THEORIES OF PAIN AND ITS APPLICATION IN PAEDIATRICS

The current definition of pain, established by the International Association for the Study of Pain (IASP) in
1986, defines pain as “an unpleasant sensory and emotional experience associated with actual or potential tissue
damage, or described in terms of tissue damage, or both.”

The theories of pain perception include the

1. Intensive theory (erb, 1874)

2. Specificity (Von Frey, 1895)
3. Strong’s theory (strong 1895)
4. Pattern theory
5. The fourth theory of pain(hardy, wolff, goodell 1940)
6. Central Summation Theory (livingstone 1943)
7. Sensory interaction theory (noordenbeos 1959)
8. Gate Control Theory (melzack and wall 1964)

INTENSIVE THEORY

This theory referred to as the intensity / summation theory. This theory defines pain, not as a unique sensory
experience but rather, as an emotion that occurs when a stimulus is stronger than usual. This theory based on
Aristotle’s concept that pain resulted from excessive stimulation of the sense of touch. Both stimulus intensity
and central summation are critical determinants. Erb proposed that the intensity of a sensation, including
pain, is directly related to the intensity of the stimulus. It suggests a linear relationship between
stimulus intensity and perceived pain intensity. It was implied that the summation occurred in the
dorsal horn cells. There must be some form of summation that occurs for the sub threshold stimuli to become
unbearably painful.
B: based on the Intensity Theory of Pain; there are no distinct pathways for low- and high-threshold stimuli.
Rather, the number of impulses in neurons determines the intensity of a stimulus. The primary afferent neurons
synpase onto wide-dynamic range (WDR) 2nd-order neurons in the dorsal horn of the spinal cord, where low
levels of activity encode innocuous stimuli, and higher levels of activity encode noxious stimuli.

SPECIFICITY THEORY OF PAIN

One of the first modern theories of pain it holds that there are specific pain receptors or pathways that transmit
signals to a “pain center” in the brain that produces the perception of pain. This theory considers pain as an
independent sensation with specialized peripheral sensory receptors (nociceptors), which respond to damage and
send signals through pathways in the nervous system to target centers in the brain. This brain center process the
signals to produce the experience of pain. Thus, it is based on the assumption that the free nerve endings are pain
receptors. This theory posits that specific nerve fibers are responsible for transmitting specific sensory
modalities, including pain.
A: based on the Specificity Theory of Pain; each modality (touch and pain) is encoded in separate pathways.
Touch and pain stimuli are encoded by specialized sense organs. Impulses for each modality are transmitted
along distinct pathways, which project to touch and pain centers in the brain, respectively. DRG, dorsal root
ganglion.

PATTERN THEORY OF PAIN

This theory considers that peripheral sensory receptors, responding to touch, warmth and other
non-damaging as well as to damaging stimuli, give rise to non-painful or painful experiences as a
result of differences in the patterns [in time] of the signals sent through the nervous system. Thus,
according to this view, people feel pain when certain patterns of neural activity occur, such as when appropriate
types of activity reach excessively high levels in the brain. These patterns occur only with intense stimulation.
Because strong and mild stimuli of the same sense modality produce different patterns of neural activity, being
hit hard feels painful, but being caressed does not.
C: the Pattern Theory of Pain posits that somatic sense organs respond to a dynamic range of stimulus
intensities. Different sense organs have different levels of responsivity to stimuli. A population code or the
pattern of activity of different neurons encodes the modality and location of the stimulus.

THE FOURTH THEORY OF PAIN (HARDY, WOLFF, GOODELL, 1940)

It stated that pain was composed of two components: the perception of pain and the reaction one has towards it.
The reaction was described as a complex physiopsychological process involving cognition, past experience,
culture and various psychological factors which influence pain perception

CENTRAL SUMMATION THEORY (LIVINGSTONE, 1943)

The theory posits that individual nerve impulses generated by noxious stimuli are integrated or summed up
within the central nervous system (specifically in the spinal cord and brain) to produce the sensation of pain.
Central Summation Theory can be seen as complementary to other theories of pain, such as the Specificity and
Pattern theories. While those theories focus on the peripheral mechanisms of pain, Central Summation Theory
emphasizes the central processes involved in pain perception.

STRONG'S THEORY (STRONG, 1895)

This theory states that pain was an experience based on the both the noxious stimulus and the psychic reaction or
displeasure provoked by sensation.

