Chapter Twenty-Three
Pain and Pain Management
"We must all die. But that I can save ( a person} from days of torture, that is what I feet
as my great and ever new privilege. Pain is a more terrible lord of mankind than even
death himself. "
Albert Schweitzer
PAIN: ACUTE AND CHRONIC 610 The Acute
Pain Model and Pain Relief 610 THE
PHYSIOLOGICAL BASIS OF PAIN
PERCEPTION 611 Nociception 611
Pain Fiber Connections in the Spinal
Cord 612 Endorphins and Descending
Pain 619 Clinical Terminology 621
PHARMACOLOGICAL MANAGEMENT
OF PAIN 623 Peripheral versus Central
Analgesics 623 Potentiators 625
Anticonvulsants and Tricyclic
Antidepressants 625 HEADACHE 625
Systems of Pain Inhibition 614 Referred
Pain 615 Phantom Pain 617 Cancer Pain 618
DESCRIPTION OF PAIN PHENOMENA 619
The Patient's Description of
Pain-Sensitive Structures 625 Symptomatic
Headaches 626 Headache Syndromes and
Their Treatment 626 Case Study 630 Key
Concepts 631
ain is a significant, often central factor for many patients. In
acute pain compared with that of the chronic pain. The second principle is
confronting pain, their experience will be highly variable. Procedures
that different approaches to pain management are effective with different
that induce agony in some will appear to be only mildly
sorts of pain. This has a bearing on the selection of an appropriate
uncomfortable to others. Some will describe their pain in clear, precise
therapeutic regimen to cope with it.
terms, while others will have difficulty pinpointing the problem. Patients
may regard their pain as a challenge, but too many are seriously debilitated,
The Acute Pain Model and Pain Relief
depressed, and almost broken by their experience.
In its most straightforward form, the experience of pain is based on the chain
P
PAIN: ACUTE AND CHRONIC
To begin our discussion, let us first note the distinction between acute pain
and chronic pain. Although the term acute is often used in clinical settings to
imply sudden and severe, in the context of pain, it refers instead to the transitory nature of the pain experience. Acute pain may range from mild to
severe, but its overall duration is relatively short, because the pain is usually
related to the progression of disease and subsequent healing. An example is
the pain associated with a fracture that heals satisfactorily or with a kidney
stone successfully removed from its point of lodgement in a ureter. By
contrast, chronic pain may also vary in severity but is of long duration (the
usual rule of thumb is six months or more). It is often subclassified on the
basis of its underlying cause. Where the pathogenesis of a
well-characterized disease underlies the experience—for example, a poorly
controlled cancer or a degenerative joint disease—the pain is termed
chronic malignant or symptomatic pain. Where no such disease or
degeneration can be identified, it is called chronic benign or chronic
nonma-lignant pain. Despite the use of the word benign, this type of pain
can be a very disabling condition in its own right. Table 23.1 presents a pain
classification scheme. Here the focus shifts from the objective nature of the
pain experience (acute versus chronic) to a combination of pain and
supposed cause that occurs in individuals.
At least two important principles emerge from the acute/chronic
categorization. The first is that in the neurophysiology of pain, significant
differences exist in the neurological processing, perception, and impact of
of events depicted in figure 23.1. Pain stimuli may directly affect a tissue's
nerve endings or indirectly cause tissue damage, releasing substances which
then depolarize the nerve endings. These fine nerve endings are called
nociceptors (noci is from the Latin to hurt). The activation of the pain fibers
associated with nociceptors is called nociception. Pain is the central sensory
experience
Table 23.1
Classification of Patients According To Their Pain
Experience and Underlying Pathology
Acute Pain
Underlying cause transitory. Treatment of pain symptomatic.
Resolution based on resolution of underlying cause. Physiological:
part of a natural or therapeutic process, vaccinations, injections, some
activity related pain, childbirth.
Posttraumatic or Postsurgery: e.g., immediate response to
whiplash, recovery from shoulder surgery. Secondary to Acute
Illness: e.g., biliary colic associated with cholelithiasis.
Chronic Pain
Underlying cause protracted or ongoing, perhaps unbeatable or not
identifiable. Long (six months?) duration. Pain is a (perhaps "the")
major focus of care.
Part Two
2
Systemic Pathophysiology
Chronic Malignant/Symptomatic Pain (underlying
pathology causes pain)
Recurrent Acute: unresolved cause, pain-free periods, only
symptomatic care available, e.g., migraine headaches.
Ongoing, Acute: pain a significant component of chronic-disease,
e.g., joint pain in rheumatoid arthritis. Ongoing, Time Limited: e.g.,
cancer pain ends with death or control of disease.
Chronic Monmalignant Pain
(pain itself and disablement that results are the major
problem, response to drugs often poor) e.g., lower back
pain.
Chronic Intractable Nonmalignant Pain Syndrome:
same as above except patient is largely disabled by pain.
Source: Adapted fron N.T. Meinhart and M. McCaffery, Pain: A Nursing
Approach to Assessment and Analysis. Copyright© 1983 Appleton & Lange.
of nociceptive input. It has two quite separate components. Pain perception,
like vision or audition, gives information about the nature, location,
intensity, and duration of the nociception. Suffering, on the other hand,
involves the reactions to pain, including varying combinations of autonomic, emotional, or behavioral responses.
Autonomic responses to intense pain typically consist of increased
heart rate and blood pressure, increased secretion of epinephrine, raised
blood glucose, decreased gastric secretions and motility, decreased blood
flow to the viscera and skin, dilated pupils, and sweating. The emotional
responses may involve fear, anger, anxiety, panic, depression, even passive
resignation. The simplest behavioral
primarily by modifying reactions to the sensory experience (autonomic,
emotional, or behavioral responses) or modulating the sensory experience
itself in indirect ways.
Stimulus
Tissue
damage
THE PHYSIOLOGICAL BASIS OF PAIN
PERCEPTION
r ■>
With an understanding of the essentials of acute and chronic pain, and a
Nociceptor
Chemical
mediators
basic model for acute pain, we can now turn to the structure and function of
the specific neurological components of pain perception.
response
f i Pain
Nociception
pathways to
brain
Sensory
experience
j
■
Suffering component
Figure 23.1 The essential aspects of acute pain processing and experience.
Pain
perception
responses are spinal cord reflexes, but behaviors may range
from lowered mobility to complex coping and avoidance behaviors.
Behavioral responses may even include maladaptive patterns of adjustment
that can complicate or even interfere with a person's recovery.
The model described in figure 23.1 best addresses the experience of
acute pain that is based on trauma or disease, which is called somatic pain.
In this case, pain is beneficial in that it informs us of danger and then
mobilizes a drive state that attempts to remove the stimulus, correct the damage, or at least reduce the intensity of the pain or suffering. Treatment that is
based on this model depends on a continued monitoring of signs and
symptoms so that changes in a patient's status may be noted, providing the
basis for a more refined or altered diagnosis. Any clinical consideration of
pain and pain relief must assume that the underlying disease is accurately
diagnosed and effectively treated.
This acute pain model is important to keep in mind because many
currently used approaches to pain management may focus less on the causes
of pain (since they may not be therapeutically accessible) and more on the
patient's response to it. Reducing the patient's level of anxiety or tension and
relieving depression or anger are a few examples. These are sometimes
called palliative pain relief methods and are designed to alleviate pain,
even if the underlying cause is not reversible. They exert their effects
Nociceptors, the finely branched nerve endings whose stimulation gives rise
to pain, all appear the same when viewed with an electron microscope. In
practice, however, some respond only to strong, mechanical stimulation,
especially by sharp objects, or to temperatures above 45° C. These endings
converge on small, fine myelinated fibers that conduct their action potentials
relatively quickly (5 to 30 m/sec). Fibers of this type are called A5 (A delta)
fibers. They are distributed only to the skin, mucous membranes, and
selected serous membranes (e.g., the parietal peritoneum). They tend to fire
immediately upon (intense) stimulation and cease firing when the stimulus
is removed, producing the sensation of sharp pain. As well, they rapidly
adapt to a stimulus. That is, you feel the needle pierce your skin but soon the
sense of sharp pain goes away, even though the needle (stimulus) remains.
