Seminar 3 – Management of Pain in Dentistry

HISTORY Word ‘pain’ is derived from latin word ‘poena’ – punishment from God. Aristotle was the first to distinguish five physical senses and considered pain to be the ‘passion of the soul’ that somehow resulted from the intensification of other sensory experience. Plato contented pain and pleasure arose from within the body giving an idea of concept that pain is an emotional experience more than a localized body disturbance. The Bible also makes reference to pain not only in relationship to injury or illness but also anguish of soul.

IntroductionPain is considered as a 5th vital sign after BP, pulse, respiratory rate and temperature. It is also one of the cardinal sign of inflammation.

According to International Association for the Study of Pain (IASP), pain is “an unpleasant sensory and emotional experience associated with actual or potential tissue damage or described in terms of such damage”.According to Monheim, pain is an “an unpleasant emotional experience usually initiated by a noxious stimulus and transmitted over a specialized neural network to the central nervous system where it is interpreted as such”.It serves as a protective function by making us aware of actual or impending damage to the body.

The most important structure that plays a crucial role in pain is the neuron which is a structural unit of nervous system, also called as nerve cell. Each consists of dendrites, axon and a cell body. Dendrites are located at the periphery and responds to the stimulation to the tissues in which they are located, carry these impulses to axon which is a long cylinder covered by a nerve membrane and then reaches to cell body through which impulse transmits to another neuron via synaptic vesicles located at neuromuscular junction at which neurotransmitter such as A-ch is present. They are of two types (sensory and motor) which have structural difference in a way that cell body is interposed at a distance from axon or main pathway of impulse transmission and provides only metabolic support while in motor neurons it plays a role in impulse transmission as well as metabolic support to neuron. They can be myelinated or non-myelinated.

Pain comprises of two components: Fast pain Slow pain

Whenever a pain stimulus is applied, firstly bright, sharp and localized pain sensation is produced called as fast pain which is followed by a dull, diffuse and unpleasant pain called as slow pain.

Peripheral nerves has different types of fibres-FIBRE TYPE FUNCTION CONDUCTION VELOCITY

(minutes / sec)SPIKE DURATION(milisec)

Myelinated Fibres

Aα Proprioception, somatic motor 30-1200.4-0.5Aβ Touch, pressure and motor function 30-120

Aγ Motor to muscle spindles 15-35Aδ Pain, temperature, touch 5-25

Myelinated fibres B Preganglionic autonomic fibres 3-15 1.2

Unmyelinated Fibres

sC (dorsal root)

Pain, temperature, touch and conducts impulses generated by cutaneous receptors

0.7-1.3 2

d γ C (sym-pathetic)

Postganglionic sympathetic fibres 0.1-2.0 2

So only Aδ and C fibres play a role in pain impulses. Aδ fibres carry fast pain while C fibres carry slow pain.

Nervous system consists of two components that is mainly responsible for pain impulse reception and reaction. Sensory component consists

a. sensory receptors – that receives stimuli from external or internal environment. b. afferent neuron – that carries impulse to brain from periphery c. neural pathways – pathway by which neuron carries impulse to brain i.e. ascending tracts in spinal cord.d. parts of brain that process the information i.e. somatosensory cortex.

Motor component consists of a. efferent neurons – that carries response from CNS to peripheryb. neural pathways – pathway by which neuron carries impulse from brain i.e. descending tracts viz pyramidal and extrapyramidal tracts.

PAIN RECEPTORSensory input from various stimuli (either external or internal) is received by specific peripheral receptors, called as nociceptors. They responds to these stimulus by acting as transducers and transmit impulses by nerve action potential along specific nerve pathways towards CNS. This process, called nociception, usually causes the perception of pain. They are found in all areas of body. External nociceptors are in tissues such as skin, cornea and mucosa. Internal nociceptors are in variety of organs such as muscle, joint, bladder, gut and continuing along the digestive tract. The cell bodies of these neurons are located in either the dorsal root ganglia or the trigeminal ganglia. The trigeminal ganglia are specialized nerves for the face, whereas the dorsal root ganglia associate with the rest of the body. The axons extend into the peripheral nervous system and terminate in branches to form receptive fields.

Development – Nociceptors develop from neural crest stem cells. Neural crest cells are responsible mainly for development of the peripheral nervous system. The neural crest stem cells split off from the neural tube as it closes, and nociceptors grow from the dorsal part of this neural crest tissue. They form late during neurogenesis.

