Pain Mechanisms: Difference between revisions
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=== Nociceptive Pain Mechanism<ref name="Smart" /><br> === | === Nociceptive Pain Mechanism<ref name="Smart" /><br> === |
Revision as of 20:27, 8 August 2018
Original Editor - Tiara Mardosas
Top Contributors - Tiara Mardosas, Carin Hunter, Jess Bell, George Prudden, Admin, Kim Jackson, Rachael Lowe, Carina Therese Magtibay, Scott Buxton, Venus Pagare, Tarina van der Stockt and Naomi O'Reilly
Pain: General Overview[1][edit | edit source]
The most widely accepted and current definition of pain, established by the International Association for the Study of Pain (IASP), is "an unpleasant sensory and emotional experience associated with acutal or potential tissue damage, or described in terms of tissue damage, or both." Although several theoretical frameworks have been proposed to explain the physiological basis of pain, not one theory has been able to exclusively incorporate the entirety of all the aspects of pain perception.
The four most influential theories of pain perception include Specificty, Intensity, Pattern and Gate Control theories of pain. However, in 1968, Melzack and Casey described pain as multi-dimensional, where the dimensions are not independent, but rather interactive. The dimensions include sensory-discriminative, affective-motivational and cognitive-evaluate components.
Pain Mechanisms[2][edit | edit source]
Determining the most plausible pain mechanism(s) is crucial during clinical assessments as this can serve as a guide to determine the most appropriate treatment(s) for a patient. Therefore, criteria upon which clinicians may base their decisions for appropriate classifications have been established through an expert consensus-derived list of clinical indicators. The tables below were adapted from Smart et al. (2010) that classified pain mechanisms as 'nociceptive', 'peripheral neuropathic' and 'central' and outlined both subjective and objective clinical indicators for each. Therefore, these tables serve as an adjunct to any current knowledge and provide as an outline that may guide clinical decision-making when determining the most appropriate mechanism(s) of pain.
Furthermore, being cognizant about the factors that may alter pain and pain perception may assist in determining the most appropriate pain mechanism for a patient. The following are risk factors that may alter pain and pain perception:
- Biomedical
- Psychosocial or Behavioural
- Social and Economical
- Professional/ Work-related
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Nociceptive Pain Mechanism[2]
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Nociceptive pain is associated with the activation of peripheral receptive terminals of primary afferent neurons in response to noxious chemical (inflammatory), mechanical or ischemic stimuli.
Subjective | Objective |
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1. Clear, proportionate mechanical/anatomical nature to aggravating and easing factors
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Peripheral Neuropathic Pain Mechanism[2][edit | edit source]
Peripheral neuropathic pain is initiated or caused by a primary lesion or dysfunction in the peripheral nervous system (PNS) and involves numerous pathophysiological mechanisms associated with altered nerve functioning and responsiveness. Mechanisms include hyperexcitability and abnormal impulse generation and mechanical, thermal and chemical sensitivity.
Subjective | Objective |
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1. Pain described as burning, shooting, sharp, aching or electric-shock-like |
Note: Supportive clinical investigations (i.e., MRI) may not be necessary in order for clinicians to classify pain as predominantly “peripheral neuropathic”
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Central Pain Mechanism[2]
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Central pain is pain initiated or caused by a primary lesion or dysfunction in the central nervous system (CNS).
Subjective | Objective |
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1. Disproportionate, non-mechanical, unpredictable pattern of pain provocation in response to multiple/non-specific aggravating/easing factors
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1. Disproportionate, inconsistent, non-mechanical/non-anatomical pattern of pain provocation in response to movement/mechanical testing
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Clinical Vignettes[edit | edit source]
The following clinical vignettes are here to supplement the above information and get those thinking about plausible pain mechanisms.
Case #1:
Patient A is a 58-year-old female, retired high school teacher. History of current complaint, approximately 1 month ago, sudden onset of low back pain after starting a season of curling and has been getting worse with walking. Patient A presents with right-sided low back pain (P1) that is a constant dull ache, 7-8/10, and anterior leg pain stopping above the R knee (P2) that is an intermittent ache for ~10-30 minutes rated at 2/10, with an occasional burning pain above the knee. P1 is aggravated by curling with R knee as lead leg, walking >15 minutes, driving >30 minutes and stairs. P2 is aggravated by sitting on hard surfaces >30minutes and sustained flexion. Coughing and sneezing does not make it worse and P1 is worse at the end of the day. General health is unremarkable. Patient A has had a previous low back injury approximately 10 years ago, underwent treatment and resolved with a good outcome. What is the dominant pain mechanism?
Case #2:
Patient B is a 30-year-old male, accountant. History of current complaint is a sudden onset of an inability to turn neck to right and side bend neck to right 2 days ago. On observation, Patient B has head resting in a position of slight L rotation and L side bend. Patient B reports a low level of pain, 2-3/10, only when trying to move head to the R, otherwise movement “is stuck”. Patient B denies any numbness, tingling or burning pain and NSAIDs ineffective. Patient B reported heat and gentle massage to ease any symptoms. Objective findings indicate only right PPIVMs and PPAVMs to have decreased range and blocked. All other cervical spine mobilizations are WNL. What is the dominant pain mechanism?
Case #3:
Patient C is a 25-year-old female student. History of current complaint is a MVA 40 days ago while going to school. Patient C was hit from behind, braced and braked with R foot, airbag inflated, checked out of the ER then home on bed rest. Since then, Patient C has had 6 visits of physiotherapy with no improvement and neck pain persisting. P1 is left C2-7 and upper trapezius, rated 3-9/10, and pain varies from a dull ache to sharp pain with occasional pins and needles, depending on neck position. P1 is aggravated by sitting and walking > 30 minutes and turning to the left. P1 occasionally disturbs sleep, particularly when rolling over in bed and coughing/sneezing does not increase pain. P1 is sometimes eased by heat and stretching. NSAIDs have no effect. X-ray day of MVA is negative, negative cauda equina, vertebral artery and cord signs. General health is generally good. Minor sprains and strains in sports, but never required treatment and no previous MVA. Patient C voices concern about fear of driving and has not been driving since the accident. Patient C has also reported an increase in sensitization in her lower extremities. What is the dominant pain mechanism?
References
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- ↑ Moayedi M, Davis KD. Theories of pain: From specificity to gate control. J Neurophysiol 2013;109:5-12. (accessed 1 April 2014).
- ↑ 2.0 2.1 2.2 2.3 Smart KM, Blake C, Staines A, Doody C. Clinical indicators of 'nociceptive', 'peripheral neuropathic' and 'central' mechanisms of musculoskeletal pain. A Delphi survey of expert clinicians. Man Ther 2010;15:80-7. (accessed 1 April 2014).