Pain and Pain Perception

Definition of Pain
Pain is defined as "an unpleasant sensory and emotional experience associated with actual or
potential tissue damage." It can be protective, defensive, or diagnostic.

Foundations for Treatment

Effective pain treatment requires a foundation based on:

1. Knowledge of the condition.

2. Theories of pain control.
3. Understanding the mechanism of action of treatment modalities.

Pain Perception
Pain perception involves several key steps:

Stimulus: An unpleasant or noxious stimulus is applied.

Receptors: Specialized somatosensory receptors, such as free nerve endings, are activated.
These receptors respond optimally to specific types of stimuli.
Transmission: Activated receptors transmit impulses to the central nervous system (CNS) via
primary afferent neurons.
Recognition: The impulses reach a higher center in the brain that recognizes the stimulus as
pain.

Theories of Pain Transmission

Specificity Theory: Proposes that specific nerve fibers and nerve endings are dedicated to
transmitting noxious stimuli. It identifies four main classes of cutaneous sensations: warm,
cold, touch, and pain.
Pattern Theory: Suggests that most cutaneous receptors are similar and respond non-
selectively to various stimuli. Painful messages are sent to the CNS when stimuli fit a specific
pattern or form, even if transmitted by fibers normally responsible for light touch, vibration,
deep touch, or temperature.
Summation Theory: Theorizes that excessive stimulation of sensory fibers results in the
transmission of noxious impulses. This can involve slow temporal summation, spatial
recruitment, and after-response mechanisms within the dorsal horn. Pathological activation
of sensory nerves can create self-exciting neuronal loops.
Sensory Interaction Theory: Postulates the existence of a specialized system that controls
sensory input, preventing summation. A rapidly conducting system inhibits a slower,
nociceptive system. If the fast system loses its inhibitory control, pathological pain states
can occur.
Nociceptors
Nociceptors are specialized receptors designed to protect organisms from tissue damage. They
are uniquely responsive to damaging or potentially damaging stimuli.

Types of Nociceptive Afferent Fibers

A delta fibers:
Fast, finely myelinated.
Rapidly accommodating.
Responsible for sharp, pricking, or electric pain (first order pain).
Found predominantly in the skin, with small numbers in joints and muscles.
Sensitive to high-intensity mechanical stimuli and some noxious temperatures.
C fibers:
Slow, small, unmyelinated.
Found in deeper skin layers and most other tissues (except the nervous system).
Sensitive to mechanical, thermal, and chemical noxious stimuli.
C polymodal fibers are free nerve endings that act as receptors and are commonly silent
until activated by noxious stimulation.
Slowly accommodating.
Responsible for dull, aching, or throbbing pain (second order pain).
Transmitter substance is likely Substance P.

Types of Pain
Acute or Fast Pain:
Short duration (minutes to several days).
Recent or sudden onset.
Usually has a demonstrable etiology and limited course.
Typically localized.
Felt within 0.1 seconds of stimulus.
May be sharp, pricking, tingling, or electric.
Protective in nature.
Example: Acute lower back pain localized to the middle of the lower back, described as
"like someone sticking an ice pack in his back."
Chronic or Slow Pain:
Long duration (months or years beyond recovery).
Felt after 1 second or more from stimulus.
Often associated with anguish, apprehension, or hopelessness.
Often of vague etiology.
May be burning, aching, or throbbing.
Example: Backache of several months' duration, poorly localized, described as a
"toothache in his back."
Referred Pain:
Pain felt at a site distant from the source of disease or injury.
Projected onto the same dermatome as the source.
Occurs when a trigger point is stimulated, causing pain to radiate to a remote site.
Components of the Pain Experience
Discrimination: Primarily processed in the Cortex and Thalamus.
Affective: Involves Limbic structures and the Thalamus.
Autonomic responses: Processed in the Reticular formation.

