From Roots to Canopy: Understanding Chronic Pelvic Pain Through a Tree-Inspired Model.

Bark is the tree’s protection or barrier from the elements. It is analogous to the adopted behaviors of an individual to protect from the impacts of CPP. These behaviors will be shaped by the individual’s epistemology and experiences [ 24 ]. It is the merging of the root, trunk, and canopy to protect from the present and future CPP experiences. In CPP, this is often considered an overprotection, as the degree of reported pain is not reflective of the degree of tissue damage [ 24 ]. The behaviors become more generalized and magnified over time [ 24 ]. This leads to long-term maladaptive management strategies.

Understanding the complexity of CPP is the first step in developing an approach to care. The biopsychosocial model describes the CPP experience through a broad lens. The neuroinflammatory model describes the CPP experience through a narrow lens. But both converge on the same outcome: the generation of CPP. The tree metaphor is useful for organizing a very complex pain presentation into a systematic, manageable approach, beginning with the roots and moving up the tree to identify which factors play a role in each individual woman. This approach can also guide history taking, physical examination, and care planning. It is recognized that other systems, such as the autonomic nervous, vascular, and endocrine systems modulate CPP, but inclusion is beyond the scope of this article. By using an approach outlined in the tree metaphor, the challenge is to identify which type of tree represents the woman seeking help; one with an extensive root system such as the aspen, one with a thick trunk such as the sequoia, or one with a large canopy such as a banyan tree. Most likely she will be an individual hybrid, as CPP is a personal experience.

Chronic pelvic pain (CPP), defined as persistent, chronic pain in the pelvic region that has lasted beyond 6 months, and is associated with negative cognitive, behavioral, emotional, and sexual consequences [ 1 ], affects millions of women globally and yet continues to be shrouded in silence. It is conservatively estimated that one quarter of women have CPP, with an underrepresentation in low-middle income countries [ 2 ]. There are many reasons why it is underdiagnosed and undertreated, ranging from gendered cultural differences that limit women seeking care to a lack of training of health practitioners [ 3 , 4 ]. A biopsychosocial model of care encompassing an interdisciplinary approach results in the best outcomes [ 5 – 7 ]. The biopsychosocial model recognizes the interconnection between biophysiological, psychological (such as thoughts, emotions, behaviors, beliefs, etc.), and social contributors in the personal experience of pain [ 8 ]. All these factors need to be recognized and addressed for the successful management of chronic pain. However, this interdisciplinary approach is not accessible to everyone, resulting in fragmented or absent care, which only accentuates women’s suffering and perpetuates these disparities. This leaves women feeling dismissed, confused, and without hope [ 9 ]. Conversely, health care providers often do not know where and whom to turn to for support, and provision of care that is beyond their training and capacity. The complexity and nuances of CPP [ 6 ] often deters practitioners from embarking on management and treatment options. However, recognizing that over 80% of women with CPP have a pelvic floor myofascial component [ 10 ] makes it imperative that every provider seeing women for urogynecological conditions be able to screen, understand, and possibly manage CPP. The key to effective diagnosis and treatment lies in appreciating the complexity of CPP, recognizing the different layers involved, and adopting an interdisciplinary approach, either directly or indirectly. This begins by shifting from seeking a singular cause of pain to recognizing the possible range of sources further influenced by various psychological, biological, and social factors. This article is aimed at increasing the understanding of CPP by bringing together both the biopsychosocial [ 10 ] and the neuroinflammatory [ 11 ] models of pain. By seeing women through different lenses and recognizing how these models reach the same conclusions when it comes to management and treatment will facilitate an approach to understanding the chronic pain experience and therefore guide an effective treatment plan. Analyzing all the factors impacting CPP is beyond the scope of this paper. But developing a framework of how to approach a woman with CPP and using this same framework for care will provide a structure. The framework will be facilitated by using the metaphor of a tree to describe CPP in an easy, relatable manner (Fig.  1 ). Fig. 1 Representation of different models Representation of different models The tree metaphor is not only a way of simplifying the understanding of a complex condition but can also be used as the foundation for history taking, physical examination, and management planning. Beginning with the roots and working up the canopy, provides a direction that ensures that the pain experience is captured.

