Clarification of the “pain neuroscience education” concept in the management of patients with persistent low back pain: A scoping review

Names used

In the literature reviewed here, several names were used to designate the PNE concept: “pain neurophysiology education”, “explain pain”, etc. The most frequently used name was “pain neuroscience education” [7, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39], which will henceforth be used in this narrative synthesis.

The context

According to some researchers, the emergence of PNE was prompted by observations of a lack of effectiveness of educational strategies and the modest effects of treatment in people suffering from chronic pain [2, 13, 40, 41]. Moseley and Butler explained these findings in terms of the counter-intuitive nature of the existing educational models: the structural tissue-based model (also covered by [42]), and the structural centralnervous system-based model [2]. The researchers suspected an amalgam between nociception and pain, implying that pain cannot be changed because a peripheral or central generator cannot be removed [2] (also covered by [13, 40]). Moseley and Butler rejected these models because of their lack of coherence, biological plausibility and clinical plausibility. The lack of coherence was due to the suggestion that pain is influenced by thoughts, emotions, behaviors, and therefore the program aims to change them. On the other hand, it is argued that the purpose is not to reduce pain. The lack of biological plausibility is due to the fact that pain can decrease, depending on the meaning given to it, through descending modulatory pathways. Finally, the lack of clinical plausibility was due to evidences showing that these programs, whose aim is not to reduce pain, have an effect on pain.

Furthermore, Moseley and Butler wondered why a patient would be motivated to commit to lasting behavioral changes if he/she believed that their pain could not be changed [2]. Other researchers hypothesize that tissue-based educational strategies (i) do not sufficiently target cognitive-behavioral aspects which are nevertheless strong predictors of pain chronicity [41], and (ii) are likely to increase levels of fear and (indirectly) pain [13, 36]. Several researchers argue that PNE is therefore designed to target these limitations, and increase the effectiveness of treatment [2, 13, 36, 41].

The initial concept

In his conceptual paper, Moseley defines PNE as an educative strategy that aims to reconceptualize someone’s meaning of pain from a neurophysiological point of view [42] (also covered by [2, 8, 13, 19, 26, 27, 38, 39, 41, 43, 44, 45, 46, 47]). Educational material is described in the Explain Pain book [8] and includes detailed information on the neurophysiology of pain (also covered by [2, 12, 13, 17, 19, 23, 28, 30, 36, 27, 38, 46, 48, 49, 50, 51]). Information is presented accurately (rather than being diluted for the sake of simplicity) and in a respectful manner that acknowledges the patient’s suffering. The objective is to reduce the threat value associated with pain (also covered by [2, 8, 13, 19, 22, 26, 27, 38, 39, 43, 44, 48, 52, 53]) by promoting deep learning of pain neurophysiology (also covered by [2, 8, 20, 36, 39, 43]) and assuming that more appropriate cognitive, behavioral responses will follow (also covered by [2, 13, 18, 19, 41, 43, 44, 45, 48, 52, 54, 55, 56, 57]). Moseley distinguishes superfical learning and deep learning; in the latter case, information is remembered and also understood, integrated in someone’s belief and attitude, and applied to solve problems (also covered by [2, 8, 28, 43]). To support deep learning, metaphors (also covered by [5, 13, 17, 23, 24, 25, 27, 28, 32, 33, 34, 36, 43, 44, 52, 53, 56, 58, 59, 60, 61]) and pictures (also covered by [5, 13, 17, 23, 32, 43, 44, 53, 58, 61, 62]) are used to present educational material. In Moseley’s publication, PNE is integrated into a multimodal approach (several treatment modalities that target different mechanisms or factors) based on its own theoretical model: the pain neuromatrix also described in Explain Pain (also covered by [2, 8, 13, 27, 27, 39]). In this model, pain is conceptualized as a protective output produced when the brain perceives that body tissues are in danger, and that action is required to protect them (also covered by [2, 8, 9, 13, 17, 43]). Pain occurs following the activation of an individual specific neuronal network called the “pain neurotag” and is experienced in the virtual body (also covered by [8, 9, 13, 43]). Chronic pain is thought to be promoted by impaired nociceptive and nonnociceptive systems (beliefs and attitudes) that increase the brain’s conviction that body tissues are in danger, thereby increasing pain neurotag activity (also covered by [8, 13, 43]). The longer the pain persists, the more the pain neurotag undergoes profound changes – including an increase in its synaptic efficacy (also covered by [8, 13, 43]). The aim of the multimodal approach is to reduce the sensitivity of the pain neurotag by (i) reducing threatening inputs (both nociceptive and nonnociceptive); (ii) activating specific components of the pain neurotag without activating the whole pain neurotag; and (iii) increasing physical and functional tolerance of the pain neurotag through graded exposure to threatening inputs by preventing flares-up (also covered by [8]). PNE is integrated in this approach by targeting a reduction in nonnociceptive inputs.

