News for Dynamic Disc Designs which includes updated research and a synthesis of the most updated studies to help efficiently engage with patients and their back and neck pain.

We take an approach that an evidence-based practitioner would take. Carefully dissecting the history of a patients complaints, weaving the mechanical and psychosocial factors and then deliver a rational and tangible approach to relieving the back pain to the patient. Our news helps keep the practitioner abreast of the latest publications related to musculoskeletal health.

At our headquarters, we dedicate weekly hours to comb through the research for those who treat back pain and neck pain and deliver it.

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.

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. 

mechanotherapy

Goal of the Study?

In this study 1, the goal is to answer how physical exercise promotes tissue healing in bone, muscle, tendon, and cartilage.

 

Why are they doing this study?

Physical therapists and other clinicians prescribe exercise to address muscle tears, non-inflammatory arthropathies and controlled loading after injuries. This practice is in line with systematic reviews and controlled trials that demonstrate how exercise and movement can benefit patients with a range of musculoskeletal problems. However, in this short article, the authors focus on what happens at the tissue level to promote the repair and remodelling of tendon, muscle, articular cartilage, and bone. They argue that mechanotransduction, which is the physiological process where cells sense and respond to mechanical loads, is the term that best describes this process. 

 

What was done?

The authors began with a literature search for the earliest reference to mechanotransduction, finding 2441 citations in Medline. However, the term is not found in the current Oxford English dictionary and lacks a formal definition. Therefore, they suggest that a useful definition of the term would be “the processes whereby cells convert physiological mechanical stimuli into biochemical responses.” They then break down the process of mechanotransduction into three parts: mechanocoupling (the physical load), cell to cell communication (the communication throughout the tissue) and cellular response (the “tissue factory”).

To determine if mechanotherapy is taught in physical therapy programs, they formed international and intergenerational focus groups. The informal results suggest that mechanotransduction was not being taught in physical therapy education programs. To address this deficiency, they re-introduce the term ‘‘mechanotherapy’’ to cover situations where therapeutic exercise is prescribed to promote the repair or remodelling of injured tissue. Using this term, they then summarize clinical studies that have shown or implied a potential for mechanotherapy to promote healing of tendon, muscle, cartilage, and bone. 

 

What did they find?

Their review of clinical studies found that exercise has a beneficial response to controlled loading after injury for tendons, muscles, cartilage, and bone. For example, one study on tendons demonstrated that tendons with Achilles tendinosis treated with exercise showed near-normal structures after almost four years. Similar findings are demonstrated with the application of mechanotherapy for muscle injury. Clinical studies illustrated that the benefits of loading include better alignment, faster regeneration, and less atrophy.  

 

Why do these findings matter?

Patients are often prescribed exercise as a form of treatment for a variety of musculoskeletal issues. Therefore, it is important to understand better how mechanotherapy can benefit patients’ healing and its value for physical therapy.

Pain Syndromes

Goal of the Study?

In this study, 1, the authors have developed a framework to differentiate Parkinson’s Disease (PD) pain from non-PD-related pain and classify PD-related pain into 3 groups based on already validated mechanistic pain descriptors – nociceptive, neuropathic and nociplastic. 

 

Why are they doing this study?

In Parkinson’s disease (PD), about 20% of patients experience chronic pain at diagnosis. This number climbs to 80% during the course of the disease. PD pain has been divided into three categories: de novo pain related to disease onset and symptoms (PD-related); previous chronic pain aggravated by the disease or treatment (PD-indirectly-related); pain that is neither caused nor aggravated by the disease (PD-unrelated). Moreover, pain is considered PD-related when one of the following applies: when occurring along with the first motor symptoms, when occurring/aggravated during the OFF stage of the disease, when occurring at the same time with choreatic dyskinesia or when improved by dopamine treatment. However, these categories have not been validated or tested, making diagnosing and treating pain in PD. In response to this need, the authors develop a classification system to define and distinguish PD-related pain from non-PD-related pain.

 

What was done?

The authors used an international, cross-sectional, multicenter study. They recruited 159 non-demented PD patients and 37 healthy controls across 4 centers. Using the mechanistic pain descriptors (nociceptive, neuropathic and nociplastic), the authors developed a PD pain classification system (PD-PCS) by including classic pain-related situations of PD into each category. The severity of PD-related pain syndromes was scored by ratings of intensity, frequency and interference with daily living activities. Finally, they did an analysis and validation of their scale.

 

What did they find?

This study provides a unifying system for pain in PD that differentiates between PD and non-PD pain and outlines a treatment-based and mechanistic classification system for PD-related pain. Using this system, the authors found that 77% of patients experienced PD-related pain, with 15% suffering more than one syndrome at the same time. PD-related pain with nociceptive, neuropathic or nociplastic components was diagnosed in 55%, 16% and 22% of participants, respectively. Mixed pain syndromes were mostly found in nociceptive pain combined with nociplastic (12.7%) or neuropathic (9.6%). Pain unrelated to PD was found in 22% of participants, versus only 5% of controls. 

Concerning the PD-PCS, the authors found that pain severity scores significantly correlated with commonly used questionnaires such as the pains’ Brief pain Inventory and McGill Pain questionnaire. They did not find that the PD-PCS scores correlated with a motor score.

Finally, they suggest that the three pain types identified by the PD-PCS are different pain syndromes and reflect different mechanistic backgrounds and, potentially, different treatment approaches.  For example, they found that patients with higher nociceptive pain scores had worse quality of life scores, but this was not found for patients with nociplastic pain. 

 

Why do these findings matter?

Better classification of pain in PD will ensure that PD patients’ pain is treated more effectively and timely, ultimately contributing to better outcomes.

 

Sagittal

Goal of the Study?

In this study 1, the authors investigated the flexion-extension range of motion (ROM) and centre of rotation (COR) of lumbar motion segments in a large population, as well as the relationship between lumbar movement and sex, age and intervertebral disc degeneration (IVD).

 

Why are they doing this study?

Research on the in vivo motion of the spine has a long history. However, many of these studies have used non-invasive technologies with inherent limitations impacting their accuracy and precision. Moreover, many studies have included a lower number of subjects, preventing the ability of the data to represent the general population.

The authors argue that radiographic techniques in this study help overcome these limitations as the images allow for better visualization of each vertebra and movement of the lumbar segments. Additionally, the use of a large sample size for this study addresses the issue of representation and is the largest study to date looking at in vivo lumbar motion. 

 

What was done?

The researchers did a retrospective study looking at the radiographs of the lumbar spine in full flexion and extension for 602 patients, with the age and sex documented for each one.  Additionally, they used MRI scans of 354 patients. 

All spinal levels between T12-L1 and L5 – S1 were analyzed, resulting in 3612 lumbar motion segments from the radiographic images. They also examined 2124 images from the MRI scans looking at disc degeneration. ROM and COR were calculated for all lumbosacral segments using the software. They then examined the associations between motion and age, sex, spinal level and disc degeneration.

 

What did they find?

The median ROM in this study was 6.6 °. The researchers found an association between age and ROM, with older individuals, have lower ROMS. They argue these findings clearly demonstrate a relationship between age and lumbar spine flexibility independent of any signs of spinal degeneration. They also found that lower ROMS were associated with disc degeneration. However, they did not find any association between sex and ROM.   

In this study, they did not find an association between the position of the COR and the spinal segment. The most common COR was at the centre of the lower endplate of the IVD or slightly lower. With degeneration, particularly severe degeneration, they found the location of the COR spread randomly around the centre of the intervertebral space.

 

Limitations?

One of the main limitations of this study was the sole focus on the flexion-extension motion of the lumbar spine rather than including information on movements of different areas of the back. 

 

Why do these findings matter?

This study comprises the largest examination of the in vivo lumbar spine in flexion-extension, paying attention to age and spinal degeneration issues. Understanding the relationship between age and spinal mobility provides patients and doctors with information to better treat back pain and instability.

Innervation

Goal of the Study?

In this study 1, the authors use a rat model to examine the time-course development of pathological joint changes and correlate them with pain-related behaviour in OA. 

Why are they doing this study?

There is a very high incidence of Osteoarthritis (OA) in the elderly population, and it is a leading cause of disability and pain. However, there is a lack of knowledge of OA’s pain mechanisms, particularly the role that neuropathic pain (NP) plays in OA.

OA has been described as a degenerative rather than an inflammatory disease. However, in recent years research has identified the many inflammatory processes that take place in OA.  Existing OA models have shown how this inflammation is supported by overexpression of nerve growth factors causing nociceptive fibres to grow into inflamed joints. This inflammatory process helps explain why there is a poor correlation between radiographic changes and pain levels in OA patients. Moreover, some patients continue to experience pain after a total joint replacement, suggesting that OA can result in neuropathic pain (NP). 