We cannot take the acute pain story and shift it to chronic pain. Acute pain is a symptom whereas chronic pain is a personal experience. The hallmark of chronic pain is that it is an unpleasant interpretation, processed in the brain, of both the internal and external environment that subsequently leads to suffering [ 1 , 5 ]. This results in patients having varying experiences to similar noxious stimuli. CPP is chronic pain experienced in the anatomical region between the umbilicus and hips [ 1 ]. There are presently no biomarkers or imaging studies to capture this experience. The often-used monodimensional pain rating scales do not adequately reflect the nature and impact of pain, nor are they reliable measures of outcomes [ 12 ]. We must therefore shift the focus on the impact of pain as this will be different for everyone. The IMPACTT statement on how to measure pain for research captures this necessity [ 13 ]. It broadly breaks down different areas to include emotional impact, physical impact, social impact, in addition to symptoms. Although many questionnaires and surveys have been developed, a simple two-point approach for beginning the conversation is pragmatic in a clinical setting [ 14 ]. This can be easily modified for pelvic pain by asking the initial screening question: how often have you experienced pelvic pain in the last 3 months? A positive response would then be followed by asking: what is the intensity of the pain, how much the pain has interfered with your enjoyment of life, and how much has it interfered with your activity (this can be modified to include intimacy and bowel and bladder function). These simple questions can provide an initial screen to open up further exploration if needed. Understanding the theories of chronic pain allows a framework that will guide assessment and management/treatment. There are several theories of chronic pain, the most common being a biopsychosocial [ 15 ] and the neuroinflammatory model of chronic pain [ 11 ]. Interestingly, both look at pain through very different lenses but then converge when it comes to chronic pain care. The biopsychosocial model of chronic pain is promoted by the International Classification of Diseases (ICD-11). It is the interplay between biological, psychosocial, and social factors, which affects emotional distress, functional disability, and social roles [ 15 ]. Conversely, the neuroinflammatory model describes the resultant biological changes in the nervous system that subsequently lead to emotional distress and functional disability [ 11 ]. The biopsychosocial model is the most frequently used CPP model [ 1 ]. Although holistic in approach, breaking it down in a more reductionist form makes integrating it into care more feasible.

One way of conceptualizing the biopsychosocial model is to envisage the model as a tree. The roots being the biological, peripheral, and/or nociceptive input, the trunk is the nociplastic pain component, with the bark protecting from a perceived or real pain threat. The trunk via tree sap relays information between the roots and the canopy in a bidirectional fashion. The canopy (leaves and branches) represents the psychosocial input. This broadly includes emotions (commonly depression, anxiety, anger), coping strategies, personality, beliefs, expectations, and previous experiences. The tree is part of the forest representing connections, support, gender expectations, and societal norms, with their associated stigma and discrimination. With this model, understanding CPP is easier by beginning with the roots, which represent nociceptive factors. Nociception refers to the sensory input from a noxious stimulus [ 16 , 17 ]. Pain is the interpretation of this stimulus. CPP can broadly originate from three nociceptive sources: the visceral system, the somatic system, and the peripheral nervous system. In addition, referred pain into the pelvis may be part of the nociceptive input. The visceral system includes common diagnoses such as painful bladder syndrome (PBS), dysmenorrhea, endometriosis, vulvodynia, and bowel disorders, including irritable bowel syndrome (IBS). The somatic system includes the muscles, fascia, skin, and bones. This includes the pelvic floor but also its interconnectedness with lumbopelvic stability and the maintenance of core stability. The peripheral nervous system will include trauma and nerve entrapment of the pudendal nerve and its branches but also the ilioinguinal, genitofemoral, hypogastric, and obturator nerves. The autonomic nervous system can also play a role in generating nociceptive stimuli. We often focus on one “diagnosis” but need to appreciate the interconnectedness of the root system. It is common that many of these pelvic pain findings coexist. Viscero–viscero sensitization results in hypersensitization in other organs owing to the convergence of innervation [ 18 ]. In women with CPP, coexistence of PBS and endometriosis is seen in 48% of women [ 19 ]. This is not the result of endometriosis implants on the bladder but of a dual convergent diagnosis. Similarly, reported IBS ranges from 30 to 70% in women with PBS [ 20 ]. The somatic system has focused on pain generated by trigger points and taut bands. However, there is increasing evidence for the role of the fascia and its impact on muscular function and pain generation [ 21 ]. The pelvic floor is also associated with low back