Pain Mechanisms: Difference between revisions
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1. Pain described as burning, shooting, sharp, aching or electric-shock-like<br>2. History of nerve injury, pathology or mechanical compromise<br>3. Pain in association with other neurological symptoms (i.e., pins and needles, numbness, weakness)<br>4. Pain referred in dermatomal or cutaneous distribution <br>5. Less responsive to simple NSAIDs/analgesics and/or more responsive to anti-epileptic (i.e., Neurontin, Lyrica) or anti-depressant (i.e., Amitriptyline) medication<br>6. Pain of high severity and irritability (i.e., easily provoked, taking longer to settle)<br>7. Mechanical pattern to aggravating and easing factors involving activities/postures associated with movement, loading or compression of neural tissue <br>8. Pain in association with other dysesthesias (i.e., crawling, electrical, heaviness)<br>9. Reports of spontaneous (i.e., stimulus-independent) pain and/or paroxysmal pain (i.e., sudden recurrences and intensification of pain <br>10. Latent pain in response to movement/mechanical stresses<br>11. Pain worse at night and associated with sleep disturbance<br>12. Pain associated with psychological affect (i.e., distress, mood disturbances) | 1. Pain described as burning, shooting, sharp, aching or electric-shock-like<br>2. History of nerve injury, pathology or mechanical compromise<br>3. Pain in association with other neurological symptoms (i.e., pins and needles, numbness, weakness)<br>4. Pain referred in dermatomal or cutaneous distribution <br>5. Less responsive to simple NSAIDs/analgesics and/or more responsive to anti-epileptic (i.e., Neurontin, Lyrica) or anti-depressant (i.e., Amitriptyline) medication<br>6. Pain of high severity and irritability (i.e., easily provoked, taking longer to settle)<br>7. Mechanical pattern to aggravating and easing factors involving activities/postures associated with movement, loading or compression of neural tissue <br>8. Pain in association with other dysesthesias (i.e., crawling, electrical, heaviness)<br>9. Reports of spontaneous (i.e., stimulus-independent) pain and/or paroxysmal pain (i.e., sudden recurrences and intensification of pain <br>10. Latent pain in response to movement/mechanical stresses<br>11. Pain worse at night and associated with sleep disturbance<br>12. Pain associated with psychological affect (i.e., distress, mood disturbances)<br> | ||
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'''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 == | == Central Pain Mechanism == |
Revision as of 22:19, 13 April 2014
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Pain: General Overview[edit | edit source]
As defined by the International Association for the Study of Pain (IASP) pain 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. Another adjunct to these theories, Melzack and Casey (1968) described pain as multi-dimensional and complex that incorporated sensory-discriminative, affective-motivational and cognitive-evaluate components. All three dimensions are not independent, but interact with one another.
Factors Affecting Pain[edit | edit source]
There are a multitude of factors that alter pain and pain perception, however, most can be grouped into the following:
- Biomedical factors
- Psychosocial or Behavioural risk factors
- Social and Economical risk factors
- Professional/ Work-related risk factors
Pain Mechanisms[edit | edit source]
Pain mechanisms are generally subgrouped into the following classifications:
- Nociceptive
- Peripheral
- Central
During clinical assessments, determing the correct pain mechanism(s) is crucial, as it will help guide choosing the most accurate and appropriate clinical treatments for each patient. The tables below have been adapted from the Smart et al. (2010) journal which utilized an expert consensus-derived list of clinical indicators to provide some indication of the criteria upon which clinicians may base such mechanistic classfications for 'nociceptive, 'peripheral neuropathic' and 'central' mechanisms of pain. 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) or pain.
Nociceptive Pain Mechanism
[edit | edit source]
Subjective | Objective |
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1. Clear, proportionate mechanical/anatomical nature to aggravating and easing factors
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Peripheral Pain Mechanism[edit | edit source]
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[edit | edit source]
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?