Introduction

Pain is probably the most fundamental and primitive sensation. It is distributed

more or less all over the body. It is protective in nature and always indicates some
serious trouble in the locality, such as a structural damage or a serious functional or
metabolic derangement.

Definition
It is difficult to define pain, as the feeling is purely subjective. It may be
succinctly described as ‘what the patient says it hurts’. Dorland’s Medical Dictionary
(1974) defined pain as ‘more or less localised sensation of discomfort, distress or
agony resulting from the stimulation of specialised nerve endings’. Fields (1987)
defined pain as ‘an unpleasant sensation that is perceived as arising from a specific
region of the body and is commonly produced by processes which damage or are
capable of damaging bodily tissue’. In other words, pain is a somatopsychic
phenomenon.
The definition proposed by the Subcommittee on Taxonomy (1986) of the
International Association for the Study of Pain (IASP) is that ‘pain is an unpleasant
sensory and emotional experience associated with actual or potential tissue damage or
described in terms of such damage’. Added to this definition is a note to emphasise
the subjective nature of pain that distinguishes and separates it from a simple
stimulation of nociceptors.

Types of pain
Many researchers have tried to classify different types of pain, and have
observed various varieties.

Clinical vs. Experimental pain

Beecher (1956) has pointed out that pain as presented by patients, so-called
clinical or pathological pain is different from experimental pain induced and studied

The Physiology of pain 1

in the laboratory. The difference is illustrated in the capacity of morphine to give
relief. Large doses of morphine does not significantly alter the brief jabs of
experimental pain, whereas a much smaller dose consistently reduces pain that has a
meaning to the patient.

Acute vs. Chronic pain

As the duration of pain input continues, the level of suffering increases even
though the intensity of input remains the same. In fact, a protracted input may sustain
a high level of input although the intensity of stimulus decreases or disappears
altogether. Pain becomes complicated and difficult to manage when it is prolonged. In
chronic pain, it is common to see a wide discrepancy between the identifiable
nociceptor source, and the amount of suffering and disability.

Somatic pain vs. Neurogenic pain

Pain emanating from a particular area may result from noxious stimulation of
the somatic structure, the nociceptive receptors, being received and transmitted by
normal components of the sensory nervous system. Such pain is referred to as
‘somatic pain’. Quite a different type of pain may emanate from the same area not due
to abnormality in the structures that comprise that area, but due to the abnormality in
the neural component that innervate the area. Such pain is known as ‘neurogenous
pain’.

Superficial pain vs. Deep somatic pain

Pain emanating from the cutaneous or mucosal tissues present clinical
characteristics that are similar to the other exteroceptive sensations. They are
precisely localisable and relate faithfully to provocation in timing, location and
intensity. In contrast, pain due to stimulation of deeper somatic and visceral structures
resemble other proprioceptive and interoceptive sensations. They are more diffusely
felt and are less responsive to provocation, and frequently initiate secondary effects
such as referred pain and muscle spasm activity.

Primary and secondary pain

If the pain emanates from the structures that hurt, it constitutes a primary
nociceptive input. If the true source of pain is located elsewhere, and the heterotropic

The Physiology of pain 2

referred pain (secondary hyperalgesia) is felt in otherwise normal structures, the area
of discomfort represents secondary pain.

Musculoskeletal vs. Visceral pain

Pain that emanates from muscles, bones, joints, tendons, ligaments and soft
connective tissue bears a close relationship to the demands of biomechanical function.
Such pain also yields a graduated response to noxious stimulation. Visceral structures,
however, are innervated by high threshold receptors so that pain is usually not felt
until threshold level is reached. Such pains therefore do not ordinarily yield a
graduated response to noxious stimulation and are not responsive to biomechanical
function.

Inflammatory pain vs. Non-inflammatory pain

Tissue injury and healing are attended by an inflammatory reaction that
includes pain. Such pain relates to the location, type and phase of inflammatory
process that prevails. Inflammatory pains therefore display a clinical timeframe that
relates to the inflammatory curve, and symptoms that relate to the confinement of
inflammatory exudate. Non-inflammatory pains do not display this type of behaviour.

Spontaneous pain vs. Stimulus evoked pain

Most primary somatic pains result from stimulation of neural structures that
innervate the site. Some pains occur spontaneously and do not require a stimulating
force. Neurogenous pain may be felt spontaneously along the peripheral distribution
of the affected nerve, while referred pains may occur spontaneously as far as the site
of pain is concerned.

Sensory reception
Pain is essentially an abnormal affective state that is aroused by the
pathological activity of a specific sensory system. Though it has proved difficult to
investigate, it is known that it is subserved by its own network of nerve fibres.
Morphological structures of the end organs subserving pain sensations are not clear.
Naked nerve endings are presumably the sense organs of pain, and are distributed all
over the body.

The Physiology of pain 3

 There are evidences suggesting that the pain receptors are modality-specific.
Pain is not produced by overstimulation of other receptors. Possibly there are specific
receptors for subserving pain sensation by specific pain stimulus, i.e. some respond to
thermal, others to mechanical and still others to chemical stimulation.

Physical stimulus
Pain is produced in the skin by many kinds of physical stimuli – thermal,
mechanical or electrical – which have the common property of being potentially or
actually harmful. The pain accompanying protective reflexes and voluntary responses
minimise the amount of damage inflicted by the noxious stimulus e.g. raising skin
temperature to 45˚C or more, exposure to cold at 0˚C, excessive pressure or tension
on the surface of the body etc.

Transmission of impulses
Pain sensations are transmitted by two types of fibres – slow fibres and fast
fibres. The slow fibres are unmyelinated dorsal root C (d.r.C) fibres having a slow
rate of conduction (0.5 – 2 m/sec) and a diameter of 0.4 to 1.2
the small myelinated A- –
velocity of 12 – 30 m/sec. According to the presence of separate types of pain fibres
and also of different conduction velocity, pain ahs been classified into two – slow and
fast.
The cell bodies of both fibre groups lie in the dorsal root ganglia of the spinal
cord; A-
dorsal root C-fibres terminate on neurons in laminas I and II. In the case of cranial
nerves, the fibres end in their respective sensory ganglia.

Neurochemical effects
The biochemical basis of nociception is becoming better understood. The
presence of a specific chemosensory pain mechanism in the human skin was
described by Dash et al (1971). Several chemicals play important role in the neural
mechanism of pain. Some of these act principally as algogenic (pain producing)
agents, some act centrally as neurotransmitters and some act in both capacities.

The Physiology of pain 4

 1. Prostaglandins
These are a group of organic acids chemically related to long-chain hydroxy-
fatty acids. There are six types, each designated by a suffix letter. Subscript numerals
indicate the degree of saturation of the side chain. Prostaglandin E2 occurs in
conjugation with inflammatory process. They sensitise the nociceptor nerve endings
to different types of stimuli, thus lowering their pain threshold to all kinds of
stimulations. Prostaglandins are required for bradykinin to act. Bradykinin, in turn,
stimulates the release of prostaglandins. There is evidence that prostaglandin-like
substances are produced in the CNS during an inflammatory reaction that produces
hyperalgesia.

2. Bradykinin
This is an endogenous polypeptide released as a part of an inflammatory
reaction. It is a powerful vasodilator and increases capillary permeability. It sensitises
some high threshold receptors so that they respond to innocuous stimuli, such as that
occurs during normal activities. It requires the presence of prostaglandins to act.

3. Serotonin

Serotonin is a monoamine released by blood platelets. It is synthesised in the

CNS and released when the brainstem is stimulated by sensory input. Peripherally,
serotonin is an algogenic agent and relates specially to vascular pain syndromes. In
the CNS, it is an important element in the endogenous anti-nociceptive mechanism.
The activation of serotoninergic pathways in the brainstem by tricyclic
antidepressants yields paralysing analgesic effect along with action in depressive
states.
4. Substance P

The substance P is a polypeptide composed of 11 amino acid residues. It is

released at the central terminals of primary nociceptive neurons and act as a transport
system, being found in distal terminals as well. Centrally, it acts as an excitatory
neurotransmitter for nociceptive impulses. It is released from spinal cord cells by

The Physiology of pain 5

stimulation of A-
are activated by noxious stimuli. Its modulating action in pain is rapid and short-lived.
5. Histamine

Histamine is a vasoactive amine that derives from the amino acid histidine. It
is a vasodilator and increases the permeability of all vessels. It has been postulated
that it also serves as a CNS neurotransmitter.
6. Other agents

A number of other substances are said to be algogenic. These include

potassium and acetylcholine as well as a variety of extraneous toxic substances.
Extrinsic algogenic substances are strong irritants which induce pain when applied to
skin and mucous membrane or when injected into the body e. g. strong acids, alkalies,
organic solvents, certain drugs (thiopentone).

The Physiology of pain 6

Pain pathways
Pain sensation from the face and the mouth is mediated centrally by way of the
afferent primary neurons that pass through the posterior roots of the fifth (trigeminal),
seventh (facial), ninth (glossopharyngeal) and tenth (vagus) cranial nerves and the
first, second and third cervical spinal nerves. To some extent, it is also by way of
visceral afferents that descend through the cervical sympathetic chain to pass through
the posterior roots of the upper thoracic spinal nerves.
All the pain fibres of the maxillofacial region terminate in the nucleus
caudalis, which is the lower caudal portion of the massive trigeminal spinal tract
nucleus. The initial synapses occur in the substantia gelatinosa of the nucleus
caudalis, where the secondary medullary (second-order) neurons begin and
considerable convergence takes place.
The secondary medullary trigeminal neuronal fibres project to the thalamus,
approximately half crossing the midline before they do so. In the thalamus, they
terminate in several nuclei and synapse occurs with third order neurons. The tertiary
neurons, after greater convergence, project to the cerebral cortex. (See Plate I)

Primary pathways
When the fibres from the sensory root of the trigeminal nerves enter the brain,
they pass through three sensory nuclei – the mesencephalic nucleus (uppermost), the
principal nucleus and the spinal nucleus (lowest), the latter two being continuous with
each other.
The mesencephalic nucleus receives fibres carrying proprioceptive impulses
from the muscles of mastication, the tongue, the orbital muscles and the periodontal
membrane. Many fibres from all the branches dichotomise to form ascending and
descending branches. The former goes to the principal nucleus carrying impulses
mediating touch and pressure. The descending branch also carries impulses mediating
touch and pressure, and runs with fibres that have not dichotomised, some of which
carry impulses mediating pain and temperature. Together, they form a distinct bundle
called the spinal tract of the trigeminal nerve, which extends to the lower end of the
medulla oblongata. Fibres from all three segments descend as far as the 2nd and 3rd
cervical segments. As they descend, the fibres pass to the spinal nucleus which lies

The Physiology of pain 7

medially. The fibres mediating touch and pressure terminate in the upper part of the
nucleus.
In the spinal tract, nerve fibres derived from the mandibular division runs
postero-medially, those from ophthalmic division run laterally and the maxillary
division fibres lie in between. This arrangement is constant, and allows for selective
cutting in patients of facial neuralgias. The fibres of the middle part of the face
terminate at the highest levels. This ‘onion peel’ distribution of innervation applies to
all three divisions of the trigeminal nerve.
The spinal nucleus is further divided into three zones
a. The nucleus oralis (uppermost – rostrally)
b. The nucleus interpolaris (intermediate)
c. The nucleus caudalis (lowest-caudally)
The nucleus caudalis is the most significant for the arrival of impulses
mediating pain. In general, the larger nerve fibres of the trigeminal nerve go to the
principal sensory nucleus and the nucleus oralis, the smaller fibres going to the
nucleus caudalis. This seems to apply also to the fibres of the dental polyp.
In the nucleus caudalis, the fibres end in the substantia gelatinosa and in the
more superficial marginal layer. The marginal layer contains projection neurons. The
substantia gelatinosa contains two kinds of interneurons, one of which is excitatory
and the other inhibitory. Thus, the morphology is similar to that of the dorsal horn of
spinal cord. Although it is known that the principal nucleus is homologous with dorsal
column nuclei, and the nucleus caudalis with the spinal cord dorsal horn, the
functional position of nucleus oralis and interpolaris have not been established.

Secondary pathways
The second order neurons of the trigeminal system form three different
pathways that ascend in the brain. Fibres from the principal sensory nucleus form the
trigeminal leminiscus which crosses the midline to travel with the medial leminiscus,
which has already crossed at a lower level. Together they go to the thalamus and end
somatotopically in the ventro-posterior position.
The other two secondary pathways take origin in the spinal trigeminal nucleus.
One of them, the neospinothalamic tract is assumed to arise from the cells which
receive the descending branches of the dichotomised primary trigeminal axons. The

The Physiology of pain 8

cells of origin of this tract receive mechanoreceptive information and also thermal and
pricking pain receptors.
The third secondary pathway from the spinal trigeminal nucleus arises from
cells whose input consists of small myelinated and non-myelinated fibres in the
trigeminal nerve coming from high threshold mechanoreceptors and thermoreception.
Their output is either to the lateral reticular formation or deeper to the medial reticular
formation, which in turn, transmits to the intralaminar nuclei of the thalamus.

Tertiary pathways
Neural impulses mediating touch and pressure are conveyed from the thalamus
via the posterior limb of the internal capsule, where they occupy a very compact area,
to the post-central gyrus of the cerebral cortex.

Representation at the cortex

The structures of the mouth and the face, including teeth, are represented at
the cortex for touch and pressure in the post-central gyrus, the primary somatic area.
The representation of the face is not inverted as often supposed.

The Physiology of pain 9

 Theories of pain
It has been suggested that pain occurs only when the rate of tissue damage is
sufficiently rapid, the damage being done particularly to the pain nerve endings.
However, traumatically caused pain is usually very rapid but does not necessarily
evoke pain, at least some considerable time afterwards.
Various theories have been put forward on how nerve impulses can give rise
to sensation of pain. There is not yet a generally accepted theory.

Intensity theory
According to this view, pain is produced when any sensory nerve is stimulated
beyond a certain level. This is true of nerves mediating the sensation of touch when
stimulated to excessive degree. In other words, pain is supposed to be non-specific
sensation, and depends only on high intensity stimulation. Thus application of heat is
pleasant, but excessive heat causes burning.
The theory does not take into account that the more intense thermal stimulus
excites additional high threshold fibres. Another example against this theory is the
case of trigeminal neuralgia, where the patient suffers excruciating pain from a
stimulus no greater than a gentle touch applied to the trigger zone.
Although the theory is not accepted, it remains true that the intensity in
stimulation is a factor in causing pain.

Specificity theory
This theory states that pain is a specific modality equivalent to vision and
hearing, just as there are Meissner’s corpuscles for the sensation of touch, Ruffini’s
end organs for the sensation of warmth etc. Associated with the peripheral pain
receptors, there are pain nerves and even a specific central apparatus, the pain centre,
in the thalamus.
The nerves concerned are small fibres of the A-
into the spinal cord, many going to the spinothalamic tract, and then conveyed to the
thalamus. In terms of this theory, there is a direct line from the receptor to the brain,
and the requisite stimulus at the receptor is necessarily followed by pain sensation.
Specialisation is known to exist in the nervous system, and there are well
known tracts in the CNS. It is accepted that C-fibres convey impulses mediating pain.
The Physiology of pain 10
But some C fibres respond to mechanical stimuli of only a few mgs of skin pressure
which does not cause pain i.e. they are not specific for nociceptive stimuli. Further,
this theory fails to explain why a person who has suffered injury during an exciting
game fails to appreciate the pain immediately.
The concept of a pain centre in the brain is incorrect (Melzack and Wall–1968,
Zimmermann-1979). Surgical disruption of nerves (trigeminal tractotomy) may fail to
abolish pain. This is because the direct line implied by this theory is bypassed and
pain may be conveyed to the higher centres through the reticular activating system.
Finally, even the concept of specific nerve endings is no longer tenable. No cutaneous
receptor has absolute specificity though they have a high degree of selective
sensitivity.

Protopathic and epicritic theory

Head and Rowers (1908) postulated the existence of two groups of cutaneous
sensory nerves extending from the periphery to the CNS, the protopathic and epicritic
systems. The protopathic system is primitive, yielding diffuse impressions of pain,
including extremes of temperature and is ungraded. The epicritic system is concerned
with touch, discrimination and small changes in temperature and is phylogenetically a
more recent acquisition.
While pointing out the difficulties of the theory, Sinclaire (1967) argued that
the perceived distinction between these ‘systems’ could be attributable to the
spinothamic and lemniscal systems. Marnford and Bowsher (1976) felt it useful to
retain the term ‘protopathic’ for the ill-defined sensory experiences evoked by the
activation of small primary afferent fibres in the absence of activity in the A-
C groups.

Pattern theory
Essentially this theory is that pain sensation depends upon the spacio-temporal
pattern of nerve impulses reaching the brain. According to Weddell (1962), warmth,
cold and pain are words used to describe reproducible spacio-temporal patterns or
codes of neural activity evoked from the skin by changes in its environment.
One form of this theory is based on the view that all or nearly all receptors are
essentially non-specialised. But their qualities are important, including the thresholds
of excitation, adaptation rates, response changes and the distribution of branches of

The Physiology of pain 11

nerve fibres. These qualities differ considerably – some are sensitive to heat, some to
pressure - and they have different adaptation rates and different stimulus strength-
response curves, different sizes and shapes of receptor fields etc. Weddell (1966) did
not completely deny the specificity theory. However, he stresses the danger of
correlating the evocation of a particular sensation with the activity produced in the
cutaneous nerve fibres by stimuli having specific physical attributes.

Gate Control theory

The Gate control theory was proposed by Melzack and Wall in 1965 and
subsequently expanded by Casey and Melzack.
According to them, pain is not due to neural activity that resides exclusively in
those pathways traditionally considered specific for pain but rather it is the result of
activity in several interacting neural systems each with its own specialised function.
In the spinal cord impulses evoked by peripheral stimulation are transmitted to three
systems.
1) The cells in the substantia gelatinosa
2) The dorsal column fibers that project toward the brain.
3) The first central transmission (T) cells in the dorsal horn.
The substantia gelatinosa function as a gate-control system that modulates
(facilitates or inhibits) the efferent patterns before they influence the T cells. The
afferent pattern in the dorsal column system act, in part at least, as a central control
trigger that activates selective brain processes to influence the modulating properties
of the gate-control system.
The T cells activate the neural mechanism comprising the action system
responsible for perception of a response to pain. The signal that triggers the action
system occurs when the output of the T cells reaches or exceeds the critical level. This
critical level of firing is determined by the afferent barrage that impinges on the T
cells and has already undergone modulation by substantia gelatinosa activity. This is
determined by a relative balance of activity between large and small peripheral fibres.
According to Melzack and Wall, the dorsal column and dorsolateral projection
pathways act as a central control trigger. They carry precise information about the
nature and location of the stimulus and conduct so rapidly that they may not only set
the receptivity of cortical neurons for subsequent afferent volleys but may by way of

The Physiology of pain 12

descending fibres influence the sensory input at the gate-control system and various
other levels. This rapid transmission makes it possible for the brain to identify,
evaluate, localise and selectively modulate the sensory input before the action system
is activated.
There is general agreement that the large cutaneous A fibres are effective in
inhibiting spinal sensory input from both large and small diameter cutaneous fibres.
Casey and Melzack have expanded the theory by taking into account more
recent physiologic and behavioural studies the further emphasise the motivational
affective and cognitive aspects of the pain experience. These pertain to neural
systems beyond the gauge and involve interaction of the neospinothalamic and
paleospinothalamic projecting systems and neocortical processes. All three forms of
activity influence motor mechanisms responsible for the complex pattern of evert
responses that characterise pain.
Despite its deficiencies the Melzack-Wall-Casey model of pain has proved to
be one of the most important development in this field. It is the most comprehensive
formulation of pain that might provide a theoretical basis for some of the pathologic
states.

The Physiology of pain 13

 Pain perception
Pain perception depends not only on the integrity of the peripheral and central
nervous pathways but also on the peripheral pain receptors and the patient's own
psyche. Ethnic and cultural factors may influence a person’s reaction to pain and may
colour the description of it. The general health, tiredness or nutritional status a person
may also have profound effect on how a person reacts to discomfort.
Everyone has experienced the phenomenon that when the mind is fully
occupied with other things, such pains are tolerable but for example in the long
reaches of the night when the mind is free to dwell on a pain it may become
intolerable. All of these matters must be kept in mind when a pain history is being
taken and this highly personal reaction often makes a diagnosis very difficult. Facial
pain is felt to be more severe and produces longer reactions because it seem a more
intimate part of one's personality, whereas the pain felt in the finger can be viewed
more objectively.
Factors which are capable of lowering the pain threshold include discomfort,
insomnia, fatigue, anxiety, fear, anger, sadness, depression, boredom, mental
isolation, social abandonment etc. At the same time, some factors would serve to raise
the threshold. They are relief of other symptoms, sleep, sympathy, understanding,
companionship, creative activity, relaxation, reduction in anxiety, elevation of mood
and drugs like analgesics, anxiolytics and antidepressants.

The Physiology of pain 14

Localisation of pain
Localisation of the source of pain is one of the most important aids to
diagnosis of disease. It is accurately localised in the skin and mucosa, but the
accuracy is lost as the source of pain sinks deep into the body. It may be said that pain
is localised primarily to the segments corresponding to the stimulated nerves and that
accuracy is superimposed on this segmental pattern. In the skin, the accuracy of
localisation of pain appears to be based on the richness of its innervation, the multiple
innervation of pain spots and on the associated nervous mechanism for accurate
localisation of touch. In deeper structures, innervation is much sparser and there is no
other sensory mode to aid in localisation of pain. In these circumstances, pain may be
felt on any part of one affected segment. Localisation of pain is believed to be a
function of cerebral cortex.
Referred pain from deep structures is that pain which occurs in addition to or
in the absence of true visceral or deep somatic pain. It is felt at a site other than that of
stimulation, in deep or superficial structures supplied by the same or adjacent neural
segments. The pain is most frequently referred to other parts of the same segment but
it may spread to adjacent segments. Pain is more commonly referred to the anterior
than to the posterior half of the body e.g. angina pectoris, peptic ulcer etc.

The Physiology of pain 15

 Methods of assessing pain
Since pain is a subjective experience that is communicated only through words
and behaviours, it is extremely difficult to measure pain. There are several
physiological and psychological factors that will influence the intensity of pain
perceived. Measuring pain is important for studying pain mechanisms in the
laboratory, and to assess treatment outcome. A number of instruments have been
developed and tested for their reliability and validity in measuring different aspects of
the pain experience.

Quantifying the pain experience

Visual analogue scale

A visual analogue scale is that represents a continuum of a particular
experience such as pain. The most common form used for assessing pain is a 10cm
line, either horizontal or vertical, with perpendicular stops at the ends. The ends are
anchored by labels ‘no pain’ and ‘worst imaginable pain’. Numbers should not be
used along the line to ensure a better, less biased distribution of pain ratings. Patients
are asked to place a slash mark somewhere along the line to indicate the intensity of
their current pain complaint. For scoring purposes, a millimetre ruler is used to
measure along the line and obtain a numerical score for the pain ratings.

McGill Pain Questionnaire

The McGill pain questionnaire is a verbal pain scale that uses a vast array of
words commonly used to describe a pain experience. Different types of pain, different
diseases and disorders, have different qualities of pain. Melzack and Torgerson (1971)
categorised the verbal descriptors into classes and subclasses designed to describe
different aspects of the pain experience. In addition, ‘affective descriptors’ such as
fear and anxiety and evaluative words describing the overall intensity of pain, were
included.
The words are listed in 20 different categories. They are arranged in order of
magnitude from less intense to most intense, and are grouped according to distinctly
different qualities of pain. The patient is asked to circle only one word in each
category that applies to them.

The Physiology of pain 16

 Melzack uses this master-list of words to derive quantitative measures of
clinical pain that can be treated statistically. It can also detect changes in pain with
different treatment modalities.

Psychological assessment
Chronic pain is the most complicated of pain experiences. Determining the
emotional, behavioural and environmental factors that perpetuate chronic pain is as
essential as establishing the correct physical diagnosis. Traditionally, the systematic
assessment of psychosocial difficulties is achieved through a psychological interview
and a battery of psychological tests. The tests designed to assess psychopathology
include the Minnesota Multiphasic Personality Inventory (MMPI), the Beck
Depression Inventory, and Symptom checklist-90.
The instruments that could be used by the clinician to evaluate the chronic
pain patient in a routine clinical setting include the Beck Depression Inventory (BDI -
1978) and the Chronic Illness Problem Inventory (CIPI -1984). These consist of
questionnaires which are easily administered, self-report and problem-oriented.

The Physiology of pain 17

 Diagnosis of orofacial pain
Every pain has its distinct and pregnant significance if one searches carefully
for it. The diagnosis of orofacial pain may prove to be one of the most challenging
and frustrating problems faced by the dental practitioner. The various organ that lie
within the face, coupled with the great variety of diseases to which they may succumb
account for many different types of facial pain. The extreme richness of the nerve
supply of the area, perhaps the richest sensory innervation of any part of the body,
also accounts for the many subtleties of pain that may be experienced in the face. Pain
may arise from the teeth, the periodontium, the jaws, joints, muscles, ligaments, nasal
cavity and accessory sinuses, eyes, ears and blood vessels. In some cases, what
presents as odontogenic pain may be the first significance of a life threatening disease.
Pain arising from disease within the cranial cavity may also be experienced in the
face, as may be referred pain from such remote sites as the heart. Cardiac effort pain
(angina pectoris) may occasionally be experienced predominantly in the neck or jaw.
It is now well recognised that pain in the face may also be associated with psychiatric
disorders such as depression.

CLASSIFICATION OF OROFACIAL PAIN SYNDROMES

I. Based on the anatomical location where pain is felt.
1. Head and neck pain - headache
- orofacial pains
- cervical pains
2. Thoracic pain
3. Abdominal
4. Extremity pain
II. Orofacial pains are classified regionally as:
1. Cutaneous and mucogingival pains.
2. Mucosal pains of the pharynx, nose and PNS.
3. Pains of dental origin.
4. Pains of the musculoskeletal structures of the mouth and face.
5. Pains of the visceral structures of the mouth and face.
6. Pains of the neural structures of the mouth and face.

The Physiology of pain 18

 7. Chronic face pain syndromes.
Pain syndromes about the mouth and face may be divided by their clinical
characteristics into three categories.
1. Somatic pain: results from noxious stimulation of normal neural structures that
innervate body tissues.
2. Neurogenous pain: is generated within the nervous system itself and is caused
by abnormality of the neural structures that innervate body tissues.
3. Psychogenic pain: results neither from noxious stimulation nor from neural
abnormality but from psychic causes.

The Physiology of pain 19

 Management of Patients in Pain

Treatment modalities
1) Cause-related therapy: consists of identification and elimination of aetiologic
factors.
2) Sensory stimulation: This is utilising the pain inhibitory affects of stimulating
certain afferent neurons.
(a) cutaneous
(b) transcutaneous
(c) percutaneous nerve stimulation.
3) Analgesic blocking: This is the use of local anaesthesia to
(a) arrest pain input
(b) interrupt cycling
(c) resolve myofascial trigger point activity
(d) induce sympathetic blockade
4) Physiotherapy: This includes cutaneous, and deep massage, exercises, deep
heat therapy, trigger point therapy, physical activity to increase "up-time".
5) Relaxation training: This includes autosedation, biofeedback training and
occlusal disengagement.
6) Placebo therapy
7) Psychotherapy: This includes counselling, hypnotherapy, and contingency
management and formal psychotherapy.
8) Neurosurgery: includes procedures as:
(a) peripheral therapy
(b) gangliolysis, rhizotomy and decompression
(c) trigeminal tractotomy.
9) Medicinal therapy: which includes
(a) analgesics
(b) anti-inflammatory agents
(c) analgesic balms
(d) antibiotics.
(e) antiherpes agents

The Physiology of pain 20

 (f) local anaesthetics
(g) anticonvulsants
(h) neuroactive drugs
(i) tranquillisers and muscle relaxants
(j) antidepressants
(k) vasoactive agents.
10) Dietary supplements
Pain management as far as somatic pain is concerned applies only to primary
sources. Heterotopic pain whether spontaneous referred pain or evoked secondary
hyperalgesia can't be treated directly. Only through identification and treatment of the
primary source can such pain be managed.

The Physiology of pain 21

 Methods to prevent pain in surgical patients
General anaesthesia
General anaesthesia is a controlled state of unconsciousness accompanied by a
partial or complete loss of protective reflexes, including the ability to maintain a
patent airway and respond purposefully to physical stimulation or verbal command,
produced by a pharmacological method, or a combination thereof. After adequate
premedication (sedatives, anxiolytics etc.) and pre-oxygenation (100% oxygen for 3
to 5 minutes), a short acting sedative is administered intravenously. An endotracheal
tube is inserted through oral or nasal cavity. Anaesthetic gases like N2O, halothane etc
can be administered through the tube to maintain the anaesthesia.

Sedation
Sedation is depressed level of consciousness which may vary from light to
deep.
Conscious sedation
Conscious sedation is a minimally depressed level of consciousness that
retains the patient’s ability to independently and continuously maintain the airway and
to respond appropriately to physical stimulation and verbal command at any time,
produced by a pharmacologic or non-pharmacologic method or a combination thereof.
The loss of consciousness should be unlikely and the drugs and techniques used
should carry a safety wide enough to render the unintended loss of consciousness
unlikely.
Common drugs used include diazepam, midazolam, pentobarbital etc. These
may be used with or without N2O –O2 supplementation.
Deep sedation
A controlled state of depressed consciousness or unconsciousness from which
the patient is not easily aroused, which may be accompanied by a partial or complete
loss of protective reflexes including the inability to independently maintain a patent
airway and respond purposefully to physical stimulation or verbal command,
produced by a pharmacologic or non-pharmacologic method or a combination thereof.

