Sclerotomes
The term "sclerotome" carries a dual meaning within medical science, leading to potential confusion if not clearly delineated. Its primary and well-established definition originates in embryology, where the sclerotome represents the ventromedial portion of the mesodermal somite. This embryonic structure undergoes differentiation to give rise to crucial components of the axial skeleton, including the vertebrae, ribs, and parts of the skull. The sclerotome's role in somitogenesis and subsequent vertebral formation is a fundamental concept in developmental biology, involving complex signaling pathways and cellular migrations.[1][2]
However, within the fields of musculoskeletal medicine and pain management, "sclerotome" is frequently used in a distinctly different, clinical sense. This usage, largely attributed to the work of Inman and Saunders in 1944, refers to a zone or area of deep somatic tissues ā primarily bone and periosteum, but sometimes extended conceptually to include ligaments, joint capsules, and deep fascia ā presumed to be innervated by a single spinal nerve root. This clinical definition is intrinsically linked to the phenomenon of referred pain originating from these deep structures. It posits that irritation or noxious stimulation of a structure within a given sclerotome can produce pain perceived not only locally but also in other tissues belonging to the same sclerotome, often at a distance from the source. It is this clinical/pain-related definition, and the concepts and controversies surrounding it, that forms the focus of this article. Understanding the embryological origin is helpful background, particularly in grasping why this specific term was adopted, but the clinical application related to pain patterns is paramount here.
Pain originating from sclerotomal tissues falls under the broader category of deep somatic pain.[3] This type of pain is typically characterized by a deep, dull, aching quality, often poorly localized by the patient and sometimes described as an expanding pressure.[4] This contrasts sharply with the qualities of superficial somatic pain (originating from skin, usually sharper and well-localized) and visceral pain (originating from internal organs, often diffuse and associated with autonomic symptoms). The clinical sclerotome concept attempts to provide a framework for understanding the specific referral patterns associated with deep somatic pain originating from skeletal and associated connective tissues.
Historical Context
Kellgren
A crucial foundation was laid by the work of J.H. Kellgren in the 1930s.[5] Kellgren conducted experiments involving the injection of hypertonic saline, a noxious stimulus, into deep somatic structures such as muscles (e.g., interspinous ligaments) and fascia in human volunteers. His meticulous observations revealed that such stimulation consistently produced pain that was deep, aching, and diffuse in quality. Critically, Kellgren noted that this pain was often felt not only at the site of injection but also referred to distant areas in patterns that were reproducible and seemed related to the segmental innervation of the stimulated structure, rather than following the distribution of peripheral nerves or dermatomes (areas of skin supplied by single nerve roots).[6] He documented these observations by creating charts depicting these "segmental pain areas". Kellgren's work established the fundamental principle that deep somatic tissues could serve as a source of referred pain with predictable, segmentally organized patterns, setting the stage for later refinements of this idea.
Inman and Saunders
(Note: actual article not able to be sourced. Hence this section uses secondary sources referencing the original study)
Building directly on this foundation, Verne Inman and John Saunders published their seminal paper, "Referred Pain from Skeletal Structures," in 1944.[7] They employed a dual methodology: meticulously documenting the pain patterns reported by patients suffering from localized skeletal pathologies, and systematically inducing pain in healthy volunteers by needling or injecting hypertonic saline into specific deep structures like periosteum, ligaments, and tendons. They observed a strong concordance between the clinical and experimental findings. It was Inman and Saunders who adopted the term "sclerotome" ā borrowed from embryology but used in a novel, non-embryological sense ā to describe these zones of referred pain. They defined a sclerotome as the territory of deep somatic tissue (bone, periosteum, ligament, tendon) innervated by a single spinal nerve segment, as identified by the characteristic pattern of pain referred from stimulating structures within that territory. Their key contribution was the creation of maps illustrating these sclerotomal zones, which they described as corresponding to spinal segments but being distinct from, and often extending beyond, the boundaries of the overlying dermatomes and underlying myotomes (muscle groups innervated by a single nerve root). Their work suggested a longitudinal organization of sclerotomes in the limbs.[8][9]
Despite the significance of their contribution, Inman and Saunders themselves acknowledged the inherent limitations in the precision of their maps, stating that "the precise segmental innervation of the sclerotomal areasā¦ cannot be given with any great precision". This early recognition of imprecision foreshadowed later critiques regarding the subjectivity inherent in mapping pain based on patient reports following artificial stimulation.
