Pain Mechanisms

Pain: General Overview

The most widely accepted and current definitions of pain established by the International Association for the Study of Pain (IASP) are:

An unpleasant sensory and sensory experience associated with or appearing to be associated with actual or potential nerve damage.[1]

Although several theoretical frameworks have been proposed to explain the physiological basis of pain, no single theory can encompass all aspects of pain perception. The four most influential dimensions of pain perception include Specificity Intensity Pattern and Gate Control theories of pain.[2] However in 1968 Melzack and Casey described pain as multidimensional in which the concepts are not independent but interactive[3]. The dimensions include perceptual-discriminative perceptual-stimulus and cognitive-test components.

Pain Mechanisms

Determining the most plausible mechanism of pain is crucial during clinical evaluation, as this can serve as a guide to determine the most appropriate treatment for the patient [4]. Thus, the criteria by which clinicians can make appropriate classification decisions A list of clinical indicators derived by expert consensus was established. The table below is adapted from Smart et al. (2010) categorized pain mechanisms as “nociceptive”, “peripheral” and “central” and outlined subjective and objective clinical per indicator. Therefore, these tables serve as an aid to any current knowledge and provide an outline that can guide clinical decision-making when determining the most appropriate pain mechanism. [5]

In addition, understanding the factors that may modify pain and pain perception may help determine the pain mechanism that is most appropriate for the patient. The following are risk factors that may modify pain and pain perception [6]:

• Biomedical
• Psychosocial or Behavioural
• Social and Economical
• Professional/ Work-related

1. Nociceptive Pain Mechanism

Nociception is classified as:

Pathological processes of surrounding organs and tissues. Pain projected to the damaged body part or referred pain. [7]

Nociception is a subclass of somatosensory. Nociception is the neural process that encodes and processes noxious stimuli. [8] Nociception refers to signals that reach the central nervous system due to stimulation of specialized sensory receptors in the peripheral nervous system called nociceptors. Nociceptors are activated by potentially noxious stimuli because nociception is a physiological process that protects body tissues from damage. Nociception is important for the body’s fight-or-flight response, protecting us from our surroundings environment.

Schematic diagram of a nociceptor showing the four regions of the cell.

Nociceptors can be activated by three types of stimuli in the target tissue – thermal (heating) mechanical (e.g. stretch/strain) and chemical (e.g. pH changes resulting from local inflammatory processes). Noxious stimuli can thus be divided into one of these three categories. Nociceptive sensation the pain is associated with activation of the primary peripheral nervous system in response to noxious chemical (thermal) mechanical or ischemic stimuli.[5][9]

The terms nociception and pain should not be used synonymously because each can occur independently of the other. Pain that results from activation of the nociceptors is called nociceptive pain. The analgesic can be classified according to the muscles that acted on the analgesic: superficial somatic ( e.g. skin) deep somatic (e.g. muscles/muscles/bones/muscles) or visceral ( internal organs).

For more information, please see: Nociception

Subjective

• Mechanical/physical properties clearly corresponding to hardening and softening factors
• Pain associated with and associated with a traumatic or pathological mechanism (inflammatory nociceptive) or movement/position dysfunction (ischemic nociceptive) .
• Pain at site of injury/dysfunction (with/without some somatic referral) .
• It is usually quick to repair or repair as expected from root canal treatment/recovery
• Responsive to simply NSAIDs/analgesics
• Usually periodic and active stimulus/mechanical stimuli; it may be a constant dull or throbbing pain at rest
• Pain associated with other signs of inflammation (i.e. swelling redness heat) (inflammatory nociceptive) .
• Absence of neurological symptoms
• Pain of recent onset
• Clear diurnal or 24h routine to symptoms (i.e. morning stiffness) .
• Absence or low correlation of psychosocial abnormalities (i.e. negative emotional dysfunction) .

Objective

• Clear mechanical/anatomical arrangement and associated pain generation on movement/mechanical testing of target muscles
• Localized pain on palpation
• Absence or expected/appropriate findings of (primary and/or secondary) hyperalgesia and/or allodynia
• Analgesic (i.e. pain relief) postural/exercise patterns
• Presence of other major signs of inflammation (swelling, redness and warmth)
• No neurologic signs; negative neurodynamic testing (ie, SLR brachial plexus tone test Tinel’s)
• Absence of maladaptive pain behaviour

2. Neuropathic Pain Mechanism

The International Association for the Study of Pain (2011) defines neuropathic pain as

Pain caused by a lesion or disease of the somatosensory nervous system. [10] .

