Understanding Pain: Definition and Context

• Pain can be defined as an unpleasant sensation and emotional response associated with actual potential tissue damage, or described in terms of such damage.
• A newer definition states that pain is an unpleasant sensory and emotional experience associated with, or resembling that associated with, actual or potential tissue damage.
• These definitions come from the International Association for the Study of Pain.

Definition Context

• Pain is a personal experience influenced by biological, psychological, and social factors.
• Pain differs from nociception and cannot be inferred from activity in sensory neurons alone.
• Individuals learn the concept of pain through life experiences.
• Respect should be given to a person's report of their pain experience.
• Pain can serve an adaptive role, or adversely affect function, social interactions, and psychological well-being.
• Expressing pain includes verbal descriptions, so inability to communicate doesn't negate the possibility of pain in humans or animals.

Key Terms

• Nociception: the encoding of painful stimulus.
• Hyperalgesia: increased pain sensitivity.
• Allodynia: Painful response to a non-nociceptive stimulus.
• Hypoalgesia: Absence of pain in response to stimulation that would normally be painful.
• Dysesthesia: an unpleasant abnormal sensation, whether spontaneous or evoked.

Pain Types by Duration

Based on the duration of symptoms, pain can be:

• Acute: caused by an event and typically lasts less than 6 months (IASP < 3 months).
• Chronic: lasting longer than 6 months (IASP > 3 months), the cause may be unknown.
• Persistent: a treatable condition versus chronic pain.

Acute Pain

• Subjective history will match symptoms and pathology.
• The patient will generally return to normal as factors leading to pain resolve.
• Possible causes include:
  • Wound
  • Disease Process
  • Invasive procedure

Chronic Pain

• Approximately one-third of U.S. residents will experiences this at some point.
• 14% of chronic pain is musculoskeletal in origin.
• Common Diagnoses of Chronic Pain
  • Chronic Spinal Pain
  • Fibromyalgia
  • Neuropathy
  • Complex regional pain syndrome (CRPS)
  • Phantom limb pain
  • Poststroke pain
  • Osteoarthritis and rheumatoid arthritis
  • Headache
  • Cancer Pain
  • Temporomandibular Joint Disorder
  • Irritable Bowel Syndrome
  • Interstitial Cystitis
• Differentiated from persistent pain

Pain Types by Symptoms, Mechanisms & Syndromes

• Nociceptive pain: mediated by nociceptors (Aδ- and C-fibers).
• Neuropathic pain: associated with nerve injury or impairment.
• Inflammatory pain: associated with inflammation.

Pain Mechanisms

• Biological Mechanisms:
  • Nociceptive: activation of nociceptors, such as in OA or ankle sprain; heat sensitivity (>100 degrees).
  • Neuropathic: pathology of the somatosensory system, such as carpal tunnel, diabetic neuropathy or complex regional pain syndrome; cold sensitivity.
  • Nociplastic: abnormal central processing, e.g. fibromyalgia.
• Psychosocial factors: e.g., depression or fear avoidance beliefs.
• Movement system: e.g., weakness and/or increased/decreased tone.

Nociceptive Pain

• It is a result of stimulation of nociceptors caused by mechanical, chemical, or thermal stimuli.
• There is a stimulus-response relationship (movement/position can lead to symptoms).
• The pain is usually felt at or near the site of injury and can be referred.
• Cutaneous stimulation causes sharp, pricking, tingling pain that is easy to localize.
• Musculoskeletal stimulation creates dull, heavy, or aching pain that is more difficult to localize.
• Visceral stimulation, like musculoskeletal pain, refers superficially and is not dependent on movement.