pain and therefore often does not work in isolation [ 22 ]. This emphasizes the importance of looking at the somatic–somatic convergence. The root system becomes more entangled in the recognition that there is also viscero–somatic convergence, which can be bidirectional [ 20 ]. It is also essential to recognize that the response to pain is protection. This protection is usually manifested as muscular bracing leading to increased muscle activity that over time can result in myalgia. At CPP centers, up to 90% of women have a musculoskeletal component to their pain [ 20 ]. Although nociceptive pain should be identified and treated, it does not fully account for the range of factors that contribute to CPP. The trunk represents nociplastic pain. This type of pain is usually more widespread and/or intense [ 17 ]. Nociplastic pain is defined as pain that is greater than expected given the amount of nociceptive input and is often accompanied by other symptoms, including sleep, memory, and fatigue issues [ 17 ]. This pain arises from an altered function of pain-related sensory pathways in the peripheral and central nervous systems (CNS), causing increased sensitivity. It is driven by ongoing inflammatory and/or neuropathic stimulus (see below for the neuroinflammatory model). Thus, it can be an amplification of peripheral nociceptive inputs or de novo neuropathic triggers (often called central sensitization), or it can come from the canopy [ 17 ]. Central sensitization is a subset of nociplastic pain and both are hallmarked by amplification of signaling. As tree sap travels up and down the trunk in a bidirectional fashion, so does nociplastic pain: it can originate from the roots, canopy, or the trunk itself. This widespread expansion pattern has also been termed hyperalgesia (increased pain response to a painful stimuli) or allodynia (painful response to a nonpainful stimulus). As these central pathways develop, the pain experience also changes and becomes less focused and more heightened. This can be seen not only in women’s difficulty in expressing their sensations but in a vagueness of their pain distribution and increasing constitutional symptoms. CPP, PBS, and IBS are commonly mixed diagnoses, with fibromyalgia, sleep disturbances, and fatigue representing both nociceptive (root) and nociplastic (trunk) contributions. This is evidenced by findings that 3–31% of women with CPP also have fibromyalgia [ 23 ]. The trunk is surrounded by bark to protect the tree. A key principle to understanding pain is to recognize that pain evolved to protect us and is not only essential but adaptive. However, chronic pain is often described as overprotection from a real or perceived threat and is therefore maladaptive [ 24 ]. It is this overprotection that leads to fear, avoidance, and difficulty in achieving personally meaningful activity. The canopy is where the interpretation and subsequent coping behaviors happen. The brain interprets all the nociceptive cues both from the body and from the external environment to conclude that this is pain. The input to the brain is phenomenal. It receives 10,000,000 bits/s from the eyes, 1,000,000 bits/s from the skin, and 100,000 bits/s from hearing, to mention but a few inputs [ 25 ]. The brain can sample only some of this information and must construct meaning from it. From an evolutionary perspective, the brain will focus primarily on threats (real or perceived). It is often compared with using a flashlight in the dark and seeing only where the beam is pointed. The beam will be pointed toward threats that reinforce the nervous system so that it becomes more heightened to these. One key concept of chronic pain is the change from a contextual experience to a more generalized concept [ 24 ]. How the brain will therefore choose to focus on certain inputs and interpret them will be influenced by three broad categories: priming [ 26 ] (previous personal experiences), emotions (often called mental health), and socio-cultural beliefs. The personal experiences can begin with epigenetics, adverse childhood events (ACEs), learned behaviors (including learned helplessness and resilience), and previous pain experiences with their subsequent outcomes. The role of neurodiversity is emerging and will play a more important role in understanding pain in the future. The more common emotions include depression, anxiety, and anger. Depression is often described as ruminating on the past, anxiety is centered on the future, and anger is focusing on perceived injustice. Bringing these emotions to the present will impact the CPP experience in a bidirectional manner and impact behavior. Social beliefs in pain intersect with gender, culture, and biases, within both the health field and society. Socio-cultural beliefs will impact behaviors, including health seeking, shame, and isolation. Social connection is crucial in recovery and managing pain. The support a woman has balances many of the other “canopy” factors and builds her resilience. Understanding how all these factors interact is important in beginning the process of treating and managing CPP. Using the metaphor of a tree can guide the way in which history taking, examination, and care planning can be broadly organized. Recognize that the metaphor is a simplification of a complex CPP condition, and everyone’s experiences will be different, as every tree is different.