It can result from damage anywhere around the nerve: the spinal cord or the supraorbital nerve.

1. Central neuropathic pain is defined as ‘pain resulting from a lesion or disease of the central somatosensory nervous system’.
2. Peripheral neuropathic pain is defined as ‘pain resulting from a lesion or disease of the peripheral somatosensory nervous system’.

The management of neuropathic pain is challenging due to the heterogeneity of its etiological symptoms and underlying mechanisms.

Peripheral neuropathic pain is initiated or caused by a primary lesion or dysfunction of the peripheral nervous system (PNS), involving a number of pathophysiological mechanisms associated with altered neurological function and responsiveness. Mechanisms include hyperarousal and abnormal impulsivity Power generation and mechanical heat and chemical sensitivity. [5] [11]

For more information see: Neuropathic Pain

Subjective

• Pain described as burning, sharp, or shock-like [12]
• History of nerve injury or mechanical injury
• Pain associated with other neurologic symptoms (i.e. needle-prick numbness and weakness)
• Pain involving dermatomes or skin distribution
• Poor response to simple NSAIDs/analgesics and/or drug responsiveness to antiepileptics (i.e. Neurontin Lyrica) or antidepressants (i.e. Amitriptyline)
• Pain of high severity and irritability (ie, being easily irritated takes longer to resolve)
• Mechanical patterns of aggravating and mitigating factors involving activities/postures associated with exercise load or compression of neural tissue
• Pain associated with other paresthesias (ie, crawling electric heaviness)
• Reports of spontaneous (i.e., unrelated to stimulus) pain and/or paroxysmal pain (i.e., sudden recurrence and intensification of pain)
• Potential pain response to exercise/mechanical stress
• Pain worse at night with sleep disturbance
• Pain associated with psychological effects (i.e. distress mood disorder) .

Objective

• Pain/signal stimulation with mechanical/movement tests (i.e. active/passive neurodynamic) stimulating/loading/compressing nerve tissue
• Triggering pain/symptoms upon palpation of the involved muscles
• Positive neurological findings (including altered reflexes sensation and nerve potential in dermatomal/myotomal or cutaneous nerve distribution) .
• Antalgic posturing of the affected limb/body part
• Positive findings of hyperalgesia (primary or secondary) and/or allodynia and/or hyperpathia in pain distribution
• Latent pain in response to movement/mechanical testing
• Clinical findings supporting an extrinsic source of neuropathy (i.e. MRI CT nerve conduction tests) .
• Symptoms of autonomic dysfunction (i.e. trophic changes) .

Note: Ancillary clinical testing (i.e. MRI) may not be necessary for clinicians to classify pain as primarily “peripheral neuropathic” .

3. Nociplastic Pain Mechanism

The International Association for the Study of Pain (2011) defines nociplastic pain as:

“Although there is no clear evidence that actual or threatened tissue damage results in activation of peripheral nociceptors, or that disease or damage to the body’s sensory systems results in pain, pain due to altered nociception”[13]

Subjective

• Disproportionate non-mechanical unpredictable pain excitation pattern in response to multiple/non-specific aggravating/relieving factors
• Pain that persists beyond expected tissue healing/pathological recovery time
• Pain out of proportion to the nature and extent of the injury or pathology
• Wide non-anatomic distribution of pain
• History of failed interventions (medical/surgical/therapeutic)
• Strongly associated with maladaptive psychosocial factors (i.e., negative emotions, poor self-efficacy, maladaptive beliefs, and pain behaviors altered by family/work/social life medical conflicts)
• Unresponsive to NSAIDs and/or more sensitive to antiepileptics or antidepressants
• Reports of spontaneous (i.e., unrelated to stimulus) pain and/or paroxysmal pain (i.e., sudden recurrence and intensification of pain)
• Pain Associated with High Disability
• More constant/unremitting pain
• Night pain/disturbed sleep
• Pain associated with other paresthesias (ie, burning, cold, crawling)
• Severe pain and restlessness (ie, being easily irritated takes a long time to resolve)
• Potential Pain Response to Exercise/Mechanical Stress in ADLs
• Pain associated with symptoms of autonomic nervous system dysfunction (skin discoloration, excessive sweating, nutritional changes)
• Often history of CNS disease/lesion (i.e. SCI)