PAIN PATHWAYSensory or ascending pathways:TRACT SITUATION FUNCTIONAnterior spinothalamic tract Anterior white funiculus Crude touch sensationLateral spinothalamic tract

Lateral white funiculus

Pain and temperature sensationVentral spinocerebellar tract Subcutaneous kinaesthetic sensationDorsal spinocerebellar tract Subcutaneous kinaesthetic sensationSpinotectal tract Concerned with spinovisual reflexFasiculus dorsolateralis Pain and temperature sensationSpinoreticular tract Consciousness and awarenessSpinoolivary tract ProprioceptionSpinovestibular tract ProprioceptionFasiculus gracilis Posterior white funiculus Tactile sensation, localization,

discriminationVibratory, conscious kinaesthetic, stereognosis sensationFasiculus cuneatus

Lateral spinothalamaic tract and fasiculus dorsolateralis are the ascending tracts employed in carrying the pain impulses from periphery to the brain. Pain impulses from pain receptors, i.e. nociceptors, are received and carried further to the brain by some neurons. These are mainly:First order neurons – they are formed by the cells in posterior nerve root ganglia. Second order neurons – they are formed by the marginal cells and cells of substantia gelatinosa situated in posterior gray column.Third order neurons – they are formed by the cells of thalamic nucleus, reticular formation, tectum and gray matter around aqueduct of sylvius.

First order neurons receive impulses from nociceptors through their dendrites and axons and finally reach spinal cord. After reaching spinal cord, fibres of fast pain synapse with marginal cells in posterior gray horn and slow pain fibres synapse with substantia gelatinosa in posterior gray horn. Then, fibres from second order neurons ascend in the form of lateral spinothalamic tract (LST) which is situated in the lateral funiculus towards medial side near the gray matter. Fibres mostly cross the midline via anterior gray commisure to the opposite side and reach anterolateral white column and ascend up while few fibres may ascend one or two segments and then cross to the opposite side and ascend in lateral column. All fibres pass through medulla, pons and midbrain towards the thalamus along with the fibres of anterior spinothalamic tract (AST) which is responsible for crude touch sensation. The majority of fibres of LST form spinal lemniscus along with the fibres of AST at the lower part of medulla. Fibres of LST terminates in the ventral posterolateral nucleus of thalamus while some fibres form collaterals and reach the reticular formation of brain stem, tectum of midbrain and gray matter surrounding aqueduct of sylvius. Fibres of fast pain are long and run as neospinothalamic fibres, a part of LST while fibres of slow pain run along with the fibres of fast pain as paleospinothalamic fibres.Then, fibres from third order neurons reach the sensory area of cerebral cortex and some fibres from reticular formation reach hypothalamus.

Motor or descending pathwaysTRACT SITUATION FUNCTION

Pyramidal Tracts

Anterior corticospinal tract Anterior white funiculus Voluntary movementsLateral corticospinal tract Lateral white funiculus

Extrapyramidal Tracts

Medial longitudinal Fasciculus

Anterior white funiculus Coordination of reflex-ocular movements and integration of movements of eyes and neck

Anterior vestibulospinal tract Anterior white funiculus Maintains muscle tone and posturePosition of head and body during acceleration

Lateral vestibulospinal tract Lateral white funiculus

Reticulospinal tract Lateral white funiculus Controls voluntary and reflex movements, muscle tone, respiration and blood vessels

Tectospinal tract Anterior white funiculus Movement of head in response to visual and auditory impulses

Rubrospinal tract Lateral white funiculus Facilitatory influence on flexor muscle toneOlivospinal tract Lateral white funiculus Movements arising due to proprioception

NEUROPHYSIOLOGY OF PAINNociception is divided into 4 steps :

a) Transductionb) Transmissionc) Modulationd) Perception

Transduction – It is the activation of nociceptor that converts mechanical energy to electrical energy. Nociceptors can be activated by :

Intense thermal and mechanical stimuli, noxious chemicals, noxious cold. Stimulation of inflammatory mediators.

