State-of-the-Art Personalized Therapy Approaches for Chronic Non-Specific Low Back Pain: Understanding the Mechanisms and Drivers

Abstract

Chronic non-specific low back pain (CNSLBP) is a debilitating condition that affects millions of people worldwide, significantly impacting quality of life and imposing a substantial socioeconomic burden. Traditional treatment approaches often rely on a one-size-fits-all strategy, failing to account for individual variations in pathophysiological mechanisms, drivers, and the principles of personalized medicine. Furthermore, an overemphasis on biomechanical findings from imaging may lead to ineffective interventions and unnecessary surgical procedures, obscuring other important factors that contribute to pain perception. While highlighting the limitations of universal treatment approaches, in this review we present a practical clinical approach aimed at elucidating the main pathophysiological mechanisms and various factors underlying the development and maintenance of CNSLBP in order to create a personalized treatment program. In conclusion, this review underscores the need for personalized therapeutic strategies that take into account the unique characteristics of each patient, recognizing the complex interaction of biological, psychological, social, and other factors that contribute to the development of individual pain. By combining a comprehensive understanding of the complexities of this condition, we aim to improve clinical outcomes and provide information on the development of effective personalized treatment algorithms, particularly in the field of neurological practice.

Key Summary Points

Why carry out this study?

Traditional treatment approaches are often based on a standard strategy that does not take into account individual differences in the pathophysiological mechanisms and drivers underlying chronic non-specific low back pain CNSLBP.

In patients with CNSLBP, we distinguish four main pain phenotypes that indirectly reflect the pathophysiological mechanisms contributing the pain syndrome: inflammation, muscle spasm, central sensitization, and disinhibition. Therefore, the choice of drugs should not be standard, but correspond to the pathophysiological mechanisms identified in a particular patient.

Eleven key pain drivers have been recognized that can modulate pain perception and alter these mechanisms: biomechanical, social and cognitive factors, anxiety, depression, catastrophization, physical activity, insomnia, obesity, hormonal imbalance, and microbiota. Each patient needs to have an individual picture of these drivers identified in order to make the right decision when choosing the appropriate treatment methods.

All therapeutic recommendations should not be formal and standard, but should be strategically targeted at the identified pathophysiological mechanisms and drivers of pain, considering their current significance and impact on the patient’s condition.

We suggest that using tools such as artificial intelligence (AI) and special applications may help patients with burden and time loss – e.g., patients can complete questionnaires before visit or use office manager’s help before attending a clinician.

Introduction

Chronic non-specific low-back pain (CNSLBP) is characterized by persistent discomfort, muscle tension, or stiffness localized in the lumbosacral region, often extending to the gluteal area, with or without radiation to the lower extremities. This condition is typically defined by the absence of a clearly identifiable specific underlying pathology or comorbidity, such as fractures, radiculopathy, ankylosing spondylitis, infections, neoplasms, or metastases [1].

The prevalence of CNSLBP has been steadily rising over the past few decades, with low-back pain now recognized as one of the leading causes of disability worldwide. In 2020, more than half a billion people worldwide suffered from low back pain, and this number is projected to exceed 800 million by 2050 [2].

This alarming increase in incidence can be attributed to several factors, each contributing to the complexity of CNSLBP management. Despite numerous clinical guidelines based on the principles of evidence-based medicine, the problem is not solved. According to a special study, only 20% of patients with back pain receive adequate care and evidence-based correct recommendations [3].

One significant issue is the undifferentiated approach to pharmacotherapy. Historically, the standardized treatment model has dominated clinical practice, where clinicians apply uniform diagnostic and therapeutic strategies to all patients. This approach does not take into account the individual pathophysiological mechanisms underlying the development of pain, as well as the existence of multiple factors influencing the perception of pain (pain drivers), thereby undermining the principles of personalized medicine [4].

In most cases, clinicians are not able to use the proposed clinical guidelines in their clinical practice because they are aimed at ‘treating pain’ rather than ‘treating the patient’. In order to implement a personalized approach to therapy it is not enough to have only Clinical Guidelines or standards. There are many patient-related factors that influence pain perception and must be taken into account (individual pain phenotype, age, gender, psychology, sleep, physical activity, cognitive function, social factors, comorbidity, etc.) [5, 6]. Mentioning complications and potential challenges of this approach to CNSLBP treatment described below, these guidelines require enough time and patients’ transparency and trust to complete a comprehensive assessment. We suggest that using tools such as artificial intelligence (AI) and special applications may help patients with burden and time loss—e.g., patients can complete questionnaires before visit or use the Office Manager’s help before attending a clinician.

