From Nociception to Pain Perception

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Pain is a common aspect of the majority of injuries and pathologies, with its protective nature causing it to interrupt all other activity and current behaviours Pain is commonly described by the International Association for the Study of Pain (IASP) as “An unpleasant sensory and emotional experience associated with actual or potential tissue damage, or described in terms of such damage” . Although, reviews have scrutinised this definition for not having a complete understanding of the nature of pain experience. Therefore, a more meaningful and clinically relevant definition has been applied as “Pain is a mutually recognizable and somatic experience that reflects a person’s apprehension of threat to their bodily or existential integrity” . Experiences of pain can be classified into three different mechanisms; Nociceptive (NP), Peripheral Neuropathic (PNP) and Centrally Sensitised (CS) and can be categorized based on each mechanism having different signs and symptoms when describing pain. Nociceptive pain refers to “chemical, mechanical or thermal stimuli producing an activation of nociceptive peripheral receptive terminals of primary afferent neurons”. Peripheral Neuropathic pain refers to pain caused by “a dysfunction or irritation within the peripheral nervous system” . The third mechanism is Central Sensitisation, which is defined as pain that “is initiated by irritation or dysfunction leading to increased sensitivity within the Central Nervous System” (CNS) . As a therapist it is critical to understand the three classifications of pain, as this will allow a clear direction to be able to understand the pain being experienced and the treatment that can be used to increase the chances of successful rehabilitation.

A 23-year-old male presented with severe pain located in his right knee, after playing in a football match where contact was made causing an internal twist of his knee. He mentioned hearing a distinct ‘pop’ sound as the contact happened. Within the subjective assessment, the patient complained of sharp and piercing pain localised to the site of injury. His right knee had a large amount of swelling in comparison to the other limb, with his VAS score being a 9/10 constantly. He had no previous injuries before this event, and red flags were cleared at the start of the assessment. The patient was active, playing for the football team at his university, training three times a week (two being football sessions and one gym session) plus one match at the weekend. The symptoms that the patient was experiencing increased when attempting to weight-bear, increasing his VAS score to 10/10. He described his pain as intensifying when attempting to move his leg into either flexion or extension. The symptoms that were being presented indicated an injury with high severity and irritability, with the nature being a consistently high and sharp pain. Therefore, an objective assessment was covered with indications of a severe injury being possible.

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The patient demonstrated limited range of motion actively when trying to perform basic ranges of flexion and extension of the knee in comparison to the other limb. He found it extremely difficult to move his leg, demonstrating aggravating and easing factors, with his VAS score remaining a 10/10. Passive range (PROM) was hardly assessed due to the severe pain that was presented during his active range (AROM). Palpation around his non-injured knee portrayed a healthy knee when comparing his injured side which demonstrated a large amount of swelling around the knee anteriorly. Palpation of the injured side was also very tender, with high amount of pain being portrayed towards the posterior/lateral side of the knee. The patient presented with low levels of strength with a Grade 1 on the Oxford Scale for Resisted Muscle Tests (RMT’s) being performed at little range. The patient demonstrated no signs of pain or irregular sensation when performing dermatomal testing. Valgus and Varus stress tests were used for the Medial and Lateral Collateral ligaments, however both presented as negative. The Posterior Cruciate ligament draw test was also performed but presented as negative. The high sensitivity and specificity of the Anterior draw, Lachman’s and Pivot shift tests presented by Benjaminse, Gokeler, van der Schans,. 2006, lead to all these tests for the Anterior Cruciate Ligament (ACL) being assessed. All three tests presented as positive, with a high amount of sag occurring after the tests, indicating an injury regarding the ACL. The patient was sent for an MRI, with results confirming a grade three tear of his right ACL, with minimal damage to his meniscus. The option the patient decided was surgery, allowing the ACL to be reconstructed. After his operation, his VAS score was an 8/10 with his range of motion remaining limited. The first stage of his 12-month recovery programme demonstrated a constant sharp ache, with pain increasing when trying to extend his leg. His comments also included being fearful to weight bear for the first three weeks, however he also commented on having a decrease in pain when becoming more educated about his injury. At 6 months of his recovery following a rehabilitation programme, his strength and range of motion had increased to an almost normal state, with his pain decreasing and working positively to the treatment that was given. Therefore, from the information gathered regarding the type of injury and pain experienced, how the pain is localised to the area and the positive effects of treatment (K.M Smart et al, 2012) lead me to believe that predominant pain mechanism presented was NP.

Injuries to the ACL are very common in sports that allow contact and where sharp turns are needed. Sports that have these factors like football is rugby, where 57% of ACL injuries occur from impact being placed on the knee (Montgomery, C et al, 2018). When having a surgical procedure on an ACL, the recovery time can last from six to nine months, following a specific rehabilitation programme to decrease the patient’s pain (Medicinenet, 2019).

