Page 27 Guide to Pain Management in Low-Resource Settings

Physiology of Pain 15

(dorsolateral tract of Lissauer) before entering the spi- ing painful sensations (“phantom pain”) and nonpainful
nal gray matter, where they make contacts with (inner- sensations (e.g., “telescoping phenomena”).
vate) the nerve cells in Rexed lamina I (marginal zone) Appreciating the complexity of the pain path-
and lamina II (substantia gelatinosa). Th e Aδ fi bers in- way can contribute to understanding the diffi culty in as-
nervate the cells in the marginal zone, and the C fi bers sessing the origin of pain in a patient and in providing
innervate mainly the cells in the substantia gelatinosa pain relief, especially in chronic pain.
layer of the spinal cord. Th ese nerve cells, in turn, in-
nervate the cells in the nucleus proprius, another area Pathophysiology of pain
of the spinal cord gray matter (Rexed layers IV, V, and
VI), which send nerve fi bers across the spinal midline Pain sensations could arise due to:
and ascend (in the anterolateral or ventrolateral part of 1) Infl ammation of the nerves, e.g., temporal neuritis.
the spinal white matter) through the medulla and pons 2) Injury to the nerves and nerve endings with scar
and innervate nerve cells located in specifi c areas of formation, e.g., surgical damage or disk prolapse.
the thalamus. Th is makes up the spinothalamic path- 3) Nerve invasion by cancer, e.g., brachial plexopathy.
way for the transmission of information on pain and 4) Injury to the structures in the spinal cord, thala-
normal thermal stimuli (<45°C). Dysfunctions in the mus, or cortical areas that process pain information,
thalamic pathways may themselves be a source of pain, which can lead to intractable pain; deaff erentation, e.g.,
as is observed in patients after stroke with central pain spinal trauma.
(“thalamic pain”) in the area of paralysis. 5) Abnormal activity in the nerve circuits that is
perceived as pain, e.g., phantom pain with cortical re-
Th e trigeminal pathway
organization.
Noxious stimuli from the face area are transmitted in
the nerve fi bers originating from the nerve cells in the Modulation of the perception of pain
trigeminal ganglion as well as cranial nuclei VII, IX, and
X. Th e nerve fi bers enter the brainstem and descend to It is well known that there is a diff erence between the
the medulla, where they innervate a subdivision of the objective reality of a painful stimulus and the subjec-
trigeminal nuclear complex. From here the nerve fi bers tive response to it. During World War II, Beecher, an
from these cells cross the neural midline and ascend to anesthesiologist, and his colleagues carried out the
innervate the thalamic nerve cells on the contralateral fi rst systematic study of this eff ect. Th ey found that
side. Spontaneous fi ring of the trigeminal nerve gan- soldiers suff ering from severe battle wounds often ex-
glion may be the etiology of “trigeminal neuralgia” (al- perienced little or no pain. Th is dissociation between
though most of the time, local trigeminal nerve dam- injury and pain has also been noted in other circum-
age by mechanical lesion through a cerebellar artery is stances such as sporting events and is attributed to the
found to be the cause, as seen by the positive results of eff ect of the context within which the injury occurs.
Janetta’s trigeminal decompression surgery). Th e existence of dissociation implies that there is a
Th e area of the thalamus that receives the pain mechanism in the body that modulates pain percep-
information from the spinal cord and trigeminal nuclei tion. Th is endogenous mechanism of pain modulation
is also the area that receives information about nor- is thought to provide the advantage of increased sur-
mal sensory stimuli such as touch and pressure. From vival in all species (Überlebensvorteil).
this area, nerve fi bers are sent to the surface layer of the Th ree important mechanisms have been de-
brain (cortical areas that deal with sensory informa- scribed: segmental inhibition, the endogenous opioid
tion). Th us, by having both the nociceptive and the nor- system, and the descending inhibitory nerve system.
mal somatic sensory information converge on the same Moreover, cognitive and other coping strategies may
cortical area, information on the location and the in- also play a major role in pain perception, as described in
tensity of the pain can be processed to become a “local- other chapters in this guide.
ized painful feeling.” Th is cortical representation of the
body—as described in Penfi eld’s homunculus—may also Segmental inhibition
be a source of pain. In certain situations, e.g., after limb In 1965, Melzack and Wall proposed the “gate theory
amputations, cortical representation may change, caus- of pain control,” which has been modifi ed subsequently