Variants of the PNE concept

Other researchers have subtly modified the initial concept. For example, Nijs’ research group adapted educational concepts from Explain Pain in a more synthetic way [63] in order to implement it in two 30-minute sessions before biopsychosocial CBT-based rehabilitation [52] (also covered by [20, 22, 26, 27, 62]. Emphasis was placed on the central sensitization concept, in order to explain chronic pain and the potential biopsychosocial factors that maintain it [52, 62]. Louw’s research group offered metaphorical and simplified adaptations of Explain Pain, together with original content [10, 13, 64]. Pain concepts were approached in a more “peripheral” way with an emphasis on the nervous system rather than the brain (e.g. pain is more related to peripheral nerve sensitization than pain neurotag sensitization), in order to avoid strong reactions like “do you think that pain is in my head?” [36]. Unlike the first publications on PNE [41, 46], Louw’s group included tissue stories (asymptomatic imaging and tissue healing) [10, 36, 37] to deconstruct Cartesian beliefs about pain before introducing an alternative view based on biology [13]. Unlike other researchers who deliver PNE in purely educational blocks [13, 36], Louw et al. offers to cut PNE into small educational pieces integrated and spread over physical therapy session (paced education) [13, 36]. According to these researchers, the objective is to better take account of the patient’s expectations so that they does not think that they are receiving “cognitive” treatment only [13]. Other educational resources from the white literature contain subtle variations on the educational content, pictures and metaphors used [65, 66]. According to Moseley and Butler, the unifying aspect of all these approaches is explanation of the key biological concepts that underlie pain, with the aim of giving the patient a functional knowledge of it [2] (also covered by [43]). Thus, patients can integrate functional knowledge of pain into their pain-related beliefs, attitudes, behaviors, treatment and lifestyle choices, in a way that reduces pain and improves function and quality of life [2] (also covered by [43]).

