Our patient education dynamic spine models help low back pain sufferers better understanding of their pain sources.

A dynamic spine model can empower a patient to help him or her get to know the motions postures and loads related to pain. Once the specific movements are identified, a patient can learn what exercises and movement strategies that will reduce their symptoms. A disc bulge is often an MRI finding but it can also tells a story about hypermobility. For lumbar spinal stenosis, it is also common for a person to have symptoms while their spine is in relative extension. The Lumbar Spinal Stenosis Model helps a practitioner deliver this important message to engage with accurate patient education.

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Low Back-related Leg Pain and Axial Loading with MRI – Using the Visual Analog Scale and Pain Drawings

Low back-related leg pain

Goal of the Study?

Low back-related leg pain is thought to be neuropathic in origin due to compromise of a nerve root(s) and is also commonly known as sciatica. In a study published in the Journal of Clinical Medicine 1 a group of authors looked to see if loading the spine during MRI imaging (axial loaded MRI) would help discern more specificity to the anatomical cause of the low back-related leg pain. These leg pain sufferers will often undergo recumbent MRI while their symptoms are in the vertical or axially loading posture. 

 

Why are they doing this study?

Many cases of sciatica can be challenging to diagnose because of the complexity of the disc mechanics and physiology. There are many nuances of sciatica, and each case can bring its own set of complexities. Learning to determine the source(s) of sciatica more accurately can be helpful in its therapeutic management.

 

What was done?

Ninety patients were recruited for this retrospective observational study. The participant’ ages ranged from 21-89 years and were screened by an orthopedic surgeon to exclude those with hip and knee problems from the study. Participants were asked to fill out a self-evaluation including the visual analog scale along with a pain drawing. Each participant was evaluated by an attending physician and underwent an axial-loaded 1.5T MRI with added weight. As a comparison, each participant.

The investigators looked for these variables:

 Cross-section of the dural sac
 Lumbar spinal stenosis grade with axial loading
 Disk herniation with axial loading
 Size of herniated disc with axial loading
 Size of hyperintensity zone with axial loading
 Ligamentum flavum ‘type’ with axial loading
 Intervertebral foraminal size with axial loading
 Foraminal stenosis
 Degenerative disc classification
 Degenerative facet arthropathy
 Edema of facet joint and effusion with axial loading
 Synovial cyst area with axial loading

 

What did they find?

The authors found that axial-loading subjects played a significant role in extracting findings that would otherwise not be seen with conventional recumbent MRI. Specifically, they found facet joint edema, atypical ligamentum flavum, was associated with low back-related leg pain.

 

Why do these findings matter?

Often, sciatica patients undergo MRI to identify a cause. However, recumbent MRI does not tell the whole picture as patients often report a worsening of symptoms when they are axially loaded. This study helped reveal the changes in the loaded state and can help clinicians make informed decisions about the symptoms patients express in a clinical setting. Understanding that the facets are under more load and the ligamentum flavum can buckle inwards towards the spinal canal can help the clinician understand the anatomy when assessing patients. Notably, the authors summarized that these axial-loaded findings could offer a dynamic picture of the instability contributing to sciatica.

 

At Dynamic Disc Designs we have developed models to help demonstrate load related changes to the spine. We believe that our models not only help the patients understand their symptoms better so they can make the appropriate adjustments to improve their sciatica, but they also help in the context of the education of spine pain in general.

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Advice and education provide small short-term improvements in pain and disability in people with non-specific spinal pain: a systematic review

Education of pain

Goal of the review?

In this review 1 the authors evaluate the effectiveness of advice/education of pain and disability in people with non-specific spinal pain. They also examine to what extent the characteristics of patients and interventions change the treatment effects.

 

Why are they doing this study?

Spinal pain is a leading cause of disability across the world. In Australia, the costs associated with chronic pain are predicted to increase from $139 billion to $215 billion by 2050. Despite the significant impact of chronic pain (spinal pain is the largest contributor), most systematic reviews are outdated and have missed critical studies and new research. Moreover, existing reviews have only looked at advice to stay active without analyzing advice on ergonomic changes or pain neuroscience education. For this reason, there continues to be much uncertainty on the effectiveness of guidance and education for the treatment of non-specific spinal pain.

 

What did they do?

The researchers did a systematic review with meta-analyses of randomized controlled trials. They included studies with participants who had non-specific spinal pain (back or neck) of any duration, interventions that focused on advice, education or information given by a healthcare professional. The review focused on two outcomes: pain and disability (primary) and adverse events (secondary). 

