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.
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 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 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.
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.
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.
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 mm. The fast fibres are the small myelinated A-d fibres having a diameter of 2–5 mm, and a conduction 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-d fibres terminate primarily on neurons in laminas I and V, whereas the 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.
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.
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.
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.
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 stimulation of A- and C afferent fibres, and excites neurons in the dorsal horns that are activated by noxious stimuli. Its modulating action in pain is rapid and short-lived.
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).
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)
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 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
- The nucleus oralis (uppermost – rostrally)
- The nucleus interpolaris (intermediate)
- 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.
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 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.
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.
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.
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.
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-d and C groups which pass 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. 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-d and C groups.
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 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 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.
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.
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.
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.
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.
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.
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
- Based on the anatomical location where pain is felt.
- Head and neck pain – headache
– orofacial pains
– cervical pains
- Thoracic pain
- Extremity pain
- Orofacial pains are classified regionally as:
- Cutaneous and mucogingival pains.
- Mucosal pains of the pharynx, nose and PNS.
- Pains of dental origin.
- Pains of the musculoskeletal structures of the mouth and face.
- Pains of the visceral structures of the mouth and face.
- Pains of the neural structures of the mouth and face.
- Chronic face pain syndromes.
Pain syndromes about the mouth and face may be divided by their clinical characteristics into three categories.
- Somatic pain: results from noxious stimulation of normal neural structures that innervate body tissues.
- Neurogenous pain: is generated within the nervous system itself and is caused by abnormality of the neural structures that innervate body tissues.
- Psychogenic pain: results neither from noxious stimulation nor from neural abnormality but from psychic causes.
Management of Patients in Pain
- Cause-related therapy: consists of identification and elimination of aetiologic factors.
- Sensory stimulation: This is utilising the pain inhibitory affects of stimulating certain afferent neurons.
- percutaneous nerve stimulation.
- Analgesic blocking: This is the use of local anaesthesia to
- arrest pain input
- interrupt cycling
- resolve myofascial trigger point activity
- induce sympathetic blockade
- Physiotherapy: This includes cutaneous, and deep massage, exercises, deep
heat therapy, trigger point therapy, physical activity to increase “up-time”.
- Relaxation training: This includes autosedation, biofeedback training and
- Placebo therapy
- Psychotherapy: This includes counselling, hypnotherapy, and contingency management and formal psychotherapy.
- Neurosurgery: includes procedures as:
- peripheral therapy
- gangliolysis, rhizotomy and decompression
- trigeminal tractotomy.
- Medicinal therapy: which includes
- anti-inflammatory agents
- analgesic balms
- antiherpes agents
- local anaesthetics
- neuroactive drugs
- tranquillisers and muscle relaxants
- vasoactive agents.
- 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.
Methods to prevent pain in surgical patients
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 is depressed level of consciousness which may vary from light to deep.
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.
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 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 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 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 current of about 3mA at the frequency ranging from 300-3000 cycles/minutes. The mechanism of action is believed to be the excitation of A-d fibres leading to the production of endorphins.
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.
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 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.
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.
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