Lower Extremity Arterial Occlusive Disease

Goal of the Study?

In this study, 1 the aim is to understand the risk factors and symptoms that contribute to patients with Lower Extremity Arterial Occlusive Disease (LEAOD) being misdiagnosed with lumbar disc herniation (LDH).

 

Why are they doing this study?

The authors argue that patients who should be diagnosed with lower extremity arterial occlusive disease are being diagnosed with LDH as there are similar symptoms. They argue it is important to understand what factors contribute to this misdiagnosis so that there is no delay in treatment and an increased economic burden to patients and society.

 

What was done?

This was a clinical study with a total of 148 patients. Group A had 126 patients who had LDH with lower extremity symptoms and whose symptoms had been relieved after lumbar surgery of posterior lumbar interbody fusion (PLIF). Group B had 22 patients with LDH with lower extremity symptoms but who had no relief after PLIF. In this group, they were diagnosed with LEOAD and their symptoms recovered after vascular treatment. The Japanese Orthopedic Association and Oswestry disability index scores were collected before surgery, six months after PLIF and sex months after vascular treatment. An evaluation of symptom relief between patients in groups A and B was then used. For each group, the researchers also collected gender, age, HBP, diabetes, smoking, coronary, pulse pressure (PP), LDH, segment and type, ankle-brachial index (ABI) and straight leg raising test (SLRT). They then used statistical software to determine the relationship between the various factors.

 

What did they find?

They found a statistical difference between the two groups in PP, ABI, central disc herniation and SLRT. The researchers found that higher PP, lower ABI, central disc herniation and negative SLRT led to an increased risk of misdiagnosis for LDH, even though these are all associated with LEAOD. Moreover, they found patients were misdiagnosed as having LDH as a way to explain lower limb symptoms even though MRI images displayed only a mild herniation. The authors argue it is important to consider other imaging exams such as CTA and MRA and sufficient patient history and physical exam to determine a diagnosis for LEAOD.  For example, skin temperature and abnormal skin colour are common in patients with LEAOD, but not LDH.

 

Why do these findings matter?

 Appropriate diagnosis is key to appropriate and timely treatment. Understanding how to differentiate LEAOD from LDH is important for good patient care.

 

minimal damage

Goal of the Study?

In this study 1, the authors evaluate the scientific validity of using the biomechanical approach to assess injury causation from minimal damage traffic crashes.

 

Why are they doing this study?

A major point of contention in civil litigation cases following traffic injury claims is related to causation. Claimants generally rely on their doctor’s expertise to explain the cause of a persistent injury following a crash. In contrast, insurers often rely on a biomechanical approach as a basis for denying any link between the crash and ongoing injuries. The theoretical basis of the biomechanical approach is that the risk of injury from a crash is the same as the forces of activities of daily living (ADLs). However, the authors argue that the literature does not support this approach. Findings of large epidemiologic studies indicate that the injury rate is significantly greater in minimal and no damage crashes than ADLs.

 

What was done?

For this review, the authors included literature from three categories: volunteer rear-impact crash testing studies, ADL studies that describe linear and angular head acceleration for various ADL activities, and observational studies of real-world impacts. They compared the occupant accelerations of minimal or no damage (3-11kph speed change or delta-V) rear-impact crash tests to the accelerations described in 6 of the most commonly reported ADLs in the reviewed studies. The injury risk observed in real-world crashes compared to the results of the pooled crash test and ADL analyses, controlling for delta-V and adjusting for test subject age and sex. 

 

What did they find?

The authors argue that the biomechanical injury causation approach is scientifically invalid. Research illustrates that both crash testing results and epidemiologic data from real-world rear crashes show that there is a substantial risk of injury even at the lowest levels of impact severity. This stands in contrast to ADLs that have virtually no risk. They found that the average acceleration forces of the head during rear-impact crash tests were several times greater than average forces experienced during ADLs. Moreover, the injury risk of real-world minimal damage rear-impact crashes was estimated to be at least 2000 times greater than for any ADL. For example, research has indicated a 54% risk of any cervical spine injury and a 6% risk of any injury lasting for more than 6 months in an 11km/h rear impact delta-V crash. For this reason, they argue that the basis underlying the biomechanical injury causation approach, which uses occupant acceleration as a proxy for injury risk, vastly underestimates the actual risk of such crashes and should not be used in practice. 