Feinstein et al
The study by Feinstein and colleagues published in 1954 sought to map the referral patterns from deep somatic tissues and challenge the assumption that such pain followed dermatomes. The researchers systematically injected a chemical irritant (hypertonic saline solution, e.g., 6%) into deep paravertebral structures (muscles and potentially associated ligaments/periosteum) at various spinal levels, from the cervical to the sacral regions, in human volunteers. This technique allowed for the controlled stimulation of nociceptors within these deep tissues, mimicking potential clinical irritation.
“The desired level for a particular injection site was first obtained by reference to adjacent bony landmarks and by palpation of the vertebral spinous processes. An intradermal wheal was raised, by the use of 1 per cent. procaine solution. This point was situated in the mid-line, midway between two adjacent spinous processes. The test injection of 0.5 to 1.0 milliliter of 6 per cent. saline solution was then made by means of a 2-inch 24-gauge needle. After the skin had been punctured, the needle was directed about 15 degrees toward either the right or the left. The depth of the insertion depended upon the adiposity of the subject, the essential requirement being the placement of the needle tip in the musculotendinous interspinous tissues. A small lead pellet was taped to the overlying skin as a marker for roetgenographic confirmation of the precise level.”
—Original description of methodology of injection by Feinstein et al
The primary outcome of the Feinstein study was the documentation and mapping of referred pain patterns originating from these deep spinal structures. The experiments demonstrated that noxious stimulation of deep somatic tissues produced pain that was often felt distally, spreading outward and downward in predictable, segmentally related zones. Crucially, these experimentally derived pain maps did not align with the well-established dermatomal charts corresponding to cutaneous innervation. Furthermore, the quality of the induced pain was consistently described as deep, aching, dull, and diffuse or poorly localized ), characteristics that strongly align with the clinical descriptions of sclerotogenous pain.
The findings provided significant early experimental evidence supporting the concept of the sclerotome as a distinct functional unit for pain referral. By demonstrating that deep somatic tissues, when irritated, produce characteristic non-dermatomal, segmentally organized referred pain patterns ), the study offered empirical validation for distinguishing sclerotogenous pain from pain arising from cutaneous or neural structures. This work, often considered alongside similar experiments by Kellgren ), helped establish the foundation for recognizing and mapping sclerotomes based on their unique pain referral characteristics, thereby informing clinical diagnosis of pain originating from structures like ligaments, periosteum, and joint capsules.
Modern Period
Further research explored pain referral patterns from more clinically relevant structures, for example the cervical zygapophyseal joints (Cooper et al). See Category:Pain Maps for a full collection of known Pain Maps. The most clinically useful studies are those that mapped pain on volunteers with noxious injection, and those that took symptomatic patients and documented pain patterns in those that had 100% relief from local anaesthetic injection (ideally validated controlled blocks). These two concepts are two of the four considerations within Bogduk's Postulates when considering whether a structure causes clinically relevant pain (particularly chronic pain).
The sclerotome concept, particularly the maps, faced skepticism from the anatomical community, partly due to the reliance on subjective pain reports rather than objective anatomical demonstration of discrete innervation territories. This initial lack of broad acceptance meant the concept and its potential implications, such as explaining patterns in congenital anomalies like thalidomide-induced dysmelia, were not widely disseminated or utilized for some time.[10]
Neurophysiological Basis
Understanding the sclerotome concept requires examining the neuroanatomical substrate ā the innervation of deep somatic tissues ā and the neurophysiological mechanisms thought to underlie the referral of pain from these structures.
A. Innervation of Deep Somatic Tissues
The tissues implicated in sclerotomal pain, namely periosteum, bone, ligaments, joint capsules, tendons, and deep fascia, are indeed innervated by sensory nerve fibers, although the density and type of innervation vary between tissues.[2] The periosteum, the membrane covering bone surfaces, is particularly noteworthy for its rich sensory innervation and high sensitivity to noxious stimuli. Anatomical studies have identified various types of nerve endings within these deep structures. These include free nerve endings, which function as nociceptors sensitive to potentially damaging mechanical (stretch, pressure) and chemical stimuli (inflammatory mediators), as well as encapsulated mechanoreceptors like Pacinian corpuscles (Type II, sensitive to vibration and pressure), Ruffini endings (Type I, sensitive to stretch and pressure, joint position), and Golgi-like endings (Type III, sensitive to tension, particularly at ligament attachments). The presence of nociceptors is critical, as their activation is the initiating event in deep somatic pain.[11]
The nerve fibers transmitting signals from these deep tissues primarily include small-diameter, thinly myelinated A-delta (AĪ“) fibers and small-diameter, unmyelinated C-fibers. While AĪ“ fibers are often associated with fast, sharp, well-localized "first pain," they also contribute to the perception of deep pain. C-fibers, which conduct signals more slowly, are predominantly associated with "second pain" ā the dull, aching, burning, poorly localized sensations characteristic of deep somatic and referred sclerotomal pain. Larger myelinated A-beta (AĪ²) fibers, primarily involved in proprioception and light touch, also innervate joint structures but are not typically considered primary pain fibers, although their inputs can modulate pain perception.