Another issue is the overestimation of biomechanical abnormalities, often identified through imaging techniques like X-rays or MRI (magnetic resonance imaging). While these findings are very valuable, they are not always the primary course of pain for every patient. Over-reliance on biomechanical factors can lead to unnecessary and ineffective physical, physiotherapeutic and manual therapies, as well as unnecessary surgical interventions [7].

Furthermore, many other contributory factors (pain drivers) in the pathogenesis of CNSLBP are often overlooked. These factors, though diverse and complex, are crucial in understanding the full spectrum of pain perception and must be considered in a comprehensive treatment strategy.

Clinical trials often aim to find a universal standard solution for all patients with CNSLBP, which is inherently wrong. The causes of pain and pathophysiological mechanisms vary significantly among individuals, requiring an individual approach. Although clinical guidelines provide a general framework for evaluation and treatment, they cannot substitute for personalized clinical decision-making [8].

In this article, we present a methodology for developing tailored therapeutic recommendations for individuals with CNSLBP, based on the detailed analysis of pathophysiological mechanisms and patient-specific pain drivers.

The proposed methodology is divided into two key parts:

I. The first part involves a comprehensive analysis of the patient’s pain phenotype, aimed at elucidating the underlying mechanisms responsible for the pain symptoms and experience.

II. The second part focuses on identifying and analyzing the specific pain drivers, which are the factors that modulate the patient’s pain perception.

It is crucial to emphasize that this approach is intended exclusively for patients diagnosed with CNSLBP, defined as those in whom specific etiologies of pain (e.g., tumors, infections such as Bechterew’s disease, osteoporosis, fractures, radiculopathy) have been ruled out at the time of evaluation. These are patients whose pain persists chronically, despite the absence of ‘red flags’ and previous unsuccessful medical interventions.

Methods

In this review article, we systematically analyzed the existing researches regarding personalized therapy approaches for CNLBP. We focused on studies published in the last 5–7 years. Comprehensive searches were conducted in multiple databases, including PubMed, Cochrane Library, Scopus, and Web of Science, using specific keywords such as "chronic non-specific low back pain," "personalized therapy," "mechanisms," and "drivers." The search was limited to articles published in English from 2016 to 2023. We included original research articles, case studies, meta-analyses, and systematic reviews that addressed personalized therapeutic interventions for CNLBP. Studies were selected based on their relevance to the topic, methodological rigor, and the clarity of their reported results. We concluded data from the suitable articles with available full texts and provided analyzed information with pictured schemes and resulting summaries. We also analyzed the approaches described in the literature mentioned in the review and applied them to simulated patients phenotypically similar to the authors’ real clinical cases. The matches of the clinical case descriptions in the “Clinical cases” section with real people are coincidental. This article is based on previously conducted studies and does not contain any studies with human participants or animals performed by any of the authors.

Pain Phenotype: Pathophysiological Mechanisms of CNSLBP

The concept of pain phenotyping refers to the clinical characterization of a pain syndrome that indirectly reflects the underlying pathophysiological mechanisms responsible for the pain. These mechanisms serve as therapeutic targets, guiding the selection of pharmacological interventions. By identifying the specific phenotype, clinicians can tailor treatments to address the precise mechanisms at play, potentially improving therapeutic outcomes from the onset of care [9].

For patients with CNSLBP, four key pathophysiological mechanisms are commonly identified, each corresponding to specific groups of drugs that are recommended based on the identification of these mechanisms (Fig. 1).

Fig. 1.

Key pathophysiological mechanisms in chronic non-specific low back pain. NSAIDs nonsteroidal anti-inflammatory drugs, SNRIs selective serotonin and norepinephrine reuptake inhibitors

Inflammation Phenotype

Characteristics: this phenotype is marked by pain or local tenderness in lower back, increased upon certain movements, referred pain, other inflammatory symptoms. Notably, patients do not experience allodynia or hyperalgesia. Clinical picture of facet joint syndrome is a typical example of inflammatory phenotype [10].

Treatment options: when inflammation is the dominant mechanism, the use of nonsteroidal anti-inflammatory drugs (NSAIDs) is typically recommended. Inflammation is a multifaceted process involving various physicochemical stages, with cyclooxygenase (COX-2) playing a critical role in acute inflammation. Therefore, NSAIDs, which inhibit COX-2, are particularly effective in managing pain linked to inflammatory process [11, 12].