 

What did they find?

In total, they included 27 trials with 7,006 participants. Most of the studies (18 in total) were assessed as being low risk of bias. Low-quality evidence from 18 trials indicated that advice had a negligible effect on pain in the short term. However, the advice provided almost no benefits at other time points. Meta-regression revealed no association between type of advice, duration of pain, location of pain, the intensity of treatment or mode of delivery with treatment effects. Moderate-quality evidence from 19 trials with 2579 participants indicated that advice had a small effect on disability in the short term, compared with no advice or placebo.

 

Why do these findings matter?

The findings suggest that advice provides some short-term improvements in pain and disability, but the effects are small and are not sufficient as the only treatment for patients with spinal pain. 

 

At Dynamic Disc Designs, we believe our models can make a large difference when pain education is delivered. We look forward to future studies using ddd models as part of the patient education of pain.

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Patient education booklet to support evidence — based low back pain care in primary care — a cluster randomized controlled trial

Goal of the study?

In this study, 1 the objective was to assess the effectiveness of a patient education booklet to overcome barriers to the delivery of recommended care for patients with low back pain. 

 

Why are they doing this study?

Low back pain is the leading cause of disability and a major health cost worldwide. One of the reasons for this is that low back pain tends to be managed without following clinical guidelines. For example, almost half of patients undergo inappropriate imaging, which drives up healthcare costs associated with increased disability. To address the barriers to implementing clinical guidelines, Australian researchers developed a patient education booklet that educates patients and their healthcare providers, reminding practitioners of guidelines and facilitating communication. 

 

What did they do?

The researchers used a cluster-randomized trial design to assess the booklet’s effectiveness with low back pain patients in primary care compared to usual care. They recruited 8 clusters, 4 for the intervention (212 participants) and 4 for the control group (203 participants), with 408 participants in the sample. The practitioners in the intervention group were provided with the booklet and a 30-minute training session. The booklet was then also provided to their patients in the intervention group. The professionals only received a short training session on the study and recruitment procedure in the control group. All consenting patients received usual care but did not get the booklet.

There were two outcomes: 1) The proportion of patients presenting with low back pain who underwent imaging examinations due to low back pain during the first three months of follow-up, and 2) Change in Patient-Reported Outcomes Measurement Information System (20 items physical functioning short form) from baseline to three-month follow-up. 

They used statistical software to analyze between-group differences. 

 

What did they find?

The patient education booklet substantially reduced the proportion of patients with low back pain who underwent imaging at 3 months, but the result was not statistically significant. It was only statistically significant when a physician was the first contacted professional. This was compared to the findings at 12 months, which resulted in an effect that was slightly larger and statistically significant. 

The researchers did not find any differences in the Patient-Reported Outcomes Measurement Information System between baseline and 3 months or 12 months. They did find a change in the number of sick days in the intervention group was less than in the control group at 3 months and 12 months. There were no statistically significant differences between the intervention and control groups in the number of healthcare appointments or patient-reported secondary outcomes.

The use of the booklet had no impact on the patient’s pain, physical functioning, disability, or quality of life compared to usual care.

 

Why do these findings matter?

Patient education often matters, and how and when it is delivered should be optimized for each patient. A custom-tailored approach to each patient should be at the forefront of each clinical encounter. This study using a booklet did not show any changes in a patient’s pain score. Something needs to change in how patient education is delivered.

 

At Dynamic Disc Designs we believe a ‘booklet’ is a dated format and practitioners can improve their patient education through the use of accurate modelling to help patients truly understand and see the causes of their specific symptoms. Fostering the right motivational movement within patients is at the hallmark of what we do. To help in the construct of tackling biomechanical causes while addressing the fears of the unknown.

 

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Evaluation is Treatment for Low Back Pain

pressure pain threshold

Goal of the study?

In this study,1 the purpose is to investigate if the physical therapy (PT) evaluation process of history taking and physical exam results in a meaningful change for patients with low back pain (LBP), even before implementing treatment interventions. 

 

Why are they doing this study?

Low back pain (LBP) is the most widely reported musculoskeletal disorder globally and has significant healthcare expenditures. In the US, LBP accounts for 25% of outpatient physical therapy (PT) visits, with an estimated 170,000 people daily seeing a PT for this issue. 

