Ganong's Review of Medical Physiology, 23rd Edition

CLINICAL BOX 11–2
Brown–Séquard Syndrome
A functional hemisection of the spinal cord causes a characteristic
and easily recognized clinical picture that reflects
damage to ascending sensory (dorsal-column pathway,
ventrolateral spinothalamic tract) and descending motor
(corticospinal tract) pathways, which is called the Brown–
Séquard syndrome. The lesion to fasciculus gracilus or fasciculus
cuneatus leads to ipsilateral loss of discriminative
touch, vibration, and proprioception below the level of lesion.
The loss of the spinothalamic tract leads to contralateral
loss of pain and temperature sensation beginning one
or two segments below the lesion. Damage to the corticospinal
tract produces weakness and spasticity in certain
muscle groups on the same side of the body. Although a
precise spinal hemisection is rare, the syndrome is fairly
common because it can be caused by spinal cord tumor,
trauma, degenerative disc disease, and ischemia.
and proprioception are reduced, the touch threshold is elevated,
and the number of touch-sensitive areas in the skin is
decreased. In addition, localization of touch sensation is
impaired. An increase in touch threshold and a decrease in
the number of touch spots in the skin are also observed after
interrupting the spinothalamic tract, but the touch deficit is
slight and touch localization remains normal. The information
carried in the lemniscal system is concerned with the
detailed localization, spatial form, and temporal pattern of
tactile stimuli. The information carried in the spinothalamic
tracts, on the other hand, is concerned with poorly localized,
gross tactile sensations. Clinical Box 11–2 describes the characteristic
changes in sensory (and motor) functions that occur
in response to spinal hemisection.
Proprioceptive information is transmitted up the spinal
cord in the dorsal columns. A good deal of the proprioceptive
input goes to the cerebellum, but some passes via the medial
lemniscus and thalamic radiations to the cortex. Diseases of
the dorsal columns produce ataxia because of the interruption
of proprioceptive input to the cerebellum.
MODULATION OF
PAIN TRANSMISSION
STRESS-INDUCED ANALGESIA
It is well known that soldiers wounded in the heat of battle often
feel no pain until the battle is over (stress-induced analgesia).
Many people have learned from practical experience that
touching or shaking an injured area decreases the pain due to
the injury. Stimulation with an electric vibrator at the site of
pain also gives some relief. The relief may result from inhibi-
CHAPTER 11 Somatosensory Pathways 177
tion of pain pathways in the dorsal horn gate by stimulation of
large-diameter touch-pressure afferents. Figure 11–1 shows
that collaterals from these myelinated afferent fibers synapse
in the dorsal horn. These collaterals may modify the input
from nociceptive afferent terminals that also synapse in the
dorsal horn. This is called the gate-control hypothesis.
The same mechanism is probably responsible for the efficacy
of counterirritants. Stimulation of the skin over an area
of visceral inflammation produces some relief of the pain due
to the visceral disease. The old-fashioned mustard plaster
works on this principle.
Surgical procedures undertaken to relieve severe pain
include cutting the nerve from the site of injury or ventrolateral
cordotomy, in which the spinothalamic tracts are carefully
cut. However, the effects of these procedures are
transient at best if the periphery has been short-circuited by
sympathetic or other reorganization of the central pathways.
MORPHINE & ENKEPHALINS
Pain can often be handled by administration of analgesic drugs
in adequate doses, though this is not always the case. The most
effective of these agents is morphine. Morphine is particularly
effective when given intrathecally. The receptors that bind morphine
and the body’s own morphines, the opioid peptides, are
found in the midbrain, brain stem, and spinal cord.
There are at least three nonmutually exclusive sites at which
opioids can act to produce analgesia: peripherally, at the site of
an injury; in the dorsal horn, where nociceptive fibers synapse
on dorsal root ganglion cells; and at more rostral sites in the
brain stem. Figure 11–5 shows various modes of action of opiates
to decrease transmission in pain pathways. Opioid receptors
are produced in dorsal root ganglion cells and migrate both
peripherally and centrally along their nerve fibers. In the
periphery, inflammation causes the production of opioid peptides
by immune cells, and these presumably act on the receptors
in the afferent nerve fibers to reduce the pain that would
otherwise be felt. The opioid receptors in the dorsal horn
region could act presynaptically to decrease release of substance
P, although presynaptic nerve endings have not been identified.
Finally, injections of morphine into the periaqueductal gray
matter of the midbrain relieve pain by activating descending
pathways that produce inhibition of primary afferent transmission
in the dorsal horn. There is evidence that this activation
occurs via projections from the periaqueductal gray matter to
the nearby raphé magnus nucleus and that descending serotonergic
fibers from this nucleus mediate the inhibition.
Chronic use of morphine to relieve pain can cause patients
to develop resistance to the drug, requiring progressively
higher doses for pain relief. This acquired tolerance is different
from addiction, which refers to a psychological craving.
Psychological addiction rarely occurs when morphine is used
to treat chronic pain, provided the patient does not have a history
of drug abuse. Clinical Box 11–3 describes mechanisms
involved in motivation and addiction.