What was done?

The researchers used a rat monoiodoacetate (MIA) model of the ankle joint. MIA results in pathological changes and pain-like behaviour common with those observed in human OA. This model has been used extensively in research and is well validated.

They injected MIA or saline into a total of 126 male rats. For this study, they used the rat ankle joint as it receives most of its nerve supply from the sciatic nerve, which is used most commonly in NP models. From this, they assessed a variety of changes, including pain-related behaviour, hypersensitivity, reaction to cold and heat, changes to normal movement, cartilage degeneration, bone degeneration, and the effects of drug treatments.

What did they find?

 Overall, the study provided a time-course view of the development of pathological changes to the joint and the associated pain-related behaviours. 

The researchers found significant innervation increases at specific periods of time that coincided with mechanical hypersensitivity at 4 weeks and pain in response to cold at 5 weeks. X-ray findings showed significant cartilage and bone degeneration and joint space narrowing at 5 and 10 weeks. 

The study also illustrated changes in sensory and sympathetic innervation of joints in the subchondral bone and synovial membrane at 5 and 10 weeks.  This increased concentration of sensory and sympathetic fibres was associated with pain-related behaviour and similar to those observed in NP models. Furthermore, they found that pain-related behaviour and extensive joint damage were associated with the expression of activating transcription factor 3 (ATF3) in the dorsal root ganglia (DRG), as well as the microglia and astrocyte changes in the dorsal horn. Using various pharmacological treatments to inhibit or block sympathetic fibres and glial could suppress pain-related behaviour. They argue that these findings suggest that multiple factors contribute to OA pain, including inflammatory changes in the joints, supporting the theory of a neuropathic component in OA.

Why do these findings matter?

As pain is the main reason patients seek medical help, effective pain management is critical to improving life quality. Therefore, understanding what causes pain will help in the development of pain management protocols and treatments. 

 

Cervical Spondylosis

Goal of the Study?

In this study, 1 the researchers investigated the association of prior cervical spondylosis (CS) diagnosis with peripheral vertigo in Taiwanese patients.

Why are they doing this study?

CS is an age-related condition resulting from deterioration in the spine, with a prevalence rate of more than 50% among those over 40 years old. While not all patients will have clinical signs of disease, symptoms can range from tingling, numbness, pain in the neck or arms, stiffness, headaches, vertigo, and balance loss.  Peripheral vertigo is often observed with CS and is one of the most common reasons patients get medical care.

The authors state that despite the wide prevalence, to date, no population-based studies are looking at the association between CS and peripheral vertigo. 

What was done?

The researchers used a case-control study design, selecting cases of peripheral vertigo and matched controls. They used the data from the Taiwan Longitudinal Health Insurance Database 2005 (LHID2005), which consists of all registration riles and medical claims data for a stratified random sample of 2 million enrollees.

They identified all those ≥ 18 years old who had received a diagnosis of peripheral vertigo between January 1, 2010, and December 31, 2016, which totalled 2,570 patients. These were compared to a control group of 7,710 patients from the same dataset (with 3 controls per one case), matching based on patient demographics such as age, sex, income, geographic location and medical comorbidities associated with increased risk of vertigo. They excluded all patients less than 18 years old and those who had never been diagnosed with peripheral vertigo.

They then used a statistical program to estimate determine the relationship between prior CS occurrence among peripheral vertigo patients versus controls. 

What did they find?

Overall, the researchers found that CS is associated with peripheral vertigo, particularly with those patients aged 45 to 64. This association is consistent with other research and may be caused by a range of issues, including cervical instability, inflammatory cytokine stimulation, and more.  They also found that CS with myelopathy (an injury to the spinal cord due to severe compression) is not associated with peripheral vertigo. 

They did not find any significant differences based on demographics. In particular, they did not find that patients over 64 years of age with CS had a higher risk of peripheral vertigo.

Limitations?

There are a few limitations outline by the authors. First, they state that claims data may not be as precise as information based on a clinical examination, resulting in some misclassification between types of vertigo. Second, there is a lack of data on potential confounding variables such as family history, lifestyle, etc. Finally, the vast majority of the study population are Han Chinese, and therefore the results may not be generalizable to other racial and ethnic groups. 

Cervical Spondylosis

Cervical model

Why do these findings matter?

As peripheral vertigo often occurs with CS, it is important to understand the relationship between the two conditions better to diagnose better and treat patients.