Nociceptive pain is the process of “chemical, mechanical or thermal stimuli activating the nociceptive peripheral sensory fibres” (Scholz, J., & Woolf, C. 2002). The activation of peripheral receptive terminals of Aδ and C fibres cause different responses from the stimuli that is placed on them. This is because the Aδ are fast conducting and the C fibres are slow conducting, meaning this inhibits different responses to nociceptive stimuli (K.M Smart et al, 2012). For example, Aδ fibres produce a pain response when responding to mechanical stimuli or changes in temperature. (Brooks and Tracey, 2005). NP is commonly referred to as ‘nerve end pain’, due to the pain being exerted from the tissues at the end of a neuron. The nerve endings become excited from mechanical, chemical or thermal stimuli, leading to injuries to any tissue such as muscles, ligaments or joints instigating nociceptive pain (Butler, D. 2000). For the process of NP to occur, there must be an impulse generated within the neuron. This occurs by an electrical impulse being triggered by a nociceptive stimulus; this stimulus triggers an action potential to occur, allowing the ion channels to open and positive ions to flow through, allowing the resting potential of the neuron to change (Butler, D. 2000). Therefore, different presentations of musculoskeletal pain can refer to stimuli such as mechanical tissue loading or compression causing tissue ischaemia; which can relate back to the mechanisms of NP (McMahon, S. B. 2005).

Within the subjective assessment of a patient, there are indicators that can refer to nociceptive pain such as the mechanism of injury (K.M Smart et al, 2012). The mechanism of injury can influence the classification of pain that is occurring. This is because with the pain also being localised to the area of injury, this suggests that there is little indication relating to pain being associated with any neurological symptoms or their experience of pain being described in a different manner, such as burning or experiencing numbness. Therefore, this suggests that the patient with a severe ACL tear experiencing pain associated with the trauma that was occurring refers to NP (K.M Smart et al, 2012). Furthermore, the patient commented on attempting to weight bear and straighten his leg caused aggravation. Different mechanisms of pain such as PNP suggest aggravating and easing factors associated with applying pressure towards neural tissue. However, with clear signs of mechanical movements such as attempting to weight bear causing aggravation, this indicates a clear nature in proportion to the pain being experienced. This further suggests the mechanism of NP being experienced. His experience regarding his rehabilitation programme further demonstrated signs of NP. With general recovery time for ACL tears after surgery being six to nine months (Medicinenet, 2019), his experience of pain was expected to decrease as the time period increased. With his pain decreasing as expected in accordance to normal time of tissue healing, this refers to NP being predominant (K.M Smart et al, 2012). This is because the time period of tissue healing is a factor regarding other mechanisms of pain, such as patients with CS experiencing pain that persists beyond the expected time of tissue healing (McMahon, S. B. 2005). Research also specifies that NP is demonstrated within the subjective assessment that a patients’ experience of pain intensifies to a ‘sharp’ pain commonly provoked by movement (Dartmouth, 2008). This is portrayed from the patient commenting on pain increasing in intensity when trying to perform flexion and extension of his leg. Although, other classifications of pain such as PNP demonstrate symptoms such as a spontaneous increase in pain without any movement occurring (K.M Smart et al, 2012).

Additionally, there are factors within the objective assessment that link to the predominant pain mechanism of the patient being nociceptive pain. NP indicates a clear and consistent nature of pain reproduction when referring to movement (K.M Smart et al, 2012). This is shown within the objective assessment when testing the patient’s AROM and PROM. His pain intensified to a VAS score of 10/10 when attempting to perform flexion and extension of his knee, and therefore his PROM could hardly be assessed due to the severity of the pain he was experiencing. This portrays a clear difference compared to mechanisms such as CS, where there is a disproportionate pattern of pain where it demonstrates as inconsistent and can result in spontaneous and severe pain (Dartmouth, 2008). Subsequent to this is the increased tenderness and pain when palpating around the site of injury. The pain remained localised to the area, with no referral symptoms, indicating the signs of NP from clinical assessment shown by K.M Smart et al, (2012). Whereas different mechanisms of pain like PNP display pain being provoked by palpation on specific neural tissues, therefore displaying NP as a dominant mechanism of pain for the ACL tear (Nee and Butler, 2006). Within an objective assessment, mechanisms of pain such as PNP portray positive neurological tests, including altered sensation and reflexes for dermatomal and myotome testing (K.M Smart et al, 2012). However, nociceptive pain presents as severe pain with an absence of neurological signs. This is shown from the patient’s dermatomal testing being negative, as well as the RMT’s being performed (myotome testing) having a Grade 1 on the Oxford Scale, demonstrating NP being displayed (Brooks and Tracey, 2005). In addition, the patient presented with signs of inflammation including a large amount of swelling anteriorly. With NP as a mechanism of pain, signs of inflammation are shown to be present as one of the indicators for NP (K.M Smart et al, 2012). On the other hand, PNP portrays no signs of inflammation being present, and instead demonstrating different factors such as having pain associated with sleep disturbance (K.M Smart et al, 2012).

