The International Association for Study of Pain (IASP) in 1994 defined pain as the subject’s conscious perception of modulated nociceptive impulses that generate an unpleasant sensory and emotional experience associated with actual damage or described in terms of such damage.
The experience of pain is usually a protective mechanism of the body. On a short-term basis, pain warns the individual that he or she is in danger so that one can alter the situation. For example when a person accidentally touches something hot he or she will alter the situation by spontaneously withdrawing from the source of injury. Long-term pain will result in immobilization of the affected part such that the individual can recover from the injury faster (for example, muscle spasm).
Pain at times can be non-beneficial, such as pain associated with cancer, psychogenic pains and neuralgias which only adds to the misery of the patient. However, interestingly these pains help the physician in diagnosis.
According to this law, exponential increase in the intensity of stimulus does not cause exponential increase in pain perceived. Though the pain perceived increases with increase in stimulus; the pain experienced is only in terms of log of the intensity of the stimulus.
For example, if a pin prick (1 unit of tissue damage) of 1 unit of intensity of stimulus results in 1 unit of pain perception; a musculocutaneous laceration (100 units of tissue damage) causing 100 units of intensity of stimulus results in 2 units of pain perception and not 100 units. Similarly, a crushing injury (1,000 units of tissue damage) causing 1,000 units of intensity of stimulus results in 3 units of pain perception and not 1,000 units.
As long as nociceptors (pain receptors) are stimulated, pain continues to be perceived as these receptors have very little or no property of adaptation. It is interesting to note that the inability to adapt to pain is beneficial in terms that a person is appraised of the injurious stimulus that causes pain as long as it persists.
Pain is poorly localized. It is said that superficial somatic pain is more localized than deep visceral pain. However this is not exactly true as the superficial injury not only excites the nociceptors but also the tactile receptors, thus helping in localizing the pain.
Pain receptors are called nociceptors (from Latin, nocere–to hurt). All nociceptors are free nerve endings (however other cutaneous receptors when stimulated excessively can result in pain). Either present in skin or any other tissues. They are more concentrated in superficial layers of skin, periosteum, arterial walls, joint surfaces, the falx and the tentorium of the cranial vault. Deep tissues are sparsely supplied with nociceptors.
|Aδ fiber||C fiber|
|1–6 μm diameter||1.5 μm diameter|
|5–30 m/s conduction velocity||0.5–2 m/s conduction velocity|
|Carries the first pain that is experienced–sharp||Carries steady dull pain|
Mechanical, chemical and thermal stimuli excite pain receptors. Fast pain is conducted by Aδ fibers which is elicited by the mechanical and thermal stimuli. The slow dull pain is conducted by the C fibers which are elicited by all three types of stimuli. It is almost always caused by release of chemicals liberated by the injured tissue. These are endogenous chemicals called algogenic (pain producing) substances. Algogenic substances stimulate nociceptors to produce pain.
It is interesting to note that commonly used NSAIDs suppresses pain by inhibiting prostaglandin synthesis. These prostaglandins by themselves cannot excite the nociceptors, i.e. prostaglandins are not algogenic but they enhance the sensitivity of the nociceptors toward the algogenic power of bradykinins and other chemical mediators of pain.
An uninhibited individual would react to acute pain by mourning and crying as seen in young children and animals. However, most individuals develop frustration, mental irritation or depression in response to long standing pain. A patient with long standing atypical facial pain will most often come to the physician with a frowning face and would often get irritated with prolonged history taking. Thus such patients should be treated both by medicines and psychological counseling.
Injury or disease causing pain results in spasm of skeletal muscle in the vicinity of the affected region. This is protective as it immobilizes the affected region and thereby puts it to forcible rest which is most essential for rapid healing. But this spasm also causes ischemia of the muscles which aggravates muscular pain.
Patients with internal derangement of temporomandibular joint (TMJ) usually exhibit spasm of the masticatory muscles of the affected side thereby preventing further damage to the affected TMJ. In such conditions apart from treating the affected site of injury, muscular spasms should be managed with physiotherapy, muscle relaxants, massage, etc.
Patients with somatic pain generally present with increased blood pressure, pupillary dilatation and tachycardia which are all the signs of sympathetic over activity. However visceral pain is associated with fall in blood pressure and vomiting.
For example, biting on a stone during mastication would immediately initiate a reflex action to keep the mouth open until an individual realizes the presence of the injurious agent (stone). Such reflex action would protect further injury to the periodontium.
Peripheral pain fibers are of two types, the fast conducting (Aδ fibers) and slow (C fibers) conducting. The fast pain is felt within 0.1 second of the application of the noxious stimulus. But it takes 1 second or more for slow pain to begin. Occasionally slow pain may take over a few minutes to begin after application of the noxious stimulus.
Though both fast and slow conducting fibers have free nerve endings as their receptors, they travel via two distinct pathways for transmitting pain signals to the central nervous system. Because of this dual pain pathway a single painful stimulus would often give a first sharp electrical pain that is generally followed by a slow dull pain. This ‘double’ pain sensation initially would cause an individual to react immediately to safeguard himself/herself. Whereas the slow pain tends to become increasingly painful over a period of time.
Sensations of mechanical and acute thermal pain are brought to the spinal cord by the first order neurons. They terminate in the lamina I (lamina marginalis) in the dorsal horns where they synapse to excite the second order neurons of the neospinothalamic tract. These fibers cross immediately to the opposite side through the anterior commissure and then travel upward in the anterolateral column of the spinal cord.
Few of these second order neurons terminate in the reticular areas of the brain stem (the reticular areas when stimulated causes excessive alertness and increases an individual’s sense perception), while most of the others travel up to the thalamus terminating in the ventrobasal complex along with the dorsal column–medial lemniscal tract. The remaining second order neurons terminate in the posterior nuclear group of the thalamus.
This pathway transmits pain, which is carried via the peripheral slow conducting C pain fibers (it also transmits very few Aδ fibers). These peripheral fibers terminate in the laminas I and II (together called substantia gelatinosa) of the dorsal horns. Most of the signals then pass through one or more additional short fiber neurons within the dorsal horns themselves before entering laminas V through VIII, also in the dorsal horn.
The next series of neurons gives rise to long axons that mostly join the fibers from the neospinothalamic tract, passing first through the anterior commissure to the opposite side of the spinal cord and then upward to the brain in the same pathway.
The electrical stimulation in the periaqueductal gray area or in the raphe magnus nucleus can almost completely suppress many strong pain signals entering the dorsal spinal roots. Stimulation of areas at still higher levels in the brain that in turn excite the periaqueductal gray can also suppress pain.
The fibers originating from the raphe magnus nucleus secrete serotonin at their nerve terminals. Finally these fibers terminate at the dorsal horns of the spinal cord. Serotonin (secreted by the fibers originating from the raphe magnus nucleus) causes the cord neurons to secrete enkephalins.
Enkephalin causes presynaptic inhibition and post synaptic inhibition of Aδ and C pain fibers at the site of synapse of the dorsal horns. This inhibition is caused by the blocking of calcium channels of nerve membrane at their terminals.
They hypothesized that pain perception was not just solely due to activation of nociceptors but due to interaction between pain conducting and non-pain conducting neurons. Non-pain conducting nerve fibers interfere with the pain conduction thus altering pain perception.
There have been various modifications of the original gate control theory. A revised version of the gate control hypothesis proposes that the projection neuron of the spinothalamic pathway when activated results in sensation of pain (Figure 2).
The projection neuron synapses with both non-nociceptive mechanoreceptors (Aα and Aβ fibers) and the nociceptive C fibers, hence activated by both. The interneuron is spontaneously active and this activation of interneuron causes inhibition of projection neuron; thus inhibiting pain perception.