You may experience some sharp pain again as the needle is withdrawn.
Essentially, these fibers carry information about sharp, pricking, acute pain
that is relatively well localized and discriminated (you know where it is and
what's causing it!).
A second population of pain fibers, smaller in diameter and
unmyelinated, are called C fibers. They are distributed to the same areas as
the A5 fibers, but with much greater density. In addition, they are very
widely distributed in deep tissue: in muscle and tendon, visceral peritoneum,
and the viscera] organs themselves (e.g., the myocardium, the stomach and
intestines). Action potentials in these fibers tend to be generated by
substances that are associated with tissue damage or insult. These impulses
travel in a continuous fashion and are therefore much slower (0.5-2 m/sec)
than those conducted over the AS fibers. As well, the initiation of firing is
not as closely related to the onset or withdrawal of the stimulus. Firing is
slow to develop, so pain may emerge some time after stimulus application,
perhaps because of the slow release or formation of the triggering substance.
Once initiated, action potential firing can persist long after the original
stimulus has been removed. C fibers carry information related to
long-lasting, burning, often called did! pain, which is poorly localized and
more diffusely distressing. Dull pain is the sort of pain that typically brings
people to seek medical attention for relief.
Chapter Twenty-Three
The Experience of Fast and
Slow Pain
A simple illustration may demonstrate this division of peripheral nociception into AS and C fibers. Using the nails
of your thumb and index finger of one hand, pinch the web of skin
between the base of two fingers on the other hand and note the
sensations. First, and within a fraction of a second, you should have felt a
sharp pain emanating precisely from the pinched area. Then, perhaps two
seconds later, a duller, less clearly localized aching or burning sensation
should have developed. These sensations were mediated first by A8 fibers
and then by C fibers, hence the commonly used terms fast and slow pain.
Pain Fiber Connections in the Spinal Cord
Like those of other sensory fibers, the cell bodies of the AS and C fibers are
found in the dorsal root ganglia. Their axons continue from the dorsal root
ganglion into the spinal cord, where they synapse with the next neuron in the
chain, called a second-order neuron. As AS and C fibers enter the cord,
some send branches (collaterals) up or down the cord for short distances.
They then travel deeper to their points of synapse (fig. 23.2a). This provides
for the involvement of several cord segments in the mediation of complex
pain reflexes (e.g., crossed extension, table 21.8).
Most of the second-order neurons pass across the cord and then
proceed toward the brain in the anterolateral-spinothalamic tract (fig.
23.2b). The term spinothalamic tract is somewhat misleading here, because
the vast majority of second-order pain fibers traveling in the
anterolateral-spinothalamic tract do not end up in the thalamus at all. Instead
they terminate in the reticular formation of the brain stem (fig. 23.2c). Here,
through the reticular activating system, they mediate an increase in general
consciousness, alertness, and attention. These are important orienting and
defense reactions to pain. They occur whatever the specific nature of the
pain stimulus and explain some of the jumpiness, irritability, and perhaps
obsessiveness of pain sufferers.
A large number of the fibers in the anterolateral system enter an area of
cells surrounding the cerebral aqueduct in the midbrain (called, therefore,
the mesencephalic periaqueductal gray matter). From here, action
potentials can be relayed to the hypothalamus and thence to the limbic
system and cerebral cortex (fig. 23.2d). This is part of the neurological basis
for the endocrine, autonomic, and emotional components of the reaction to
pain. The pain pathway, thought to be the evolutionarily most primitive, is
one that activates cells in the region of the dorsal midbrain (fig. 23.2e). (This
area is called the tectum of the midbrain and is associated with orienting
responses to visual and auditory stimuli.) In response, these cells appear to
promote
Activation ot motor
neurons
Activation of
inhibitory
interneurons
1 f
f "1 Extensors
■ relax
i
Flexors
contract
3
Pain and Pain Management
Flexor-Withdrawal
Physiology
Reflex
The neural explanation of the flexor-withdrawal reflex involves
action potentials generated in A8 fibers by cutaneous receptors. The
action potentials pass into the dorsal horn, where they
synapse with excitatory second-order neurons, which in turn synapse with
Alpha motor neurons in the ipsitateral ventral horn. These motor neurons
then stimulate the contraction of flexor muscles that draw the stimulated
area away from the source of the painful stimulus. These same AS fibers
simultaneously synapse with inhibitory interneurons (box fig. 23.1) that
produce relaxation of the related extensor muscle group to facilitate the
flexion of the limb.
A 5 input
Flexor
withdrawal retlex
Box Figure 23.1
The flexor-withdrawal reflex depends on activation of flexors at the same
time that extensors are inhibited.
spinal cord motor mechanisms, thereby enhancing spinal reflexes and
facilitating behavioral responses.
Neospinothalamic Pain Pathways
Many AS fibers synapse immediately upon entering lamina I, the first of
five layers or laminae of the cord's dorsal horn. Axons from the cell bodies
in this layer cross the cord and travel the anterolateral-spinothalamic system
to their destinations (fig. 23.3). About one-third of A5 fibers terminate in the
posterior nuclear group in the thalamus. These fibers have been called the
neospinothalamic pain system to denote that this is an evolutionarily
advanced and sophisticated pain discrimination pathway. The effectiveness
and
4
Part Two
Systemic Pathophysiology
Figure 23.2 An overview of the essential neuronal interrelations for dull and sharp pain perception. Letters a through e are keyed to the text. The
shaded areas of the spina! cord represent the anterolateral-spinothalamic tracts.
specificity of neospinothalamic pain discrimination is due to the
convergence on these same thalamic nuclei of the medial lemniscal fibers
that carry highly differentiated sensory information for light touch,
two-point discrimination, stretch, etc. Pain discrimination is enhanced
through the addition of these sensations to the relatively well-discriminated
AS impulses. Because the posterior nuclear group of thalamic nuclei provide
direct access to the primary and secondary somatosensory cortex, conscious
appreciation of sharp, well-discriminated, and localized pain is realized.
Activity in AS fibers is the principal factor in eliciting pain-induced
spinal reflexes. In the simplest of these, the flexor-withdrawal reflex,
touching something sharp or hot causes rapid withdrawal of the stimulated
limb. The withdrawal occurs so rapidly that it is accomplished even before
we become conscious of the sensation of pain. This reflex minimizes
exposure to the potentially harmful stimulus. In the crossed-extension
reflex, reflex extension of the opposite limb is added to the
flexor-withdrawal reflex. For example, if you step on a tack, you will
simultaneously lift the pricked foot and extend the other leg so that your
weight is borne on the unstimulated foot.
Paleospinothalamic Pain Pathways
The C fibers have a slightly more complex fate in the cord: they synapse in
either lamina II or V. But they form a major input to a much more
complicated local processing system that feeds into a separate pain pathway
that originates in lamina V. Fibers from cell bodies in lamina V pass into the
ascending reticular system, the mesencephalic periaqueductal gray matter,
and the midbrain tectum, as do the
Chapter Twenty-Three
A 5 nociceptors (sharp pain)
C nociceptors
(dull pain)
1 r
f\
Dorsal horn
intemeurons
Paleospinothalamic pathways
Neospinothalamic
pathways
Higher perception
centers
Acute sharp pain
Chronic
Figure 2.?..?
The general scheme for underlying perception dull pain
of the two types of pain.
fibers from lamina I. But, as well, some continue to the thalamus,
particularly its intralaminar nuclei, from which they diffusely project to
various parts of the cortex. The number of fibers arriving at the thalamus is
small compared with the vast number of original C fibers, and there is also
little overlap or convergence with fibers arising from A5. For these reasons,
discrimination and localization of pain in this system is quite imprecise. The
pathways involved are called the paleospinothalamic pathways.
The spinal cord processing of information that feeds into the
paleospinothalamic pathway is shown in figure 23.4. It shows the array of
interconnections in the laminae of the dorsal horn that make possible the
varieties of pain fiber activity. Incoming AS fibers synapse in lamina I, then
cross the cord to ascend in the contralateral spinothalamic tract. C fibers end
in either lamina II or lamina V. Another element is the lamina V neuron
itself. It receives inputs from C and second-order A5 fibers. A portion of
these lamina V neurons contribute to the paleospinothalamic pathway.