PNE as an educational approach

Researchers have variously defined PNE as a cognitive [13, 23, 32, 38, 71], cognitive-behavioral [48, 53, 58, 68] and/or educational [2, 12, 14, 17, 18, 19, 28, 31, 33, 37, 38, 40, 46, 48, 57, 60] approach for explaining pain to patients from a neurophysiological viewpoint [2, 12, 13, 17, 19, 23, 27, 28, 30, 31, 36, 38, 46, 48, 49, 50, 51]. Moseley and Butler stated that PNE can refer to a set of educational strategies that aim to change someone’s understanding of what pain is and what its purpose is [2] (also covered by [40]). More precisely, the researchers consider that PNE involves changing someone’s conception of pain from a marker of tissue injury to the perceived need to protect bodily tissues [2] (also covered by [7, 28, 40]) with a neurobiological perspective (e.g. brain output, sensitive nervous system) [17, 27, 37, 60]. Pain is presented as an emerging (rather than linear) phenomenon that is counter-intuitive when viewed against dominant structural models [2] (also covered by [42]). That is why Moseley and Butler argue that PNE challenges existing concepts based on optimizing learning and multimedia strategies, rather than simply delivering information [2]. To deliver it, several researchers believe that clinicians must first have a reconceptualization of pain according to the neuroscience model of pain [2, 36, 40, 43, 67]. By emphasizing a change in the concept of the patient’s pain, PNE differs from educational approaches to pain neuroscience that consider nociception and pain to be analogs (e.g. osteoarthritis equals pain; also covered by [40]). The researchers also differentiate between PNE and strategies that seek to teach coping strategies (e.g. pacing, goal setting, problem solving, and relaxation training) – with which PNE can nevertheless be combined (also covered by [40]). Lastly, PNE differs from approaches that focus on psychosocial aspects of pain [2] and can only be delivered through a biopsychosocial paradigm, with the integrated treatment of peripheral and central nociceptive drivers [2] (also covered by [8, 13, 26, 27]). Lotze and Moseley differentiate between PNE and pain education provided in CBT based programs because the latter are limited to applying science (e.g. teaching that pain does not equal injury) rather than covering pain science itself (e.g. teaching why pain does not equal injury) [40]. Louw et al. conceptualized PNE as a cognitive restructuring strategy integrated into a physical therapy, like a behavioral component of CBT [13]. However, some researchers point out that PNE can use experiential elements from other approaches (e.g. exercise, graded motor imagery, and manual therapy) to reinforce previously integrated educational concepts [38, 40, 43, 60]. While PNE was evaluated as the sole therapy in some clinical trials [19, 23, 28, 35, 44, 45, 46, 47, 48], Moseley and Butler argue that this is not its intention; rather, the goal is to increase adherence to biopsychosocial rehabilitation, in order to reduce pain and disability [2] (also covered by [7, 8, 13, 17, 18, 36, 43, 47, 52]). In the literature reviewed here, PNE has been combined with several other approaches, such as exercise/activity therapy [2, 8, 9, 10, 13, 19, 20, 22, 25, 26, 27, 29, 30, 31, 32, 34, 36, 38, 39, 41, 43, 45, 53, 54, 56, 58, 61, 63, 64, 65, 66, 68, 69], manual therapy [10, 13, 19, 22, 30, 32, 33, 36, 41, 51, 60, 64, 70], relaxation/meditation techniques [10, 13, 24, 27, 34, 36, 58, 64, 65, 69, 56], hypnosis [67], sensory retraining [71], and dry needling [49]. However, several researchers recommend that this management should include multimodal therapy based on cognitive-behavioral reactivation [2, 13, 20, 26, 27, 39, 40, 42, 58, 62].