Often the biopsychosocial model of pain can be intimidating, especially as many health care providers have been trained using a biological model of illness. The neuroinflammatory model of pain can explain the neurosensory dysfunction that results in the CPP experience. There continues to be emerging evidence showing complex interactions between the neural and immune systems. Interestingly, we can use the same tree metaphor. The roots represent the peripheral neuroimmune nociceptive inputs that end in the dorsal root ganglion (DRG), the trunk represents the neuroinflammation in the spinal cord that results in nociplastic activation, and the canopy is the role of neuroinflammation in other factors affecting the meaning of these inputs, such as depression, anxiety, and memory. The nociceptors in the peripheral nervous system are myelinated Aδ fibers and unmyelinated C fibers [ 11 , 27 ]. They respond to thermal, mechanical, or chemical stimuli [ 11 ]. Peripheral inflammation lowers their threshold and will occur following degranulation of neutrophils and subsequent migration of macrophages and mast cells [ 11 ]. The fibers are activated by inflammatory mediators, proinflammatory cytokines and chemokines, and Toll-like receptors (TLRs) [ 27 ]. Conversely, the nociceptor nerves release neuropeptides that activate the immune system [ 27 ]. The result is the potential of perpetuating the nociceptive cycle. TLRs are also known to activate macrophages but also microglia and astrocytes [ 11 ]. The ensuing neuroimmune communication via inflammatory mediators and TLRs, is a fine balance between resolving or perpetuating these peripheral inputs. Perpetuation will lead to hyperalgesia. The myelinated Aδ fibers and unmyelinated C fibers synapse in the DRG to secondary neurons in the dorsal horn (nerves that relay impulses between the peripheral nervous system and the brain). These neurons are important for the establishment of nociplastic pain [ 11 ]. The peripheral neurons release Substance P, glutamate, and calcitonin gene-related peptide (indirectly) [ 11 , 27 ]. These excite dorsal root nerves via the NMDA receptor [ 11 ]. Inhibitory pathways modulate the effects through GABAergic receptors but also serotonin, norepinephrine, and endogenous opioids [ 11 ]. In chronic pain, the balance is more excitatory than inhibitory. The subsequent neuroinflammation results in activation of glial cells, migration of immune mediators (neutrophils, mast cells, macrophages), and the release of neuropeptides (chemokines and cytokines) [ 27 ]. Glial cells (astrocytes, microglia, and oligodendrocytes), especially microglia, are responsible for the neuroplasticity (structural changes) of the CNS seen in people with chronic pain [ 11 , 27 ]. Microgliosis (microglial activation) occurs in the dorsal horn and reinforces the connections to the peripheral nervous system [ 11 ]. It is thought that these cells may have “molecular pain memory,” which explains the potentiation with repeated pain exposures and the vulnerability to pain over time [ 11 ]. Microglial cells decrease second-order neuron excitability, thus creating central sensitization. Astrocytes are thought to maintain central sensitization through their numerous impacts on neurons, inflammatory mediators, and ability to produce neuroplastic changes [ 11 ]. The glial cells are reminiscent of tree sap: they can change and be changed by the bidirectional input from the brain (canopy) and from the peripheral nervous system (roots). Neuroinflammation, both peripherally and centrally, results in leakiness of the blood–brain barrier, allowing peripheral cytokine and immune-cell entry; glial-cell activation, especially microglia and astrocytes; and cytokine release [ 11 , 27 , 28 ]. Microglial cells and astrocytes are found in the brain and can cause changes. Microglial cells affect dopaminergic pathways (known as the reward system) [ 11 ]. Neuroinflammation and microglial cell activation is known to play a role in major depression and anxiety [ 11 , 28 ]. The glial cells are central in the development of memory and cognition [ 28 ]. Conversely, depression, stress, decreased sleep, and poor diet are known to trigger neuroinflammation [ 28 ]. These are all factors that further impact CPP and strengthen the bidirectionality of the neuroinflammation.