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Torrecampo, Karleen Lara J.

DMD-2C

Assignment:

1. What is pain?

Pain is an unpleasant feeling that is conveyed to the brain by sensory


neurons. The discomfort signals actual or potential injury to the body.
However, pain is more than a sensation, or the physical awareness of pain; it
also includes perception, the subjective interpretation of the discomfort.
Perception gives information on the pain's location, intensity, and something
about its nature. The various conscious and unconscious responses to both
sensation and perception, including the emotional response, add further
definition to the overall concept of pain.

2. Theories of pain

a. Specificity

Descartes' pain pathway.

In his 1664 Treatise of Man, René Descartes traced a pain pathway.


"Particles of heat" (A) activate a spot of skin (B) attached by a fine thread
(cc) to a valve in the brain (de) where this activity opens the valve, allowing
the animal spirits to flow from a cavity (F) into the muscles that then flinch
from the stimulus, turn the head and eyes toward the affected body part,
and move the hand and turn the body protectively. The underlying premise
of this model - that pain is the direct product of a noxious stimulus activating
a dedicated pain pathway, from a receptor in the skin, along a thread or
chain of nerve fibers to the pain center in the brain, to a mechanical
behavioral response - remained the dominant perspective on pain until the
mid-nineteen sixties.

b. Pattern

Specificity theory (dedicated pain receptor and pathway) has been


challenged by the theory, proposed initially in 1874 by Wilhelm Erb, that a
pain signal can be generated by stimulation of any sensory receptor,
provided the stimulation is intense enough: the pattern of stimulation
(intensity over time and area), not the receptor type, determines whether
nociception occurs. Alfred Goldscheider (1894) proposed that over time,
activity from many sensory fibers might accumulate in the dorsal horns of
the spinal cord and begin to signal pain once a certain threshold of
accumulated stimulation has been crossed. In 1953, Willem Noordenbos
observed that a signal carried from the area of injury along large diameter
"touch, pressure or vibration" fibers may inhibit the signal carried by the
thinner "pain" fibers - the ratio of large fiber signal to thin fiber signal
determining pain intensity; hence, we rub a smack. This was taken as a
demonstration that pattern of stimulation (of large and thin fibers in this
instance) modulates pain intensity.

c. Gate Control

Melzack and Wall introduced their "gate control" theory of pain in the
1965 Science article "Pain Mechanisms: A New Theory". The authors
proposed that thin ("pain") and large diameter ("touch, pressure, vibration")
nerve fibers carry information from the site of injury to two destinations in
the dorsal horn of the spinal cord: the "inhibitory" cells and the
"transmission" cells. Signals from both thin and large diameter fibers excite
the transmission cells, and when the output of the transmission cells exceeds
a critical level, pain begins. The job of the inhibitory cells is to inhibit
activation of the transmission cells. The transmission cells are the gate on
pain, and inhibitory cells can shut the gate. When thin (pain) and large
(touch, etc.) fibers, activated by a noxious event, excite a spinal cord
transmission cell, they also act on its inhibitory cells. The thin fibers impede
the inhibitory cells (tending to leave the gate open) while the large diameter
fibers excite the inhibitory cells (tending to close the gate). So, the more
large fiber activity relative to thin fiber activity coming from the inhibitory
cell's receptive field, the less pain is felt. The authors had conceived a neural
"circuit diagram" to explain why we rub a smack.
They pictured not only a signal traveling from the site of injury to the
inhibitory and transmission cells and up the spinal cord to the brain, but also
a signal traveling from the site of injury directly up the cord to the brain
(bypassing the inhibitory and transmission cells) where, depending on the
state of the brain, it may trigger a signal back down the spinal cord to
modulate inhibitory cell activity (and so pain intensity). This was the first
theory to offer a physiological explanation for the previously reported effect
of psychology on pain perception.

3. Methods of pain control

a. Removing the cause


b. Blocking the pathway of painful impulses
c. Raising the pain threshold
d. Preventing pain reaction by cortical depression
e. Using psychosomatic methods

4. Innervations

Pain messages are two-way traffic. Inhibitory effects are achieved through
the descending pathways, which reach from the conscious brain down to the
gates in the subconscious brain and the spinal cord. The reason for this is
that the gates are places where the flow of pain messages can be controlled
or influenced (Wells & Nown 1998). By sending responses back to the
periphery, the brain can ordered the release of chemicals that have
analgesic effects, which can reduces or inhibit pain sensation.