Peripheral Neuropathic Pain

• Caused by lesion or disease affecting peripheral nerves.
• Can be worsened by activities that compress or stretch involved nerves.
• Symptoms include pain with active/passive movement of the involved limb; tenderness to palpation of the involved nerve; tenderness/inflammation of tissue enervated by the involved nerve

Nociplastic/Central Sensitization

• A clear anatomical correlate is not present, is worsened by the cold, and is spread or worsened without apparent cause.
• Pain is associated with fatigue, sleep disturbance, impaired physical/mental functioning, phantom pain; also swelling/stiffness and depression.
• Patients may experience pain flare-ups which are out of proportion to triggering activity and can last for several days.
• Signs of Sensitization
  • Sensitivity to normally innocuous stimuli (allodynia).
  • Pain intensity/duration out of proportion to the stimulus (hyperalgesia).
  • Pain is perceived in an area beyond the typically affected area.
  • Spontaneous/evoked unpleasant sensations aside from pain (dysesthesia).
  • Pain from repeated subthreshold stimuli (hyperpathia).
• Diagnoses: fibromyalgia, osteoarthritis, rheumatoid arthritis, temporomandibular disorders, whiplash, low back pain, and pelvic pain.

Psychosocial Pain

• Triggered by cognition, emotion, context, and environment.
• It should not be considered "imaginary pain," but may not correlate with the condition of the body's tissues.
• Commonly seen in persons who have had lasting injuries, which typically persist for more than several months.
• Similarities to Nociplastic Pain:
  • the pain is spreading or inconsistent, without anatomically correlate.
  • Significantly affected by mood or environment.
  • Flares up, lasting days, without reason.
• Differences:
  • no allodynia, no hyperpathia, and no sensitivity to cold.

Referred Pain

• It is felt in a location different from the injury.
• Local tenderness, hyperalgesia, or allodynia distinguishes nociceptive/local neuropathic pain from psychosomatic, central, and referred pain.
• Possible Mechanisms: Convergence and unmasking.
• Typical Patterns: Dermatomes, myotomes, sclerotomes, and viscerotomes.

Referred Pain Mechanism, Convergence

• Convergence describes one neuron receiving impulses from two peripheral neurons, resulting in the central pathways not being able to distinguish between the sources.

Referred Pain Mechanism, Unmasking

• Unmasking describes otherwise silent or latent synaptic connections being activated by nociceptive sensory nerve fibers.
• In the brainstem, nociceptive afferent nerve fibers branch extensively terminating on many different second order neurons.
• Some of these synaptic connections are latent.
• Latent synapses may become active after prolonged and/or intense stimulation (muscle trauma).
• Transmits signals that convey information from regions unrelated to the source of the noxious peripheral stimulus.

Additional Pain Types

• Deep Somatic pain: deep achy feeling often differing from the site of pathology may be caused by cancer.
• Radiating pain: irritation of nerves and nerve roots radiating pain to the lower extremities (LE) and foot when associated with herniated disc or contusion of the sciatic nerve.

Pain from Start to Finish, Nociception

1. Injury to cell.
2. Release prostaglandins, leukotrienes and substance P (receptors).
3. Stimulate nociceptors (A and C fibers).
4. Pain response (neural pathways).

Peripheral Factors

Sensory receptors include: Meissner's corpuscles, Merkel's corpuscles, Pacinian corpuscles, Ruffini corpuscles, Hair Follicles, Nociceptors/ free nerve endings, Krause's end bulbs, Muscle spindles, Golgi tendon organs.

Receptor Behavior

• Phasic receptors: respond when stimulus is increasing or decreasing
• Tonic receptors: respond to stimulus as long as the stimulus is present.
• Accommodation: decrease in generator potential and frequency with prolonged/repeated stimulation.