Summary of Ascending Pain Processing
Much of the neural activity generated by pain stimuli feeds into the
ascending reticular system to increase alertness, attentiveness, and readiness
to identify and respond to stimuli (spinoreticular component). A portion of
the input ends up in the periaqueductal gray region of the midbrain, gaining
access to the hypothalamus and therefore both the limbic and endocrine
systems. Some excitation arrives at the tectum of the midbrain and thereby
increases the motor responsiveness of spinal cord mechanisms that enhance
reflex activity (spinotectal component). The strictly "spinothalamic"
component is divided into two elements: a highly discriminated
neospinothalamic pathway that provides direct access to the specialized
sensory cortex, and a less well-discriminated paleospinothalamic pathway
that appears to play an important role in the mediation of chronic pain.
Figure 23.5 presents these principles in schematic form.
Endorphins and Descending Systems of Pain
Inhibition
We have already noted the role of pain in alerting us to danger and activating
some coping responses. Once this role has been served, however, it is
Pain and Pain Management
5
desirable to limit the pain and much therapeutic effort is devoted to this goal.
One long-standing approach has been the use of narcotic agents, e.g.,
morphine, to dull the pain. Most narcotics are derived from plants and
produce their effects by binding to specific receptors in the brain stem. Once
the presence of such receptors was discovered, an intriguing speculation
arose. Presumably they would have developed in a system that used some
internally produced substance that would bind to them; it was just a
coincidence that plant-derived narcotics were sufficiently similar to bind to
the same receptors (fig. 23.6). This speculation has proved to be correct, and
the presence of endogenous morphinelike substances is now well
established. Certain of them, known as endorphins, are the subject of much
study in their role as pain inhibitors.
The actual inhibitory effects of the endorphins are achieved indirectly.
Endorphin receptors are richly distrib uted in the brain stem. When activated
by endorphins, they promote the flow of action potentials down the cord, to
lamina II of the dorsal horn. The arrival of these action potentials triggers the
release of another member of the endorphin group called leucine
enkephalin. This is a key step, in that leucine enkephalin exerts an
inhibitory effect at the synapses between A8 and C inputs to their
second-order neurons. In this way, the descending pathways are able to limit
pain inputs to the higher perception centers (fig. 23.7). The principal
inhibitory effect of this descending system is on the paleospinothalamic
pathways and their contribution to dull, aching pain. Since this is the case,
we might predict that exogenous substances that can bind to endorphin
receptors would be most effective against this type of pain, and this is,
indeed, the case.
Another approach to analgesia uses harmless electrical stimulation of
the skin that overlies the painful area, the peripheral nerve that serves the
area, or the dorsal horn
6
Part Two
Systemic Pathophysiology
Diffusely
to cortex
Cingulum
nsula
Neospinothalamic
pathway
Paleospinothalamic
pathway
- Long-acting inhibition
(leucine enkephalin 7
Short-acting inhibition +
Excitation (serotonin)
To muscle
Figure 23,4 Scheme of AS and C nociceptor synapses in the dorsal horn of the spinal cord. Shading highlights the horn's laminae, designated by
Roman numerals. Most output from lamina V passes to higher perception centers via contralateral spinothalamic tracts. Ipsilateral tracts omitted for
clarity.
into which its input is relayed. This method is known as transcutaneous
electric nerve stimulation (TENS). Its analgesic effects are thought to
derive from the direct or indirect stimulation of the endorphin system. Yet
another technique, used when pain is severe and unresponsive to other
analgesics, is stimulus-produced analgesia. It involves the placement of
electrodes directly within the brain stem, from where their stimulus directly
activates the descending pathways that induce pain inhibition.
Referred Pain
As a later section will show, adequate observation of a patient's pain
experience requires a precise description of the pain and its localization.
This can be quite straightforward, e.g., a burning sensation at the incision
site. But it can also be puzzling, e.g., the radiating pains in the left axilla and
arm that are associated with a heart attack. In such cases, it is important to
recognize that all pain is really "felt" in the brain. The mind projects that
perception of
Chapter Twenty-Three
Pain and Pain Management
7
Nociceptor
input
Spinal cord
inierneurons
Reticular
activating
system
Tectum of
midbrain
Thalamus
and cortex
Periaqueductal
gray matter
c
. •>
Endocrine
system ^ J
Hypothalamus
J
Increased
alertness
Enhanced
reflex action
Increased pain
response
capability
Figure 23.5
Autonomic and
emotional
responses
Summary of the components of the system for processing nociceptor input to the central nervous system.
pain to an area of the body that is in many cases, but not always, the same as
the spot whose stimulation gave rise to the sensation in the first place.
Sensations arising at the skin or in the mucous membranes and in some of
the parietal serous membranes are quite accurately projected. When a
mosquito bites you in the back of the leg you know exactly where to swat,
without even looking. On the other hand, pain arising from internal organs,
visceral pain, is not nearly this accurately projected. It may be perceived as
arising on the skin surface or in muscles quite remote from the site of
nociception. In this case the sensation is called referred pain.
The most widely accepted explanation for referred pain is based on the
concept of dermatomes. Each of these is the area of skin supplied by a
single spinal nerve. This means that cutaneous stimuli from a given
dermatome produce action potentials that are always delivered to the
corresponding spinal cord segment. The relationship is very straightforward
during early embryonic development (fig. 23.8a), when each of the
dermatomes lies directly over its corresponding cord segment. However, as
development
CNS receptor
Perception of
sharp and
dull pain
Sz3
Exogenous narcotic
Endorphin
i
Pain inhibition
Figure 23.6 Essential mechanism whereby exogenous narcotics work via
the endogenous analgesia receptors of the central nervous system.
8
Part Two
Systemic Pathophysiology
Exogenous e n d o f
p h i n -like narcotic
analgesic
Endorphin
Binding of
brain stem
receptors v J
C2
3
\
4
( \ Action
potentials
to dorsai horn
\
1
f- ■
Fn ko
release
v. J
Paleospinothalamic
inhibition
(a
)
Suppression of
dull-aching
pain
Figure 23.7 Essential elements of the descending analgesic system
used by narcotics.
proceeds and limb buds emerge and differentiate, the spatial relationship
between dermatome and cord becomes distorted (fig. 23.86). Even though
some parts of the dermatomes are stretched some distance from their cord
segment, the connecting nerves elongate to maintain the links previously
established. As you might expect, the situation is actually somewhat more
complex, because there is some overlap in the actual distribution of
dermatomes. The treatment here is simplified only to make the point.
The connection between this developmental pattern and referred pain
is that the sensory nerves from various body organs enter the cord at points
that coincide with those of a given dermatome. Early sensory input from a
given dermatome seems to become a reference that higher processing
centers rely upon. Since most pain-related input is from the skin,
interpretation centers seem to "assume" that all input is from the skin. When
an organ is damaged, its pain afferents are interpreted as originating in the
skin of the reference dermatome. For example, impulses entering the cord at
levels Tl to T4 or T5 from pain receptors stimulated by myocardial ischemia
are interpreted as impulses from dermatomes associated with T1-T4. Hence
the referred pain that is characteristic of cardiac ischemia: chest pains on the
left side (including the shoulder and axilla), which radiate down the left arm
Table 23.2
Typical Surfaces to Which Selected Organs Refer Pain
Organ
Heart
Esophagus
Stomach
Bile duct/Gall bladder
Pancreas
Large bowel
Kidney/Ureter
Bladder/Test is
Uterus
Appendix
(b)
Figure 23.8 Dermatome migration during embryologic development,
( a ) At about 4 weeks, the dermatomes are quite uniform and correspond
closely to cord segments. Note early limb buds, ( b ) By week 16,
dermatomes C6-T1 have migrated with the developing arms.
and perhaps from the base of the neck into the jaw. The general, but not
invariable, left localization is presumably due to the entry of the majority of
the fibers carrying pain information from the heart into the left side of the
spinal cord. (Some people with myocardial ischemia will report bilateral
pain, and—rarely—a person may report principally right-sided pain. Some
typical patterns of pain referral are presented in table 23.2.)