With a shift toward a biopsychosocial model, more focus has been put on the therapeutic alliance (TA) and its impact on patient outcomes. TA is essentially the working social connection between a patient and clinician, blending clinical skills, verbal and non-verbal communication, a sense of warmth, collaboration, and trust. There is increasing evidence that TA and trust play a significant role in patients’ pain outcomes before any formal treatment is started.

 

Evaluation

 

What did they do?

This observational study included 34 patients with LBP with/without leg pain who went to four different outpatient PT clinics over a 3-month period. They had one PT at each site do the history taking and physical exam, and a different PT does the outcome measurements. Before the examination, all participants completed a demographic survey, disability index, and outcome measurements, including pain (low back and leg; numeric pain rating scale – NPRS), fear-avoidance beliefs (FABQ), Pain catastrophization (PCS), lumbar flexion, nerve sensitivity – pressure pain thresholds (PPT). After completing this pre-assessment, history taking and physical exams were done on each patient. 

All data were analyzed using statistical software.

 

What did they find?

This study found that for patients with LBP, the process of history taking and a physical exam had a significant therapeutic effect regarding fear-avoidance, pain catastrophization, movement and sensitivity of the nervous system. However, while some changes met or exceeded clinically significant differences, these were not correlated to physical exam duration and perceived connection by the PT.

Following history taking, the authors also found that NPRS for leg pain, PCS, trunk flexion, and PPT measurements showed a significant change from the initial intake. While adding a physical exam generated some improvement, only active trunk flexion and PPT for the low back were significantly improved compared to the measurements after history taking alone. Overall, they found that history taking resulted in the most significant changes seen in the evaluation process. The authors suggest that in line with existing research, this finding may result from the fact that history-taking happens at first contact and therefore provides an opportunity for a connection to alleviate patient fears and establish a TA. 

They did not find that the PT’s connection with the patient altered changes in pain or function.

 

Limitations?

The main limitation of this study is the study design. Being observational, the findings cannot speak to any causal relationships between the changes and outcome measures. Additionally, as there were no strict controls on the history taking and physical exam, with each PT doing them their own way may have affected the findings.

 

Why do these findings matter?

Understanding what factors provide the most significant treatment outcomes for patients with LBP can help address patient pain and function and reduce overall healthcare costs.

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Low Back Pain — Epidemiology, causes and risk factors

Low back pain

Goal of the review?

In this paper, 1 the authors provide a research-based overview of the epidemiology, causes, and risk factors. They also describe the clinical presentation and diagnostic criteria, and treatment options for low back pain.

 

Overview

Epidemiology and Socioeconomic burden

The economic impact of lower back pain is widely significant, with estimates of £2.8 billion in the UK and $100 billion in the US. Almost two-thirds of the economic costs from lower back pain stem from indirect costs such as loss of productivity. One study done in 195 countries found low back pain the leading cause of productivity loss in 126 countries. 

Low back pain can be classified as mechanical, neuropathic or nociplastic. Studies have shown that the prevalence of neuropathic pain ranges from 16% and 55% in patients with chronic lower back pain. One systematic review illustrated the prevalence of low back pain to range from 11.9% – 23.3 %, increasing with age and most common in middle-aged to older women.

 

Pathogenesis

There is a multitude of factors and causes of lower back pain. These include disc degeneration, radicular (neuropathic) pain, facet arthropathy, myofascial pain, sacroiliac joint pain, spondyloarthropathies (ankylosing spondylitis and psoriatic arthritis), and nociplastic pain (non-specific low back pain).

Low back pain

Professional LxH Model and the Lumbar Spinal Stenosis Model — helping patients understand their source(s) of low back pain.

 

Brain change, behavioural and genetic factors

Low back pain can be caused by changes in the brain, such as alterations in blood flow and changes to white and grey matter in the brain. Behavioural factors can also play a role. Studies show the role that emotion and emotional experiences can have on low back pain. For example, negative expectations, depression, and anxiety have been shown to predict poor pain outcomes in patients. Finally, there are also genetic factors that contribute to low back pain. Research has illustrated that heritability contributed to 26% lifetime prevalence of low back pain, 36% for functional limitations and 25% to pain intensity.

 

Clinical presentation, diagnosis, and screening

Low back and leg pain can be a manifestation of intervertebral disc herniation. Often, this type of pain will resolve itself in a few weeks. However, some patients can have recurring pain for up to two years. 

A large percentage of back pain is non-specific and resolves without any formal diagnosis. However, most guidelines recommend that patients have a physical exam and that history is taken. Some patients may require a neurological exam or vascular-focused exams to differentiate different types of claudication. Routine imaging is not required for most lower back pain cases. However, CT scan, MRI, and x-ray can be useful depending on the case.

