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THE SKIN SENSES
Proceedings of the First International Symposium
on the Skin Senses
Held at The Florida State University
in Tallahassee, Florida
Compiled and Edited by
DAN R. KENSHALO, Ph.D.
Department of Psychology
The Florida State University
Tallahassee, Florida
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N-1
Chapter 20
SENSORY, MOTIVATIONAL, AND CENTRAL
CONTROL DETERMINANTS OF PAIN
A New Conceptual Model*
R. MELZACK AND K. L. CASEY]
T
HE PROBLEM OF PAIN,
since the beginning of the century, has been
dominated by the concept that pain is a sensory experience. Yet pain has a
unique, distinctly unpleasant, affective quality that differentiates it from
sensory experiences such as sight, hearing, or touch. It becomes overwhelm-
ing, demands immediate attention, and disrupts ongoing behavior and
thought. It motivates or drives the organism into activity aimed at stopping
the pain as quickly as possible. To consider only the sensory features of
pain, and ignore its motivational and affective properties, is to look at only
part of the problem, and not even the most important part at that (Cantril
and Livingston, 1963; Chapman, Dingman, and Ginzberg, 1965) . The
theory that pain is a sensory modality is relatively recent. The traditional
theory of pain in the 19th century (Marshall, 1894; Dallenbach, 1939) held
that it is an affective
quale —
the opposite of pleasure — rather than a sensa-
tion, and emphasized the unpleasant affect (or "feeling") that forces the
organism into action. That pain is comprised of both sensory and affective
dimensions was clear to Sherrington who proposed simply that "mind
rarely, probably never, perceives any object with absolute indifference, that
is, without 'feeling' . . . affective tone is an attribute of all sensation, and
among the attribute tones of skin sensation is skin pain" (Sherrington,
1900, p. 974) .
The remarkable development of sensory physiology and psychophysics
since Sherrington's time has given momentum to the concept of pain as a
sensation and has overshadowed the role of affective and motivational
processes. The sensory approach to pain, however, valuable as it has been,
fails to provide a complete picture of pain processes. Even the concept of
pain as a perception, with full recognition of past- experience, attention,
and other cognitive determinants of sensory quality and intensity (Barber,
1959; Livingston, 1953; Melzack, 1961) , still neglects the crucial motiva-
*Supported by contract SD-193 from the Advanced Research Projects Agency of the U. S. De-
partment of Defense.
(Supported by U. S. Public Health Service Special Fellowship from the National Institute of
Mental Health, now at the Department of Physiology, University of Michigan.
423-
PAIN
SENSATION
REACTIONS TO PAIN
PAIN
FIBERS
PAIN
CENTER
EVALUATION
AND
PERCEPTION
MOTIVATION
AND
AFFECT
424
The Skin Senses
tional dimension. Our purpose here is to present a model of the sensory,
motivational, and cognitive determinants of pain.
THE NEED FOR A NEW APPROACH
The neglect of the motivational features of pain underscores a serious
schism in pain research. Characteristically, textbooks in psychology and
physiology deal with "pain sensation" in one section and "aversive drives
and punishment" in another, with no indication that both are facets of
the same phenomenon. This separation reflects the widespread acceptance of
von Frey's (1895) specificity theory of pain, with its implicit psychological
assumption (see Melzack and Wall, 1962) that "pain impulses" are trans-
mitted from specific pain receptors in the skin directly to a pain center in
the brain, so that sensory quality is determined solely by activity of the
center. Although there is convincing physiological evidence (Iggo, 1960;
Zotterman, 1959) that specialization exists within the somesthetic system,
the clinical, physiological, and psychological evidence reviewed by Melzack
and Wall ,1962; 1965) is overwhelmingly against the assumption that
activity in one type of receptor, fiber, or spinal pathway elicits only one
kind of sensation. Moreover, the concept of a pain center implies a "man-in-
the-brain" who hears the alarm-bell ring, evaluates the meaning of the in-
put, decides on a response strategy, and pushes the appropriate response
button. To avoid this sort of animistic thinking, we must postulate rela-
tionships among sensory, motivational, and cognitive systems to account for
the facts of behavior.
Figure 20-1. Conceptual
model of pain sensation and reactions to pain.