SENSORY INTERACTION THEORY (NOORDENBOS, 1959)

Multisensory Integration: According to the Sensory Interaction Theory, pain perception is not solely
determined by nociceptive (pain-related) signals. Instead, it involves the integration of multiple sensory
modalities. Role of Other Sensory Inputs: The theory emphasizes that sensory experiences such as touch,
temperature, and proprioceptive feedback can influence the perception of pain. For example, a gentle touch or a
change in temperature might modulate the intensity or quality of a pain sensation.

GATE CONTROL THEORY OF PAIN

Melzack has proposed a theory of pain that has stimulated considerable interest and debate and has certainly been
a vasy improvement on the early theories of pain. According to his theory, pain stimulation is carried by small,
slow fibers that enter the dorsal horn of the spinal cord; then other cells transmit the impulses from the spinal
cord up to the brain. These fibers are called T-cells. The T-cells can be located in a specific area of the spinal
cord, known as the substantial gelatinosa. These fibers can have an impact on the smaller fibers that carry the
pain stimulation. In some cases they can inhibit the communication of stimulation, while in other cases they can
allow stimulation to be communicated into the central nervous system.

For example, large fibers can prohibit the impulses from the small fibers from ever communicating with the
brain. In this way, the large fibers create a hypothetical "gate" that can open or close the system to pain
stimulation. According to the theory, the gate can sometimes be overwhelmed by a large number of small
activated fibers. In other words, the greater the level of pain stimulation, the less adequate the gate in blocking
the communication of this information.

D: the Gate Control Theory of Pain proposes that both large (A-fibers) and small (C-fibers) synpase onto cells in
the substantia gelatinosa (SG) and the 1st central transmission (T) cells. The inhibitory effect exerted by SG cells
onto the primary afferent fiber terminals at the T cells is increased by activity in A-fibers and decreased by
activity in C-fibers. The central control trigger is represented by a line running from the A-fiber systerm to the
central control mechanisms; these mechanisms, in turn, project back to the Gate Control system. The T cells
project to the entry cells of the action system. , excitation; , inhibition. Figure is reproduced with permission from
Perl (2007).
Pain Theory Explanation
Specificity Pain is a distinct sensation
Theory (19th with specific receptors
century - Von (nociceptors) responding
Frey) to damage. Signals
transmit to the brain's
"pain center."
Intensive Theory Pain intensity is
(19th century - proportional to tissue
Erb) damage. Implies a linear
relationship between
stimulus intensity and
perceived pain intensity.
Central Pain results from the
Summation integration of neural
Theory (1943 - signals within the central
Livingston) nervous system (spinal
cord and brain).
Sensory Pain perception involves
Interaction the interaction of various
Theory (1959 - sensory modalities, not
Noordenbos) solely determined by pain-
related signals.
Gate Control Pain perception is
Theory (1965 - regulated by a neural
Melzack and Wall) "gate" in the spinal cord
influenced by sensory
input, emotions, and
cognition.
Pattern Theory Pain depends on patterns
(20th century - of neural activity in
Livingston) response to stimuli.
Different patterns create
different sensations,
including pain.
Example Application in Pediatric Pain
Management
Touching a hot Tailoring interventions based on
stove - nociceptors developmental stages, using specific
respond to burn. strategies for different types of pain
in children.
Deep paper cut - Assessing and managing pediatric
more intense cut, pain based on the severity of tissue
more pain. damage, guiding appropriate
interventions for acute and chronic
pain in children.
Stubbing toe - Developing comprehensive pain
signals integrated management strategies addressing
in the CNS. both peripheral and central
sensitization processes in pediatric
patients.
Feeling less pain Designing holistic pain management
when held gently approaches considering sensory
during a interactions, optimizing pain relief,
procedure. and comfort in pediatric patients.
Rubbing a Implementing multidisciplinary
bumped knee - approaches, including distraction and
activating large relaxation techniques, to modulate
fibers. pain perception in pediatric patients.
Feeling pain when Considering sensory factors (touch,
hit hard but not temperature) in pediatric pain
when caressed. assessment and incorporating
sensory-based interventions for pain
 MECHANISM OF PAIN:

 Pain sensation involves series of complex interactions between PNS & CNS
 Pain sensation modulated by excitatory and inhibitory neurotransmitters released in response to stimuli.
 Sensation of pain is composed of 4 basic processes
 Transduction
 Transmission
 Modulation
 Perception