Different screening tools have been developed that assist in preventing and treating low back pain, identifying patients prone to chronic pain, and distinguishing neuropathic from non-neuropathic pain.

 

Prevention and Treatment

Research demonstrates that a combination of exercise, education and ergonomic changes are effective as prevention strategies for lower back pain. These behavioural, non-pharmacological approaches are also used as first-line treatment. This can include clarification-oriented and exposure-based interventions that can help patients self-manage their pain and pain behaviours. 

For patients whose pain persists, pharmacological and procedural options can be explored. The American College of Physicians Guidelines recommends that treatment begins with non-steroidal anti-inflammatory drugs (NSAIDs) and muscle relaxants, tramadol, or duloxetine as second-line treatment and opioids as the last choice. Due to the addictive potential and negative side effects, opioid treatment is not recommended for most patients. 

There are also non-pharmacological interventions for low back pain. Steroid injections in the foramen, between the vertebrae, and in the sacroiliac joints have positive therapeutic effects. Other interventions such as facet joint blocks and radiofrequency are used but have mixed evidence supporting them. Spinal cord stimulation has shown positive outcomes and can be cost-effective, depending on the patient. 

When other interventions have not been successful, surgery may be an option for some patients. Research shows that for herniated nucleus pulposus, surgery can provide relief for a period but does not result in long-term benefits. For patients with lumbar spinal stenosis, decompression surgery can provide substantial improvement compared to a traditional approach.

 

Conclusions

Low back pain is globally prevalent and increasing as lifestyles become more sedentary. Lower back pain is a complex condition with various factors; therefore, diagnosis and treatment can be challenging. Existing research provides important evidence that can be used to develop inter-disciplinary and multimodal approaches to treatment and diagnosis. 

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The neurobiology of skeletal pain

Neurobiology

Goal of the review?

In this review 1, the authors focus on recent advances in understanding the nociceptive and neuropathic components of pain, as well as treatments for skeletal pain. 

 

Why are they doing this review?

Skeletal pain neurobiology is widely prevalent and has a significant impact on an individual’s quality of life and the broader society, as it is a leading cause of work disability. For this reason, the authors argue that understanding the mechanism that drives skeletal pain is critical to the prevent and treat pain.

 

What did they find?

Primary afferent sensory nerve fibres that innervate the skeleton

Unlike the skin innervated by various sensory nerve fibres, including A-beta, A-delta, C-fibers and others, the adult skeleton (bone and joint) is predominantly innervated TfkA+ sensory nerve fibres and CGRP.

While the same nociceptive nerve fibres innervate bone and joint, the density, pattern, and morphology are very different. For example, the periosteum (tissue enveloping the bones) has the largest sensory nerve fibres with A-delta and C-sensory nerve fibres that detect injury or alteration. In contrast, the articular cartilage of the knee and temporomandibular joint lack any innervation by sensory nerve fibres or vascularization by blood vessels. Therefore, it is believed that pain from a joint injury must come from the ligaments, synovium, and muscle.

Skeletal pain is also driven by the innervation of adrenergic and cholinergic sympathetic nerve fibres. Research has shown that these regulate bone destruction, bone formation and more, and therefore may play a significant role in disease progression in cartilage, bone, and skeletal pain.

Additionally, studies have shown that following injury to the skeleton, there is an interaction between sensory and sympathetic nerve fibres that may play a role in OA and complex regional pain syndrome. 

 

Nociceptive and neuropathic components of skeletal pain

Bone fractures and injury to articular cartilage are characterized by sharp stabbing pain and a lesser dull aching pain. Following injury, A-delta and C-fibers in the synovium and subchondral bone are sensitized. Normally non-noxious loading and movement of the joint are perceived as noxious stimuli. However, as articular cartilage lacks innervation, the location of the nerves driving pain is not known. Moreover, there is no clear correlation between the extent of joint destruction and the frequency and severity of joint pain. 

Research suggests there may be a neuropathic component in different types of skeletal pain. For example, in some types of cancer pain, the tumour cells destroy the distal ends of sensory nerve fibres that innervate the skeleton, which is then accompanied by an increase in movement-based pain. Another mechanism of neurobiology pain may arise from the sprouting of sensory and sympathetic nerve fibres. In mouse models of bone cancer, the number of nerve fibres per unit increased exponentially in a way not normally seen in bone.  

