when their attention was directed away from those sensations.

The study, led by Dr Nofar Mizrachi and conducted in collaboration with Prof Menachem Rottem, a clinical immunologist, involved 57 healthy volunteers across three preregistered experiments. Participants underwent a standardised procedure that produced a small, temporary inflammatory response in the skin. They were then instructed either to focus on sensations from the affected area or to direct their attention elsewhere. The researchers measured the inflammatory response for 20 minutes as it unfolded, along with physiological measures such as heart-rate variability, skin temperature and autonomic activity.

The effect was substantial and highly consistent: nearly 90% of participants showed a smaller inflammatory response when they focused on the affected area, with responses approximately 1.5-fold smaller under internal attention compared with distraction. Differences emerged within minutes, with the response also showing faster return toward baseline.

“What was particularly striking was that directing attention toward the inflamed area changed not only what participants experienced, but the inflammatory response itself,” said Dr Rozenkrantz. “This raises the possibility that our subjective experience of what is happening in the body is not only a passive process, but may be actively contributing to how physiological responses are regulated.”

The researchers identified two complementary pathways that contributed to the effect. One involved sensory signals coming from the inflamed tissue. The other was a top-down mechanism through which attention continued to influence inflammation even when sensory signals were reduced using a local anesthetic.

Together, the findings suggest that attention can influence inflammation through both sensory and top-down pathways. More broadly, they suggest that the way the brain prioritises signals from the body may have consequences for how the body regulates itself.

The experiments involved healthy volunteers and a controlled model of acute skin inflammation. Whether the same mechanisms apply to chronic inflammation, autoimmune disease, wound healing or other conditions remains to be determined. The team’s next step is to identify the precise brain and immune pathways involved and determine whether similar effects occur in other physiological systems.

Source: EurekAlert!

Categories : Pain Management RheumatologyTags :

Exercise Helps Hip Arthritis Pain, but Perhaps Less than We Thought

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A new Cochrane review finds that exercise may improve pain and function, but the benefits may fall short of what patients would notice in daily life.

Hip osteoarthritis is a condition affecting millions of people worldwide and a leading cause of chronic pain and disability. Exercise is widely recommended as a first-line treatment for managing hip arthritis pain.

Led by researchers from University of Sydney and University of Melbourne, the findings show exercise produces small improvements in pain and physical function for people with hip osteoarthritis, but those improvements may not be large enough to make a meaningful difference to patients.

The review included 18 clinical trials involving 1368 people. Participants were mostly women (63%) and were aged between 53 and 74 years, meaning findings may not apply to younger people. Exercise programmes in the included studies varied widely, lasting between two and 52 weeks and covering a range of types including strengthening, aerobic, and mind-body approaches.

Compared with no treatment or usual care, exercise probably reduces pain by around 7 points on a 100-point scale. However, experts generally consider an improvement of at least 12 points necessary for patients to notice a meaningful difference in daily life. Physical function showed a similar pattern. The authors note, however, that these thresholds were derived largely from knee and mixed osteoarthritis populations, and may not entirely reflect the hip osteoarthritis experience.

Quality of life, arguably the outcome patients care about most, showed little to no improvement with exercise regardless of the comparison used.
 

“Exercise is recommended as a primary treatment for hip osteoarthritis, and this review doesn’t overturn that, but it does suggest we should be honest with patients that the average benefit may be modest, and that we need better-designed trials to understand who benefits most and from which type of exercise.”

— Michelle Hall, co-lead author from the University of Sydney. 


This update analysed results differently from its 2014 predecessor, which pooled all available data together and found high-quality evidence that exercise slightly reduced pain. The new review separated trials according to what exercise was being compared against.

When exercise was tested against a placebo or sham treatment, the evidence for pain relief weakened considerably. And adding exercise on top of another treatment made little difference either. While no single type of exercise came out on top, the authors caution that the evidence to answer that question properly simply isn’t there yet.

Not a recommendation away from exercise

The review stops short of saying exercise is ineffective or should be abandoned as a recommendation. Exercise carries broad health benefits beyond arthritis, is low-cost, and is unlikely to cause harm. 

Most studies included in this review were small and unblinded, which may have influenced outcomes. Because pain and function were largely self-reported, and participants knew whether they were exercising, exercise may appear more effective than it truly is.

The authors call for larger, better-designed trials to give patients and clinicians a clearer picture of what exercise can realistically achieve for hip osteoarthritis specifically.
 

“There just isn’t a huge body of evidence out there. For some people struggling with hip pain, exercise can really be their only hope, but I also don’t want to give patients false hope. It’s important future research is done with larger, better-quality trials, examining what types of exercise work specifically for different people.” 

— Belinda Lawford, co-lead author from the University of Melbourne. 