To conclude, the patient demonstrated indications of NP in his subjective and objective assessments. This is shown from factors such as the mechanism of injury and tissue healing time within the subjective assessment. His treatment and experience of pain indicated that NP was present (K.M Smart et al, 2012). Moreover, features like the pain on palpation and the nature of his pain within the objective assessment portray that NP was a dominant pain mechanism (Nee and Butler, 2006). However, it is important to note that an experience of pain is not always demonstrated as black and white. Considerations need to be made regarding psychological and social factors which can have unique outcomes concerning a pain experience and how pain is communicated (Hadjistavropoulos, 2011). Therefore, a therapist must understand models such as the Biopyschosocial model to recognise that there will be cases where an experience of pain does not relate to the damage that has been caused (Eccleston, C. 2001).



  1. Benjaminse, A., Gokeler, A., & van der Schans, C. P. (2006). Clinical diagnosis of an anterior cruciate ligament rupture: a meta-analysis. Journal of orthopaedic & sports physical therapy, 36(5), 267-288.
  2. Butler, D. S. (2000). The sensitive nervous system. Noigroup publications.
  3. Chung, K. S., & Noonan, B. (2006). A practical review of the mechanisms of pain and pain management following ACL reconstruction. Orthopedics, 29(11).
  4. Cohen M, Quintner J, van Rysewyk S. Reconsidering the international association for the study of pain definition of pain. Pain Rep 2018;3:e634–37.
  5. (2008). Chapter 19: Pain. [online] Available at: [Accessed 2 Dec. 2019].
  6. Dubin, A. E., & Patapoutian, A. (2010). Nociceptors: the sensors of the pain pathway. The Journal of clinical investigation, 120(11), 3760-3772.
  7. Eccleston, C. (2001). Role of psychology in pain management. British journal of anaesthesia, 87(1), 144-152.
  8. Hadjistavropoulos, T., Craig, K. D., Duck, S., Cano, A., Goubert, L., Jackson, P. L., . . . Fitzgerald, T. D. (2011). A biopsychosocial formulation of pain communication. Psychological Bulletin, 137(6), 910-939. doi:10.1037/a0023876
  9. H. Merskey, N. Bogduk. Classification of chronic pain, (2nd ed.), IASP Press, Seattle (1994)
  10. IASP. Pain terms: a list with definitions and notes on usage: recommended by the IASP Subcommittee on Taxonomy. PAIN 1979;6:249.
  11. McMahon, S. B. (2005). Inflammatory mediators and modulators of pain. Wall and Melzack’s textbook of Pain, 49-72.
  12. Montgomery, C., Blackburn, J., Withers, D., Tierney, G., Moran, C., & Simms, C. (2018). Mechanisms of ACL injury in professional rugby union: A systematic video analysis of 36 cases. British Journal of Sports Medicine, 52(15), 994-1001. doi:10.1136/bjsports-2016-096425
  13. Nee, R. J., & Butler, D. (2006). Management of peripheral neuropathic pain: integrating neurobiology, neurodynamics, and clinical evidence. Physical Therapy in sport, 7(1), 36-49.
  14. Physiopedia. (2019). Pain Mechanisms. [online] Available at:
  15. Raynor, M. C., Pietrobon, R., Guller, U., & Higgins, L. D. (2005). Cryotherapy After ACL Reconstruction–A Meta-analysis. The journal of knee surgery, 18(02), 123-129.
  16. Ribigan, A. C. , Bajenaru, O. L. , Antochi, F. A. , Bajenaru, O. A. & NA., (2019). Nociceptive pain unmasking a serious pathology – paraneoplastic hypertrophic osteoarthropathy. Medicine, 98(23), e15900. doi: 10.1097/MD.0000000000015900.
  17. Scholz, J., & Woolf, C. (2002). Can we conquer pain?. Nature Neuroscience, 5(S11), 1062-1067. doi: 10.1038/nn942
  18. Smart, K. M., Blake, C., Staines, A., & Doody, C. (2009;2010;). Clinical indicators of ‘nociceptive’, ‘peripheral neuropathic’ and ‘central’ mechanisms of musculoskeletal pain. A delphi survey of expert clinicians. Manual Therapy, 15(1), 80-87. doi:10.1016/j.math.2009.07.005
  19. Smart, K. M., Blake, C., Staines, A., Thacker, M., & Doody, C. (2012). Mechanisms-based classifications of musculoskeletal pain: Part 1 of 3: Symptoms and signs of central sensitisation in patients with low back (±leg) pain. Manual Therapy, 17(4), 336-344. doi:10.1016/j.math.2012.03.013
  20. Smart, K. M., Blake, C., Staines, A., Thacker, M., & Doody, C. (2012). Mechanisms-based classifications of musculoskeletal pain: Part 2 of 3: Symptoms and signs of peripheral neuropathic pain in patients with low back (±leg) pain. Manual Therapy, 17(4), 345-351. doi:10.1016/j.math.2012.03.003
  21. Smart, K. M., Blake, C., Staines, A., Thacker, M., & Doody, C. (2012). Mechanisms-based classifications of musculoskeletal pain: part 3 of 3: symptoms and signs of nociceptive pain in patients with low back (±leg) pain. Manual therapy, 17(4), 352-357.
  22. Torn ACL Symptoms, Recovery Times, Treatment & Surgery. (2019), from   
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