Phantom Pain
In connection with the physiological basis of pain, we should touch on the
puzzling pain experience called phantom pain. Phantoms are tactile and
movement perceptions that
Chapter Twenty-Three
Site of Referred Pain
Usually left shoulder and
axilla, with radiation
down inside of left arm;
also radiation from neck
to jaw
Pharynx, lower neck and
arm, substernum near
heart
Pain and Pain Management
9
Epigastric region, usually between umbilicus and xiphoid process
Midepigastric region, radiating to tip of right scapula
Midback, sometimes low epigastric region
Hypogastric region, lower abdomen, and periumbilical area
Edge of rectus abdominis muscle below level of umbilicus, radiation to flank and groin
Suprapubic region
Low abdomen or low back and side
Initially near umbilicus, then shifting to lower right as parietal peritoneum becomes involved
remain after a part of the body has been amputated. There can be a very real
sense that the leg, for example, is still there, has bulk and weight, can be
moved at will, gets itchy, or, to the great distress of the amputee, is a source
of extreme pain. Phantoms can exist for any lost body part (e.g., breasts,
hands, legs), but the greater the extent of cortical representation, the more
likely it is that there will be a phantom.
Phantoms are more common in adults than children, and are thought to
be
quite
unusual
in
young
children. They may also occur when an area has been denervated, for
example in a spinal cord injury that severs all cord pathways at T12. Some
people with spinal cord lesions experience such realistic phantoms, capable
of "movement" and apparent sensation, that the phenomena can be quite
disturbing.
There is great variability in the persistence of phantoms. Some are only
briefly apparent after an amputation, some fade or shrink gradually, some
persist or reoccur for years. In emergency situations, a long-dormant but
realistic phantom may arise with unfortunate consequences. For example, a
person may reach out with a nonexistent arm to fend off a flying object.
Sensory reeducation can help a great deal in coping with phantoms
connected to nerve damage. Where repeated opportunities for reeducation of
the cortex exist, for example in the paraplegic who repeatedly has his legs
stimulated with clearly no corresponding sensation, the phantom tends to
fade. Such reeducation may not be possible if the limb is missing, and the
phantom may then persist, but the proximal portions (which are more poorly
represented on the cortex than the distal portions) may fade, with a
subsequent shrinking of the phantom.
can be extremely variable, depending on its specific source. Tumor masses
impinging on neural structures can cause pain ranging from sharp and
stabbing neuralgias (table 23.4) to diffuse paresthesias. Invasion and
displacement of functional tissue (bone, muscle, skin) can result in dull
aching pain that becomes more severe with tumor progression. Compression
of or growth into a tubular structure can cause pain in a variety of ways.
Backing up of glandular secretions can cause distention and pain before the
organ slows or shuts down its secretion. If the tube is a ureter, pain may be
the only sign before the kidney is
irreparably damaged. Masses in or near
the esophagus can render swallowing painful, and stenosis of the gut can
lead to distention and diffuse
Impediments to Accurate and Complete Pain Reporting
Pain is not associated with all phantoms but when it does occur it can
be a very troubling problem. Many amputees have transient phantom pain,
and about 5-10% of this special population have serious, persistent phantom
pain. The circumstances that bring on the phantom pain will vary. For some
it comes without warning, or it may be associated with fatigue, pressure
sores, or a poorly fitting prosthesis. In other cases, stimulation or irritation of
certain consistent trigger points will be the cause.
The approaches that have been used to treat phantom pain present a
catalogue of modern pain treatment, ranging from physical and electrical
stimulation (including acupuncture), through peripheral and spinal nerve
sections and blocks, psychosurgery, psychotropic drugs, and megavitamin
therapy, to a host of psychologically based approaches. The results vary
from approach to approach, and even more from patient to patient.
Individuals experiencing such pain will possibly require extensive and
highly specialized referral, assessment, and care.
Cancer Pain
Part of the problem with cancer is that many forms can be well advanced
before they produce definitive symptoms, including pain, and some people
never experience pain generated by their cancer. The pain, when produced,
If
Effective
communication
about
pain
requires
a
positive desire and capacity on the patient's part
to
send
accurate
information
and
an
equivalent
capacity and desire in the health care team to
J
receive it. The following points are worth con£
sidering if pain assessment or management is
not going well. The first step is to look more closely at the
person who is in pain. Some individuals may be playing the good patient
role, not wishing to trouble you, or, at a simpler level, they may simply be
misinformed about the sort of pain to expect and what input from them is
required. On the other hand, the patient who has learned to cope with the
chronic pain associated with arthritis or chronic pelvic inflammatory disease
may well have a fear of wearing out the listener. This person is probably at
least as common as the person who likes to complain. And some unfortunate
people will have lapsed into a learned helplessness, defeated by their pain
and without the optimism that an attempt at communication requires.
Other patients may have specific reasons for concealing pain. Perhaps
they are anxious to protect their family from the severity of their pain or the
progression of disease they think it represents. Perhaps they fear that a report
of intense pain will cause postponement of long-awaited surgery, in the
same way a systemic infection might. Some people harbor common misconceptions about narcotic analgesics: that they will become addicted; that
taking narcotics for pain when it is less severe will build up a tolerance so
that the drug will not be effective later when they really need it; that the
withdrawal from the narcotic will be worse than the pain. Or they may
associate narcotics with addicts and degeneracy. Whatever the underlying
concern, by sensitive and supportive questioning you may be able to help the
patient to identify it so that you can address it.
A more subtle problem arises when dealing with people of different
cultures and social backgrounds, whose behavior may be affected by deeply
ingrained differences in the ways they understand, relate to, and express
themselves about pain. If people produce pain behaviors that are
recognizable and familial' to us, we are more likely to believe the expression
as genuine and act to alleviate it. It is important, therefore, to make
allowances for social and cultural differences when interpreting pain
reports.
Chapter Twenty-Three
pain. Arterial occlusion may result in ischemic pain, the nature of which will
depend on the structure or organ occluded (if visceral, then referred pain,
etc.). Venous or lymphatic blockage can lead to diffuse dull aching. A lung
tumor growing into a bronchus can lead to infection in the unventilated
region. This can produce dull chest pain or extend to the pleural membranes,
producing the sharp pain of pleurisy. Advanced cancer, especially that
accompanied by extensive necrosis as tumors outgrow their blood supplies,
can produce excruciating pain. Potent central analgesics like morphine,
given in appropriate doses and intervals, are necessary to help the patient
cope. These efforts may be supplemented with therapeutic blocking of
peripheral nerves where appropriate. In some cases even these measures are
inadequate.
DESCRIPTION OF PAIN PHENOMENA
Compared with sights or sounds, the perception, expression, and effect of
pain sensations are subject to great variability both between individuals and
within a given person. But this complexity shouldn't be allowed to interfere
with effective clinical observation. Pain associated with disease processes or
trauma can provide important clues to suggest or confirm diagnoses. And
here, every detail can be meaningful: What is it like? Does it change or
move? Is the pain clearly localized? To what events or circumstances is it
related? What makes it better or worse? All of this data has to be evaluated
in the context of the medical, personal, and social history within which it
occurs. When evaluating what the patient says, it is helpful to bear in mind
that "real pain" can't be distinguished from "imaginary pain," since the only
true pain to the patient is what is felt.
The Patient's Description of Pain
The patient's verbal description of pain can present problems, either because
the pain itself is difficult to describe (diffuse, wandering, etc.) or because of
imprecision or variation in the patient's use of words. Some commonly used
words that seem to denote clearly different subjective pain qualities are
presented in table 23.3. The clusters of adjectives denote particular qualities
of pain perception (e.g., intensity, timing, or location, etc.) and, where
appropriate, the specific words have been scaled. With regard to one quality,
changes in the intensity may be quite clear to the patient, especially when
they are rapid, but this aspect of pain perception is greatly affected by
fatigue, stress, lack of effective support, or inadequate management. The
sensation of pain may be constant, while the perception of its intensity
increases as the person becomes worn out.