Damaged tissue release bradykinin, potassium, histamine, serotonin and arachidonic acid. Arachidonic acid produce prostaglandins and leukotrienes by cyclooxegenase and lipoxygenase enzyme respectively. Synergistic effect of BK, PG, LK increases plasma extravasation and produce edema which in turn replenishes release of inflammatory mediators. PG stimulate nociceptors directly, LK stimulate nociceptors indirectly by increasing PMN that releases chemical mediators and stimulates nociceptor, BK contributes by causing sympathetic nerve terminal to release PG thus stimulates nociceptor. Sympathetic nerve terminal release another PG in response to its own neurotransmitter (norepinephrine). Such ongoing inflammatory state causes physiologic sensitization of nociceptors thus generating a response even to a non-painful stimuli and exaggerated response to noxious stimuli.

Transmission – It is the process by which peripheral nociceptive information is relayed to CNS. First order neuron synapses with the secondary order neuron from where impulse is carried to higher structures of brain. Repeated or intense C fibre activation brings specific changes on N-methyl-D-aspartate receptors resulting in central sensitization, thus, response of secnd order neurons increases as well as size of the receptive field also increases.Modulation – It is the mechanism by which transmission of impulse to the brain is reduced. Nociceptive transmission is influenced by :

Descending inhibitory systems that originate supraspinally Periaqueductal gray Nucleus raphe magnus Nucleus tractus solitarius Locus ceruleus/subceruleus Endogenous opioid peptides

Endogenous opioid peptides are naturally occurring pain-dampening neurotransmitters and neuromodulators employed in suppression and modulation of pain because they are present in large quantities in areas of brain associated with these activities.Perception – It is the subjective experience of pain. It is the sum of complex activities in CNS that may shape the character and intensity of pain perceived and ascribe meaning to pain.

THEORIES OF PAIN1. Intensity Theory2. Specificity Theory 3. Pattern Theory4. Gate Control Theory

1. Intensity theory – It was given by Erb in 1874. According to this theory, pain is a non-specific sensation and pain is produced only whenever there is stimulation of high intensity but this theory is not accepted as in trigeminal neuralgia, patient can suffer excruciating pain even when the stimulus is no greater than gentle touch provided it is applied in trigger zone. Although it is not accepted but this is fact intensity of stimulation is a factor in causing pain.

2. Specificity theory – It was given by Von Frey in 1895. According to this theory, body has a separate sensory system for perceiving pain, just as it does for hearing and vision i.e. Meissner corpuscles for sensation of touch, Ruffini end organs for warmth, Krause end organs for cold, similarly, specialised peripheral sensory receptors called nociceptors for pain, which respond to damage and send signals through pathways along the nerve fibres in the nervous system to target centres in the brain. These brain centres process the signals to produce the experience of pain. It got disapproved as it does not account for the wide range of psychological factors that affect our perception of pain. For example, soldiers may report little or no pain in relation to a serious wound in war time that would otherwise be excruciating.

3. Pattern theory – It was given by Goldschneider in 1920. He proposed that there is no separate system for perceiving pain and the receptors for pain are shared with other senses, such as of touch. This theory considers that peripheral sensory receptors, responding to touch, warmth and other non-damaging as well as to damaging stimuli, give rise to non-painful or painful experiences as a result of differences in the patterns of the signals sent through the nervous system. Thus, according to this view, people feel pain when certain patterns of neural activity occur, such as when appropriate types of activity reach excessively high levels in the brain. These patterns occur only with intense stimulation. Because strong and mild stimuli of the same sense modality produce different patterns of neural activity. It suggested that all cutaneous qualities are produced by spatial and temporal patterns of nerve impulses rather than by separate, modality specific transmission routes.

4. Gate control Theory – It was given by Ronald Melzack and Patrick Wall in 1965. According to this theory, there is variation in relative input of neural impulses along the large and small fibres. Small fibres carry the impulses to posterior gray horn of spinal cord and relay impulses to the cells of substantia gelatinosa from where it is transmitted to higher centres of brain while large fibres carry impulses and relay them to the marginal cells of posterior gray horn as cells of substantia gelatinosa terminate on small fibres just when large fibres are about to synapse on it, thus resulting in reduction / stoppage in the ongoing activity of impulse transmission. This theory also states that large fibres has the ability to modulate synaptic transmission of small fibres within the dorsal horn i.e. if a large fibre is carrying a impulse of temperature or pressure and small fibre is carrying a pain impulse, activation of large fibre can prohibit transmission of small fibre impulses from ever communicating with the brain. In this way, large fibres creates a hypothetical gate that can open or close the system to pain stimulation. There are 3 factors on which depends the opening and closing of gate:

a) Amount of activity in pain fibres – Greater the noxious stimulti, less adequate will be the gate in blocking the impulse.