Muscle Spasm Phenotype

Characteristics: this phenotype is identified by symptoms such as muscle tension, increased muscle tone, thickening or shortening of the muscle, reduced range of motion and soreness upon palpation, often accompanied by abnormal motor postures [13, 14].

Treatment options: pharmacological strategies for this phenotype include muscle relaxants (e.g., tolperisone, tizanidine, cyclobenzaprine), along with manual therapy, kinesiotherapy, taping, and massage. It is crucial for patients to understand that muscle spasms often arise from musculoskeletal weaknesses due to poor posture or improper movement patterns. Thus, while initial treatment focuses on muscle relaxation, long-term management must include biomechanical correction, muscle strengthening, and training to prevent recurrence [15, 16].

Central Sensitization Phenotype

Characteristics: central sensitization is characterized by hyperalgesia, allodynia, pain disproportionate to the injury, non-anatomical pain distribution, and diffuse hypersensitivity on palpation [17]. This condition is often associated with psychological factors such as negative emotions and social stressors. Central sensitization involves the hyperexcitability of central sensory neurons, representing a form of neuroplasticity in response to peripheral or central disturbances. This mechanism is a key contributor to chronic pain syndromes and can be present in different types of pain: nociceptive, neuropathic and nociplastic pain.

Treatment options: pharmacotherapy for this phenotype often includes gabapentinoids like pregabalin or gabapentin. Additionally, non-pharmacological interventions such as psychotherapy, social support, physical activity, sleep hygiene, and patient education are vital components of the treatment strategy [18–20].

Disinhibition Phenotype

Characteristics: disinhibition is characterized by chronic pain lasting over a year, often with anxiety, depressive disorders, sleep disturbances, and social maladaptation [21, 22]. Usually, the pain becomes widespread and does not correlate with peripheral changes in paravertebral tissues. No relationship of pain with movement is observed. Patients report no efficacy of any previous treatments with NSAIDs and physiotherapy. This phenotype indicates a deficiency in descending antinociceptive pathways, which is a significant factor in chronic pain conditions, including low back pain [23].

Treatment options: in this scenario, selective serotonin and norepinephrine reuptake inhibitors (SNRIs) such as duloxetine are recommended due to their dual role in providing central analgesic effects and addressing comorbid depression and anxiety [24].

By identifying these phenotypes through clinical assessment, healthcare providers can tailor treatments to the specific mechanisms involved in a patient’s pain. This approach enhances the effectiveness of therapy by addressing the root causes of pain, rather than applying a one-size-fits-all treatment model. This phenotyping framework also underscores the complexity of CNSLBP, where multiple pain mechanisms may coexist. In such cases, a combination of therapeutic strategies might be necessary to achieve optimal pain management [25].

Pain Drivers in Patients with CNSLBP

CNSLBP is a complex, multifactorial condition resulting from the interplay of various biological, psychological, social, and other factors. The assessment of these factors, which significantly influence pain perception and shape the clinical presentation—such as the severity, dynamics, progression, and prognosis of the pain syndrome—are referred to as “pain drivers.”

Besides modified drivers described below, it is highly important to draw special attention to non-modified but significant factors of pain perception such as nationality and culture, age, race, and gender. Recent studies emphasize impact given by ethical, psychological and racial differences to perceive pain [26]. Also, patients’ age showed its meaning to pain sensitivity: pain threshold increased in response to heat stimuli in the older participants compared to younger [27]. Despite the importance of these factors, we will not focus on them in the treatment of chronic pain later in this article, as our attention will be directed towards modified pain factors that can be influenced by non-pharmacological therapies.

Each identified driver can modulate pain perception and alter the pathophysiological mechanisms of pain through specific neuro-endocrine-immune pathways. For example, even with well-chosen pharmacotherapy that addresses the pain phenotype, the overall success of rehabilitation may be compromised if factors such as anxiety and/or depressive disorders, high levels of catastrophizing, insomnia, low physical activity, obesity, hormonal imbalances, or cognitive dysfunctions are not properly addressed or are underestimated.

We have identified 11 key pain drivers that appear to be the most significant and impactful (Fig. 2). While other drivers may exist, these are deemed essential for consideration. Evaluating these factors in a screening context is crucial and can significantly enhance the development of personalized rehabilitation strategies for patients with CNSLBP.

Fig. 2.

Key pain drivers

Each driver relates to its possible impact on chronic pain and can by identified by appropriate diagnostic tools (Table 1). Each of these 11 pain drivers is essential to evaluate, as they are closely linked to the underlying mechanisms of chronic pain development. Without addressing these factors, the treatment of patients with chronic pain will not be fully effective. Recognizing and incorporating these key pain drivers into the treatment plan is important for improving patient outcomes and managing pain more effectively.

Table 1.

Description of key pain drivers in CNSLBP

Pain driver	Impact on pain	Evaluation
Biomechanics	Biomechanical factors play a crucial role in the onset of CNSLBP and directly influence the severity and chronicity of back pain [28, 29]. For instance, inappropriate spinal load distribution and muscle weakness can exacerbate pain, leading to increased intensity and reduced pain tolerance over time [30]. Specific cases include individuals with chronic CNSLBP exhibiting altered posture control and impaired movement coordination, even during periods without active pain [31]	Diagnosis of biomechanical factors contributing to CNSLBP typically involves a thorough physical examination, including posture analysis, assessment of muscle strength, and evaluation of spinal alignment. Imaging techniques such as MRI (magnetic resonance imaging) and CT (computed tomography) scans may be used to detect structural abnormalities like intervertebral disc degeneration or facet joint dysfunction [32] A consultation with a physiotherapist might be necessary
Social factors	Social determinants such as occupation, socioeconomic status, and social support significantly affect the clinical presentation of CNSLBP [33]. Stressful work environments, lack of social support, and low socioeconomic status can contribute to the chronicity of CNSLBP and impair the patient’s ability to cope with pain. The intensity and duration of pain are often exacerbated by these factors, leading to prolonged disability and reduced quality of life [34]	Social factors are assessed through patient interviews and questionnaires designed to evaluate stress levels, work conditions, and social support systems [35]. Understanding these factors is essential for developing a comprehensive treatment plan that addresses both the physical and psychosocial aspects of CNSLBP
Cognitive impairment	Chronic pain has been shown to negatively impact various cognitive domains, including memory, attention, and executive function, through its direct effects on the central nervous system [36, 37] In many cases, cognitive impairment in chronic pain patients is a result of both the primary disease causing the pain as well as the direct effects of chronic pain on the CNS (central nervous system) [38] Cognitive dysfunction can also alter therapeutic options, as it directly affects pain reporting, pain behavior, and pain coping strategies. Pain expression and behaviors accompanying pain can vary significantly between patients with cognitive dysfunction	- The Mini-Cog and the Montreal Cognitive Assessment Scale can be used to screen for cognitive function in chronic pain patients [39] - Patients with positive screening results merit further evaluation for possible dementia - In patients with dementia, the PAINAD scale (Pain Assessment in Advanced Dementia Scale) can be used to assess pain Pain therapy in patients with cognitive impairment should take into account current recommendations for the prevention and treatment of cognitive impairment [40]
Anxiety	Anxiety is commonly observed in patients with CNSLBP, manifesting through increased muscle tension, impaired movement, avoidance behaviors, and reduced pain tolerance [41, 42]. This creates a cycle where pain increases anxiety, which in turn intensifies the pain. Clinical studies frequently show that patients with high anxiety levels are more likely to develop chronic CNSLBP [30]	Anxiety in patients with CNSLBP is typically diagnosed using psychological assessments like the Hospital Anxiety and Depression Scale (HADS) or the Generalized Anxiety Disorder 7-item scale (GAD-7) [43]. These tools help quantify the impact of anxiety on pain perception and guide the management strategy [44] A consultation with a psychotherapist might be necessary
Depression	Depression is a significant comorbidity in patients with CNSLBP, characterized by symptoms such as persistent sadness, loss of interest in activities, and fatigue. Depression amplifies the perception of pain and decreases pain tolerance [45]. The condition can reduce patients’ motivation for treatment adherence, leading to worse outcomes [46]. Clinical evidence suggests that depression can increase both the intensity and duration of pain episodes [47]	Depression in patients with CNSLBP is diagnosed using different standardized tools, for example the Patient Health Questionnaire-9 (PHQ-9) [48]. Early detection and treatment of depression are essential for improving pain outcomes and overall quality of life in these patients A consultation with a psychotherapist might be necessary