Pain generally starts with a physical event; a cut, burn, tear, or bump
(Catalano, 1987). The sensation of pain usually depends on the activation of
a set of neurons that includes primary afferent nociceptors, interneurons in
the spinal cord, cells of the ascending tracts, thalamic neurons and neurons
of the cerebral cortex. Hence, the pain system involves a set of ascending
pathways that convey nociceptive information from peripheral nociceptors to
higher levels of the central nervous system, as well as descending pathways
that modulate that information (Bromm & Desmedth, 1995).

The term nociception refers to the process by which pain information is


carried from the periphery sense receptors in the skin and in the viscera to
the cerebral cortex through network of neuronal relays (Karoly & Jensen
1987). Exteroceptors on the body surface and propioceptors within the body
are specialized neurons that receive stimulation; mechanical (e.g. pressure),
chemical, electrical, or thermal (i.e. hot-cold sensitive).

The body is equipped with mechanical nociceptors at the periphery (so-


called first-order neurons), which project to second-order neurons in the
spinal cord and medulla, which then carries the sensory information (in the
form of electrical impulse) to the thalamus, where it synapses with third-
order neurons that transmit the impulse to the cortex.

Second-order neurons sends their sensory inputs to the thalamus via two
ascending pathways: the dorsal column medial-lemniscal system and the
anterolateral system (includes the spinothalamic, spinoreticular, and
spinotectal fibers). The former transmits impulse involving position sense,
touch, and pressure. The latter pathway is involved in pain transmission
(Karoly & Jensen 1987).

The spinal cord is the central concourse along which all pain messages
travels to and from the brain (Catalano, 1987). For example, when you stub
your toe and your peripheral nerves register alarm, this acute pain is
immediately relayed along the nerve fibers of your foot and leg to the
substantia gelatinosa located within the dorsal horn of the spinal cord. The
cells in the substantia gelatinosa relay this "fast pain" message along the
neospinothalamic and terminating in the thalamus and the cortex (see
diagram 4) (Catalano, 1987). The cortex is the region in which thoughts are
processed.

In contrast, chronic pain moves along a different and slower tract, called
the paleospinothalamic tract. This "slow pain" is generally dull, aching,
burning, and cramping (Catalano, 1987). Slow pain follows the same path as
the fast pain through the spinal cord, but once in the brain, it separates and
terminate in the hypothalamus and the limbic structures (Catalano, 1987).
The hypothalamus is responsible for stimulating the release of stress
hormones. The limbic structures are the places where emotions are
processed.

Just as there is an ascending pain pathway from the body to the brain,
there is a descending pathway that allows the brain to modulate pain
sensory. The brain uses this pathway to send chemical substances and nerve
impulses back down to the cells in the spinal cord to act against the pain
message sent up by the pain receptors. Hence, the primarily role of the
descending pathway is to send chemical messages from the brain to close
the gates in the spinal cord to ascending messages (Catalano, 1987, Wells &
Nown, 1998).

Descending inhibitory processes are of great interest in the research


arena. Hence, it has been extensively studied by scientists. For instance,
descending inhibitory processes have been investigated in anesthetized
animals (Zimmerman 1984). It was found that the firing of dorsal horn
neurons in response to noxious skin heating can be inhibited by stimulation
in the periaqueductal gray (PAG) and the lateral reticular formation (LRF) in
the midbrain. In addition, inhibition of the spinal cord neurons can also be
achieved by electrical stimulation in other regions of the brain, such as the
raphe nuclei, the locus coeruleus, and various regions of the medullary
reticular formation (for review, see Willis 1982; Mokha 1983; Morton et al.
1983; Gebhart et al. 1984), as well as sites in the hypothalamus, septum,
orbital cortex, and sensorimotor cortex (Zimmerman 1984). At the present it
is not clear to what extent these different descending systems cooperate and
interact, what their normal physiological functions are, and how they can be
activated other than by focal electrical stimulation.