Studies investigating the specific innervation patterns of joints like the hip, knee, and ankle reveal considerable complexity. For instance, the knee joint capsule receives branches from the femoral, obturator, tibial, and common fibular nerves.[12] The hip joint capsule is innervated by branches of the femoral, obturator, sciatic, and superior gluteal nerves.[13] This complex innervation, often involving contributions from multiple peripheral nerves derived from several different spinal cord segments, presents a challenge to the simple concept of discrete sclerotomes innervated by a single spinal segment. While deep tissues are undeniably innervated, the presumed strict segmental specificity implied by sclerotome maps lacks clear anatomical validation through nerve tracing studies.
B. Mechanisms of Deep Somatic Referred Pain
Several neurophysiological mechanisms have been proposed to explain why stimulation of deep somatic structures causes pain perceived in areas distant from the source.
The most widely accepted explanation is the Convergence-Projection Theory. This theory posits that primary afferent neurons innervating deep somatic structures (e.g., a spinal ligament or facet joint), which typically have a relatively low density of innervation, converge onto the same population of second-order neurons in the dorsal horn of the spinal cord as primary afferents from other somatic regions (e.g., skin or muscle in the buttock or thigh), which often have a higher density of innervation or provide more frequent input. When the deep structure is noxiously stimulated, the resulting signals activate these shared second-order neurons. Ascending pathways transmit this information to higher brain centers (e.g., thalamus, somatosensory cortex). However, because these central neurons normally receive more input from, or have a larger cortical representation corresponding to, the area with denser innervation, the brain misinterprets the origin of the signal and "projects" the sensation of pain to that more commonly represented or densely innervated somatic area. This mislocalization results in the perception of referred pain.
Central Sensitization also plays a significant role, particularly in persistent or intense pain states.[14] Prolonged or intense nociceptive barrage from injured or inflamed deep tissues can lead to neuroplastic changes within the central nervous system, primarily at the level of the dorsal horn. This involves increased excitability of second-order neurons, a reduction in their activation threshold, and an expansion of their receptive fields. Neurotransmitters like glutamate (acting on NMDA receptors) and substance P, along with various neuromodulators, contribute to this process.[15] Central sensitization can amplify the perceived intensity of pain, cause normally non-painful stimuli to be perceived as painful (allodynia), and contribute to the spread of pain beyond the initially affected area, including the phenomenon of referred hyperalgesia (increased sensitivity in the area of referred pain). It has been proposed that central sensitization might "unmask" previously ineffective or latent synaptic connections between afferents from the primary site and neurons receiving input from the referred zone, further facilitating the referral phenomenon.[14] While convergence-projection explains the basic mislocalization, central sensitization helps account for the amplification, spread, and altered quality often seen in chronic referred pain states, potentially contributing further to the variability in patterns.
Other contributing mechanisms have been suggested, including the peripheral branching of single primary afferent neurons (dichotomizing axons) that innervate structures in both the primary site and the referred area, although evidence for this is less robust for somatic-to-somatic referral compared to viscerosomatic referral.[14] Convergence-facilitation, where subthreshold inputs from different sources summate on a common neuron to reach firing threshold, may also contribute.
The quality of deep somatic referred painātypically described as deep, aching, dull, gnawing, or like an expanding pressure, and often difficult to precisely localize - aligns well with the characteristics of pain mediated predominantly by C-fiber nociceptors. The referred pain often has a delayed onset compared to any local pain experienced at the site of stimulation.