In clinical settings where pain diagnosis and management is a central
task, protocols incorporating such verbal and other pain assessment scales
and questions are often used to standardize the documentation of the
patient's pain experience. These ensure consistency and thoroughness and.
Pain and Pain Management 10
Part Two
11
Table 23.3
Systemic Pathophysiology
Adjectives Used to Describe Pain. The Clusters Suggest Differing Intensities of a Variety of
Independent Qualities of Pain
Onset or Specific Nature of Pain?
1) numb
2a) penetrating
Intensity?
2b) tearing
dull
boring
rasping
tingling
piercing
gnawing
pricking
stabbing
lacerating
sharp
(referred to as
cutting
"lancinating")
Time Component?
1) constant
periodic
intermittent
2) brief
3) steady
flickering
la) generalized
diffuse
pulsing
focal
"The pain is"
"The painful area is"
mild
bothersome
discomforting
moderate
tender
sore
hurting
smarting
intense horrible
excruciating
unbearable
Spatial Quality?
aching
splitting
blinding
lb) deep
superficial
2) fixed
spreading
radiating
throbbing
jumping
pounding
shooting
enduring
Tension or Pressure?
1) tugging
Temperature?
3) tight
1)
hot
2) cool
pulling
pinching
burning
taut
pressing heavy
scalding
squeezing
searing
(referred to as
2) cramping
wrenching
crushing suffocating
Emotional/Visceral Aspects?
1) haunting
fearful
3) sickening
nauseating
frightful
terrifying
"causalgia")
Impact of Pain?
annoying
troublesome
nagging
4) miserable
punishing
wretched
tiring
grueling
exhausting
agonizing
cruel
debilitating
killing
vicious
2) distressing
Source: Adapted and modified from R. Melzack, The McGill Pain Questionnaire, McGill University, Montreal, 1975.
cold
freezing
Chapter Twenty-Three
with the inclusion of pain pictures like the one in figure 23.9a, give the
patient an easier vehicle for self-expression than simple self-report. With
children the use of a pain intensity rating scale like the faces in figure 23.9b
ensures a consistency and accuracy well beyond that from verbal reports.
Clinical Terminology
The need for precision in describing the varieties of pain experience has
given rise to an elaborate terminology (table 23.4). For a phenomenon as
complex as pain, a variety of medical terms have evolved. We can relate to
many of these terms because we have experienced the acute pain with which
they are associated.
The term somatic pain describes a potentially tissue-damaging
stimulus that leads to the activation of nociceptors, the transmission of this
information to the brain, and its interpretation there. This transmission and
interpretation can be straightforward, as it is with stepping on a tack, or
Table 23.4
Pain and Pain Management
more complex, as with the referred pain of myocardial infarction. In every
such case, there is a significant stimulus (e.g., myocardial ischemia) and a
fairly predictable response (e.g., perception of pain in the left axilla and
superficial chest, etc.). In chronic pain, the satisfactory explanations for an
individual's pain experience are most often made in terms of a complex
interaction between altered neural input and/or processing and
social/psychological and behavioral factors. The special case of pain that is
due to altered neural input or processing, is sometimes called neuropathic
pain (i.e., pain associated with neuropathy). Table 23.5 contrasts the
characteristics of somatic and neuropathic pain.
Although acute pain and somatic pain are often associated (as are
chronic pain and neuropathic pain), we must be clear that the terms are not
synonyms. Acute and chronic strictly denote patterns of onset and duration,
while somatic and neuropathic propose different physiological mechanisms
for the production of pain.
Definitions for Medical Terms Applying to Selected Peripheral and Central Neuropathies and Altered
Perception of Sensation Sometimes Associated
Symptoms
Paresthesias
Dysesthesia Hyperpathia
Hyperesthesia
Hyperalgesia
Allodynia
12
13
Part Two
Systemic Pathophysiology
Definitions
Formication
Causalgia
Hemianesthesia
Peripheral Nerve
Syndromes
Focal peripheral
neuropathy
Neuralgia
Trigeminal Neuralgia (Tic
douloureux) Root avulsion
Generalized
neuropathy
peripheral
Postherpetic
pain
Myofascial pain
General term referring to any of a variety of spontaneous abnormal sensations and sensitivities including
(but not restricted to) burning, numbness, pricking, tingling, increased sensitivity to somatic sensation.
Ongoing background aching or burning sensation in the absence of apparent stimulus.
General term applied to increased and sometimes abnormal sensitivity to stimuli (includes hyperesthesia,
hyperalgesia, and allodynia).
Extreme sensitivity to touch.
Exaggerated sensitivity to painful stimuli.
Condition in which a variety of stimuli (e.g., light touch, breeze on the skin) are perceived as intensely painful.
A spontaneous sensation like insects (ants) crawling on the skin.
Continuous burning, searing sensation in which a variety of stimuli can cause pain (allodynia) often initially accompanied by
flushing of the skin; most common following peripheral nerve injury. Chronic causalgia is associated with vasoconstriction.
Loss of sensation from one side of the body, usually from a CVA.
Peripheral nerve damage due to trauma, vascular compromise, compression, etc; will affect sensory and motor function; not
necessarily painful,
Pain in the distribution of a single peripheral nerve; usually combines ongoing aching and burning with intermittent sharp pain.
A neuralgia in the distribution of the fifth (trigeminal) cranial nerve; principal symptom is intermittent intense, paroxysmal,
lancinating pain; triggered by eating, cold air current, talking, or spontaneous. Severe trauma to spinal roots at the level of the
cord caused by wrenching trauma to a limb; chronic pain common.
Damage to peripheral nerves, may be principally sensory or sensorimotor, symmetric or asymmetric, diffuse or focal;
classically a diffuse peripheral neuropathy is symmetric and distal with a "glove-and-stocking" anesthesia (i.e., loss of
sensitivity to pain first in the feet then the hands) accompanied by a variety of paresthesias.
Following or during active herpes zoster infection; sudden lancinating pain, perhaps background of causalgia; can be
elicited by light touch, cold, sometimes spontaneous.
Following injury or disease in a joint and/or associated muscles some patients develop "fibromyositis" with pain elicited by
muscle contraction. This myofascial pain may be a factor in lower back and neck pain, and temporomandibular joint disorders.
Syndromes
Attributable
to Central Lesions
Multiple sclerosis
Tabetic pain
Acute spinal cord
trauma
Thalamic pain
syndrome
Table 23.5
Often associated with a variety of paresthesias.
Associated with lesions to posterior roots and dorsal columns caused by syphilis (tabes dorsalis); skin
and joint sensation impaired, paresthesias and dysesthesias.
A variety of paresthesias and dysesthesias as well as autonomic dysfunctions occur.
Damage to the thalamic nucleus involved in the referral of discriminative sensation (ventroposteriolateral nucleus) causes
intense, paroxysmal pain, often causalgia, in the limbs opposite the lesion.
Comparison of the Principal Differences between Somatic Pain (Arising from Tissue Damage) and
Neuropathic Pain (Arising as a Result of Faulty Neural Input and/or Processing)
Somatic Pain
1. Pain stimulus usually identified easily.
2. Surface pain well localized; if visceral, felt in predictable referral areas.
3. Pain characteristics match previous pain experience.
4. Analgesics usually effective.
Neuropathic Pain
1. Pain stimulus difficult to identify.
2. Pain often difficult to localize, felt in unusual referral sites.
3. Pain qualities unusual in patient's experience,
Chapter Twenty-Three
14
Pain and Pain Management
4. Poor response to analgesics.
NSAIDs
PHARMACOLOGICAL
MANAGEMENT OF PAIN
Pharmaceutical agents that limit pain, analgesics, are the mainstay of pain
management in most medical and nonmedical settings. Broadly speaking,
Acetaminophen
analgesics act peripherally, attenuating or blocking the generation of pain
signals in the tissues, or they act centrally, raising thresholds for pain
transmission at a variety of sites in the central nervous system.
Arachidonic acid
Peripheral versus Central Analgesics
Peripheral analgesics act by blocking the production of prostaglandins,
particularly prostaglandin E2 (PGE2). PGE2 appears to mediate nociception
by sensitizing pain receptors to the stimulating effect of bradykinin.