The assumption that pain is a primary sensation has relegated motiva-
tional and cognitive processes to the role of "reactions to pain" (see Fig.
20-1) , and has made them only "secondary considerations" in the whole
pain process (Hardy, Wolff, and Goodell, 1952; Sweet, 1959). But the notion
that motivational and cognitive processes must follow the primary pain
Sensory, Motivational, and Central Control Determinants
425
sensation fails to account for even relatively simple data. For example,
Beecher's observation that most American soldiers wounded at the Anzio
beachhead "entirely denied pain from their extensive wounds or had so
little that they did not want any medication to relieve it" (Beecher, 1959,
p. 165) is interpreted by specificity theorists (Beecher, 1959; Sweet, 1959) to
mean that their joy at having escaped alive from the battlefield blocked
only their reaction to pain, but not pain sensation itself. If this is the case,
then pain sensation is not painful, even after extensive bodily damage.
Rather than face the paradox of nonpainful pain (Nafe, 1934) , it seems
more reasonable to say simply that these men felt no pain after their exten-
sive injuries, that the input was blocked or modulated by cognitive activities
before it could evoke the motivational-affective processes that are an inte-
gral part of the total pain experience.
The motivational-affective dimension of pain is brought clearly into
focus by clinical studies on frontal lobotomy and by reported cases of "con-
genital insensitivity to pain" and "pain asymbolia." Patients with frontal
lobe lesions (Freeman and Watts, 1948) rarely complain about severe
clinical pain or ask for medication. Since lobotomy does not disrupt sensory
pathways — indeed, sensory thresholds may be lowered (King, Clausen, and
Scarff, 1950) — its predominant effect appears to be on the motivational-
affective dimension of the whole pain experience. The aversive quality of
the pain and the drive to seek pain relief both appear to be diminished.
Similarly, people reported to be congenitally insensitive to pain appear to
have no sensory loss and are able to feel pricking, warmth, cold, and pres-
sure. They give accurate reports of increasing intensity of stimulation, but
the input, even at intense, noxious levels, seems never to well up into frank
pain. The evidence (Ford and Wilkins, 1938; McMurray, 1950; Sternbach,
1963) suggests that it is not the sensory properties of the input but rather
the motivational-affective properties that somehow fail to operate. Finally,
patients exhibiting "pain asymbolia" (Rubins and Friedman, 1948; Schilder
and Stengel, 1931) are able to appreciate the spatial and temporal properties
of noxious stimuli; for example, they recognize pin pricks as sharp, but fail
to withdraw or complain about them. The sensory input never evokes the
strong aversive drive and negative affect characteristic of pain experience
and response.
The gate control theory of pain proposed by Melzack and Wall (1965)
provides the basis for consideration of the motivational dimension of pain
in addition to its more obvious sensory dimension. The theory suggests that
there exists, in the spinal cord, a gate control system that modulates the
amount of input transmitted from the peripheral fibers to dorsal horn trans-
mission (or T) cells (Fig. 20-2) which project to the anterolateral pathway.
CENTRAL
CONTROL
GATE CONTROL SYSTEM
ACTION
SYSTEM
INPUT
S
426
The Skin Senses
The number of impulses transmitted, per unit time, by the T cells is deter-
mined by the ratio of large and small fiber inputs, and by brain activities
which influence the gate control system through central control efferent
fibers. The output of the T cells is monitored centrally over a prolonged
period of time. When it reaches or exceeds a critical intensity level, it
triggers the action system — those neural areas responsible for the complex,
sequential patterns of behavior and experience characteristic of pain. We
propose here to examine in more detail the consequences of the T-cell
output at the brain level and to relate it to the sensory and motivational
dimensions of pain.
Figure 20-2. Schematic diagram of the gate control theory of pain mechanisms:
L,
the
large diameter fibers; S, the small diameter fibers. The fibers project to the substantia
gelatinosa (SG) and first central transmission (T) cells. The inhibitory effect exerted by
SG on the afferent fiber terminals is increased by activity in
L
fibers and decreased by
activity in S fibers. The central control trigger is represented by a line running from
the large fiber system to the central control mechanisms. These mechanisms, in turn,
project back to the gate control system. The T cells project to the entry cells of the
action system. ±, excitation;—,inhibition (Fig. 4, Melzack, R., & Wall,
P.