 

Neurochemical and structural changes to the Central Nervous System (CNS)

Little is known about the mechanisms that drive central sensitization in skeletal pain. However, it is thought to result when chemical, electrophysiological, and pharmacological systems that transmit and modulate pain are changed in the spinal cord and higher brain centers. 

 

Potential treatments for skeletal pain

The authors point out that while analgesics are needed to control pain better, an important therapeutic approach could induce bone or cartilage formation following injury. There are currently two classes of drugs to treat age-related bone loss: antiresorptive and osteoanabolic. However, both classes of drugs have limitations. 

Recent findings have outlined several new therapeutic targets for treating bone loss. Two of these inhibitory proteins that show promise are: sclerostin and Dickkopf-1. A Phase 1 study demonstrated that a dose of anti-sclerostin antibody increased bone density in the hip and spine in healthy men and postmenopausal women.

One question the researchers raise is how much neurobiology pain should be relieved. While it is beneficial for cancer patients to have their pain eliminated, the same is not true for patients with skeletal pain due to OA, bone fracture or ageing. The elimination of all pain could lead to overuse and more deterioration. Therefore, finding a treatment that could block pain while at the same time promoting bone formation and healing is critical. 

 

Why do these findings matter?

Understanding the causes of skeletal pain will help lead to more effective and targeted treatments. 

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Lumbar Spinal Stenosis — A Clinical Update and Approach to Patient Care with a Lumbar Spinal Stenosis Model

Lumbar Model with NervesJerome Fryer

Goal of the Study?

Lumbar spinal stenosis affects approximately 11% of the population, primarily in the adult population.1 In this article, the authors worked to provide a clinical update giving practitioners a “what you need to know” perspective on the ins and outs of clinical practice.

 

Why are they doing this study?

Because of its prevalence and challenge to accurately diagnose, it is important to understand the clinical presentation of lumbar spinal stenosis from a symptomatology standpoint. This careful attention to a patient’s symptoms can help guide an appropriate care plan. The clinical challenge can be cloudy as other conditions like vascular claudication can lead even the best clinicians down the wrong diagnostic path.

 

What was done?

A review of the anatomy is important when understanding the clinical symptoms of lumbar spinal stenosis. In this clinical update, the authors revisit the degenerative changes of the spinal canal and the intervertebral foramen related to spacing and the nerves that travel through these spaces.

Spinal Canal Spacing, Lumbar Spinal Stenosis Education Model

Lumbar spinal stenosis model

 

What did they find?

As the discs lose height, the associated anatomical changes can lead to narrowing. Degenerative discs lose height over time, and in doing so, the facets approximate, leading to hypertrophy of the bony architecture. Facet arthropathy (as seen in the Lumbar Spinal Stenosis Dynamic Disc Model) can take up valuable spinal real estate for lateral recess and intervertebral foramen; furthermore, discs lose height, discs bulge. And with this bulging, just as a tire bulges when it loses air pressure, it can often take up spinal canal spacing. This can also lead to the ligamentum flavum bulging itself (also thought of as buckling or thickening), encroaching on the valuable room the vasculature around the cauda equina must have to function.

The classic presentation is the patient reporting of not being able to distance walk as they have previously. They also report that standing often generates lower leg symptoms or buttock/leg weakness and relief of these symptoms by sitting and/or using the upper extremities to offload and flex the spine, like that seen with the shopping cart posture.

The authors point out that lateral recess stenosis and foraminal stenosis can mimic radiculopathy as seen in sciatica related to a disc herniation and report that a combination of these symptoms and subtypes is common.

 

How is Lumbar Spinal Stenosis Diagnosed?

A careful history and examination are at the roots of a proper diagnosis. Imaging has been relatively unreliable and likely due to the static nature of MRI and CT. It is suggested that clinicians can ask suspected patients to walk or to have patients extend the lumbar spine for thirty seconds to recreate the symptoms.

The authors have created these points and to be mindful of patients over 50 present with these symptoms:

  • pain in lower extremities/buttocks while walking
  • flexion to relieve
  • relief if using the upper extremities to push down and generate lumbar flexion like that seen using a shopping cart or riding a bicycle
  • unsteady motor disturbance while walking
  • tingling or numbness in the legs while walking
  • pulses equal and bilateral in lower extremities
  • low back pain

 

How do Clinicians Talk about Lumbar Spinal Stenosis with their patients?

Lumbar Spinal Stenosis Model

What tools do you use to educate your patients?

 

 

 

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