Mapping the Sclerotomes
Following the initial work of Kellgren and later Inman and Saunders, various charts purporting to map sclerotomes have been produced and are sometimes used in clinical or educational contexts. These maps typically depict the referred pain zones associated with stimulation of deep structures presumed to be innervated by specific spinal segments (e.g., C1 to S3). In the limbs, these zones are often shown as somewhat overlapping longitudinal bands. For example, some maps suggest the proximal femur and knee region receive innervation primarily from L3, L4, and L5, while L5, S1, and S2 extend to the foot. However, the scientific validity and clinical utility of these maps are subjects of significant debate, stemming from methodological issues and a lack of robust corroborating evidence.
A. Methodological Criticisms and Limitations
The primary method used to generate the original sclerotome maps involved inducing pain, typically by injecting hypertonic saline into deep tissues, and recording the subjective location and quality of the pain reported by volunteers. This methodology carries inherent limitations. Firstly, accurately localizing deep, diffuse, aching pain is intrinsically difficult for subjects, introducing uncertainty into the mapping process. Secondly, the original studies often lacked clarity regarding the precise number and location of points stimulated, and the number of subjects tested for each segment. Thirdly, injecting fluid, even in small volumes, carries the risk of stimulus spread to adjacent tissues or structures potentially innervated by different segments, confounding the results. These methodological concerns raise questions about the accuracy and reproducibility of the original maps.[9]
Perhaps the most significant criticism is the persistent lack of subsequent anatomical or physiological validation. Despite the clinical use of the term, decades after Inman and Saunders' work, there remains little direct evidence from anatomical tracing studies or neurophysiological recordings to confirm the existence of discrete, sharply defined territories of bone or periosteum exclusively innervated by single spinal segments. Reviews, notably by Ivanusic, have consistently concluded that robust evidence supporting discrete spinal segmental innervation patterns for the skeleton is lacking.[9]
B. Variability, Overlap, and Reliability Issues
Compounding the methodological issues is the observation of significant inter-individual variability in referred pain patterns. Even under controlled experimental conditions, the location and extent of referred pain elicited by stimulating the same structure can differ considerably between individuals. This inherent variability makes the creation of a single, universally applicable sclerotome map problematic. Furthermore, the proposed sclerotomal zones exhibit extensive overlap, meaning that a given area of perceived pain could potentially originate from structures innervated by multiple different spinal segments, severely limiting the map's diagnostic specificity.
The only exception often cited is the relative consistency observed in referral patterns from cervical zygapophyseal (facet) joints. Studies involving provocative injections into these joints have shown more predictable patterns of neck and shoulder pain referral compared to patterns elicited from lumbar structures. This suggests that while some deep structures might have more consistent referral patterns, it does not validate the entire concept of discrete, map-able sclerotomes across all spinal levels. Consequently, the reliability of using existing sclerotome maps to accurately infer the specific spinal segment or structure responsible for a patient's pain is considered low, especially outside the cervical spine.
C. Comparison with Dermatome Maps
A comparison with dermatomes highlights the relative weakness of the evidence supporting sclerotomes. Dermatomes are defined as areas of skin supplied by sensory fibers from a single spinal nerve root. The mapping of dermatomes, while also subject to variations and overlap, rests on a more diverse and arguably more objective evidence base. Methods have included observing the distribution of rashes in herpes zoster infections (which follow nerve pathways), mapping sensory deficits after surgical dorsal rhizotomy (cutting specific nerve roots), assessing sensation changes after nerve blocks, and nerve conduction studies.[16] Similarly, myotomes (muscles innervated by a single root) have been mapped using observations in patients with polio or spinal cord injuries, and confirmed with electromyography (EMG). In contrast, sclerotome mapping relies almost exclusively on the interpretation of subjective pain referral following artificial stimulation.
Consequently, the dermatome and myotome concepts, despite their own acknowledged limitations, are considered to have a more substantial historical and scientific foundation. While dermatome maps published in textbooks also show inconsistencies and significant inter-individual variability exists, they are generally accepted as more reliable clinical tools for localizing neurological lesions affecting specific nerve roots or spinal cord levels. Sclerotome maps, on the other hand, are frequently described as inconsistent and less reliable for pinpointing the origin of deep somatic pain.
Spatially, sclerotomes are conceptualized as relating to deep structures underlying the skin and are often depicted as extending beyond the corresponding dermatome. Crucially, the patterns are distinct; sclerotomal pain explicitly does not follow dermatomal distributions. This distinction is fundamental to the concept's proposed clinical utility in identifying non-radicular sources of pain. The core issue remains the significant gap between the observation of deep referred pain and the inference of discrete, anatomically defined sclerotomal territories ā the evidence supports the former but provides weak validation for the latter. The maps appear to represent general tendencies rather than precise anatomical zones.