b) Amount of activity in peripheral fibres - These fibers are called as Aβ fibres and carry information about harmless stimuli or mild irritation such as touching, rubbing, or lightly scratching the skin. Activity in these fibers tends to close the gate in the presence of noxious stimuli and thus inhibits the pain perception. This explains the reason behind the relief of pain when gentle massage or heat is applied to sore muscles.

c) Impulses that descends from the brain – Impulses sent by neurons located in brainstem and cortex can open or close the gate. The effects of some brain processes opens or closes the gate for all inputs from any areas of the body. But the impact of other brain processes may be very specific, applying to only some inputs from certain parts of the body. This explains the reason behind the fact that people who are hypnotized or distracted, by competing environmental stimuli, may not notice the pain of an injury.

CLASSIFICATION OF PAIN

CONTROL / MANAGEMENT OF PAINPain can be controlled in several ways:Non-pharmalogical interventions

1. Bed rest2. Distraction3. Therapeutic modalities

a) TENSb) Superficial heatc) Ultrasoundd) Cryotherapye) Acupuncture

4. Exercise5. Hypnosis

Pharmacologic interventions1. Non-opioids analgesics2. Opioids analgesics

Non pharmacologic interventions1. Bed rest – Bed rest may be beneficial to allow for reduction of significant muscle spasm brought on with

upright activity.2. Distraction – It is nothing but just diversion of one’s attention from pain to something else as people has a

ability to turn their attention away from objects and events.3. Therapeutic modalities

a) TENS (Transcutaneous Electrical Nerve Stimulation) – It is the local stimulation of of sore sites and strong neurologic sites in the region of pain, followed by stretching of the stiff muscle. Electrodes are placed directly on the skin. It is used in chronic pain conditions not in acute pain.

b) Superficial heat – It is superficial heating modality limited to a depth of 1-2 cm. Deeper tissues are not heated because of the thermal insulation of subcutaneous fat and increased blood flow that dissipates heat. It diminishes the pain and decreases local muscle spasm. There is a new emerging concept among it is Continuous low level heat therapy that allows for active use of therapeutic heat resulting in pain reduction, decreased muscle stiffness, improved flexibility, and decreased disability.

c) Ultrasound – It is a deep heating modality and is effective in heating structures where superficial heat cannot reach. It is not indicated in acute inflammatory conditions where it may severe or exacerbate the inflammatory response.

d) Cryotherapy – It is the reduction of intramuscular temperature to 3O - 7OC by application of cold. It works by decreasing nerve conduction velocity along pain fibres with a reduction of muscle spindle activity responsible for mediating local muscle tone. It can be achieved by application of ice, continuously via adjustable cuffs attached to cold water dispensers etc. It is applied over a region for 15-20 min and 3-4 times/day. It is mostly effective in acute phase of treatment.

e) Acupuncture – It is a most common form of strong counterstimulation that can be used for chronic pain. it involves the local needling in sore sites and strong neurologic sites in the region. 30 min of low frequency electrical stimulation i.e. 2-3 Hz is added by clipping the stimulator directly to the inserted needle.

4. Exercise5. Hypnosis – It is a formalized method of applying the techniques of attention modification, paced breathing

and muscle relaxation. The process of helping a patient to reach hypnotic state is called induction.

Pharmacologic interventionsAccording to WHO analgesic ladder, 1986 for mild pain – Non opioids with or without adjuvantsfor moderate pain – Weak opioids with non opioid (with or without adjuvants)for severe pain – Strong opioids with non opioid (with or without adjuvants)Adjuvants include antidepressants, antiepileptics, sodium channel blockers, and N-methyl-D-aspartate receptor antagonists.