Catastrophization	Catastrophization contributes to chronic CNSLBP by increasing the perceived severity of pain and leading to greater disability [49]. This cognitive distortion leads to a perception of pain as overwhelming and uncontrollable [43]. This psychological factor is associated with worse treatment outcomes, as patients are less likely to engage in active pain management strategies. Studies show that high levels of catastrophization correlate with increased pain intensity and longer-lasting pain episodes [50]	The Pain Catastrophizing Scale is a widely used tool for diagnosing catastrophization in patients with CNSLBP. It measures the extent to which patients focus on and magnify their pain experiences, providing insights into their cognitive patterns [51] A consultation with a psychotherapist might be necessary
Physical activity (hyper- and hypodynamia)	Physical activity levels, whether excessive or insufficient, have a direct impact on the presentation of CNSLBP. Both extremes of physical activity influence pain intensity and duration [44]. Hypodynamia contributes to the chronicity of CNSLBP by weakening the musculoskeletal support system, while hyperdynamia can exacerbate pain through repetitive strain injuries. Clinical studies illustrate that a balanced level of physical activity is crucial for managing CNSLBP effectively [52]	Assessment of physical activity in patients with CNSLBP involves evaluating their exercise habits, posture, and movement patterns [53]. Tools like the International Physical Activity Questionnaire (IPAQ) help quantify activity levels and guide treatment recommendations [54] A consultation with a physiotherapist might be necessary [55]
Insomnia (sleep–wake cycle disorders)	Insomnia and sleep disturbances are common in patients with chronic CNSLBP, presenting as difficulty falling asleep, frequent awakenings, and non-restorative sleep [45]. Sleep disorders exacerbate pain by disrupting the body’s natural healing processes and increasing inflammatory responses. Chronic insomnia leads to heightened pain perception and a lower pain threshold, creating a vicious cycle that perpetuates pain [56]. Clinical observations show that patients with CNSLBP and insomnia report higher pain levels and greater functional impairment. In addition, in this condition, patients have a disruption of circadian rhythms, which in turn leads to impaired synthesis of melatonin, among other analgesic effects [57] In some cases, melatonin might be good option to improve sleep and reduce pain [58]	Insomnia is diagnosed in patients with CNSLBP through sleep questionnaires such as the Pittsburgh Sleep Quality Index (PSQI) and polysomnographic studies. These tools help identify sleep disturbances and their impact on pain, allowing for targeted interventions [59] Correction of the sleep–wake cycle will undoubtedly contribute to better rehabilitation
Hormonal imbalance	Hormonal fluctuations, especially reductions in estrogen, are linked to increased pain sensitivity and chronicity of CNSLBP [60]. These imbalances can lead to accelerated degeneration of intervertebral discs and other spinal structures, exacerbating pain [49]. Case studies reveal that hormone replacement therapy (HRT) may not always alleviate CNSLBP, and in some instances, may worsen it [61]	Hormonal imbalances are diagnosed through blood tests measuring levels of estrogen, progesterone, and other relevant hormones [62]. These tests help determine the role of hormonal factors in the patient’s CNSLBP and guide treatment options, including the potential use of HRT. A consultation with an endocrinologist might be necessary
Obesity	Obesity is frequently associated with CNSLBP, presenting as increased mechanical load on the spine, poor posture, and limited mobility [62]. Obesity exacerbates CNSLBP through both biomechanical and inflammatory pathways. Excess weight increases spinal compression, leading to accelerated degeneration of intervertebral discs, while systemic inflammation associated with obesity heightens pain sensitivity [63]. Clinical evidence shows that obese individuals are more likely to develop chronic CNSLBP, with higher pain intensity and greater disability [64, 65]	Diagnosis of obesity-related CNSLBP involves assessing body mass index (BMI), waist-to-hip ratio, and bioimpedance analysis [66]. These assessments are critical for developing a weight management plan that alleviates CNSLBP. A consultation with an endocrinologist and nutritionist might be necessary
Microbiota	Gut microbiota, or dysbiosis, can exacerbate CNSLBP by promoting systemic inflammation, which in turn influences pain mechanisms [67]. Clinical signs include chronic inflammation and gastrointestinal symptoms that may be linked to musculoskeletal pain [68]. Changes in the gut microbiome may also affect psychological factors such as anxiety and depression, further complicating CNSLBP management. Case studies highlight the emerging concept of the “gut–spine axis,” where microbiota imbalances are linked to intervertebral disc degeneration and chronic pain [64]	Diagnosis of microbiota-related CNSLBP involves analyzing of food habits, diet, gastrointestinal symptoms. The stool samples can help to identify dysbiosis and its potential impact on inflammation and pain Understanding the microbiome’s role in CNSLBP can lead to novel treatment strategies, such as probiotics or dietary interventions [69] A consultation with a nutritionist might be necessary