Clinical Significance
Despite the significant criticisms regarding their scientific validation and mapping precision, the concept of sclerotomes persists in clinical discourse and holds some perceived relevance for musculoskeletal physicians and physiatrists. Its potential utility lies primarily in providing a framework for understanding deep, aching pain patterns that do not conform to typical dermatomal distributions associated with radiculopathy.[2]
A. Potential Diagnostic Utility
The sclerotome concept prompts clinicians to consider deep somatic structures as potential pain generators when faced with diffuse, poorly localized pain. It suggests that pain felt in the buttock, thigh, or even calf, in the absence of clear neurological signs, might originate not from nerve root compression, but from irritation of structures like lumbar zygapophyseal (facet) joints, sacroiliac joints, intervertebral discs, or spinal ligaments. For example, pain referred to the posterior calf from an L5-S1 disc, without the typical S1 dermatomal numbness or reflex changes, might be interpreted as sclerotomal (discogenic) pain.[17] Similarly, knee pain without local knee pathology might raise suspicion of referred pain from hip structures, potentially corresponding to L3, L4, or L5 sclerotomal patterns.[18] The concept aims to add an element of "depth" to sensory mapping, acknowledging that structures beneath the skin have their own patterns of segmental innervation and pain referral.
B. Guiding Interventions
Anatomical knowledge derived from sclerotomal concepts, however imprecise, has been proposed as a guide for diagnostic and therapeutic procedures. For instance, understanding the likely segmental innervation of a painful bone or joint region might inform the selection of levels for diagnostic nerve blocks or radiofrequency ablation procedures aimed at treating chronic pain originating from structures like facet or sacroiliac joints. The "modified Mayo block,"[2] mentioned in relation to lower extremity sclerotomes, exemplifies this idea of using sclerotomal anatomy to target peripheral nerve blockade, although specific details of this technique are limited in the provided materials. Pain mapping procedures, involving systematic palpation or stimulation of specific structures (like pelvic ligaments) and recording the resulting pain distribution, are sometimes used to identify potential sclerotomal contributions to conditions like chronic pelvic pain.[19]
C. Illustrative Examples and Controversial Applications
Case reports and clinical descriptions sometimes invoke sclerotomal patterns to explain observed symptoms.[17] Beyond common musculoskeletal pain, the sclerotome concept has controversially been applied to explain the distribution of lesions in rare bone conditions like melorheostosis[9] and the patterns of skeletal defects in thalidomide-induced dysmelia. Proponents argue that the congruence between the observed defects and published sclerotome maps supports the biological reality of sclerotomes and suggests a role for sensory nerves in limb morphogenesis However, critics point to the weak evidence for sclerotomes themselves and the lack of other diseases conforming to these patterns, questioning the validity of these associations. These applications highlight the concept's use in attempting to explain poorly understood phenomena but also underscore its controversial status.
D. Critical Evaluation of Clinical Utility
While the concept that deep somatic structures refer pain in non-dermatomal, segmentally related patterns is valid and clinically important, the practical utility of specific sclerotome maps for diagnosis is highly questionable. The lack of anatomical proof, the questionable methodology of the original mapping studies, and, most importantly, the high degree of inter-individual variability and map inconsistency severely limit their reliability. Other than a few exceptions (e.g. cervical facet joint pain), clinically observed pain patterns only loosely approximate published dermatome or sclerotome charts, and attempting to identify the specific spinal level involved based solely on these patterns provides very limited diagnostic accuracy.
Therefore, while sclerotomal charts might serve as a conceptual reminder that structures like facet joints, discs, or ligaments can cause referred pain, relying on their specific boundaries to pinpoint a diagnosis is likely to be misleading. The primary clinical value of considering sclerotomal pain lies not in precise mapping, but in broadening the differential diagnosis for patients presenting with deep, aching, diffuse pain, prompting the clinician to thoroughly assess potential deep spinal or other somatic sources rather than prematurely concluding the pain is purely muscular, radicular (if neuro signs are absent), or psychogenic.
Characteristics of Sclerotomal Pain
Pain quality: Pain arising from deep somatic structures like bone, periosteum, ligaments, fascia, and joint capsules, when referred, typically exhibits specific qualities. The pain is predominantly described as deep, dull, aching, or gnawing, and may have a sensation of expanding pressure. It is characteristically poorly localized and diffuse, spreading over relatively wide areas, making it difficult for the patient to pinpoint with a single finger.