Non opioid analgesics are classified as :A. Nonselective COX inhibitors

1. Salicylates: aspirin2. Propionic acid derivatives: ibuprofen3. Anthranilic acid derivatives: mephenamic acid4. Aryl-acetic acid derivatives: diclofenac5. Oxicam derivatives: piroxicam6. Pyrrolo-pyrrole derivative: ketorolac7. Indole derivative: indomethacin8. Pyrazolone derivatives: phenylbutazone

B. Preferential COX-2 inhibitorsNimesulide, meloxicam, nabumetone

C. Selective COX-2 inhibitorsCelecoxib, valdecoxib

D. Analgesic-antipyretics with poor anti-inflammatory action1. Paraaminophenol derivative: paracetamol2. Pyrazolone derivatives: metamizol3. Benzoxazocine derivative: nefopam

PG, prostacyclin and thromboxane A2 are produced from arachidonic acid by enzyme cyclooxegenase which exists in the constitutive(COX-1) and inducible(COX-1) isoforms. Non opioid analgesics inhibits COX-1 COX-2 nonselectively or COX-2 selectively.Salicylates acts by obtunding peripheral pain receptors and prevents PG mediated sensitization of nerve endings. They raise the threshold to pain perception.Propionic acid derivatives inhibit PG synthesis, platelet aggregation and prolongs bleeding time.Anthranilic acid derivatives inhibits COX and antagonise certain actions of PGs.Aryl-acetic acid derivatives inhibits PG synthesis and has short lasting antiplatelet action.Oxicam derivatives lowers PG concentration in synovial fluid and inhibits platelet aggregation.Pyrrolo-pyrrole derivative and Indole derivative inhibits PG synthesis.Selective COX-2 inhibitors inhibits only COX-2 without affecting COX-1 function. They do not depress thromboxane A2 production by platelets thus platelet aggregation remains undepressed but reduce PG production by vascular endothelium.

Opioids analgesics are classified as :1. Natural opium alkaloids: morphine, codeine2. Semisynthetic opiates: diacetylmorphine, pholcodeine3. Synthetic opiods: pethidine, fentanyl, tramadol

Opioid analgesics exert their actions by interacting with specific receptors present on neurons in CNS and in peripheral tissues. They inhibit the release of excitatory transmitters from primary afferents carrying impulses. Action at supraspinal sites in medulla, midbrain, limbic and cortical areas alter processing and interpretation of pain impulses and send inhibitory impulses through descending pathways to the spinal cord.Mu receptors are located widely throughtout the CNS especially in the limbic system and thalamus, striatum, hypothalamus and midbrain.Kappa receptors are located primarily in the spinal cord and cerebral cortex.Delta receptors are mainly present in dorsal horn of spinal cord.

Antidepressants are classified as :1. Reversible inhibitors of MAO-A: Moclobemide2. Tricyclic antidepressants

a) NA + 5-HT reuptake inhibitors: imipramineb) Predominantly NA reuptake inhibitors: desipramine

3. Selective serotonin reuptake inhibitors: fluoxetine, sertraline4. Atypical antidepressants: trazodone, mianserin

It is known that descending pain modulation pathways release serotonin (5-hydroxytryptamine or 5-HT) and norepinephrine (NE) to suppress pain transmission. The depressed patient has a dysfunctional 5-HTor NE system, which likely implies a dysfunctional 5-HTor NE pain modulation pathway. This may explain comorbid pain symptoms in patients with depression.

Antiepileptics are classified as :1. Barbiturate: phenobarbitone2. Deoxybarbiturate: primidone3. Hydantoin: phenytoin4. Iminostilbene: carbamazepine5. Succinimide: ethosuximide6. Aliphatic carboxylic acid: valproic acid7. Benzodiazepines: diazepam8. Phenyltriazine: lamotrigine9. Cyclic GABA analogue: gabapentin10. Newer drugs: vigabatrin

They limit neuronal excitation and enhance inhibition. Various sites of action include CNS voltage-gated ion channels involved in pain transmission (i.e. sodium and calcium channels), the excitatory receptors for glutamate including N-methyl-D-aspartate receptors, and the inhibitory receptors for GABA and glycine.

CLINICAL ASPECTS1. Tooth ache can be due to

a. Pulpitis (acute / chronic)b. Periapical pathology

2. TMD – Limitation of opening, episodes of joint locking, pain with mandibular dysfunction, facial pain and headache.Management

a. Physical therapy – application of moist heat or cold compressionb. Pharmacotherapy - analgesics, nonsteroidal anti-inflammatory drugs (NSAIDs), local anesthetics,

oral and injectable cortico steroids, sodium hyaluronate injections, muscle relaxants, botulinum toxin injections, and antidepressants.

NSAIDS - Commonly used NSAIDs include ibuprofen and naproxen, celecoxib. Local anesthetics – They are primarily used when a myofascial trigger point is present.