PNE as a theoretical model

In their narrative review, Moseley and Butler stated that PNE refers to both an approach and a theoretical model from which to consider the treatment of pain [2]. This theoretical model was described initially in Explain Pain [8] and then adapted in several publications [26, 27, 39, 40, 42] and educational resources [9, 10, 13, 43, 63, 64, 65, 66, 68]. The model’s main tenet is that pain is a marker of the brain’s perceived need to protect the body’s tissues, rather than a marker of tissue injury [2] (also covered by [8, 9, 13, 43, 65, 66]). More specifically, pain is produced following the activation of a set of neural networks in the brain called the pain neurotag [42] (also covered by [8, 9, 13, 43, 68]). Pain occurs when the brain concludes (after a probabilistic evaluation of all nociceptive inputs (including immune and endocrine molecules that stimulate nociceptors and tissues) and nonnociceptive inputs (cognitive, emotional, sensory and social factors) that body tissues are in danger and action is required to protect them [42] (also covered by [2, 8, 9, 13, 43, 65, 66, 68]). Hence, pain is conceptualized as a perception combined with other perceptive responses (e.g. thoughts, emotions, and feelings) and neurobiological responses (e.g. sympathetic, endocrine and motor responses) that seek to protect and maintain homeostasis [43] (also covered by [8, 9, 13]). Through descending nociceptive pathways and the hypothalamic-pituitary-adrenal axis, this physiological reaction can influence peripheral processes such as blood flow, tissue healing and the inflammatory response; in turn, these peripheral processes influence the information analyzed by the brain within a circular system [43] (also covered by [8, 9, 13]). As a result, nociceptive information is neither necessary nor sufficient to produce pain: nociceptors are danger detectors and not pain detectors [8] (also covered by [2, 10, 13, 42, 43, 63, 64, 65, 66]). This concept implies that pain can occur in the absence of tissue damage if the brain’s analysis concludes that tissues are in danger (i.e. powerful danger perception). Conversely, tissue damage can occur without causing any pain if the brain concludes that its tissues are safe (i.e. strong safety perception). Excluding certain particular contexts, pain is conceptualized as a protector that is triggered before tissues get injured; in other words, there is a buffer zone between the pain threshold and the tissue tolerance threshold [8] (also covered by [9, 43]). In this model, chronic pain is contrasted against acute pain as being more related to central nervous system sensitivity (including the pain neurotag and the second-order neuron in the dorsal horn) rather than the state of the tissues, which heal linearly – at least after three to six months [8] (also covered by [9, 10, 13, 26, 42, 43, 63, 64, 65, 66]). The brain relies on erroneous information about the state of the tissues, and the pain neurotag is likely to be activated by events that are usually insufficient to activate it (e.g. light movement, thoughts, and emotions) [8] (also covered by [9, 13, 43]). Pain becomes overprotective, increasing the buffer effect between it and the tissue tolerance threshold [8] (also covered by [9, 43]). Central nervous system sensitization can help to make sense of persistent, disproportionate, widespread pain states or those triggered by non-physical factors [8] (also covered by [9, 13, 43]. According to the researchers, this central sensitization is favored by the persistence of factors that accentuate danger perception (e.g. beliefs of vulnerability, catastrophic thoughts, and fear of movement [2, 8, 9, 13, 26, 40, 42, 43, 65]), maladaptive behaviors (e.g. avoidance of fear, and perseverance despite pain) [8, 9, 10, 13, 63, 64, 66], factors disrupting homeostasis (e.g. sleep disturbance, sedentary behavior, and comorbidities) [10, 26, 64, 65, 66] or other overactive protective systems [10, 26, 64, 65, 66]. Protective systems (including the nervous system) are considered to be plastic and adaptable, meaning that chronic pain reversibility is biologically plausible whatever the state of the body tissues [43] (also covered by [8, 9, 10, 13, 64, 65, 66]). Active coping and evidencebased treatment strategies that include PNE are designed to promote this reversibility and recovery [43] (also covered by [8, 9, 10, 13, 26, 27, 39, 40]). This model offers a metaphorical rationale for conceptualizing pain management by integrating treatment of peripheral and central nociceptive contributors (see the initial concept). This theoretical framework has been built from a wide range of anecdotes (e.g. various facts of people who suffered from serious injuries without experiencing pain, or people who felt pain without evidence of injuries), other theories (e.g. Melzack’s neuromatrix theory, Bayesian predictive coding theory, and conceptual change theory) and scientific research (e.g. work on central sensitization, neuroimaging studies, asymptomatic imaging studies, and so on) [2] (also covered by [8, 13]).