Distribution: The distribution relates segmentally to the source structure but does not follow classical dermatomes. Referral typically follows an axial-to-distal pattern (e.g., spine to limb) and rarely extends distal to the knee or elbow.
Absence of neurology: A key distinguishing feature is the general absence of objective neurological deficits such as numbness, distinct paresthesia (pins and needles), muscle weakness, or reflex changes. While some sources mention numbness or tingling as possible associated symptoms , these are not considered primary features indicative of nerve root compromise as seen in radiculopathy. Provocation testing often reveals increased pain when the source structure is stressed or palpated, whereas pressure on the area of referred pain typically does not exacerbate the symptoms.
| Somatic Referred | Radicular | |
|---|---|---|
| Primary Source | Bone, periosteum, ligament, joint capsule, fascia, disc annulus | Dorsal nerve root / Dorsal Root Ganglion (DRG) |
| Pain quality | Dull, deep ache, or pressure-like, perhaps like an expanding pressure | Shooting, lancinating, or electric-shocks |
| Relation to back pain | Referred pain is always concurrent with back pain. If the back pain ceases then so does the referred pain. If the back pain flares then so does the leg pain intensity and spatial spread. | Not always concurrent with back pain. |
| Distribution | Anywhere in the lower limb, fixed in location, commonly in the buttock or proximal thigh. Spread of pain distal to the knee can occur when severe even to the foot, and it can skip regions such as the thigh. It can feel like an expanding pressure into the lower limb, but remains in location once established without traveling. It can wax and wane, but does so in the same location. | Entire length of lower limb, but below knee > above knee. In mild cases the pain may be restricted proximally. |
| Pattern | Felt in a wide area, with difficult to perceive boundaries, often demonstrated with an open hand rather than pointing finger. The centres in contrast can be confidently indicated. | Travels along a narrow band no more than 5-8 cm wide in a quasi-segmental fashion but not related to dermatomes (dynatomal). |
| Depth | Deep only, lacks any cutaneous quality | Deep as well as superficial |
| Neurological signs | Not characteristic | Favours radicular pain, but not required. |
| Neuroanatomical basis | Discharge of the peripheral nerve endings of AĪ“ and C fibres from the lower back converge onto second order neurons in the dorsal horn that also receive input from from the lower limb, and so the frontal lobe has no way of knowing where the pain came from. | Heterotopic discharge of AĪ“, AĪ², and C fibres through stimulation of a dorsal root or dorsal root ganglion of a spinal nerve, typically in the presence of inflammation, with pain being felt in the peripheral innervation of the affected nerve |
Resources
References
- ā Monsoro-Burq, Anne-Helene (2005). "Sclerotome development and morphogenesis: when experimental embryology meets genetics". The International Journal of Developmental Biology. 49 (2ā3): 301ā308. doi:10.1387/ijdb.041953am. ISSN 0214-6282.
- ā 2.0 2.1 2.2 2.3 Meyr, Andrew J.; DiPrimio, Raymond (2009-05-01). "Lower-Extremity Sclerotomes". Journal of the American Podiatric Medical Association. 99 (3): 232ā235. doi:10.7547/0980232. ISSN 8750-7315.
- ā "Pain Tracts and Sources (Section 2, Chapter 7) Neuroscience Online: An Electronic Textbook for the Neurosciences | Department of Neurobiology and Anatomy - The University of Texas Medical School at Houston". nba.uth.tmc.edu. Retrieved 2025-04-13.
- ā "Sclerotome Pain Referral Pattern Chart". Clinical Charts and Supplies (in English). Retrieved 2025-04-13.
- ā Kellgren. On the distribution of pain arising from deep somatic structures with charts of segmental pain areas. 1939
- ā Bogduk, Nikolai (2009-12). "On the definitions and physiology of back pain, referred pain, and radicular pain". Pain. 147 (1): 17ā19. doi:10.1016/j.pain.2009.08.020. ISSN 0304-3959. Check date values in:
|date=(help) - ā Inman, Verne T.; deC. M. SAUNDERS, John B. (1944-05). "REFERRED PAIN FROM SKELETAL STRUCTURES". The Journal of Nervous and Mental Disease (in English). 99 (5): 660. ISSN 0022-3018. Check date values in:
|date=(help) - ā Gadet, Ph. (2020-02-11). "Segmental innervation: a graphic synthesis of correspondence between dermatomes, myotomes, sclerotomes and viscerotomes. Systematic review of existing works and publications about dermatomes, myotomes, sclerotomes and viscerotomes aimed to design a graphic synthesis of somato-visceral correspondences". Russian Osteopathic Journal (3ā4): 150ā163. doi:10.32885/2220-0975-2019-3-4-150-163. ISSN 2220-0975.