D.,
Science,
1965,
150, 971.
Copyright 1965 by the American Association for the Advancement of
Science) .
THE DETERMINANTS OF PAIN
The output of
the dorsal horn T cells is transmitted toward the brain
by fibers in the anterolateral spinal cord and is projected into two major
brain systems: (a) via neospinothalamic fibers into the ventrobasal and
GATE
CONTROL
SYSTEM
INPUT
S
SENSORY-DISCRIMINITIVE
SYSTEM
(SPATIO-TEMPORAL ANALYSIS)
N
MOTIVATIONAL-AFFECTIVE
SYSTEM
(CENTRAL
INTENSITY MONITOR)
CENTRAL CONTROL PROCESSES
MOTOR
MECHANISMS
Sensory, Motivational, and Central Control Determinants
427
posterolateral thalamus and the somatosensory cortex; and (b) via medially
coursing fibers, that comprise a paramedial ascending system, into the
reticular formation and medial intralaminar thalamus and the limbic sys-
tem (Mehler, 1957; Mehler, Feferman, and Nauta, 1960) . Electrical stimu-
lation of the tooth at noxious intensities evokes activity in both projection
systems (Haugen and Melzack, 1957; Kerr, Haugen, and Melzack, 1955;
Melzack and Haugen, 1957) , and discrete lesions in each may strikingly
diminish pain perception and response (Melzack, Stotler, and Livingston,
1958) . We propose the following (Fig. 20-3) : (a) that the selection and
modulation of the sensory input through the neospinothalamic projection
system provides, in part at least, the neurological basis of the sensory-
discriminative dimension of pain; (b) that activation of reticular and limbic
structures through the paramedial ascending system underlies the powerful
motivational drive and unpleasant affect that trigger the organism into
action, and (c) that neocortical or higher central nervous system processes,
such as evaluation of the input in terms of past experience, exert control
over activity in both the discriminative and motivational systems.
We
assume that these three categories of activity interact with one another to
provide perceptual information regarding the location, magnitude, and
spatiotemporal properties of the noxious stimulus, motivational tendency
toward escape or attack, and cognitive information based on analysis of
1
Figure 20-3. Conceptual model of the sensory, motivational, and central control determin-
r
ants of pain. The output of the T cells of the gate control system projects to the sensory-
discriminative system (via neospinothalamic fibers) and the motivational-affective
system (via the paramedial ascending system) . The central control trigger (comprising
the dorsal column and dorsolateral projection systems) is represented by a line running
from the large fiber system to central control processes. These, in turn, project back to
the gate control system, and to the sensory-discriminative and motivational-affective
systems. All three systems interact with one another, and project to the motor system.
428
The Skin Senses
multimodal information, past experience, and probability of outcome of
different response strategies. We assume, moreover, that all three forms of
activity influence motor mechanisms responsible for the complex pattern of
overt responses that characterize pain.
The Sensory Determinants
Physiological and behavioral studies suggest that the sensory-discrimin-
ative dimension of pain is subserved, at least in part, by the neospinothal-
amic projection system. Neurons in the ventrobasal thalamus, which receive
a large portion of its afferent flow, show discrete somatotopic organization
(Poggio and Mountcastle, 1963) even after dorsal column section (Perl and
Whitlock, 1961) . In clinical studies, Cook and Browder (1965) have shown
that surgical section of the dorsal columns, long presumed to subserve vir-
tually all of the discriminative capacity of the skin sensory system, produced
no permanent change in two-point discrimination and localization in seven
patients. Moreover, Semmes and Mishkin (1965) found that monkeys with
lesions of the sensorimotor cortex show marked deficits in form and rough-
ness discriminations on the ipsilateral side. Since the cortical input from the
dorsal column-lemniscal pathway is almost entirely contralateral, the deficit
appears to be attributable to injury of the cortical projection of the neo-
spinothalamic system.
These data, taken together, suggest that the neospinothalamic projec-
tion of the T-cell output has the capacity to process information about the
spatial, temporal, and magnitude properties of the input. This capacity, to
be sure, may be strongly influenced by, and in part dependent upon, the
activity of the dorsal column-medial lemniscal system which projects to the
dorsal horns (Ramon y Cajal, 1952) and the ventrobasal thalamus. We pro-
pose, then, that the selection and modulation of the sensory input during
transmission through the neospinothalamic projection system provide the
neural basis for the sensory-discriminative dimension of pain.