PNE as an overall approach to care

While PNE is mostly described as a specific educational intervention, some researchers give it a broader definition [13, 43]. Moseley and Butler describe PNE as a way of thinking about pain based on an understanding of a theoretical model [43]. According to Louw et al., PNE can be described as an overall approach that permeates all facets of care [13]. Other researchers describe this type of an approach implicitly in the selected literature (e.g. pain neuroscience approach, pain neuromatrix approach or PNE plus) [12, 26, 27, 36, 39, 42, 55, 60]. According to some researchers, pain reconceptualization leads clinicians to observe patients and manage them through the prism of pain mechanism [12, 26, 27, 39, 40, 42, 55], the biopsychosocial model [2, 36, 42] or danger and safety evidence (including tissues) [40, 43]. Patients can be observed through this lens from the initial assessment and throughout their treatment [40] (also covered by [12, 13, 26, 27, 39, 42, 43, 55]). According to Lotze and Moseley, the unifying principle is always being aware of providing evidence of safety [40]. For example, Lotze and Moseley state that a friendly attitude, being perceived as an expert, spending time focusing on the person and their needs, and explaining pain and rehabilitation in an understandable manner are all elements that can provide evidence of safety [40]. On the same lines, Louw et al. recommend conducting an in-depth interview, conscientiously examining the patient, and taking care to explain the test results in a reassuring manner when appropriate [36]. According to Louw et al. PNE in the broad sense can represent a general language for communicating with the patient [13]. Several researchers recommend adjusting communication during treatment in a way that remains consistent with the educational model [13, 22, 38, 40, 60]. Communication has to use safe language while limiting the use of words, metaphors and explanatory models reflecting the structural model of pain, which are likely to increase danger perception [12, 13, 22, 36, 43]. Several researchers argue that exercise therapy must be adapted and include a time- or load-contingent approach, rather than symptomcontingent approach [40] (also covered by [26, 27, 38, 39, 42, 60]), and can include discussion of pain cognition before and after exercise to facilitate pain reconceptualization [20, 26, 27, 38, 39, 62].

Key characteristics of PNE

The theoretical model

PNE is based on its own theoretical model which includes biological concepts that underlie pain and its management. The model predicates that education, reassurance, and graded exposure have important roles in the therapeutic approach. The objective is to help patients reconceptualize their pain, reduce the associated perceived threat (thus reducing the activation of protective systems), and increase adherence to biopsychosocial rehabilitation (thus desensitizing the central nervous system). This model distinguishes PNE from other educational and CBT-based approaches, and is one of its key characteristics. More details are given in the “context” and “initial concept” sections.