- ā 9.0 9.1 9.2 9.3 Ivanusic, Jason J. (2007-10-18). "The evidence for the spinal segmental innervation of bone". Clinical Anatomy. 20 (8): 956ā960. doi:10.1002/ca.20555. ISSN 0897-3806.
- ā McCredie, J.; Willert, H.-G. (1999-01). "Longitudinal limb deficiencies and the sclerotomes". The Journal of Bone and Joint Surgery. British volume. 81-B (1): 9ā23. doi:10.1302/0301-620x.81b1.0810009. ISSN 0301-620X. Check date values in:
|date=(help) - ā "Review of Pain". Journal of Anesthesia & Critical Care: Open Access. 6 (2). 2016-11-10. doi:10.15406/jaccoa.2016.06.00221.
- ā Nyland, John; Brosky, Tony; Currier, Dean; Nitz, Art; Caborn, David (1994-01). "Review of the Afferent Neural System of the Knee and Its Contribution to Motor Learning". Journal of Orthopaedic & Sports Physical Therapy. 19 (1): 2ā11. doi:10.2519/jospt.1994.19.1.2. ISSN 0190-6011. Check date values in:
|date=(help) - ā Short, Anthony J.; Barnett, Jessi Jo G.; Gofeld, Michael; Baig, Ehtesham; Lam, Karen; Agur, Anne M.R.; Peng, Philip W.H. (2017-11). "Anatomic Study of Innervation of the Anterior Hip Capsule". Regional Anesthesia and Pain Medicine: 1. doi:10.1097/aap.0000000000000701. ISSN 1098-7339. Check date values in:
|date=(help) - ā 14.0 14.1 14.2 Jin, Qianjun; Chang, Yuxin; Lu, Chenmiao; Chen, Lunhao; Wang, Yue (2023-06-28). "Referred pain: characteristics, possible mechanisms, and clinical management". Frontiers in Neurology. 14. doi:10.3389/fneur.2023.1104817. ISSN 1664-2295.
- ā Chen, Jiatong (Steven); Kandle, Patricia F.; Murray, Ian V.; Fitzgerald, Lauren A.; Sehdev, Jasjit S. (2025). "Physiology, Pain". StatPearls. Treasure Island (FL): StatPearls Publishing. PMID 30969611.
- ā Downs, Mary Beth; Laporte, Cindy (2011-06). "Conflicting Dermatome Maps: Educational and Clinical Implications". Journal of Orthopaedic & Sports Physical Therapy (in English). 41 (6): 427ā434. doi:10.2519/jospt.2011.3506. ISSN 0190-6011. Check date values in:
|date=(help) - ā 17.0 17.1 Simmons, J. W.; Ricketson, R.; McMillin, J. N. (1993-10). "Painful lumbosacral sensory distribution patterns: embryogenesis to adulthood". Orthopaedic Review. 22 (10): 1110ā1118. ISSN 0094-6591. PMID 8265218. Check date values in:
|date=(help) - ā NIIMI, Masachika; ABO, Masahiro; MIYANO, Satoshi (2015). "Referred Pain to the Knee in Hip Diseases : A Case Series Study". The Japanese Journal of Rehabilitation Medicine. 52 (3): 202ā206. doi:10.2490/jjrmc.52.202. ISSN 1881-3526.
- ā Torstensson, Thomas; Butler, Stephen; Lindgren, Anne; Peterson, Magnus; Eriksson, Margaretha; Kristiansson, Per (2015-03-20). "Referred Pain Patterns Provoked on Intra-Pelvic Structures among Women with and without Chronic Pelvic Pain: A Descriptive Study". PLOS ONE (in English). 10 (3): e0119542. doi:10.1371/journal.pone.0119542. ISSN 1932-6203. PMC 4368679. PMID 25793999.CS1 maint: PMC format (link)
- ā Bogduk et al. Medical Management of Acute and Chronic Low Back Pain: An Evidence Based Approach. Elsevier Science. 2002