 

Why do these findings matter?

The results of this review challenge the use of the biomechanical approach and illustrate how it underestimates the risk of minimal damage crashes on those involved. 

persistent pain

Goal of the Study?

In this study, 1 the authors try to understand the mechanisms involved in the peripheral and central sensitization associated with inflammatory pain. To do this, they used models of inflammation to examine the expression and internalization of the substance P receptor (SPR) in the spinal dorsal horn.

 

Why are they doing this study?

Chronic inflammation is responsible for various illnesses of which pain is paramount including arthritis, back pain and other joint disorders. To date, the neurochemical changes that occur within the spinal cord that contribute to the creation and continuance of inflammation are poorly understood. 

 

What was done?

The authors used four models of inflammation, which they produced by injecting the hind paw with formalin to look at acute pain, carrageenan to look at short-term pain and complete Freund’s adjuvant (CFA) to examine long-term pain. They also examined the neurochemical changes in an animal model of polyarthritis induced by CFA injection into the base of the rat’s tail. They then compared this data to past electro-physiological and behavioural data to examine and illustrate the changes in the amount and/or site of release of SPR from primary sensory neurons, the number and location of SPR expressing spinal neurons that are activated by this released Substance P (SP) and the populations of neurons showing up-regulation of the SPR.

 

What did they find?

They looked at three types of inflammatory pain: acute, short-term and long-term, to demonstrate how SPR internalization may show the role of ongoing sensory neuron input to acute and persistent pain states. Overall, they found a unique neurochemical signature that characterizes each type of inflammatory pain within the spinal cord.

Formalin injection to examine acute pain resulted in a two-phase response with early and short pain response, followed by a longer and more persistent pain. They found that there is ongoing sensory nerve input from C fibres and the release of SP in the spinal cord during both phases. Unlike formalin-induced inflammation, when carrageenan was injected as a way to examine short-term inflammatory pain, the researchers found that SPR internalization was observed early after injection. Still, no ongoing SPR internalization was seen 3 hours after injection. The researchers found that both short- and long-term pain is characterized by a lack of spontaneous SP release from primary afferents, as well as an increase in both the number and the location of SPR-IR spinal neurons that are triggered in response to stimuli. However, the major difference found between short- and long-term pain is that in the latter, there is up-regulation of SPR on neurons in the spinal cord that is not seen in other types of pain. They argue this may contribute to the central sensitization observed in long-term inflammatory pain

 

Why do these findings matter?

Understanding mechanisms of pain provide potential pathways for targeted treatment for patients impacted by different types of pain.

Pathophysiology

Goal of the Study?

In this paper, [Pathophysiology of musculoskeletal pain: a narrative review], the authors provide a review of the various pathophysiology mechanisms of musculoskeletal pain and how they interact to promote the transition from acute to chronic pain. 

 

Why are they doing this review?

Chronic musculoskeletal pain is defined as pain felt in the musculoskeletal tissues that last for more than 3 months and is characterized by functional disability and emotional distress. It is a secondary type of pain caused by different conditions such as infection or auto-inflammatory processes that lead to systemic inflammation or structural changes to joints, muscles or tissues. 

Chronic musculoskeletal pain is prevalent in the general population, with approximately 37% of the US population impacted and an economic burden of $635 billion per year. Outside of the US, the prevalence ranges from 18.6% in Switzerland to over 45% in Italy and France.

 

What did they find?

In the review, the authors illustrate how many factors and processes interact to produce musculoskeletal pain. Research illustrates that bones, joints and muscles, including the ligaments, capsules and menisci, are innervated by a network of sensory nerve fibres including, Aδ and C fibres. These fibres’ stimulation can drive musculoskeletal pain through mechanical distortion, local acidosis, and increased bone medullary pressure. This then drives the promotion of inflammatory mediators such as nerve growth factor (NGF), pro-inflammatory cytokines interleukin (IL) 1ß, IL-6, tumour necrosis factor- α chemokines. Moreover, the interaction between immune and nervous systems and glial stimulation further promotes these inflammatory mediators that magnify and sensitize pain signals and lead to cortical remodelling.