Read the review

By Mia Parkinson

Source: Cochrane

Categories : Pain ManagementTags :

Researchers Demystify the Molecular Mechanisms of General Anaesthesia

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Left: Surface model of the bacterial sodium channel NavMs with one of the four subunits coloured light blue and the others grey. The anaesthetic sevoflurane (coloured spheres) sits in a pocket at the interface of two adjacent subunits. Right: Close-up of the binding pocket. The semi-transparent surface exposes the underlying ribbon and a tyrosine amino acid (light blue), which is key to binding sevoflurane (coloured sticks). Credit: Dr Karl Herold

Researchers at Weill Cornell Medicine and Birkbeck, University of London, have identified a site where a commonly used anaesthetic binds to sodium ion channels, revealing a molecular mechanism that may explain how these drugs dampen communication between neurons. Ion channels are proteins that regulate the flow of charged particles across cell membranes, enabling neurons to generate electrical signals. By reducing this signalling, inhaled anaesthetics help suppress brain activity, producing unconsciousness and immobility during surgery.

The findings, published June 19 in Nature Communications, shed light on a longstanding mystery: For 175 years, doctors have safely used inhaled anaesthetics to render patients unconscious, but didn’t fully understand how these drugs work.

“Sodium channels are critical for communication between neurons in the brain, and anaesthesia breaks down that communication,” said Dr Hugh Hemmings, senior associate dean for research and chair of the Department of Anesthesiology at Weill Cornell, who co-led the research. “So, there’s good reason to believe that the unconsciousness produced by volatile anaesthetics is related to their effects on sodium channels.” 

The study provides the first atomic-level view of how the anaesthetic sevoflurane binds to sodium channels and stabilises them in an inactive state. “The insights we gain from this study may enable us to design safer, more selective anaesthetics, with fewer side effects,” said Dr Karl Herold, co-first author and senior research associate at Weill Cornell.

Anaesthetising a bacterial counterpart

As far back as the 1970s, scientists suspected that inhaled, volatile anaesthetics could interact with ion channels – in particular, the voltage-gated sodium channels that play a crucial role in cell-to-cell communication throughout the nervous system. But determining how this interaction inhibits neuronal activity has been challenging because mammalian sodium channels were too large and complex for detailed structural analysis.

The researchers turned to a marine bacterium, Magnetococcus marinus, that uses voltage-gated sodium channels to swim toward nutrients and oxygen. Although structurally simpler than their mammalian counterparts, the bacterial channels operate similarly and share the same sensitivity to anaesthetics. “Volatile anaesthetics bind through weak, low-affinity interactions that are very hard to capture structurally,” Dr Herold said. “A bacterial channel that behaves like ours but is small enough to crystallise lets us finally see where sevoflurane sits and how it holds the channel inactive.”

Discovering a binding pocket

The Weill Cornell team joined forces with Birkbeck researchers, co-senior author Dr Bonnie Ann Wallace and co-first author David Hollingworth. The UK-based researchers have extensive expertise in structural analysis of these bacterial channels bound to a variety of drugs, including those that affect neuronal activity.

Using high-resolution X-ray crystallography, the researchers captured detailed snapshots of sevoflurane bound to the channel. They discovered that the anaesthetic tucks into a small pocket at the edge of the channel’s pore-forming region, but away from the pathway through which sodium ions flow. Binding in this pocket stabilises the channel in an inactive state, making it less likely to open and allow sodium ions through, thereby reducing a neuron’s ability to transmit electrical signals.

This interaction is key to the drug’s molecular effects. When the researchers altered a single amino acid in the binding pocket, sevoflurane could no longer bind effectively and lost its ability to keep the channel in its inactivated state.

The researchers are now working on translating their findings to the mammalian system. “The bacterial channel is just a testing ground,” Dr Hemmings explained. “If naturally occurring mutations affecting anaesthetic binding exist in humans, studying them could help explain why some people respond differently to anaesthesia and may provide new insights into the biology of consciousness.”

“As anaesthesiologists, it’s our responsibility to understand how these drugs work, so we can resolve issues when people don’t react well to anaesthesia,” said Dr Hemmings, who is also anaesthesiologist-in-chief at NewYork-Presbyterian/Weill Cornell Medical Center.

Source: Weill Cornell Medical Center

Categories : Obstetrics & Gynaecology Pain ManagementTags :

Epidurals Not Linked to Increased Harm for Newborns or Children

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Study provides strong evidence that epidural analgesia in labour is safe for newborns, say researchers

Photo by Duda Oliveira

Having an epidural during labour is not associated with clinically significant increased risks of harm to newborn babies, including brain injury, severe breathing problems, sepsis and death, or cerebral palsy later in childhood.

The researchers say these findings “support widening availability and equitable access to epidural analgesia as a safe component of intrapartum care.”

Epidural analgesia in labour provides effective pain relief and may help reduce complications in mothers after giving birth, but evidence of its effect on newborn and child health is limited.

To address this, researchers analysed data for 495 695 births in Scotland over a 13 year period (2007-2019) to examine whether epidural analgesia during labour was associated with serious neurological conditions occurring within 28 days of birth.