Pain Modulation
Pain can be modified or controlled through various mechanisms. Key theories and methods
include:

Gate Theory of Pain Control (Melzack and Wall, 1965)

Concept: A "physiologic gate" exists in the substantia gelatinosa of the dorsal horn of the
spinal cord.
Mechanism: This gate's opening or closing is influenced by the relative activity in large-
diameter (A delta) and small-diameter (C) sensory fibers.
Activity in large fibers tends to inhibit transmission (closes the gate).
Increased activity in small fibers tends to facilitate transmission (opens the gate).
Pain Perception: When the gate is open, inhibitory activity is lost, allowing pain perception.
When closed, pain sensation is blocked at the cord level.
Closing the Gate: Stimulation of large, superficial sensory fibers (A delta) can close the gate.
This can be achieved through:
Transcutaneous Electrical Nerve Stimulation (TENS)
Massage
Stroking
Heat
Cold
Vibration
Modifications: The theory has been modified to include that both mechanoreceptive and
nociceptive afferents can evoke inhibition, not all nociceptive neurons receive input from both
fiber types, and not all primary nociceptive afferents have the same central effects.
Descending control systems and local interneurons also modulate impulse transmission.
Significance: While not a complete explanation, the Gate Theory has been the basis for many
treatment protocols, especially TENS.

Release of Endogenous Opiates

Concept: The body releases "naturally occurring morphine-like substances" (endogenous
opiates) that suppress pain.
Key Substance: Beta-endorphin (approximately 48 times the strength of morphine),
dynorphin, and enkephalin.
Production: Primarily produced in the anterior lobe of the pituitary gland.
Effect: Systemic inhibitory effect, involved in degrading pain-producing chemicals.
Enhancement: Production is enhanced by:
Vigorous exercise
Deep relaxation
Acupuncture
Low-frequency, high-intensity electrical stimulation (Low TENS)
Manipulation (mild increase in beta-endorphin levels)
Counter-irritation
Concept: The pain-relieving effect of painful stimuli; essentially, "pain inhibits pain."
Mechanism: A more intense or distracting painful stimulus can temporarily override or mask
the original pain.
Examples:
Fracturing a toe to distract from a headache.
Application of painful cold (ice massage).
Painful electrical stimulation ("hypalgesia by hyperstimulation").
Requirement: Electrical acupuncture point stimulation may need to be as strong as the
patient can tolerate for a reliable effect.

Exogenous Pharmaceuticals
Mechanism: Various chemical agents help relieve or prevent pain.
Non-steroidal anti-inflammatory drugs (NSAIDs) block inflammation.
Some block impulse transmission by interfering with synaptic relay.
Others reduce muscle tension and provide sedation.
Caution: While effective, some pharmaceuticals can interfere with the healing process or
cause adverse effects if over-relied upon.

Nerve Block (Conduction Block)

Concept: High-frequency electrical stimulation may block sensory stimulus transmission.
Frequency-Dependent Conduction Block Theory: Proposes that a pain-transmission neuron
can be rendered inactive by delivering impulses at a specific frequency. If an impulse is
delivered before all ionic channels in the neuron respond, no action potential is generated,
and pain is not felt. This is analogous to muscle fatigue caused by certain electrical
stimulation parameters.

Quality of Pain
Pain can be described using various terms, often categorized by the type of sensation:

Group 1: Flickering, Quivering, Pulsing

Group 2: Jumping, Flashing, Shooting
Group 3: Pricking, Sharp, Pinching
Group 4: Boring, Gritting, Pressing, Drilling, Lacerating
Group 5: Gnawing

Pain Terms
Visceral Pain: Pain originating from diffuse stimulation of pain nerve endings in viscera (e.g.,
chemical damage, smooth muscle spasm).
Causalgia: A syndrome of sustained burning pain.
General Pain: Pain associated with a lesion of the CNS.
Hyperalgesia: An increased response to a normally painful stimulus.
Hypoalgesia: A decreased sensitivity to pain stimulation.
Analgesia: Absence of pain in response to a normally painful stimulus.
Neuralgia: Pain in the distribution of a nerve.
Myalgia: Muscle pain.
Noxious Stimulus: A stimulus capable of causing damage to normal tissue.
Nociceptors: Receptors preferentially sensitive to noxious stimulation or stimuli that would
become noxious if prolonged.
Pain Threshold: The least amount of pain a person can recognize.
Pain Tolerance Level: The greatest level of pain a person can endure.
Allodynia: Pain caused by a stimulus that does not normally induce pain.
Paraesthesia: An abnormal sensation.
Neurogenic Pain: Pain arising from nerve injury.
Psychogenic Pain: Pain felt due to a psychological disorder.