Neural Transmission - Afferent Neuron Classification

• Aα fibers: Type I; subgroup 1a; 13-22 micrometers diameter; 70-120 m/s velocity; proprioceptive (muscle spindle) mechanoreceptor; involved in muscle velocity and length change/shortening during rapid speed.
• Aα fibers: Type I; subgroup 1b; proprioceptive mechanoreceptor; involved in muscle length information from touch and Pacinian corpuscles.
• Aβ fibers: Type II; Muscle; 8-13 diameter; 40-70 m/s velocity; receptors are those in muscle including the Meissner corpuscle, Merkel cell, Pacinian corpuscle, Ruffini ending, hair follicle, Paciniform endings, muscle spindle.
• Aβ fibers: Type II; Skin; receptors are those in skin including the Meissner corpuscle, Merkel cell, Pacinian corpuscle, Ruffini ending, hair follicle, Paciniform endings, muscle spindle.
• Aδ fibers: Type III; Muscle; 1-4 diameter; 5-15 m/s velocity; 75% mechanoreceptors and thermoreceptors (free nerve endings); involved in temperature change.
• Aδ fibers: Type III; skin; velocity is 5-15 m/s; 25% nociceptors, mechanoreceptors, and thermoreceptors (hot and cold).
• C Fibers: Type IV; muscle; 0.2-1.0 diameter; 0.2-2.0 m/s velocity; 50% mechanoreceptors and thermoceptors (free nerve endings); involved in touch and temperature.

Nociception

• Fast Pain (A-fibers δ): larger, faster-conducting a-delta afferents in skin. Brief, well-matched stimulus (pricking, sharp) and well localized.
• Slow Pain (C-fibers): C fibers originate in skin and deeper tissue, causing aching, throbbing, burning pain that poorly localized.

Neural Transmitters

• Neurotransmitters like acetylcholine pass information between neurons.
• They also may facilitate or inhibit synaptic activity.
• Types of neurotransmitters are serotonin, norepinephrine, substance P, enkephalin, and B-endorphin.
• Serotonin blocks pain messages is the efferent pathways.
• Enkephalin inhibits depolarization of 2nd order nociceptive nerve fibers.

Nociception Hyperalgesia

• Primary Hyperalgesia: Peripheral mechanism - Peripheral sensitization, decrease receptor threshold, increased response to suprathreshold and expansion of receptive field. May also involve less of central inhibition and sympathetic NS in chronic pain.
• Secondary Hyperalgesia: Central mechanisms (after several hours). Chemicals increase in concentration to increase the size of the pain area and hypersensitivity. Sensitivity to mechanical, but not heat, stimuli.

Mechanisms of Pain Control

• Blocking ascending pathways (gate control).
• Activating descending pathways.
• Releasing ẞ-endorphin and dynorphin.

Neuropathways

• A beta fibers are responsible for the release of enkephalin, which blocks the pain pathway and decreases the perception of this sensation.

Pain Assessment

• Is used to identify type of pain.
• Is used to quantify the intensity; also to evaluate what effect it has on the patient’s level of function.
• Used to assess psychosocial aspect of pain.
• Patient self report is considered the golden standard.

Pain Scales

• Visual Analog Scale
• Numeric Pain Rating Scale (NPRS: eleven-point scale; "rate your pain on a scale of 0 to 10, 0 being no pain at all and 10 being the worst pain imaginable.")
• Pain Charts: use figures to allow for visualization and specificity.
• McGill Pain Questionnaire

Pain Management

• Treatment Models:
  • Biomedical Model: Pain has a physiological cause that clinicians treat.
  • Biopsychosocial Model: accounts for the interaction of biological (nociception), psychological (pain appraisal, pain behaviors, coping mechanisms), and sociocultural variables (social roles for pain and illness).
• Cognitive Influences:
  • Modulate pain perception via descending systems (behavior modification, focusing, hypnosis, suggestion)
  • Facilitating/inhibiting Pain Perception (past experience, culture, anger, fear, and aggression)
• Modalities:
  • TENS/massage stimulates large diameter afferents
  • Cold can decrease pain fiber transmission
  • Stimulate small diameter afferents and descending pain control with acupressure, deep massage, TENS, or trigger points, and also the release of endogenous opioids via small fiber stimulation (TENS).
• Therapeutic:
  • Electrical energy (electrical stimulation/ iontophoresis)
  • Electromagnetic energy (SWD, MD, IR, UV, LLL)
  • Ultrasound and also mechanical methods (massage, compression, traction)