The Motivational Determinants
There is reason to believe that the brain stem reticular formation and
the limbic system, which receive projections from the paramedial ascending
system, are responsible for the aversive drive and affect characteristic of
pain. The term "paramedial ascending system" is used in this paper to refer
to the spinoreticular, spinomesencephalic, and paleospinothalamic compo-
nents of the anterolateral somatosensory pathway. The paramedial ascending
system and the structures with which it connects are not organized to pro-
vide discrete spatial or temporal information. There is little or no evidence
for spatial information transfer to the reticular formation (Amassian and
DeVito, 1954; Bach-y-Rita, 1964; Bell, Sierra, Buendia, and Segundo, 1964)
Sensory, Motivational, and Central Control Determinants
429
or medial thalamus (Albe-Fessard and Bowsher, 1965; Albe-Fessard and
Kruger, 1962; Casey, 1966; Kruger and Albe-Fessard, 1960) , where somato-
sensory input, though predominant, is mixed with other sensory inputs
(Bell
et al.,
1964; Scheibel, Scheibel, Mollica, and Moruzzi, 1955; Starzl,
Taylor, and Magoun, 1951).
The striking feature of the paramedial ascending system is its strategic
relation to the limbic system and associated structures (Fig. 20-4) . Its
fibers penetrate the medial brainstem reticular formation and the midbrain
central gray (Mehler
et al.,
1960; Bowsher, 1957) , which are reciprocally
interconnected. The midbrain central gray is part of the "limbic midbrain
area" (Nauta, 1958) that (a) projects diffusely to the adjacent reticular
formation and mesencephalic tegmentum (Weisschedel, 1937) ; (b) con-
nects reciprocally with the hypothalamic region via Schutz's fasciculus and
thus permits interaction with the limbic forebrain areas by way of the
medial forebrain bundle; (c) connects with the medial and intralaminar
thalamic nuclei, and (d) receives connections from the granular frontal
cortex (Nauta, 1964) . Thus the phylogenetically old paramedial ascending
system, which is separate from but in parallel with the newer neospino-
thalamic projection system, gains access to the complex circuitry of the
limbic system.
It is now well established that many limbic system structures play an
important role in aversive drives or similar pain related behavior. At the
mesencephalic level, stimulation in a region which includes the central
gray, the ventral tectum and dorsal tegmentum produces strong aversive
drive and behavior typical of responses to naturally occurring painful
stimuli (Delgado, 1965; Hunsperger, 1956; Olds and Olds, 1963; Spiegel,
Kletzkin and Szekeley, 1954) . Lesions of the central gray and adjacent mid-
brain tegmentum, in contrast, produce marked decreases in responsiveness
to noxious stimuli (Melzack
et al.,
1958; Skultety, 1958) . At the thalamic
level, "fear-like" responses, associated with escape behavior, have been
elicited by stimulation in the dorsomedial and adjacent medial-intralaminar
nuclei of the thalamus (Roberts, 1962) . In the human, lesions in the medial
thalamus have provided relief from intractable pain (Hecaen, Talairach,
David, and Dell, 1949; Mark, Ervin, and Yakovlev, 1963) .
Limbic forebrain areas have also been implicated in pain related pro-
cesses. Electrical stimulation of the hippocampus, fornix, or amygdala may
evoke escape or other attempts to stop stimulation (Delgado, 1955; Delgado,
Rosvold and Looney, 1956) , as well as defensive reactions (Hilton and
Zbrozyna, 1963; MacLean and Delgado, 1953) . After ablation of the amyg-
dala and overlying cortex, cats show marked changes in affective behavior,
including decreased responsiveness to noxious stimuli (Schreiner and Kling,
1953) . Surgical section of the cingulum bundle, which connects the pos-
430
The Skin Senses
L
Sensory, Motivational, and Central Control Determinants
431
terior frontal cortex to the hippocampus, also produces a loss of "negative
affect" associated with intractable pain (Foltz and White, 1962) . This evi-
dence indicates that limbic structures, although they play a role in many
other functions (Pribram and Kruger, 1954) , provide a neural basis for the
aversive drive and affect that comprise the motivational dimension of pain.
