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.




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.



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.

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.



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.



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.



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. 

disc herniations, sequestered lumbar disc herniation

Goal of the article?

The goal of this study, 1 is to examine why there is an increasing incidence of disc herniation in young people. 


Why are they doing this review?

Disc herniation is often the result of natural degeneration changes accompanied by age as the vertebral discs lose water and become less resilient and less responsive to dynamic shock. However, increasingly, disc herniations are appearing in younger people. The cause of this early degeneration is most likely from inactivity sustained by static compressive loads, as well as other factors such as smoking, obesity, familial predisposition and other factors like prolonged sitting. As this can have long-term implications, understanding causes and potential treatments of early degeneration is critical to minimizing the negative outcomes for individuals and society at large.


What was done?

This is a prospective study with a total of 33 young patients, all with extruded lumbar disc herniations managed by conservative or surgical approaches between 2017 and 2018. On average, patients were 25 years old. In addition to age, the researchers asked each patient about smoking, familial predisposition, sporting activity, and occupation. They measured pain using a visual analog scale (VAS) and measured patients’ BMI. All patients had lumbar MRI imaging.


Helping patients understand compressive loads with a Dynamic Disc Model


What did they find?

The researchers found that 18 patients (8 females and 10 males) had a disc extrusion at the L5-S1 level, 12 patients (8 females and 4 males) had a disc extrusion at the L4 and L5 level, and 3 patients had a disc extrusion at both the L4-L5 and L5-S1 levels. Motor deficits were detected in 4 patients who then required surgical treatment. For these patients, three procedures involved the L4-L5; one had right L5 radiculopathy and motor deficit, while the others were on the left side. 

The remaining 29 patients were treated conservatively with physical therapy and pain medication. They were given information on ergonomics and help with stopping smoking. In follow-up, the VAS scores were reduced, and all patients had lost weight. However, only three patients had quit smoking.

When the researchers looked at occupations, they found that all patients sat during the day and lacked movement. They also found that 61% of the patients were smokers and the mean BMI was 32.5 kg/m2.  Additionally, in line with existing research, this study found that familial predisposition with lumbar disc herniation played a role. 


Why do these findings matter?

Understanding factors contributing to early disc degeneration can help patients make lifestyle changes that can postpone pain and mobility issues. 

Disc Nucleus

Goal of the review?

The goal of the article, 1 explores the molecular level of intervertebral disc degeneration. Specifically, the authors examine the correlation between proteolytic enzymes, microvascular formation, or neve fibre ingrowth in the intervertebral disc nucleus. 


Why are they doing this review?

To aid in diagnosis and treatment, the authors argue that it is important to understand the molecular level of disc degeneration and the functional changes that accompany degenerative IVD. By measuring the extracellular matrix components, such as collagen in the disc nucleus tissue, the relationship between the degrees of degeneration of the intervertebral disc (IVD) is analyzed. 



What was done?

They selected 40 patients for the case group, all of whom had degenerative disc nucleus pulposus (NP) and were admitted to the hospital. The inclusion criteria for this group were the presence of lumbar degenerative disease and cervical spondylosis. Additionally, they selected 20 healthy subjects for the control group, with inclusion criteria of cervical vertebra and lumbar vertebra injury caused by trauma. There was no significant difference in demographic characteristics, including age, gender, and other variables. 

The researchers took blood and NP tissue from each participant and stored the samples at 80º. They then carried out H&E staining and immunohistochemical staining to observe cathepsins such as aminopeptidase and vascular endothelial positive cells. Finally, they used statistical software to determine correlations.


What did they find?

In the normal group, the researchers found that following H&E staining, chondrocytes were clustered in the cartilage depression, and matrix staining was more uniform. In contrast, the chondrocytes were reduced for the case group, and the nucleus was stained or disappeared. When looking at immunohistochemical staining results, the normal group had little or no expression of aminopeptidase N (APN) and leucine aminopeptidase (LAP). However, in the patient group, APN and LAP were expressed in the degenerative IVD. These are important findings as a positive correlation between APN and LAP and degenerative changes to the IVD. Research shows that degenerative changes in the IVD tissue are associated with neovascularization. The appearance of proteolytic enzymes such as APN in the IVD and the relationship between microvessel formation and nerve in growth in the IV illustrate changes at the molecular level of disc degeneration. Moreover, the NP tissue was immunohistochemically stained with CD31-labeled VEGF, and the endothelial cells were stained singly or in clusters.


Why do these findings matter?

Understanding molecular changes to the IVD will help to diagnose better and treat issues related to degenerative IVD.


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. 


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.

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?