Myofascial trigger points are usually detected in the mastication muscles. The trigger point injection technique involves locating the trigger point, which is usually found in a taut band of muscle, and needling the area.

TMJ injections - Intracapsular injection of corticosteroids significantly reduces TMJ pain. It is indicated for acute and painful arthritic TMJ that has not responded to other modalities of treatment. The use of triamcinolone or dexamethasone, in addition to 2% lidocaine without epinephrine. The quantity of steroid injections should be carefully considered due to the possibility of bone resorption in the site of injection.

Muscle relaxants – It can be prescribed for acute muscle tension associated with TMJ disorders. A commonly used and effective muscle relaxant is cyclobenzaprine, started at lower dosages (5–10 mg) and taken 1–2 hours before bedtime.

Antidepressants - Tricyclic antidepressants like amitriptyline and nortriptyline. They have anti-nociceptive effects.

Occlusal appliance therapy – They are processed acrylic devices that are used for the purpose of equally distributing jaw parafunctional forces, reducing the forces placed on the masticatory muscles, and protecting the occlusal surfaces of the teeth from chronic nocturnal bruxing.

c. Surgical intervention - When non-surgical therapy has been ineffective, surgical recommendations, such as arthrocentesis and arthroscopy, depend on the degree of internal derangement. Arthrocentesis is a conservative treatment that involves an intra-articular lavage with or without deposit of corticosteroids that is useful when there are intra-articular restrictions to movement. Arthroscopy is a closed surgical procedure that is useful in hypomobility due to joint derangement58 as well as fibrosis. Arthrotomy is an open surgical procedure that modifies joint anatomy.

d. Acupuncture – It involves the stimulation of acupuncture points that are thought to stimulate the flow of energy believed to be blocked.

3. Trigeminal neuralgia – It is a chronic paroxysmal neuropathic pain condition that is described as a severe, lancinating, and electric-like unilateral pain. There is usually a trigger zone in the trigeminal distribution which, when stimulated, can result in an excruciatingly painful attack. The etiology is vascular compression that may result in focal demyelination. The superior cerebellar artery compression on the trigeminal root is responsible for attacks of TN pain.Management

a. Pharmacological intervention – Antiepileptic medications are the drugs of choice for the management of TN. First-line medications – Carbamazepine, Oxcarbazepine, and GabapentinSecond-line medications – Baclofen and Lamotrigine

b. Surgical intervention – If pain attacks recur and medications are no longer effective, neurosurgical options such as microvascular decompression or gamma knife radiosurgery may be considered.

4. Glossopharyngeal neuralgia – It is a rare condition associated with pain in the area supplied by the glossopharyngeal nerve including nasopharynx, posterior part of the tongue, throat, tonsil, larynx, and ear.Management

a. Pharmacological intervention – Antiepileptic medications are the drugs of choice for the management.

b. Surgical intervention – If medication management fails, then microvascular decompression, radiofrequency thermocoagulation, gamma knife radiosurgery, or rhizotomy.

5. Peripheral trigeminal neuropathic pain – It can arise as a result of a traumatic nerve injury resulting in chronic aching, continuous burning like pain at the site of the injury. ManagementTopical medications can be used. Capsaicin is a common locally acting pharmacologic agent that can be utilized in cream or gel form, normally at a concentration ranging from 0.025%–0.05% mixed with benzocaine 20% and applied with the use of a stent that covers the affected area (neurosensory stent). Cream may also include analgesics/sedatives such as ketamine, NSAIDs such as diclofenac, anticonvulsant drugs such as gabapentin and carbamazepine, and tricyclic antidepressant medications such as nortriptyline and amitriptyline.

6. Centralized trigeminal neuropathic pain - Prolonged stimulation of peripheral nociceptors may eventually lead to central neural changes. The pain in these cases is described as continuous, aching, and burning. ManagementCentrally acting systemic medications are used. Antiepileptic drugs, such as gabapentin and valproic acid, in combination with tricyclic antidepressants such as amitriptyline, may reduce pain.

7. Atypical odontalgia – It is a centralized trigeminal neuropathy often localized in a tooth or tooth area. If the pain is localized to a peripheral origin, a topical medication can be used and a neurosensory stent can be fabricated. Systemic approaches such as tricyclic antidepressants, calcium channel blockers (pregabalin and gabapentin), sodium channel blockers (carbamazepine), and antiepileptics such as topiramate can be used.