Blocking PGEj formation therefore leads to reduced peripheral pain stimulation for a given level of pain-producing bradykinin. You may recall from
chapter 2 that both PGE, and bradykinin are produced in an inflammatory
response. Along with other substances, they are responsible for the delayed
but prolonged vasodilation and increased vascular permeability that promote
the delivery of cells and plasma products to the site of injury. Bradykinin is
generated from a plasma precursor. Prostaglandins, on the other hand, are
generated from cell-membrane-derived arachidonic acid. Cyclooxy-genase,
the enzyme responsible for prostaglandin production from arachidonic acid,
is inactivated by aspirin, acetaminophen, and nonsteroidal
anti-inflammatory drugs. These drugs will produce analgesia (by raising the
threshold for bradykinin stimulation of nociceptors) at levels lower than
those required to reduce the inflammation (fig. 23.10).
Central analgesics, by contrast, are narcotic drugs. As noted earlier,
narcotics bind to a variety of receptors in the cord, brain stem, and cerebrum
that are the normal receptors for certain endogenously produced
morphinelike neurotransmitters, including the endorphins. These receptors
are thought to be involved in mediating pain and some aspects of pleasure or
reward. A variety of natural and synthetic narcotics are used, alone or in
combination with substances intended to focus their action more effectively,
to impede or block pain signals once they have entered the central nervous
system.
Nonnarcotic Analgesics
Although usage does vary, it is typical to refer to aspirin, acetaminophen,
and nonsteroidal anti-inflammatory drugs (NSAIDs)—in other words, to the
peripheral analgesics— as nonnarcotic analgesics. Aspirin (acetylsalicylic
acid— ASA) is one of a group of salicylates that are potent peripheral
analgesics. Unfortunately, it tends to irritate the gastric mucosa more than
other salicylates (enteric-coated preparations avoid some of this); it can also
depress platelet numbers and function, and is associated with Reye's
syndrome in children. Acetaminophen doesn't have these risks, but on the
other hand, it is not a very effective anti-inflammatory agent.
Nonsteroidal anti-inflammatory drugs (NSAIDs) are generally equal
or superior to ASA in analgesia. They act by interfering with prostaglandin
production in the same
Tissue
damage
PGEn
Figure 23.10 Mechanism underlying the analgesics
that act peripherally to limit nociception, The three most Bradykinin
commonly used analgesics block the formation of PGE2
( H ) to limit nociceptor responses and reduce pain.
r
Enhanced
nociceptor
response
way as ASA. Their antiplatelet effect is rapidly
i I
reversible, unlike that of ASA, and some are less f
irritating to the gastric mucosa. They are used with tow Pain
iJ
back pain, migraine, postoperative pain, cancer pain, and
dysmenorrhea.
Table 23.6 lists some common nonnarcotic
analgesics. There is a limitation to the analgesia provided
by these drugs, so they are best used to control mild to
moderate pain. Also, unlike narcotics, many are effective
antipyretics (i.e., they can control fever). They do not cause sedation, nor do
they lead to tolerance or dependence. For these reasons, it is usually
recommended that maximum use be made of nonnarcotic analgesics for any
pain that has a
Table 23.6
Selected Analgesic Agents Commonly Encountered in
Clinical Settings
Nonnarcotic Analgesics
Acetylsalicylic acid (ASA, aspirin)
Magnesium trisalicylate Acetaminophen
Nonsteroidal anti-inflammatory drugs (NSAIDs): Ibuprofen Naproxen
Indomethacin
Narcotic Analgesics
Mild to moderate pain:
Codeine
Oxycodone
Propoxyphene Moderate to
severe pain:
Meperidine
Pentazocine
Morphine
Hydromorphone
Methadone
Levorphanol
Nalbuphine
Cyclooxygenase
1 1
f > Inflammation
peripheral component. Incidentally, as far as we know, headaches are
Aspirin
generated in tissue external to the brain's neural tissue, i.e., vessels, the dura,
muscles, etc. In this sense headache is "peripheral" and therefore often
Chapter Twenty-Three
responds to nonnarcotic analgesics. A more detailed discussion of headache
appears at the end of this chapter.
Narcotic Analgesics
By binding to the central nervous system endorphin receptors, narcotics
activate the descending analgesia pathways, which work at the level of
nociceptor input to second-order neurons in the pain pathways. There are
different endorphin receptors distributed throughout the CNS. Each narcotic
(see list in table 23.6) will have a different pattern of affinities with these
receptors and thereby a different set of actions mediated by the receptors.
There is no significant foundation to the fear of developing addiction
from the use of narcotic analgesics. Appropriate dose levels, to meet the
need for analgesia, can be closely monitored and any dependence that does
emerge can be readily dealt with by gradual withdrawal. Prolonged
administration of narcotics does, however, lead to tolerance, the decreased
effect of a given dose over time. When it occurs, as in cancer patients, it can
be overcome by adjusting dosage and frequency of administration while
monitoring for any CNS effects, such as respiratory depression,
Although widely used, the synthetic narcotic meperidine (Demerol)
has significant hazards. Normeperidine is produced as a metabolite of the
breakdown of meperidine. It is much more slowly cleared from the tissues
than meperidine and therefore accumulates in the plasma. It can produce
tremors, anxiety, myoclonus (exaggerated tendon reflexes), and generalized
seizures, particularly in patients with compromised kidney function, who
can't excrete it. Codeine and oxycodone are morphinelike substances suitable for treating moderate pain. They are often used effectively in
combination with nonnarcotic analgesics.
Potentiators
Potentiators are medications administered with an analgesic, to enhance the
effect of a given dose. The theory is that, in this way, greater analgesia can
be achieved without increasing side effects or risk of toxicity. In fact, these
drugs may act in different ways. Some are actually additive drugs, i.e.,
medications that have an analgesic effect on their own that is added to that of
the primary analgesic. Hydroxyzine (Atarax, Vistaril), an antihistamine, is
probably an example. Other drugs, e.g., cimetidine (Tagamet), appear to
potentiate by interfering with the normal metabolic breakdown of analgesics
in the liver. The result is slower clearance and higher plasma drug levels.
The same effect can be achieved with more control by simply increasing the
dose of analgesic or its frequency of administration, or both.
Other potentiators, e.g., phenothiazines, have varied effects on pain.
The phenothiazine chlorpromazine (Thorazine), a drug whose primary use
is as an antipsychotic, has some analgesic effect. However, the most popular
phenothiazine (Phenergan), an antihistamine, is ineffective or even an
antianalgesic. There probably are no dependable pure potentiators for
narcotics, with the possible exception of aspirin and acetaminophen, which
appear to potentiate codeine. On the other hand, adding 100-200 mg of
caffeine (a strong cup of coffee contains about 150 mg) to either
acetaminophen or ASA (650 mg) will significantly improve analgesia.
Anticonvulsants and Tricyclic Antidepressants
Neuropathic pain presents real challenges to pharmacological management
because it seldom responds to either narcotic or nonnarcotic analgesics. The
sharp, stabbing pain of trigeminal neuralgia and some other focal neuralgias
is often controlled by anticonvulsants (carbamazepine, pheny-toin, or
clonazepam), while tricyclic antidepressants can be effective in controlling
the pain arising in postherpetic neuralgia and peripheral nerve injury. Recall
that one of the descending pain limitation systems causes the release of
leucine enkephalin in the dorsal horn of the cord. Some tricyclic
Pain and Pain Management
15
antidepressants enhance this effect. Whatever their route of action, these
substances appear to be analgesic, whether or not the person is depressed.
HEADACHE
Headache is a relatively common form of pain experience. Although it may
be temporarily completely disabling, the vast majority of headaches are
benign, nonprogressive disorders. Headaches associated with excess alcohol
use, smoking, stress, or fatigue are best treated by taking two aspirin and,
rather than calling the physician in the morning, avoiding the cause in the
future. Headache is the unfortunate accompaniment of a variety of medical
disorders: fever of any cause, food poisoning, carbon monoxide poisoning,
diseases producing hypercapnia (e.g., chronic lung disease),
hypothyroidism, and others. In some syndromes, headache is the central
complaint. These are various forms of migraine, cluster headaches, and
tension headaches. Finally, in some cases headache is symptomatic of some
serious underlying pathology.