Bone pain can also be caused by the increase in sensory nerve fibres where there are injuries. During bone healing, nerves sprout around the injury site and then pull back when it is healed. However, when bones don’t heal (as in osteoarthritis), the injured area remains hyper-innervated, and heightened pain sensitivity occurs. 

Finally, research has indicated that sex, age, psychosocial factors, beliefs and thoughts influence gene expression and the experience of musculoskeletal pain. For example, women experience higher pain sensitivity than men and have a different biologic response to tissue damage with higher cytokine production than men, which means a stronger inflammatory response and higher pain levels. 

 

Why do these findings matter?

Understanding the pathophysiology of musculoskeletal pain, which includes biological and demographic and psychological factors, is critical to developing pain management treatments and strategies for patients.

smartphone overuse

Goal of the Study?

In this study, 1, the aim was to investigate the association between nuchal (neck) pain, psychological impairment and smartphone overuse (SO) in office workers.

 

Why are they doing this study?

The use of smartphones is prevalent, with most people spending multiple hours a day using them for work and personal life. The prolonged use of smartphones can lead to neck disorders due to users’ neck flexion posture as they look at the screen for prolonged periods of time. Most smartphone tasks require users to stare downwards and hold their arms out in front of them, making the head move forward and causing an excessive anterior curve in the lower cervical vertebrae and an excessive posterior curve in the upper thoracic vertebrae to maintain balance. This forward head posture (FHP) may increase stress on the cervical spine and neck muscles. Research has shown that incorrect posture of the neck and head is associated with chronic musculoskeletal pain. Therefore, the increased use of smartphones at work is an important aspect of the study.

 

What was done?

The authors conducted a cross-sectional report of a cohort study between May 2018 and July 2019, with 1602 office workers (575 males and 1027 females). To be included in the study, participants had to be at least 18 years of age and have more than 4 years of smartphone use. People were excluded if they had a history of cervical trauma or any congenital abnormalities in the spine. 

The researchers assessed a range of data including demographics, abnormal symptoms of pain in the neck, physical activity and psychological behaviour — using scales to measure smartphone addiction, depression, anxiety and stress, as well as physical activity.  Multiple regression was used to evaluate the relationships.

 

What did they find?

The overall prevalence rate for neck pain was 30.1%, with significantly more females and younger workers reporting neck pain than others in the sample. The researchers also found with higher physical activity, less neck pain was reported. Those with vigorous, moderate and light activity had different reported neck pain levels with 7%, 25.5% and 31.5%, respectively. 

The prevalence for SO was 20.3% and was more common in younger male workers. Office workers with SO showed a higher prevalence of neck pain (62.9%) than people without SO. Additionally, single office workers had 1.6 times more risk for SO compared to married workers. Overall, those with SO were approximately 6 times more likely to have neck pain.

The researchers also found a significant correlation between neck pain and depression, anxiety and stress, with 26.6% of the workers with severe depression, 31.3% severe anxiety and 36.6% severe stress. Moreover, those with severe depression had a 70% more chance of neck pain

 

Why do these findings matter?

With the increasing reliance on smartphone use in modern life, the relationship between SO, neck pain, and psychological suffering found in this study is important information. The authors argue that there is a need for research on preventing the negative outcomes of SO. 

 

degenerative joint disease

Goal of the Study?

In this study 1, the authors investigate degenerative joint disease in the spine and major peripheral joints (shoulder, elbow, hip and knee) in chimpanzees, lowland gorillas and bonobos.

 

Why are they doing this study?

Degenerative joint disease is one of the most common pathological musculoskeletal conditions in human populations. It has also been observed in a variety of nonhuman animals, including nonhuman primates. Existing research has illustrated degenerative disease in chimpanzees, gorillas, orangutans, gibbons, macaques, baboons and probosci’s monkeys. Overall, prevalence has been reported as quite low in wild monkeys (with some exceptions) compared to colony-reared Old-World monkeys. 

The authors want better to understand the evolutionary basis of degenerative joint disease. 

 

What was done?