Objective

• Disproportionately inconsistent non-mechanical/non-anatomic pain excitation patterns in response to motor/mechanical testing
• Positive findings of hyperalgesia (primary secondary) and/or allodynia and/or hyperalgesia in the distribution of pain
• Diffuse/non-anatomical pain/tenderness
• Active identification of psychosocial factors (i.e. catastrophic fear avoidance behavioral distress)
• No signs of tissue damage/pathology
• Latent pain in response to exercise/mechanical testing
• Disuse atrophy of muscles
• Symptoms of autonomic nervous system dysfunction (i.e. skin discoloration sweating) .
• Antalgic (i.e. pain relieving) posture/movement pattern

Central Pain Mechanism

The International Association for the Study of Pain (2011) defines Central Sensitization as:

increased response of nociceptors in the central nervous system to normal or low level afferent input resulting in: Hypersensitivity to stimuli.[13]

This type of pain does not respond to most medications and often requires a tailored care plan that includes addressing potential contributors to persistent pain (lifestyle cognitive functioning). work life factors) .

This type of pain is initiated either by a primary lesion or dysfunction in the central nervous system (CNS).[5][14]

Generally the pain can be defined as an increased response of nociceptors in the central nervous system to normal or low levels of afferent input[15] resulting in:

1. Hypersensitivity to stimuli.[16]
2. Responses to non-threatening stimuli.[10][17]
3. Increased pain response evoked by stimulation outside the injured area an expanded receptive field..[18]

Watch the 2 minute video below on central sensitization

For more information see: Central Sensitization

Subjective:

Objective:

Clinical Vignettes

The following clinical vignette complements the above information and encourages consideration of plausible mechanisms of pain.

Case #1: Patient A is a 58-year-old retired female high school teacher. Current History of Complaints Sudden low back pain approximately 1 month ago after starting a curling season and getting worse with walking. Patient A presents with right low back pain (P1), a Constant dull pain 7-8/10 and pain in the front of the leg that stops above the R knee joint (P2), this is intermittent pain for about 10-30 minutes, rated 2/10, with occasional burning pain above the knee. R knee curl aggravates P1 when walking >15 min on the front leg and driving >30 min and stairs. P2 is Sitting on a hard surface for more than 30 minutes with continued flexion can aggravate the condition. Coughing and sneezing didn’t make it worse, and P1 was worse at the end of the day. General health was not apparent. Patient A had a low back injury about 10 years ago and recovered after receiving treatment a good result. What is the primary pain mechanism?

Case #2: Patient B is a 30 year old male accountant. The current complaint is an inability to turn the neck to the right and bend the neck to the right suddenly onset 2 days ago. During observation, Patient B’s head rests in a slight L-rotation and L-side flexion position. Patient B reports low Pain 2-3/10 only when trying to move head to R, otherwise movement “stuck”. Patient B denied any numbness, tingling or burning sensation, and denied that NSAIDs were ineffective. Patient B reported that heat and gentle massage relieved any symptoms. Objective results show that only correct PPIVM and The scope of PPAVM is reduced and blocked. All other cervical mobilizations are WNL. What is the primary pain mechanism?

Case #3: Patient C is a 25 year old female student. The history of the current complaint is the MVA from school 40 days ago. Patient C was hit from behind, braced and immobilized with the R foot bladder inflated, checked out of the ER and returned home to bed rest. Patient C has since had 6 sessions of physical therapy No improvement, neck pain persists. P1 was on the left C2-7 and upper trapezius, graded 3-9/10, pain ranged from dull to sharp pain with occasional pins and needles depending on neck position. P1 aggravated by sitting and walking for > 30 minutes and turning to the left. P1 Occasionally Coughing/sneezing without increased pain disrupts sleep, especially when turning over in bed. P1 is sometimes relieved by heat and stretching. NSAIDs are not effective. X-rays on the day of the MVA were negative, as were the cauda equina vertebral artery and spinal cord signs. General health is good. minor sprain and stress during exercise, but never needed therapy and had no previous MVA. Patient C expressed concern about his fear of driving and had not driven since the accident. Patient C also reported increased sensitivity in her lower extremities. What is the primary pain mechanism?