THE LANCET • Vol 353 • June 19, 1999 2145
Although the precise mechanism s of viscera l pain differ
between different organs an d organ systems, there seem to
be two common princip les that ap ply to all visceral pa in. The
first principle is that the neurological mechanisms of visceral
pain differ fr om those involved in soma tic pain, and theref ore
findings in somatic pain rese arch ca nnot necessarily be
extrapolated to visceral pain. The second principle is
t h a tt h e psychophysics—the percep tion and p sychological
processing—of visceral pain also dif fers from that of somatic
pain. The differences between the mechanisms of somatic
and visceral pain are not only of scientific interest, but are
also relevant to clinical management.
Visceral pain has five important clinical characteristics:
(1) it is not evoked from all viscera (organs such as liver,
kidney, most solid viscera, and lung parenchyma are not
sensitive to pain); (2) it is not always linked to visceral
injury (cutting the intestine causes no pain and is an
example of visceral injury with no attendant pain, whereas
stretching the bladder is pa inful and is an e xample of pain
with no injury); (3) it is diffuse and poorly localised; (4) it
is referred to other locations; and (5) it is accompanied
with motor and autonomic reflexes, such as the nausea,
vomiting, and lower-back muscle tension that occurs in
renal colic (panel).1The mechanisms responsible for these
clinical features of visceral pain have been reviewed
p r e v i o u s l y .1 , 2
The fact that visceral pain cannot be evoked from all
viscera and that it is not always linked to visceral injury
h a s led to the notion that some viscera l ack afferent
innervation. We now know, however, that these features
are due to the functional properties of the peripheral
receptors of the nerves that innervate certain visceral
organs and to the fact that man y viscera are innervate d b y
receptors that do not evoke conscious perception and,
thus, are not sensory receptors in the strict sense. Visceral
pain tends to be diffuse because of the organisation
o f visceral nociceptive pathways in the central nervous
system, particularly the absence of a separate visceral
sensory pathway and the low proportion of visceral afferent
nerve fibres, compared with those of somatic origin (figure 1 ) .3
The nausea and diaphoresis that accompanies angina is an
example of autonomic responses provoked by visceral pain
that serve as a warning to the individual to “slow down”.
Transmission of visceral pain
In the past few years there hav e been new insights into the
neural mechanisms of the clinical features of visceral pain
that have challenged the established paradigm.
Traditionally, the two schools of thought among pain
researchers were: that the viscera are innervated by separate
classes of sensory receptors, some concerned with
autonomic regulation and some co ncerned with sensation,
including pain; or that internal organs are i nnervated by a
single and homogeneou s class of sensory receptors that at
low freq uencies of act ivation send n ormal regulatory signals
and at high frequencies of activ ation, induced by intense
stimuli, signal pain. The first theory extends the concept of
nociceptors used in descriptions of somatic pain to the
visceral domain.4However, our research and that of others
indicates that there are two distinct classes of nociceptive
sensory receptors that innervate internal organs.5The first
class of receptors have a high threshold to natural stimuli
(mostly mechanical). The encoding function—the relation
between stimu lus intensity and nerve a ctivity—of these
high-thresho ld rec eptors is ev oked en tirely by stimuli within
the noxious range. To date, high-threshold receptors have
been identified in the he art, vein, lung and airways,
oesophagus, bil iary system, sm all intestine, colon, ureter,
PAIN
Lancet 1999; 353: 2145–48
Departamento de Fisiología, Universidad de Alcalá, Alcalá de
Henares, E-28871 Madrid, Spain (F Cervero MD, J M A Laird PhD)
Correspondence to: Prof Fernando Cervero
(e-mail: ffcervero@fisfar.alcala.es)
Visceral pain
Fernando Cervero, Jennifer M A L a i r d
Pain
Visceral pain is the most common form of pain produced by disease and one of the most frequent reasons why patients
seek medical attention. Yet much of what we know about the mechanisms of pain derives from experimental s tudies of
somatic not visceral nociception. The conventional view is that visceral pain is simply a variant of somatic pain, a view
based on the belief that a single neurological mechanism is responsible for all pain. However, the more we learn about
the mechanisms of somatic and visceral pain, the more we realise that although these two processes have much in
common, they also have important differences. Although visceral pain is an important part of the normal sensory
repertoire of all human beings and a prominent s ymptom of many clinical conditions , not much clinical resea rch has
been done in this field and there are few clinical scientists with expertise in the management of visceral pain. Instead,
visceral pain is usually treated by a range of specialists who take quite different approaches to the management of this
type of pain. Thus, the management of visceral pain is frequently unsatisfactory. In this review, we consider visceral pain
as a separate form of pain and examine its distinct sensory properties from a clinical perspective. We describe recent
research findings that may change the way we think about visceral pain and, more importantly, may help develop new
procedures for its management.
Sensory characteristics of visceral pain and related
mechanism
Psychophysics Neurobiology
Not evoked from all viscera Not all viscera are innervated by
“sensory” receptors
Not linked to injury Functional properties of visceral
“sensory” afferents
Referred to body wall Viscerosomatic convergence in
central pain pathways
Diffuse and poorly localised Few “sensory” visceral afferents.
Extensive divergence in central
nervous system
Intense motor and autonomic Mainly a warning system, with a
reactions substantial capacity for amplification