Only women who delivered a single baby vaginally or via unplanned caesarean section between 24 and 42 weeks of pregnancy were included in the analysis.

Further measures included other severe newborn illness, sepsis, low Apgar score (a routine test of a baby’s health) five minutes after birth, death within 28 days of birth, and cerebral palsy diagnosed at any point during childhood.

Factors such as mother’s age, ethnicity, weight, existing pre-eclampsia or diabetes, smoking history, birth location and gestational age at birth, were also taken into account.

Of nearly 500 000 women included in the study, around one in four had an epidural during labour. Overall, serious neurological conditions were rare, affecting fewer than 1 in 1000 babies. These conditions occurred at the expected rate and were no more common among babies whose mothers had an epidural compared with those who did not.

No association was found between epidural analgesia in labour and serious neurological conditions, other severe newborn illness, sepsis, low Apgar score at five minutes, death at 28 days, or cerebral palsy in childhood.

This is an observational study so no firm conclusions can be drawn about cause and effect, and the authors acknowledge that the study was limited to women delivering in Scotland, a predominantly white population, so the findings may not apply to more ethnically diverse populations or other healthcare settings.

However, this was a large study with long term follow-up of newborn and childhood outcomes, and results were consistent after additional analyses across various groups including women considered to have high risk pregnancies and preterm births, supporting the reliability of the findings.

As such, the authors conclude: “These results should reassure parents and clinicians that epidural analgesia use in labour is safe for babies and support informed, evidence based decision making about analgesic options in labour.”

Source: The BMJ Group

Categories : Pain ManagementTags :

Melatonin May Help Ease Chronic Muscle and Joint Pain, New Study Suggests

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Dipa Kamdar, Kingston University

Melatonin is best known for helping us sleep. But a new study suggests it might have another surprising use: easing muscle and joint pain.

Produced naturally by the pineal gland in the brain at night, melatonin helps regulate the body’s sleep-wake cycle. That’s why this hormone is widely used as a treatment for insomnia and jet lag.

Sleep and pain are closely linked (poor sleep can make pain feel worse, and pain can make sleep harder). But melatonin may also reduce pain directly. Researchers believe it dampens pain signals in the brain and spinal cord, reduces inflammation, calms overactive nerves and protects cells from oxidative stress – the cellular wear and tear caused when harmful molecules build up.

In the new study, researchers combined the results of 23 clinical trials involving over 2,000 participants to identify overall patterns. These trials looked at melatonin for long-term muscle and joint pain as well as pain after surgery.

Overall, melatonin reduced both pain and sleep problems in people with chronic muscle and joint pain. But the improvements were modest. On average, pain scores fell by about nine points on a 100-point scale. That’s within the range reported for some anti-inflammatory drugs in similar studies, although the two treatments haven’t been directly compared.

Melatonin’s effects may also depend on whether people already have sleep problems or other long-term health conditions. Most of the chronic pain studies included people who already had poor sleep to begin with, but none of the trials looked at results separately for people with and without sleep issues. Because of this, it’s unclear whether melatonin works better for people who struggle with sleep or whether the effects are similar for everyone.

The findings were much less convincing for pain after surgery. Melatonin did not make a noticeable difference to pain or sleep. One analysis found a tiny improvement (about 2.5 points on a 100-point pain scale), but this is far below what would matter to patients recovering from surgery.

The benefits in chronic muscle and joint pain are modest. Based on the current evidence, melatonin should be seen as a possible add-on treatment rather than a replacement for established therapies. The evidence suggests melatonin could complement treatments such as physiotherapy, exercise and anti-inflammatory medicines rather than replace them.

What we still don’t know

There is also still a lot we don’t know. The trials in this study used a wide range of doses, from 1mg to 10mg, and the researchers couldn’t determine which dose worked best.

There were hints that longer treatment helped more in chronic pain, but this was based on only a few studies. There is also very little evidence on the effectiveness of higher doses, even though they appear safe in other studies.

Melatonin is widely used and generally considered safe for short-term use, but it can cause side-effects, such as daytime sleepiness, dizziness, headaches and nausea.

People with liver or kidney conditions, or those with autoimmune conditions like rheumatoid arthritis, should speak with a doctor or pharmacist before taking it.

It is also worth noting that melatonin is regulated very differently around the world. In the US, melatonin is sold as a dietary supplement, meaning people can buy it easily in supermarkets and online without medical advice. But in the UK, melatonin is a prescription-only medicine and is only licensed for short-term sleep problems and jet lag.

For now, the findings suggest melatonin may offer modest relief for some people with chronic muscle and joint pain, particularly if poor sleep is part of the problem. It’s unlikely to replace established treatments, but it could eventually earn a place alongside them. Larger, well-designed trials will be needed before doctors can say with confidence who is most likely to benefit.

Dipa Kamdar, Senior Lecturer in Pharmacy Practice, Kingston University

This article is republished from The Conversation under a Creative Commons license. Read the original article.