Though the brain contains billions of neurons,
it does not contain any receptors for pain. When you have a headache,
the pain you feel is in the blood vessels that supply blood to the brain, and
not in the neurons that make up the brain itself. When these blood vessels contract
or dilate in abnormal ways, the pain receptors in their walls are translated into
pain impulses, which are then perceived by your brain.
Each of the spinal nerves emerging from the spinal
cord through the space between two vertebrae consists of two types of fibres:
sensory fibres, which come from the dorsal root of the nerve, and motor fibres,
which come from its ventral root. Every person has 8 cervical spinal nerves (C1
to C8), 12 thoracic spinal nerves (T1 to T12), 5 lumbar spinal nerves (L1 to L5),
and 5 sacral spinal nerves (S1 to S5). The skin area innervated by a given spinal
nerve is called its dermatome.
ASCENDING PAIN PATHWAYS
You close a door on your
finger. You bump your shin on a chair. You burn your arm on the toaster. In all
three cases, you experience a pain
withdrawal reflex first, then an acute sensation of pain, and then a duller
In order to understand the difference between
these two types of pain—fast or acute pain and slow or dull pain—before
we look at the neural pathways by which the pain signals reach the brain, we must
look at where these signals start and what kind of nerve fibres they travel over.
of all, in contrast to other types of sensory fibres such as those for the sense
of touch, which have specialized structures (such as Pacinian and Messner corpuscles)
at their endings, nociceptive fibres (the fibres that carry pain signals) have
none. Instead they have what are known as free nerve endings. These free nerve
endings form dense networks with multiple branches that are regarded as nociceptors,
that is, the sensory receptors for pain. These nociceptors respond only when a
stimulus is strong enough to threaten the body’s integrity—in other
words, when it is likely to cause an injury.
are various types of nerve fibres (axons)
whose free endings form nociceptors. These fibres all connect peripheral organs
to the spinal cord, but differ greatly both in diameter and in the thickness of
sheath that surrounds them. Both of these traits affect the speed at which
these axons conduct nerve impulses: the greater the diameter of the fibre, the
thicker its myelin sheath, and the faster this fibre will conduct nerve impulses.
Using these two criteria, the following types of sensory fibres can be distinguished.
Note that axons that have the same diameters as these
A alpha, A beta, A delta and C fibres but that arise from the muscles and tendons
rather than from the skin are also designated groups I, II, III, and IV.
difference between the speeds at which the two types of nociceptive nerve fibres
(A delta and C) conduct nerve impulses explains why, when you are injured, you
first feel a sharp, acute, specific pain, which gives way a few seconds later
to a more diffuse, dull pain.
This time lag is directly
attributable to the difference in the conduction speeds of A delta and C fibres:
their messages do not reach the brain at exactly the same time. “Fast pain”,
which goes away fairly quickly, comes from the stimulation and transmission of
nerve impulses over A delta fibres, while “slow pain”, which
persists longer, comes from stimulation and transmission over non-myelinated C
fibres. In relative terms, A delta fibres carry messages at the speed of a messenger
on a bicycle, while C fibres carry them at the speed of a messenger on foot. C
fibres are estimated to account for about 70% of all nociceptive fibres.
The activation thresholds for the different
types of sensory fibres are different too. In other words, some fibres require
more intense stimuli in order to begin generating nerve impulses. These differences
in activation thresholds have been clearly shown in experiments where an electrical
current was used to directly stimulate a sensory nerve, which contains nerve fibres
of all kinds.
When applied at low intensity, the
current caused the subjects to experience a tactile sensation, but no pain, because
it is the A beta fibres that are activated first. When the current’s intensity
was increased, nerve impulses were generated in the A delta fibres, and the subjects
experienced a brief, tolerable, highly localized sensation of pain. Increasing
the current further activated the C fibres, and, as you might expect, the subjects
reported experiencing intense, diffuse pain.
experiments, the A delta and C fibres were blocked selectively, and the differences
in the timing of the neural activity measured in the nerve confirmed the role
of each type of fibre in the two components of pain.
But scientists know that these pathways are not
perfect and do not always transmit pain signals intact and undistorted from the
body’s periphery to the brain. The nociceptors can be highly activated without
an individual’s experiencing pain—for example, when athletes or soldiers
are injured or wounded but
feel practically no pain in the heat of action. Or in your everyday life,
haven’t you sometimes cut yourself without realizing it, because your attention
was so focused on the task at hand? Or to cite another example, there is the placebo
effect, where simply believing that a medication works can reduce the sensation
of pain, even though the medication actually contains no active ingredients.
understand what makes all these phenomena possible, we must look at what are known
as the descending pain-control pathways: neural pathways that
descend from the central structures of the nervous system and diminish the pain
signals travelling up the the ascending pathways from the body to the brain.
all human perceptions are subject to varying degrees of modulation by these central
structures, the power of these top-down
mechanisms is greatest when it comes to controlling pain. As described above,
these descending pain-control mechanisms can sometimes even completely eliminate
certain forms of pain.
These mechanisms thus imply
a tremendous paradigm
shift. They mean that pain pathways cannot be seen as direct links between the
pain receptors in the body and “pain centres” in the brain. Instead,
these pathways are better described in terms of concurrent ascending and descending
influences—a veritable symphony of neural activity occurring simultaneously
in both directions. And it is when this delicate balance tips in favour of the
excitatory nociceptive messages that an individual experiences pain. Pain thus
becomes less of a reflexive response to an injury and more of an “opinion”
that the body forms about its physical integrity. This understanding has yielded
major advances in the treatment of pain, because researchers can now seek ways
to potentiate these descending pathways that inhibit pain.
theory now recognized as best describing the mechanisms involved in the descending
control of pain is called the gate-control theory of pain. In this theory,
the primary metaphor is that at each of the main relay points along the ascending
pain pathways, there are “gates” that can be closed to make it harder
for nociceptive impulses to get through. Thus, depending on how open the gates
are at each of these relay points, the same level of activity in a nociceptor
will not always lead to perception of the same intensity of pain.
There are three types of controls
that can play this role of a biological gate or filter reducing the transmission
of pain impulses: