pain pathway, theories of pain, pain receptors

1. 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.
Introduction
Pain 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 30-120
0.4-0.5Aβ Touch, pressure and motor function 30-120
Aγ Motor to muscle spindles 15-35
Aδ 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.

2. 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 periphery
b. neural pathways – pathway by which neuron carries impulse from brain i.e. descending tracts viz pyramidal
and extrapyramidal tracts.
PAIN RECEPTOR
Sensory 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 PATHWAY
Sensory or ascending pathways:
TRACT SITUATION FUNCTION
Anterior spinothalamic tract Anterior white funiculus Crude touch sensation
Lateral spinothalamic tract
Lateral white funiculus
Pain and temperature sensation
Ventral spinocerebellar tract Subcutaneous kinaesthetic sensation
Dorsal spinocerebellar tract Subcutaneous kinaesthetic sensation
Spinotectal tract Concerned with spinovisual reflex
Fasiculus dorsolateralis Pain and temperature sensation
Spinoreticular tract Consciousness and awareness
Spinoolivary tract Proprioception
Spinovestibular tract Proprioception
Fasiculus gracilis Posterior white funiculus Tactile sensation, localization,
discrimination
Vibratory, 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.

3. 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 pathways
TRACT SITUATION FUNCTION
Pyramidal
Tracts
Anterior corticospinal tract Anterior white funiculus Voluntary movements
Lateral 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 posture
Position 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 tone
Olivospinal tract Lateral white funiculus Movements arising due to proprioception
NEUROPHYSIOLOGY OF PAIN
Nociception is divided into 4 steps :
a) Transduction
b) Transmission
c) Modulation
d) 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.

4. 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 PAIN
1. Intensity Theory
2. Specificity Theory
3. Pattern Theory
4. 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.

5. 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

6. CONTROL / MANAGEMENT OF PAIN
Pain can be controlled in several ways:
Non-pharmalogical interventions
1. Bed rest
2. Distraction
3. Therapeutic modalities
a) TENS
b) Superficial heat
c) Ultrasound
d) Cryotherapy
e) Acupuncture
4. Exercise
5. Hypnosis
Pharmacologic interventions
1. Non-opioids analgesics
2. Opioids analgesics
Non pharmacologic interventions
1. 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. Exercise
5. 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.

7. Pharmacologic interventions
According to WHO analgesic ladder, 1986
for mild pain – Non opioids with or without adjuvants
for 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: aspirin
2. Propionic acid derivatives: ibuprofen
3. Anthranilic acid derivatives: mephenamic acid
4. Aryl-acetic acid derivatives: diclofenac
5. Oxicam derivatives: piroxicam
6. Pyrrolo-pyrrole derivative: ketorolac
7. Indole derivative: indomethacin
8. Pyrazolone derivatives: phenylbutazone
B. Preferential COX-2 inhibitors
Nimesulide, meloxicam, nabumetone
C. Selective COX-2 inhibitors
Celecoxib, valdecoxib
D. Analgesic-antipyretics with poor anti-inflammatory action
1. Paraaminophenol derivative: paracetamol
2. Pyrazolone derivatives: metamizol
3. 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, codeine
2. Semisynthetic opiates: diacetylmorphine, pholcodeine
3. 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.

8. Antidepressants are classified as :
1. Reversible inhibitors of MAO-A: Moclobemide
2. Tricyclic antidepressants
a) NA + 5-HT reuptake inhibitors: imipramine
b) Predominantly NA reuptake inhibitors: desipramine
3. Selective serotonin reuptake inhibitors: fluoxetine, sertraline
4. 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: phenobarbitone
2. Deoxybarbiturate: primidone
3. Hydantoin: phenytoin
4. Iminostilbene: carbamazepine
5. Succinimide: ethosuximide
6. Aliphatic carboxylic acid: valproic acid
7. Benzodiazepines: diazepam
8. Phenyltriazine: lamotrigine
9. Cyclic GABA analogue: gabapentin
10. 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.

9. CLINICAL ASPECTS
1. 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 compression
b. 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 Gabapentin
Second-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.

10. 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.
Management
Topical 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.
Management
Centrally 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.