9
8
Neuromatrix theory: In 1999, Melzack and Wall pre-
sented a newer theory of pain, consistent with the idea of
gate control that addresses some of these unanswered
questions. This “new and improved” theory, the neuro-
matrix theory, says that each person has a genetically
built-in network of neurons called the “body-self neuro-
matrix. Just as each person is unique in physical appear-
ance, each person’s matrix of neurons is unique and is
affected by all facets of the person’s physical, psycho-
logical, and cognitive makeup, as well as his or her ex-
perience. Thus, the pain experience does not reflect a
simple one-to-one relationship between tissue damage
and pain.
sheath. The C fibers are the ones that produce constant
pain. According to the gate control theory, stimulation
of the fibers that transmit non-painful stimuli can block
pain impulses at the gate in the dorsal horn. For exam-
ple, if touch receptors (A beta fibers) are stimulated,
they dominate and close the gate. This ability to block
pain impulses is the reason a person is prone to immedi-
ately grab and massage the foot when he or she stubs a
toe. The touch blocks the transmission and duration of
pain impulses. Since the mechanosensory pathway as-
cends ipsilaterally in the cord, a unilateral spinal lesion
will produce sensory loss of touch, pressure, vibration,
and proprioception below the lesion on the same side.
The pathways for pain and temperature, however, cross
the midline to ascend on the opposite side of the cord.
This pattern is referred to as a dissociated sensory loss
and (together with local dermatomal signs; helps define
the level of the lesion.
Pain Pathways and Transmission
Previously, pain pathways were seen as having three
components:-
•
•
•
A first order neurone (cell body in dorsal root
ganglion) which transmits pain from a peripheral
receptor.
A second-order neurone in the dorsal horn of the
spinal cord, which axon crosses the midline to
ascend in the spinothalamic tract to the thalamus.
A third-order neurone projects to the postcentral
gyrus (via the internal capsule).
Regulators of Pain
Chemical substances that modulate the transmission of
pain are released into the extracellular tissue when tissue
damage occurs. They activate the pain receptors by irri-
tating nerve endings. These chemical mediators include
histamine, substance P, bradykinin, acetylcholine, leu-
kotrienes and prostaglandins. The mediators can produce
other reactions at the site of injury, such as vasoconstric-
tion, vasodilatation, or altered capillary permeability.
For example, prostaglandins induce inflammation and
potentiate other inflammatory mediators. Aspirin a non-
steroidal anti inflammatory medications, and the new
cyclooxygenase-2 (COX-2) inhibitors block cyclooxy-
genase-2, the enzyme needed for prostaglandin synthe-
sis, thus reducing pain. Consequently, these medica-
tions are often prescribed for painful conditions due to
inflammation.
This scenario, while partially correct, is now known to
be horribly over-simplified. The pathways that carry
information about noxious stimuli to the brain, as might
be expected for such an important and multifaceted
system, are complex. The major pathways are
summarized in the following figure which omits some of
the less well understood subsidiary routes. Because
projections from non-nociceptive temperature-sensitive
neurons follow the same anatomical route, they are
included in this description, even though they are not
part of the pain system. Nociceptors, or pain receptors,
are free nerve endings that respond to painful stimuli.
Nociceptors are found throughout all tissues except the
brain, and they transmit information to the brain. They
are stimulated by biological, electrical, thermal,
mechanical, and chemical stimuli. Pain perception
occurs when these stimuli are transmitted to the spinal
cord and then to the central areas of the brain. Pain
impulses travel to the dorsal horn of the spine, where
they synapse with dorsal horn neurons in the substantia
gelatinosa and then ascend to the brain.
Fibers in the dorsal horn, brain stem, and peripheral tis-
sues release neuromodulators, known as endogenous
opioids that inhibit the action of neurons that transmit
pain impulses. β-endorphins and dynorphins are types of
natural opioid-like substances released, and they are
responsible for pain relief. Endorphins are the modula-
tors that allow an athlete to continue an athletic event
after sustaining an injury. Endorphin levels vary from
person to person, so different persons experience differ-
ent levels of pain. This endogenous opioid mechanism
may play an important role in the placebo effect. A pla-
cebo is an inactive substance or treatment used for com-
parison with “real” treatment in controlled studies to
determine the efficacy of the treatment under study. De-
spite the lack of any intrinsic value, placebos can and do
produce an analgesic response in many persons. Placebo
analgesia can affect nociceptive mechanisms in the cor-
tex of the brain and descending pathways of the spinal
cord.
Two types of fibers are involved in pain transmission:
The large A delta fibers produce sharp well-defined
pain, called “fast pain” or “first pain,” typically stimu-
lated by a cut, an electrical shock, or a physical blow.
Transmission through the A fibers is so fast that the
body’s reflexes can actually respond faster than the pain
stimulus, resulting in retraction of the affected body part
even before the person perceives the pain.
Classification of Pain
After this first pain, the smaller C fibers transmit dull
burning or aching sensations, known as “second pain.”
The C fibers transmit pain more slowly than the A fibers
do because the C fibers are smaller and lack a myelin
Pain can be divided into
(
A) nociceptive (B) neuropathic (C) a mixture of these