Intimately related to the brain areas involved in aversive drive and
sometimes overlapping with them are regions that are involved in approach
responses and other behavior aimed at maintaining and prolonging stimula-
tion. Such regions include the lateral hypothalamus, medial forebrain bun-
dle, and septum (Olds and Milner, 1954; Olds and Olds, 1963) . Stimula-
tion of many of these areas, as well as some of the limbic forebrain structures,
yields behavior in which the animal presses one bar to receive stimulation
and another to stop it. These effects, which may be due to overlap of
"aversive" and "approach" structures, are sometimes a function simply of
intensity of stimulation, so that low level stimulation elicits approach and
intense stimulation evokes avoidance (Grastyan, Czopf, Angyan, and Szabo,
1965) . In addition, complex excitatory and inhibitory interactions among
these areas (Olds and Olds, 1962; Stuart, Porter, and Adey, 1964; Tsubo-
kawa and Sutin, 1963) may explain why aversive drive to noxious stimuli
can be blocked by stimulation of positive reward areas in the lateral hypo-
thalamus (Cox and Valenstein, 1965) .
These psychophysiological data leave little doubt that the neural areas
comprising the paramedial, reticular, and limbic systems are involved in the
motivational and affective features of pain. The manner in which these
areas are brought into play deserves consideration. The fact that there are
inputs from other sensory systems as well as the cutaneous system (Bell
et al.,
1964) indicates that these areas are not activated exclusively by noxi-
ous stimuli. Moreover, the somatic input has access to areas involved in
Figure 20-4. Schematic diagram of the anatomical foundation of the proposed pain model.
On the right•
thalamic and neocortical structures subserving discriminative capacity. On
the left:
reticular and limbic systems subserving motivational-affective functions. Ascend-
ing pathways from the spinal cord (SC) are (a) the dorsal column-lemniscal and dorso-
lateral tracts
(right ascending arrow)
projecting to the somatosensory thalamus (SST)
and cortex (SSC) , and (b) the anterolateral pathway
(left ascending arrow)
to the
somatosensory thalamus via the neospinothalamic tract, and to the reticular formation
(stippled area),
the limbic midbrain area (LMA) and medial thalamus (MT) via the
paramedial ascending system. Descending pathways to spinal cord originates in somato-
sensory and associated cortical areas (AC) and in the reticular formation. Polysynaptic
and reciprocal relationships in limbic and reticular systems are indicated. Other abbrevi-
ations: FC — frontal cortex; LFS — limbic forebrain structures (hippocampus, septum,
amygdala, and associated cortex) ; H — hypothalamus. (Adapted from Nauta, W. J. H.,
Brain,
1958, 81, 319.)
432
The Skin Senses
approach or avoidance, and some areas can produce both. On what basis
are aversive rather than approach mechanisms triggered by the input?
We propose that these systems function as a
central intensity monitor;
that their activities are determined, in part at least, by the intensity of the
T-cell output (the total number of active fibers and their rate of firing) after
it has undergone modulation by the gate control system in the dorsal horns.
The output of cells in the medial brainstem may be facilitated by the sum-
mation of input from spatially separate body sites and by the interaction
of temporally dispersed inputs (Amassian and DeVito, 1954; Bell
et al.,
1964) . The poststimulus discharge activity of some of these cells lasts for
many seconds (Casey, 1966) , so that their activity may provide a measure
of the intensity of the total T-cell output over relatively long periods of
time. Essentially, both forms of summation transform discrete spatial and
temporal information into intensity information. We propose that the
output of these cells, up to a critical intensity level, activates those brain
areas subserving positive affect and approach tendency. Beyond that level,
the output activates areas underlying negative affect and aversive drive.
We suggest, therefore, that the drive mechanisms associated with pain are
activated when the somatosensory input into the motivational-affective
system exceeds the critical level. This notion fits well with Grastyan's
(Grastyan
et al.,
1965) observations that animals seek low-intensity electrical
stimulation of some limbic system structures, but avoid or actively try to
stop high-intensity stimulation of the same areas. Signals from these limbic
structures to motor mechanisms set the stage for response patterns that are
aimed at dealing with the input on the basis of both the sensory informa-
tion and cognitive processes.