In turn, the interneuron synapses with the projection neuron, C fibers, Aα and Aβ fibers. When the non-nociceptive mechanoreceptors (myelinated and fast conducting Aα and Aβ fibers) are stimulated they cause two effects: (i) activation of interneuron and (ii) activation of projection neuron.
When both non-nociceptive mechanoreceptors and nociceptors are simultaneously activated, the mechanoreceptors being myelinated fast conducting fibers, the signals from these fibers reach interneuron and projection neuron first before C fibers can conduct signals. In these instances the Aα and Aβ fibers stimulate the interneuron before C fibers can inhibit the same. Thus the net effect is no pain.
Studies indicate that the C fiber system responsible for itching may not be the same responsible for pain. Surprisingly tickling sensation in general is regarded as pleasurable whereas itching and pain are regarded as unpleasant sensations.
3. Usually if the referred pain is felt outside the nerve that mediates the pain, it is generally felt cephalad to the nerve (upward and toward the head) and not caudally. However in severe pain the excitatory effects are felt caudal to the site of initiating input.
Bell (1989) has classified orofacial pain as follows:
It is generally a physiologic response to an injury. It persists as long as the noxious stimulus is present. Acute pain almost always subsides within the time period required for the process of normal healing.
Merskey and Bogduk (1994) described chronic pain as a persistent pain that is not amenable, as a rule, to treatments based on specific remedies, or to the routine methods of pain control such as non-narcotic analgesics.
In common parlance chronic pain is regarded as pain that persists way beyond the normal time required for the process of normal healing. Pain is said to be chronic in nature when it lasts over 3 months. It is generally associated/ influenced by psychological, emotional, social and cultural factors.
The diagnosis and management of orofacial pain begins with a comprehensive patient history. The most expeditious way to obtain such a history is via a detailed patient questionnaire and detailed patient-physician interview.
Assessment of pain can be achieved by certain subjective and objective methods. Some widely accepted subjective methods include the use of McGill Pain Questionnaire (long/ short), visual analog pain scale (VAS), brief pain inventory. The faces pain scale and the pain diagram.
During the patient interview the clinician should obtain the following data: mode of onset, duration, location of the pain, quality or character of the pain, intensity of the pain, frequency of the painful episodes, aggravating and relieving factors if any, radiation or referral patterns, any other associated symptoms and history of any medical consultations/use of medications for the same.
The pain quality or character can be expressed using the widely accepted McGill Pain Questionnaire (Figure 4). This questionnaire will help the patient to describe how exactly he/she feels about the pain by selecting an appropriate adjective from a list in the questionnaire.
The intensity of pain can be quantified using the visual analog scale (VAS). The VAS is a 10 cm long line with 0 marked on one end (represents no pain) and 10 at the other end (represents worst possible pain). The linear scale has markings from 0 to 10 at 1 cm intervals. The patient is encouraged to mark a point along this scale that correlates with the intensity of pain experienced. For convenience pain intensity can be categorized as mild (score 1–1), moderate (score 4–4) and severe for scores 7–7 (Figure 5).
Figure 6 Faces pain scale. Score the chosen face 0, 2, 4, 6, 8 or 10, counting left to right, so ‘0’ = ‘no pain’ and ‘10’ = ‘very much pain’. Do not use words like ‘happy’ and ‘sad’. This scale is intended to measure how children feel inside, not how their face looks. From PAIN, 2001, 93, 173–173 ‘The Faces Pain Scale-Revised: toward a Common Metric in Pediatric Pain Measurement’, by CL Hicks, CL von Baeyer, PA Spafford, I van Korlaar and B Goodenough. Reprinted with permission of the International Association for the study of Pain®.
Following the history, physical examination should be undertaken. A thorough physical examination of the head and neck, including the TMJ, maxillary sinus, masticatory muscles along with the accessory muscles, salivary glands and the oral cavity should be performed.