CNSLBP chronic non-specific low back pain

Clinical Cases

The treatment of CNSLBP should not be limited to the rote application of drugs or methods prescribed by clinical guidelines and standards. Instead, we advocate for a methodology that involves a thorough analysis of the underlying mechanisms and drivers of pain, facilitating the implementation of a personalized approach in routine clinical practice. This methodology would enable clinicians to select therapeutic interventions that are specifically tailored to the needs of each patient, rather than relying solely on treatments that are generally deemed beneficial for low back pain according to randomized controlled trials (RCTs), meta-analyses or expert opinions.

To illustrate our methodology, we present three clinical cases, all presenting with a common diagnosis of CNSLBP with similar clinical profiles, yet differing in their underlying mechanisms and contributing drivers. These distinctions require tailored therapeutic approaches. Each patient reports a persistent history of low-back pain, unrelated to any other specific pathology, with pain intensity measured at 6–7 on the Visual Analogue Scale (VAS).

Patient M.: A 45-year-old male IT specialist presents with chronic low-back pain that began five years ago following a fall on ice. The trauma was not associated with severe spinal injury. Over time, the patient developed persistent pain exacerbated by movement, particularly during verticalization, rotation, and extending. The pain often radiates to the buttocks and posterior thighs. The patient is overweight (BMI (Body Mass Index) of 32), leads a sedentary lifestyle due to the demands of his office job, and has a diet high in calories but low in fruits and vegetables. He also reports insomnia, which he believes exacerbates his pain perception.

Clinical examination reveals limited lumbar spine mobility, pain on rotation and extension, tenderness and significant pain upon palpation in projection of facet joints. The VAS score is 6/10. Radiographic imaging of the lumbar spine and MRI reveal minimal degenerative disc changes without herniation.

Patient C.: A 37-year-old female web designer reports constant, dull low-back pain localized to the thoracolumbar and lumbosacral regions. The pain, which has been present for several years, has recently intensified, became permanent, causing significant concern. The patient has been under considerable stress due to the threat of job loss, leading to daily anxiety and bad mood. She is now depressed, fearful of movement, avoids physical activity to protect her back, and spends much of her time at home. The patient expresses concern that her pain might require surgical intervention, as it does not fully resolve with NSAIDs.

Upon examination, there is slight tenderness in the lumbar and thoracic spine regions. No radiation of pain, no muscle tension, no pain upon movements and palpation, no allodynia. The patient rates her pain as 6/10 on the VAS. Radiographic imaging shows no specific abnormalities, and MRI of the lumbar spine reveals minimal degenerative changes without evidence of herniation.

Patient T.: A 40-year-old male office worker presents with back and gluteal pain that first appeared after prolonged static loading. Since then, the pain has recurred, often disrupting his sleep. He describes the pain as intensive and aching, accompanied by marked muscle tension and movement difficulties. During the consultation, the patient appeared agitated, frequently interrupted the conversation, and struggled to articulate his thoughts. He also reported recent memory issues.

Examination findings include pain in the lumbar region, exacerbated by movement and prolonged sitting, with a VAS score of 7/10. There is increased muscle tone in the lumbar muscles, pain upon palpation of muscles. Although the neurological status is generally normal, there are notable signs of social withdrawal and anxiety, with the patient expressing concerns about cognitive decline.

These three patients in general clinical practice probably would receive a standard treatment, involving combination of NSAIDs, muscle relaxants, increased physical activity, physiotherapy, massage, the manual therapy. However, a more precise approach using estimation of pain phenotype and pain drivers allows to recommend to everyone only necessary and appropriate for his condition medications and non-medical therapeutic recommendations.

Patient M.

Pain Phenotype

The onset of pain symptoms is clearly linked to trauma, with a predominant biomechanical factor in the past. The clinical phenotype suggests an inflammatory mechanism, with pain linked to movement and localized in specific regions. Thus, the primary therapeutic approach should involve anti-inflammatory treatment, such as NSAIDs.