This investigation’s skeletal materials are drawn from two samples of chimpanzees, a sample of lowland gorillas and a small sample of bonobos. The samples from the chimpanzees are from Gombe National Park, Tanzania, while the other materials are from museum materials originally collected in west/central Africa. In total, 5807 sample surfaces for vertebral osteophytosis (VOP), 12,479 surfaces for spinal osteoarthritis (OA) and 1211 joints for evaluation of peripheral joint OA.

The human osteological samples are from two areas, Central California and a group of Inuit from Alaska.

The presence of VOP was based on a determination of osteophyte development. OA presence was based on hypertrophic development and changes to joint spacing. The severity of VOP and OA was scored based on slight, moderate or severe.

 

What did they find?

All apes display significantly less spinal disease compared to humans. The authors suggest that this is most likely related to movement on two legs. Among the African apes, gorillas are slightly more involved in the spine than chimpanzees with almost no spinal degeneration. Both bonobos and gorillas have significantly more involvement than chimpanzees in the cervical and thoracic regions (but the sample size for bonobos is so small that it is hard to say there is any significance).  As with previous research, the authors found that colony reared Old World monkeys, such as macaques, have higher OA levels than other free-ranging apes. The authors argue that the variation between humans and African apes in VOP and OA prevalence may be explained by human longevity.

 

Why do these findings matter?

This study can help understand basic processes in degenerative joint disease among humans and our closest relatives in a broader evolutionary context. 

 

Dynamic Sitting Exercise

Goal of the Study?

The objective of this study [1. An Evaluation of an Innovative Exercise to Relieve Chronic Low Back Pain in Sedentary Workers] was to examine the effectiveness of a unique supported dynamic lumbar extension with the abdominal drawing-in maneuver (ADIM) technique on stature change, deep abdominal muscle activity, trunk muscle fatigue and pain intensity during prolonged sitting in chronic low back pain (CLBP) participants.

 

Why are they doing this study?

Low back pain (LBP) is a global issue among the working population. In Thailand, where this study is based, the prevalence of LBP across various occupations is approximately 83%, and 60% of workers in call centers have reported that their LBP is aggravated by sitting during the workday. 

Previous research has demonstrated that continuous sitting results in trunk muscles’ contraction, causing muscle fatigue and reducing muscular support to the spine. This increases stress on ligaments and intervertebral discs, ultimately leading to LBP. Existing research, such as that by lead author Jerome Fryer (the CEO of Dynamic Disc Designs Corp.) et al. (2010), has demonstrated the value of the dynamic sitting exercise on restoring disc height. Moreover, the ADIM technique has been shown to be effective in reducing the spinal lumbar load in patients with chronic LBP. 

 

What was done?

This is the first study investigating the combined use of a supported lumbar extension with the ADIM technique on stature recovery in CLBP patients.

They recruited 30 patients (15 males and 15 females) between the ages of 20-39 years old. All participants included had CLBP lasting more than 3 months, had low to moderate pain levels and reported sitting for at least 2 hours at work.

The participants were randomly assigned to one of two groups: 1) control – sitting without exercise; 2) sitting with supported dynamic lumbar extension with the ADIM technique. The control group sat for a 41-minute testing period. The intervention group sat in a neutral posture for 27 seconds; at the 28th second, they straightened their lower back and drew in their lower abdomen and extend their lumbar spine with their upper limbs supported to transfer the spinal load to the upper limbs, with their chest up slightly and chin in for 5 seconds. Participants were then repositioned to a neutral position and relaxed their lower abdomen for 3 seconds. This was completed 3 times over the 41-minute sitting period.

 

What did they find?

This study found that a dynamic lumbar extension with the ADIM technique protected from the detrimental effects on stature change and deep trunk muscle fatigue that can result from prolonged sitting. They found the intervention significantly reduced stature loss compared to the control group. Additionally, they found that this combined approach prevented an increase in pain intensity during prolonged sitting in people with CLBP. 

 

Limitations?

This study has several limitations, including the use of young participants, setting the study in a laboratory rather than the workplace, self-reported data, lack of consensus on body positioning, and limiting the findings to immediate effects rather than long-term outcomes.

 

Why do these findings matter?

Clinicians can implement this intervention for patients who sit for long periods of time as a way to prevent LBP problems.