Pain-Sensitive Structures
A knowledge of the structures of the head that are capable of generating pain
is helpful in understanding the pathophysiology of headache. The bone of
the skull and much of the dura, arachnoid, and pia are insensitive, as is all
the brain itself. By contrast, the venous sinuses and tributary veins, the dura
at the base of the brain, and the arteries within the meninges and the
subarachnoid space are highly sensitive to any stimulation that can produce
the sensation of pain. Similarly, certain nerves (e.g., trigeminal, vagus,
upper cervical) generate pain when inflamed, compressed, or under tension.
Superficial tissues are also capable of generating pain that is experienced as
headache: skin, connective tissues, muscles, arteries, and periosteum of the
skull. Other sensitive structures are the eye, the ear, and the nasal and sinus
cavities.
Headaches can thus be produced by mechanical stimulation (traction,
dilatation, distention) of intracranial or extracranial arteries, large
intracranial veins, venous sinuses or associated dura, the nasal cavity, and
the paranasal sinuses. Inflammation or irritation of the meninges and raised
intracranial pressure, as well as spasm, injury, or inflammation of
extracranial muscles, can also result in headache. For an intracranial mass to
generate pain, it usually has to stretch or displace vessels, nerves, or dura at
the base of the brain. This can occur well in advance of any change in
intracranial pressure (that is, while the tumor may still be quite small).
Symptomatic Headaches
Brain tumor produces headaches in about two-thirds of all patients.
Sometimes the pain is triggered by activity or postural changes (e.g.,
stooping), but there may be no provoking factor. Typically, headaches due
to tumors are deep seated, variably throbbing, perhaps "aching" or
"bursting," and occur with increasing frequency and severity. They may last
minutes to an hour or more and occur once to many times per day, in some
cases accompanied by forceful (projectile) vomiting. Rest will sometimes
diminish the pain.
Headaches that are precipitated by cough or exertion are usually
benign, although they raise the question of some intracranial mass (e.g., a
tumor, an arteriovenous malformation—AVM) or developmental
abnormality. The mechanism is presumably the increase in intrathoracic
pressure during cough or exertion, which both raises the intrathoracic blood
pressure and impedes venous drainage.
With arteriovenous malformation or aneurysm, there is little
correlation between the size and the progression of the pathology and the
nature of the symptomatic headache. Hemorrhage of an AVM or aneurysm,
however, produces a highly symptomatic headache; rapidly developing,
extremely severe, lasting many days, and localizing in the occiput and neck.
Chapter Twenty-Three
Blood turbulence detected by auscultation and blood in the CSF are
diagnostic. Those that survive the hemorrhage are candidates for surgical
correction of the defective vasculature before a more serious rebleed occurs.
Headache that follows trauma, for example concussion or whiplash
injury, is varied. It can be severe and chronic, with either continuous or
intermittent pain. There is often also giddiness, vertigo, or tinnitus (ringing
or whistling in the ears), and sometimes there is posttraumatic nervous
instability, a condition of agitated restlessness and hypersensitivity not
directly associated with headache. Headache immediately following trauma
may signal the development of a subdural hematoma. In such cases, the
headache is supplanted by drowsiness, confusion, stupor, and then coma.
Headache that is due to inflammation and blockage of the paranasal
sinuses can result from the pressure of accumulated fluid; alternatively, as
fluid is reabsorbed, the exit may remain blocked from tension on the mucous
membranes, a condition leading to the so-called vacuum sinus headache.
Headache of ocular origin (perhaps due to eyestrain) tends to be steady and
aching and located in the orbit, forehead, and temple. It often occurs after
sustained use of the eyes in close focusing and resolves with appropriate
corrective lenses.
The headache of meningeal irritation, whether caused by inflammation
from infection or by irritation from the breakdown of blood from a
subarachnoid bleed or other cause, has an acute onset and becomes severe
and generalized (or bioccipital or bifrontal). As with other meningeal signs,
it worsens if the head is bent forward and is often accompanied by a stiff
neck. Lumbar puncture produces an immediate headache upon arising from
the procedure; in this case the pain is attributable to the loss of fluid and
consequent tension placed on dural, venous, and arterial structures at the
base of the brain as it sags within the cranial space.
Headache Syndromes and Their Treatment
There are several headache syndromes which, while nonprogressive and for
the most part benign, can be cruelly disabling. They require diagnosis and
appropriate symptomatic care.
Tension Headaches
This is one of the most common of headache syndromes. It is also one of the
most poorly understood, and is often ineffectively treated. The sufferer
experiences a bilateral, generalized sense of nonthrobbing pressure,
fullness, or tightness that is characteristic. Onset is gradual and the headache
can persist in continuous or variable intensity day and night for days, weeks,
even years. At one time the pain was thought to develop from muscle
tension associated with stress, but careful studies using electromyography
have failed to support that theory. In some cases, however, relaxation
training using muscle tension biofeedback has apparently been effective in
treating these hard-to-manage headaches. Since fatigue, nervous strain, and
worry tend to provoke episodes of tension headache, strategies that reduce
stress, improve coping, or restrain reactions, as with antidepressant or
antianxiety drugs, will tend to reduce their incidence or severity.
Nonnarcotic analgesics (e.g., aspirin or acetaminophen) may lessen the
intensity of the pain but rarely get rid of it, and sufferers often take 6-8 pills
a day with little effect.
Migraine Headaches
These headaches, with throbbing-to-dull pain often accompanied by nausea
and vomiting, are frequently localized to one side of the head perhaps behind
one eye or ear, and hence the French term migraine, derived from the Latin
hemicrania—half the skull. Perhaps 20-30% of the population have some
degree of migraine, with females being three times as susceptible. About
60% of migraine sufferers have a relative in the immediate family that has
Pain and Pain Management
16
shared the complaint. Onset is often in childhood and adolescence or young
adulthood, and most people experience extensive relief with middle age.
Women are more likely to have the migraine begin during the premenstrual
part of their cycle. During pregnancy the headaches typically lessen.
Although the pathophysiology has yet to be fully defined, all the variants of
migraine appear to result from arteriolar constriction and decreased cerebral
blood flow. These variants include classic migraine, common migraine, and
complicated migraine.
Classic migraine follows a typical course. The person may have
premonitory symptoms hours before the attack: a sense of elation or energy
or foreboding, cravings, drowsiness, or depression. Visual disturbances like
scintillations, light sensitivity, bright zigzag lines or scotomas (blind spots)
affecting one or both visual fields and even extending to blindness, or
dizziness and tinnitus signal the start of the attack. These symptoms,
sometimes called the prodrome, develop slowly, at least over minutes, and
may spread or change. As with other symptoms of migraine, the gradual
time course of development allows us to distinguish these symptoms of
onset from epileptic phenomena. The pain and photophobia that follow the
prodome are often so extreme that the person must withdraw to a darkened
room to wait it out or sleep it off. The throbbing pain behind one eye or ear
becomes a dull generalized ache, and the scalp may be sensitive. The
duration is hours to one or two days, and bouts may recur at irregular
intervals of weeks or months.
In common migraine the headache is not preceded by the visual or
other symptoms but otherwise follows the same course. An additional
feature may be frequent nausea and occasional vomiting, which give rise to
the name sick headache.
Complicated migraine, also sometimes called neurological migraine,
is distinguished by the presence of neurological symptoms other than (and
perhaps in addition to) the visual symptoms of classic migraine. These may
include unilateral numbness and tingling of the lips, face, hand, or leg,
which may deepen to weakness or paralysis imitating a stroke. The person
also may have difficulty speaking or understanding speech. Such symptoms
may occur before or during the aching phase of the headache and may
spread slowly over a period of minutes; they usually resolve in minutes or
hours.
The condition is termed "complicated" for another reason. Some
people experience long-term, even permanent neurological deficits:
hemianopsia, hemiplegia or hemianesthesia, or eye movement defects.