Pain Drivers

A sedentary lifestyle is the main cause of physical inactivity, which necessitates the use of therapeutic exercise and increased daily activity. Dietary imbalances require nutritional counseling, and obesity warrants an endocrinological consultation and hormonal assessment. The potential role of gut microbiota in the patient’s pain and emotional state should also be considered. For sleep disturbances, referral to a sleep specialist is recommended. Each identified mechanism and its associated drivers clearly indicate specific therapeutic interventions (Fig. 3). Therefore, along with taking NSAIDs, this patient should follow above recommendations to correct pain drivers, which contribute to pain.

Fig. 3.

Main pain drivers for patient M.

Patient C.

Pain Phenotype

The long-term duration of pain, combination of persistent pain, depression and significant anxiety symptoms indicate a disinhibitory mechanism of pain. The questionnaires confirmed elevated anxiety and depression levels, supporting the use of SNRIs like duloxetine to address the mechanism of disinhibition.

Pain Drivers

Pronounced anxiety, catastrophizing tendencies, and low mood levels require cognitive-behavioral therapy and psychological counseling. Autogenic training and meditation can help manage anxiety and catastrophizing. Reduced motor activity requires structured physical therapy (Fig. 4). Therefore, along with taking duloxetine this patient should follow above recommendations to correct pain drivers, which contribute to pain.

Fig. 4.

Main pain drivers for patient C.

Patient T.

Pain Phenotype

The pain profile is characterized by pronounced muscle tension and reduced movement functionality, indicative of a muscle spasm mechanism. Muscle relaxants are therefore recommended as the primary treatment.

Pain Drivers

The patient’s phenotype is shaped by cognitive decline, hypodynamia and insomnia. Recommendations include cognitive enhancement strategies, increased physical activity, physiotherapy, and sleep correction. The patient’s social withdrawal may also require social support services (Fig. 5). Therefore, along with taking muscle relaxant, this patient should follow above recommendations to correct pain drivers, which contribute to pain.

Fig. 5.

Main pain drivers for patient T.

By addressing both the mechanisms and drivers of pain in particular patient, we can provide more effective, personalized therapeutic interventions for patients with CNSLBP. Moreover, continuous monitoring of therapy is crucial. As the patient’s life circumstances evolve, the contribution and role of specific drivers may change, necessitating timely adjustments to the therapeutic regimen. This dynamic approach ensures that the therapy remains relevant and effective over time.

Conclusions

The current paradigm for treating CNSLBP, which is based on a biopsychosocial approach, is conceptually sound but often remains theoretical and underutilized in clinical practice. Although the call for personalized therapy is well founded, it is rarely realized in practice due to the lack of specific tools and techniques that allow clinicians to accurately identify and select the most appropriate therapeutic interventions, including pharmacological and non-pharmacological options, for individual patients.

To bridge this gap, an analysis of the individual pattern of pain mechanisms and drivers is necessary. Such an analysis would allow for the formulation of well-founded recommendations for both drug and non-drug therapies tailored to the patient’s unique clinical profile. Each therapeutic recommendation should be strategically targeted to address the identified mechanism and driver, considering their current significance and impact on the patient’s condition.

By adopting this methodology, we can move from a “one-size-fits-all” approach to a truly personalized therapeutic strategy that addresses the unique needs of each patient. This approach has the potential to significantly enhance and improve the effectiveness of CNSLBP treatment in clinical practice.

Author Contributions

Andrey Danilov conducted the primary research and drafted the initial manuscript Anastasiia Badaeva Alexey Danilov, Anastasiia Kosareva, Ksenia Popovskaya, Viacheslav Novikov contributed to the reviewing and critical revision of the manuscript. All authors reviewed and approved the final draft of the submitted manuscript.

Funding

No funding or sponsorship was received for this study or publication of this article. The Rapid Service Fee was waived for the authors.

Data Availability

Data supporting the findings of this study are available from the corresponding author upon reasonable request.

Declarations

Conflict of interest

Anastasiia Badaeva, Anastasiia Kosareva, Ksenia Popovskaya, Viacheslav Novikov declare that they have no conflicts of interest. Alexey Danilov and Andrey Danilov are Editorial Board members of Pain and Therapy. Alexey Danilov and Andrey Danilov were not involved in the selection of peer reviewers for the manuscript nor any of the subsequent editorial decisions.

Ethical Approval

This article is based on previously conducted studies and does not contain any studies with human participants or animals performed by any of the authors.