The Central Control Determinants
There is convincing evidence that pain is influenced by cognitive or
"higher central nervous system" activities. Anticipation of pain (Hill,
Kornetsky, Flanary, and Wilker, 1952a) , anxiety and attention (Hill
et al.,
1952b) , suggestion and placebos (Beecher, 1959; Melzack, Weisz, and
Sprague, 1963) , cultural background (Chapman and Jones, 1944) , evalua-
tion of the meaning of the pain-producing situation (Beecher, 1959) , hyp-
nosis (Barber, 1959) , early experience (Melzack and Scott, 1957) , and
prior conditioning (Pavlov, 1927; 1928) all have a profound effect on pain
experience and response. These activities, which are subserved, in part at
least, by neocortical processes, may affect both sensory and affective experi-
ence or they may modify primarily the affective-motivational dimension.
Thus, excitement in games or war appears to block both dimensions of pain
(Livingston, 1953; Beecher, 1959), while suggestion (Melzack
et al.,
1963;
Sensory, Motivational, and Central Control Determinants
433
Hardy
et al.,
1952) and placebos (Beecher, 1959) may modulate the motiva-
tional-affective dimension and leave the sensory-discriminative dimension
relatively undisturbed.
Cognitive functions, then, are able to act selectively on sensory process-
ing or motivational mechanisms. In addition, there is evidence that the
input is localized, identified in terms of its physical properties, evaluated in
terms of present and past experience, and modified before it activates the
sensory or motivational systems. Men wounded in battle may feel little pain
from the wound but may complain bitterly about an inept vein puncture
(Beecher, 1959). Dogs that repeatedly receive food immediately after the
skin is shocked, burned, or cut soon respond to these stimuli as signals for
food and salivate, without showing any signs of pain, yet howl as normal
dogs would when the stimuli are applied to other sites on the body (Pavlov,
1927; 1928) .
The system performing these complex functions of identification, evalu-
ation, and selective input modulation must conduct rapidly to the cortex
so that somatosensory information has the opportunity to undergo further
analysis, interact with other sensory inputs, and activate memory stores and
preset response strategies. Moreover, it must be able to act selectively on
the motivational and sensory systems in order to influence their response
to the information being transmitted over more slowly conducting pathways.
Melzack and Wall (1965) have proposed that the dorsal-column and dorso-
lateral (Morin, Kitai, Portnoy, and Demirjian, 1963) projection pathways
act as a
central control trigger
to form the input or "feed-forward" limb of
this loop. The fast-conducting pathways have grown apace with the cerebral
cortex (Bishop, 1959) , carry precise information about the nature and
location of the stimulus, adapt quickly to give precedence to phasic stimulus
changes rather than prolonged tonic activity, and they conduct rapidly
(Morse and Towe, 1964; Kennedy and Towe, 1962) to the cortex so that
their impulses may begin activation of central control processes.
Corticofugal influences are known to act, via pyramidal and other central-
control fibers, on portions of the sensory-discriminative system such as the
ventrobasal thalamus (Shimazu, Yanagisawa, and Garoutte, 1965) and on
the dorsal column nuclei (Jabbur and Towe, 1961; Magni, Melzack, Moruz-
zi, and Smith, 1959; Winter, 1965) . Moreover, the powerful descending
inhibitory influences exerted at the dorsal horns of the spinal cord (Hag-
barth and Fex, 1959; Hagbarth and Kerr, 1954) can affect the gate control
system (Melzack and Wall, 1965) so that the input may be modulated
before it is transmitted to both the discriminative and motivational systems.
The motivational-affective system can be influenced by neocortical (French,
Hernandez-Peon, and Livingston, 1955) and limbic forebrain (Adey, Se-
04
The Skin Senses
gundo, and Livingston, 1957; Adey, Dunlop, and Sunderland, 1958; Her-
nandez-Peon and Hagbarth, 1955) structures acting on the brain stem reticu-
lar formation. Information from other modalities could enter into the
central control process via both projections (Casey, Cuenod, and MacLean,
1965; Cuenod, Casey, and MacLean, 1965) . The frontal cortex may play a
particularly significant role in mediating between cognitive activities and
the motivational-affective features of pain since it receives information via
intracortical fiber systems from virtually all sensory and associational cortical
areas (Crosby, Humphrey, and Lauer, 1962) and projects strongly to reticu-
lar (Newman and Wolstencroft, 1959) and limbic (Nauta, 1964; Ward and
McCulloch, 1947) structures. The effects of lobotomy, which are character-
ized by lowered affect and decreased drive for narcotics and other methods
of pain relief, could be due to a disruption of the regulating effects of central
control processes on activity in the reticular and limbic systems (Melzack,
1965) .