Educational content

PNE’s educational content is intended to promote the reconceptualization of pain [41]. The content covers broad pain concepts explained through neuroscientific knowledge [40, 43]. In their narrative review, Moseley and Butler describe the key biological concepts that PNE can include: the variable relationship between nociception and pain (also covered by [8, 9, 10, 13, 63, 64, 65, 66, 68]), the powerful influence of context on pain (also covered by [8, 43, 65]), sensitization of the nociceptive system when pain persists (also covered by [8, 13, 26, 36, 43, 52, 58, 60, 65, 66]), the coexistence of several protective systems (including pain) (also covered by [8, 9, 13, 43]), the potential influence of other protective systems (sympathetic, endocrine, immune and motor systems) on pain (also covered by [8, 9, 13, 43]), the adaptability/trainability of our biology (also covered by [8, 9, 10, 13, 43, 63, 64, 65, 66, 68]), the knowledge that a return to normal is likely to be slow (also covered by [43]) [2]. In Explain Pain Supercharged, Moseley and Butler add some further concepts: pain is normal, personal and always real (also covered by [8, 10, 13, 63, 64, 65, 66, 68]), there is danger receptor and no pain receptor (also covered by [8, 9, 13, 63, 64, 65, 66, 68]), pain depends on the balance between danger and safety (also covered by [8, 9, 10, 13, 42, 63, 64, 65, 66, 68, 73]), pain involves distributed brain activity (also covered by [8, 9, 13, 26, 43, 52, 64]), learning about pain can help the individual and society (including that knowing pain can ease pain) and active treatment strategies promote recovery (also covered by [2, 8, 9, 10, 13, 63, 64, 65, 66]) [43]. In Recovery strategies, Lehman addresses some subtle variations of the original concepts (e.g. pain is more about sensitivity than damage, several factors can influence sensitivity, and the body is strong and adaptable) and adds other key messages: different mobility does not mean pain (also covered by [10, 69]), the body does not need to put back in place (also covered by [10]), and no movement should be banned forever [66]. Historically, the knowledge used to explain this broader pain concept was limited to pain neuroscience information [41, 42, 47]. According to Louw et al., it can include information about nociception and nociceptive pathways (e.g. neurons, action potentials, synapses, and primary and secondary nociceptors) [8, 13, 26, 32, 42, 43, 46, 47, 52, 63, 65, 66], spinal inhibition (also covered by [2, 8, 9, 10, 13, 26, 42, 43, 46, 52, 63, 64, 64, 66, 68, 72]), spinal facilitation (also covered by [2, 8, 13, 26, 42, 43, 45, 50, 52, 63, 65, 70]), peripheral sensitization (also covered by [8, 13, 26, 32, 33, 36, 43, 46, 47, 52, 58, 65]), central sensitization (also covered by [8, 13, 26, 28, 32, 33, 36, 43, 47, 52, 53, 58, 59, 60, 62, 63, 65, 68]) and nervous system plasticity [2, 8, 9, 10, 13, 18, 26, 32, 33, 35, 43, 52, 63, 64, 65, 66]. The role of the brain (e.g. the pain neuromatrix theory, and pain as a brain output based on danger perception) is also covered by many researchers [2, 13, 18, 20, 26, 31, 32, 33, 42, 43, 52, 73]. The virtual body (Penfield’s homunculus) is mentioned by some researchers [8, 13, 43, 51, 68]. However, PNE can include content on tissues and anatomy if it promotes the de-education of pain misconceptions or reinforces educational concepts (see the section on variants of the PNE concept). On the same lines, content on biomechanics (e.g. spinal curves, leg length discrepancies, etc.) [10, 66], physical factors (e.g. posture, load bearing, strength, and flexibility) [10, 66, 69, 70] can be found in some educational materials. Louw et al. added that PNE can also include content on beliefs (e.g. fear avoidance) and psychosocial factors (e.g. catastrophism, fear of movement, hypervigilance, and avoidance and perseverance behaviors) that influence pain [13] (also covered by [5, 8, 10, 18, 31, 32, 33, 34, 36, 52, 53, 56, 58, 61, 63, 64, 65, 66, 70]). Other biopsychosocial factors such as lifestyle factors (e.g. a sedentary lifestyle and sleep hygiene) [13, 65, 66, 70] and comorbidities [66] are considered by some researchers to contribute to nervous system sensitivity in a biopsychosocial model. Specific content related to low back pain is found in some studies [17, 36, 56, 61, 69], patient education books [8, 10, 66], and clinicians education books [13, 43]. These variations of content allow for taking into account anatomical (e.g. the solidity of the lumbar spine with “it’s not out, never out”), neurophysiological (e.g. the solid but sensitive nature of the lumbar spine with “the jewels of the crown”), pathoanatomical (e.g. disc degeneration with “stable platform”), diagnostic (e.g. the meaning of the nonspecific low back pain label with “back pain is like pimples”), or therapeutic particularities by integrating it and representations around the management of persistent low back pain (e.g. posture, ergonomics, etc.) [43]. However, Moseley and Butler have pointed out that PNE does not include simplistic explanations such as gate control theory or the conflation of nociception and pain (e.g. pain is caused by structural damage to the central nervous system, and nerves send pain messages to the brain) [2]. Lastly, several publications did not consider the presentation of treatment options to be part of PNE [12, 23, 24, 25, 39, 44, 45, 46, 47, 48, 68, 71]; in contrast, other publications [28, 32, 33, 34, 53, 56, 60, 61, 69, 73] and educational resources [8, 9, 10, 13, 43, 64, 65, 66] encompassed treatment with a pain neuroscience perspective (i.e. with the objective of desensitizing the nervous system).