Furthermore, some people experience the neurological symptoms without
headache. Children may'have nausea, abdominal pain, and vomiting without
headache or may have intense spells of vertigo. Adults may have these
symptoms or localized pain, bouts of fever, or mood disturbances. Migraine
must be considered when other explanations for these symptoms have been
ruled out. Diagnosis is made even more difficult because some older adults,
with no earlier history of migraine, will develop migrainous neurological
symptoms that resemble those of transient ischemic attacks.
The pathophysiological basis to migraine has not been established.
The older theory was that the pain is caused by the vasodilation and vascular
distention that follows a prodromal episode of vascular spasm and ischemia,
but this theory has been shown to be incorrect. During the evolution of an
attack, studies of cerebral blood flow show a slow drop in cerebral
perfusion, usually beginning in the occipital region. Throughout the attack
there are areas of hypoperfusion, and there is no evidence of localized or
generalized dilation or hyperperfusion. Current explanations of migraine
center on a defect in the neural regulation of vascular tone that in some way
involves serotonin released locally from platelets. Antiserotonin drugs like
methy-sergide are effective in arresting attacks, while drugs that trigger
serotonin release, like reserpine, precipitate attacks. Many other
neurotransmitters that affect vascular tone are being considered for their
contribution to migraine.
Chapter Twenty-Three
Conventional medical control of migraines depends on treating the
acute attack at its first sign, using ergot preparations (ergot is derived from a
mold affecting rye grain). Once the pain becomes intense, codeine sulfate
may control it, but aspirin and acetaminophen are ineffective. The new
antiserotonin drug sumatriptan, unlike other migraine medications available
by prescription, can often arrest a migraine even after it has started to
evolve. While expensive and not universally effective, for some it offers
control that was formerly accessible only through the emergency ward.
Cluster Headaches
These headaches are so named because they tend to occur nightly for weeks
to a few months (in a cluster). Although the underlying mechanisms may be
quite different from those causing migraine, cluster headaches are usually
described as a migraine variant. Men are four times as likely as women to
Pain and Pain Management
17
have them, in contrast to the pattern with migraines. Two or three hours
after falling asleep the person awakens with steady, intense pain in one orbit
and flowing tears. The nostril on the same side is plugged and later begins to
run. The affected pupil may be constricted, the eyelid drooped, and the
cheek flushed and edematous. The attack may last from ten minutes to two
hours. The majority of people with cluster headaches show no history of
migraine.
Cluster headaches are very difficult to treat effectively. If stress or
fatigue is implicated, efforts are made to reduce it. Some people can
interrupt an excruciating attack by administering oxygen or using an inhaled
ergot preparation. Prophylactic administration of the tricyclic antidepressant
amitriptyline is the method of choice, while methysergide, corticosteroids
like prednisone, and the antidepressant lithium are used with very resistant
cases.
Case Study
A 35-year-old male carpenter suffered an injury at work while lifting a
heavy object. He stopped work and saw a physician, who identified muscle
spasm and a reduced range of spinal mobility. Based on her diagnosis of low
back strain, she prescribed a benzodiazepam drug as a muscle relaxant and a
codeine/acetaminophen agent for pain, and recommended rest and a return
for evaluation in two weeks. At that time improvement was minimal and a
regimen of physiotherapy was implemented, along with continuation of the
drug regimen, which the patient requested for his pain. Improvement failed
to materialize over the next several weeks, and an orthopedic specialist was
called in for an assessment. X-rays and a CT scan indicated some evidence
of low lumbar degeneration. The specialist recommended that the man not
return to his occupation and that he approach the worker's compensation
agency, which provides benefits in cases of work-related disability, for
retraining in some less strenuous work.
The carpenter's approach to the compensation agency led to an
assessment by an agency physician some 16 weeks after the initial injury.
He found the patient to have been continuing with his medications and to
have developed a marked degree of hostility and depression. He further
found significant disagreement between the patient's complaints of pain and
loss of movement and any objective findings. The patient was also quite
deconditioned from the lack of normal activity during the past weeks. On
some probing interrogation and reference to the agency's files, the physician
discovered that the patient had a history of a broken home, work injury
claims, and alcohol and drug abuse. Because he couldn't work his wife had
been forced to work in a disagreeable, low-paying job, and their family was
rapidly becoming dysfunctional.
Rather than defer to the man's demands for further medical
consultations and surgery to prevent his becoming a cripple, the doctor
prescribed a low-dose antidepressant and withdrawal of the narcotic
medication, suspecting it had been enhancing the patient's pain by endorphin
depletion. He also arranged for a program of physiotherapy aimed at
restoring conditioning and persuaded the man to accept some family
counseling. As a result of this regimen, the patient reported loss of half his
pain two weeks after withdrawal of the narcotics, and significant overall
improvement after six weeks of gradually increased physical activity.
Between family counseling and the employer's willingness to accommodate
a gradual return to work, he achieved full resumption of work and a greatly
improved home situation 25 weeks postinjury.
Commentary
Had this patient had a family physician aware of his history, recovery might
have occurred much sooner. The pattern of an insecure upbringing,
substance abuse, and depression are indicators of an increased likelihood of
developing the pattern of chronic pain and disability behavior seen in this
case. The depletion of endorphins and a resulting increase in passive pain
should have been recognized earlier as being related to the extended use of
narcotics and benzodiazepine agents. Endorphin replenishment following
withdrawal of these agents was speeded by the antidepressant agent
prescribed. It was also sound practice not to assume too quickly that the
patient was motivated solely by a desire for a large insurance compensation
award, and to attempt some degree of rehabilitation and renewal of
self-esteem. Unfortunately, not all such cases resolve as successfully.
Chapter Twenty-Three
Pain and Pain Management
18
Key Concepts
1.
Acute and chronic pain differ in their neurological processing,
6.
impact, and treatment (pp. 610-611).
The pain that may accompany cancer is highly variable in both nature
and pathological basis (pp. 618-619).
2. Pain stimuli can produce physiological and psychic arousal, a variety
of orienting responses, precise localization (via the neospmothalamic
pathway), or chronic pain responses (via the paleospinothalamic
pathway) (pp. 612-613).
7.
pain have given rise to a precise and detailed vocabulary (pp.
619-622).
8.
3. Narcotics produce their analgesic effects by binding to endorphin
receptors in the brain stem, thereby stimulating fibers that release a
neurotransmitter that inhibits pain signals as they enter the cord.
TENS and stimulus-produced analgesia probably induce the same
neurotransmitter release (pp. 614-615).
The complexity and variability of the experience and causation of
Peripheral analgesics inhibit the production of prostaglandins,
thereby raising the pain threshold (p. 623).
9.
Narcotics act centrally and, depending on their binding
characteristics, can produce respiratory depression, euphoria, and
other effects (pp. 623-625).
10.
4. Referred pain is of great clinical diagnostic utility (pp.
A minority of headaches are symptomatic of serious underlying
pathology, and in some conditions the pattern and localization of pain
615-617).
is quite characteristic (pp. 625-626).
5. Phantom pain illustrates the role of central processing in pain
perception and is a significant clinical problem (pp. 617-618).
11.
A variety of headache syndromes, while nonprogressive and not
life-threatening, can produce significant disability (pp. 626-627),
REVIEW ACTIVITIES
1. Recall your last significant experience with pain. Go through each
cluster in table 23.3 and choose the appropriate terms to describe
your experience.
2.
Make a copy of table 23.4. Cut up the paper in such a way as to
separate all the symptoms from their definitions, and keep them in
one pile. Do the same with the peripheral and central syndromes,
only mix them up. Now attempt to unite symptoms and definitions,
separate peripheral from central syndromes, and unite each
syndrome with its definition.
3. The point was made that acute pain is processed preponderantly by
the neospinothalamic pathway, while chronic pain is processed via
the paleospinothalamic pathway. In table form, list the features
common to both pathways. Then list the ways in which they differ.
4. Find a few people who experience migraine or tension or cluster
headaches (if you're unfortunate, one of them may be you!). Question
them about their pain experience and try to classify their headaches.