PAIN EXPERIENCE AND RESPONSE
The word "pain" is a label, a category, signifying a multitude of differ-
ent, unique experiences. Pain varies along both sensory-discriminative and
motivational-affective dimensions. The magnitude or intensity along these
dimensions, moreover, is influenced by cognitive activities, such as evalua-
tion of the seriousness of the injury. If injury or any other noxious input
fails to evoke aversive drive, the experience cannot be labelled as pain.
Conversely, anxiety or anguish without somatic input is not pain. Pain
must be defined in terms of its sensory, motivational, and central control
determinants. Pain, we believe, is a function of the interactions of all three
determinants, and cannot be ascribed to any one of them. It would be just
as wrong to say that the limbic system is the "pain center" as to ascribe that
function to the posterior thalamus. Clearly, each of the central nervous sys-
tem areas involved in the total pain experience has specialized functions. In
a model such as this, "function" does not reside in any one area. Rather,
each specialized portion of the brain contributes to experience and response
as a whole.
We believe that the complex sequences of behavior that characterize
pain (Melzack and Wall, 1965) are determined by sensory, motivational,
and cognitive processes acting on motor mechanisms. By "motor system"
(Fig. 20-3) we mean all of the brain areas that contribute to overt behavioral
response patterns, including motor cortex, basal ganglia, and response-
producing mechanisms in the hypothalamus, brain stem, and ventral horns.
There is reason to postulate an intensity monitor immediately after the
spinal gate which is capable of integrating the output of the dorsal horn
Sensory, Motivational, and Central Control Determinants
435
T cells so that activity beyond a critical level may elicit responses normally
classified as "reflexes." Even reflexes, however, are influenced by cognitive
processes. If we pick up a hot cup of tea in an expensive cup we are not
likely simply to drop the cup, but jerkily put it back on the table, and
then
shake our hand.
The therapeutic implications of the model should be obvious; but
because of the historical emphasis on the sensory dimension of pain, they
are not obvious at all. The surgical and pharmacological attack on pain
might well profit by redirecting thinking toward the neglected and almost
forgotten contributions of motivational and cognitive processes. Pain can
be treated not only by trying to cut down the sensory input by anesthetic
block, surgical intervention and the like, but also by influencing the motiva-
tional-affective and cognitive factors as well. Relaxants, transquillizers, seda-
tives, suggestion, placebos, and hypnosis are known to influence pain, but the
historical emphasis on sensory mechanisms has made these forms of therapy
suspect, seemingly fraudulent, almost a sideshow in the mainstream of pain
treatment. Yet, if we can recover from historical accident, these methods
deserve more attention than they have received.
ACKNOWLEDGMENT
We are grateful to Dr.
P.
D. Wall of the Massachusetts Institute of Tech-
nology for his valuable criticisms and suggestions.
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DISCUSSION
DR.
ZOTTERMAN:
In the introduction to your very interesting paper you
said that a man can be stabbed and he does not feel much pain? Does that
mean that you believe that there is a very strong stimulation or excitation
of peripheral nerve fibers which in some way generally induce pain in this
case?
DR.
MELZACK:
There is an intense input that, under normal circum-
stances, will induce pain.
DR.
ZorrERmAN: How do you know that?
DR. MELZACK:
There is every reason to believe that it is not otherwise.
Do you claim that after lesions of your skin, there is not a massive discharge
in the afferent fibers?
DR. ZOTTERMAN: No, that depends upon the kind of stimulus. But this
case is when people are in shock or they are dying, or they are run through.
I do not think there is much stimulation of afferent fibers in this case. It
takes some time to develop this intense stimulation of the fibers which I
would call nociceptive fibers. You have no evidence for that. That is the
first thing. The next thing, as I understand, you said you have large fibers
and small fibers involved when you produce pain. Which of those are the
more essential for the production of pain?