Optimization of learning strategies

According to Moseley and Butler, PNE refers to the quality of the content taught and how the content is taught [2]. They argue that deep learning requires the optimization of learning strategies [2] (also covered by [13, 36, 43]) and is thus a key feature of PNE. While a few studies have assessed the value of delivering educational materials alone [73], several researchers (i) acknowledge that this strategy alone does not produce significant behavioral changes and clinical effects and (ii) recommend that education be guided by a healthcare professional [13, 43]. Although a lecture format is described in some clinical trials [17, 45, 48, 54, 56, 61, 69], several researchers do not recommend this learning approach [13, 22, 43, 53, 62]. Moseley and Butler argue that it places the learner in a passive role that does not promote conceptual change [43]. They recommend a constructivist approach, placing the clinician as a guide and the patient in an active position seeking to make sense of the information presented to him/her [43]. To this end, some researchers present educational concepts in a conversational, interactive style [13, 22, 23, 26, 38, 40, 43, 56, 57, 61, 63]. Nijs et al. used a Socratic dialogue [39]. According to Moseley and Butler, learning a concept produces a neurotag associated with that concept, whose influence can be strengthened by the use of metaphors (strengthening of the synaptic efficiency of the neurotag), visual aids (increasing the precision of the neurotag), repetition and variation of modalities to present the same concept (increasing the mass of the neurotag) [43]. That’s why many researchers state that the message can be presented with metaphors [5, 13, 17, 18, 20, 23, 24, 27, 28, 32, 33, 35, 36, 42, 43, 44, 52, 53, 56, 60, 61], examples [13, 20, 23, 26, 28, 36, 44, 46, 47, 52, 60] and/or stories [13, 43]. Pictures can also be used, to illustrate the therapist’s discourse [5, 13, 17, 23, 32, 43, 44, 53, 58, 62]. They can be prepared in advance [34, 47, 61] or drawn freehand [13, 35, 42, 46, 50]. According to these researchers, this content can take the form of a graph [18, 28, 32, 42], a diagram [47, 50, 52, 56, 61, 62], a video [13, 18, 23, 34, 43] and/or a photo [13]. PowerPoint presentations [24, 28, 32, 33, 49, 52, 54, 69], books, booklets, and brochures [2, 8, 9, 10, 13, 20, 27, 31, 52, 56, 63, 64, 66, 68, 69, 73] are frequently used to present these pictures. Other researchers use websites [27, 65, 69], video servers [23, 24, 34], infographics [18], posters [13] and/or educational cards [13]. Moseley and Butler recommend that the messages must be understandable (also covered by [20, 26, 38, 40, 43, 56, 61]), coherent (also covered by [38, 40, 43, 48]), attractive, and plausible [43]. Many researchers also recommend that educational content should be individualized [18, 20, 24, 31, 32, 36, 43, 49, 55, 59]. For example, several researchers argue that this content should take the patient’s concerns into account [13, 24, 36, 43, 58]. According to the researchers, the content must take account of their signs and symptoms [13, 36, 43, 55, 71], beliefs [43], experiences [20], motivation to change [55], and/or intellectual abilities [26]. Other educational strategies are used by various researchers, such as prompting the patient to read educational material [20, 28, 31, 47, 52, 62, 69, 71, 72] or ask questions [13, 36, 26, 28, 49, 50, 69], self-explanation [18, 36, 26, 43, 52, 58], cognitive homework [13, 23, 36, 49, 57], paced education [13, 36, 43], quiz [26, 52, 58], and explanatory feedback [43]. Finally, according to Blickenstaff et al., experiential learning can reinforce (conceptual) change [38], that is why several researchers describe the use of experiential elements from other therapeutic approaches to reinforce the accommodation of education concepts [13, 38, 39, 43, 60].