The Physiology of pain 22

 The combination of intravenous midazolam, fentanyl, N2O –O2, and small
increments of methohexital are widely used for deep sedation. Intramuscular ketamine
produces excellent deep sedation for approximately 30 minutes.

Local anaesthesia
Local anaesthesia is the use of a potent drug to produce temporary loss of all
modalities of sensation in a limited region of the body. Local analgesia is the loss of
sensation of pain. This can be achieved by surface application or infiltration and
regional injection of drugs. A local anaesthetic drug is placed near the sensory nerves
so as to temporarily prevent the conduction of pain impulses to the brain.
Surface analgesia may be achieved by topical application of the analgesic
drugs, the main methods of application being pastes, solutions, sprays, jet injectors,
lozenges and mouthwashes. The injectable local anaesthetics are used either as an
infiltration or as a regional block.

Acupuncture analgesia
Acupuncture analgesia is thought to have originated in China about 3000 or
more years ago. It makes use of acupuncture needles inserted at various sites on the
body based on the ancient meridian theory. The needles are twirled at 100-200
cycles/min, or instead stimulated by an electrical acupuncture machine which uses a
-3000 cycles/minutes. The
mechanism of action is believed to be the excitation of A-
production of endorphins.

Hypnotism
Hypnotism induces a trance-like state in which the patient’s attention is
focussed on the operator so that awareness of other stimuli such as pain is markedly
reduced, or not felt at all. This is method is of use only in susceptible and co-operative
patients. Also, it may initially be time-consuming.

Audio-analgesia
Described by Gardner and Licklider (1959), this method uses loud sounds to
produce insensitivity to pain in some patients. The patient wears stereophonic
earphones and controls the volume and type of sound. He increases the volume of

The Physiology of pain 23

sound when the pain becomes uncomfortable. The explanations to the success of this
method are relaxation, need for concentration, stimulation of other sensory tracts etc.

Electric anaesthesia (anelectrotonus)

In 1950, Suzuki described a method of blocking nerve conduction in the
peripheral part of the pain pathway by use of a direct electric current. The
physiological basis of this is that a pain impulse is accompanied by a negative
potential, and depolarisation of the nerve fibre is prevented by introducing as positive
potential due to a direct electrical current. The best results with this technique are
obtained in children less than 10 years of age.

Anaesthesia by cold air

When a part of the body becomes sufficiently cold, pain sensation is abolished
due to the inability of nerve fibres to conduct action potentials at low temperatures.
This principle of lowering the temperature of the tissues to achieve anaesthesia is used
in clinical situation by spraying on a volatile material such as ethyl chloride. As it
evaporates, it removes heat from the tissues due to its latent heat of evaporation, and
thus chills them.

Conclusion
A surgeon should be aware of the physiologic and psychological aspects of
pain and anxiety as it applies to the patient. There is a vast array of diseases that
manifest with painful symptoms clinically. Adequate clinical assessment and
diagnosis are the keys to successfully manage such conditions.
Pain caused by surgical procedures is an anathema to the patients. The surgeon
should be aware of the different methods to alleviate the sufferings of the patient and
should apply them to situations as necessary.

The Physiology of pain 24

 References

1. Samson Wright’s Applied Physiology.

2. Local analgesia in dentistry. 3rd edition. DH Roberts and JH Sowray. 1987.
3. Miller’s Anaesthesia Vol. I
4. Monheim’s Local Anaesthesia and Pain Control in Dental Practice.
5. Review of medical physiology. 14th edition. WF Ganong. 1989.
6. Orofacial pain –classification, diagnosis and management – Welden E Bell
7. Dental pain. Dental Clinics of North America. October 1987.
8. Differential diagnosis and management of craniofacial pain. B Jaeger. In
Endodontics. 4th edition. JI Ingle, LK Bakland (ed)
9. Management of Pain and Anxiety. J Weaver. In Principles of Oral and
Maxillofacial Surgery (ed) LJ Peterson, RD Marciani. AT Indresano. 1997.
10. Office anaesthesia evaluation manual. 3rd edition. American Association of
Oral and Maxillofacial Surgeons. 1986.
11. Burcket’s Oral Medicine: diagnosis and treatment. 9th edition. (eds) MA
Lynch, VJ Brightman, MS Greenberg. 1994.

The Physiology of pain 25