Major Neurotransmitters are divided into two types - small rapid acting molecules like acetylcholine, norepinephrine, glutamate, and aspartate that are excitatory, and larger slower acting molecules like GABA, glycine, and dopamine that are inhibitory. Neurotransmitters are involved in various functions in both the central and peripheral nervous systems, and imbalances can lead to conditions like depression, Alzheimer's disease, and Parkinson's disease.
EPANDING THE CONTENT OF AN OUTLINE using notes.pptx
Major Neurotransmitters and Their Functions
1. Major Neurotransmitters
Biogenic amines
– Acetylcholine
– Monoamines
• Catecholamines – Dopamine, Norepinephrine,
Epinephrine
• Serotonin
Amino Acids
– Glutamate, GABA, Glycine
Neuropeptides
– Substance P
– Opioid peptides
• endorphin, enkephalin
Nitric Oxide
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2. Neurotransmitters are divided into 2 types-
• Small rapid acting molecules –Acetylcholine,
Norepinephrine, Glutamate,
Aspartate,
Serotonin(excitatory)
- GABA, Glycine, dopamine(Inhibitory)
• Larger slower acting molecules-
Substance P, Endorphins
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3. Acetylcholine
Produced by-
In Brain
-Motor cortex, the basal ganglion
In PNS
– Motor neurons
– Parasympathetic
• Both pre- and postganglionic neurons
– Sympathetic
• pre-ganglionic neurons
• some post-ganglionic neurons that innervate sweat
glands and blood vessels
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4. • Acetylcholine is a very widely distributed excitatory
neurotransmitter that triggers muscle contraction and
stimulates the excretion of certain hormones. In the
central nervous system, it is involved in wakefulness,
attentiveness, anger, aggression, sexuality, and thirst,
among other things.
• Alzheimer’s disease is associated with a lack of
acetylcholine in certain regions of the brain
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5. Norepinephrine
• Norepinephrine is a neurotransmitter that is important
for attentiveness, emotions, sleeping, dreaming, and
learning.
• Norepinephrine is also released as a hormone into the
blood, where it causes blood vessels to contract and
heart rate to increase.
• Norepinephrine plays a role in mood disorders such as
manic depression.
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7. Glutamate
• Glutamate is a major excitatory neurotransmitter
secreted by presynaptic terminals in many sensory
pathways as well as in many areas of the cortex and is
associated with learning and memory. It is also thought
to be associated with Alzheimer’s disease, whose first
symptoms include memory malfunctions.
Aspartate
It is secreted by presynaptic terminals in many sensory
pathways in the dorsal horn. It is thought to always cause
excitation
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8. • Serotonin contributes to various functions, such as regulating body
temperature, sleep, mood, appetite, and pain. Depression, suicide,
impulsive behaviour, and aggressiveness all appear to involve
certain imbalances in serotonin.
• It is released by blood platelets
• In CNS is synthesized from L-Tryptophan and released from
nucleus magnus when stimulated from sensory input.
• Peripherally it is an algogenic agent
• In CNS it is an important chemical in the endogenous
antinoniceptive mechanism.
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10. • Dopamine is an inhibitory neurotransmitter involved in
controlling movement and posture. It also modulates
mood and plays a central role in positive reinforcement
and dependency.
• The loss of dopamine in certain parts of the brain causes
the muscle rigidity typical of Parkinson’s disease.
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12. Glycine
It is secreted by many areas of spinal cord and likely to be
secreted in the trigeminal spinal nucleus.It is probably
always an inhibitory transmitter.
HISTAMINE
Vasoactive amine derived from histadine
Also a vasodilator and increases small vessel permeability
Causes contraction of smooth muscles in the lungs
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13. • GABA (gamma-aminobutyric acid) is an inhibitory
neurotransmitter that is secreted by the neurons in the
spinal cord,cerebellum,basal ganglia, and parts of the
cortex.
• GABA contributes to motor control.It also regulates
anxiety.
• Some drugs that increase the level of GABA in the brain
are used to treat epilepsy and to calm the trembling of
people suffering from Huntington’s disease.
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14. Substance P
• Belongs to family of proteins called tachykinins
• 11 amino acids polypeptide
• Found in primary afferent nerve endings (C
fibres),substantia gelatinosa of cord, substantia nigra
• Roles in– pain transmission / inflammation,
nausea,mood/depression, migraine
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15. ENDORPHINS
• Endorphins can be found in the pitutary gland, in other parts of the
brain, or distributed throughout the nervous system.
• Stress and pain are the two most common factors leading to the
release of endorphins. Endorphins interact with the opiate receptors
in the brain to reduce our perception of pain and act similarly to
drugs such as morphine and codeine. In contrast to the opiate
drugs, however, activation of the opiate receptors by the body's
endorphins does not lead to addiction or dependence.
• In addition to decreased feelings of pain, secretion of endorphins
leads to feelings of euphoria, modulation of appetite, release of sex
hormones, and enhancement of the immune response. With high
endorphin levels, we feel less pain and fewer negative effects of
stress
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17. Contents-Part-I
The Nature of Pain
• Definition
• Neural anatomy of orofacial pain
• Neurophysiology of orofacial pain
• Central processing and Psychology of pain
Clinical considerations of pain
• Measurement of Pain and Disability
• History of Orofacial pain
• Orofacial Pain Clinical examination
• Establishing the pain category
• Confirmation of clinical diagnosis
Classification of orofacial painwww.indiandentalacademy.com
18. PART-II
• Clinical pain Syndromes
• General Considerations in Managing
Orofacial pains.
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20. • Somatic Pain
Noxious impulses being received and transmitted
by normal components of the sensory nervous
system.(normal neural structures –abnormal
somatic structures)
• Neuropathic Pain
Noxious impulses originating from an abnormality
in neural structures.(abnormal neural structures -
normal somatic structures)
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22. Superficial Somatic Pain
1. The pain has a bright, stimulating quality.
2. Subjective localization of the pain is excellent and
anatomically accurate.
3. The site of pain identifies the correct location of its source.
4. Response to provocation at the site of pain is faithful in
incidence, intensity, and location.
5. The application of a topical anesthetic at the site of pain
temporarily arrests it.
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24. Mucogingival pains of the mouth
Etiology-
• Trauma
• Allergic
• Local infections
• Systemic conditions
• Or may present as burning mouth syndrome
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25. • Since the pain of Mucogingival origin is an expression of
primary hyperalgesia of the tissue that hurt, application
of a topical anaesthetic to those tissues arrests the pain
due to action of the medication on the receptors and pain
fibres in the mucogingival tissues.
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26. Burning Mouth Syndrome (Glossodynia)
(Mucogingival pain)
Burning sensations accompany many inflammatory or
Ulcerative diseases of the oral mucosa, but the term
“burning mouth syndrome” (BMS) is reserved for describing
oral burning that has no detectable cause. The burning
symptoms in patients with BMS do not follow anatomic
pathways, there are no mucosal lesions or known
neurologic disorders to explain the symptoms,and there are
no characteristic laboratory abnormalities.
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28. • Dysgeusia (particularly an abnormally bitter taste) has
been reported by 60% of BMS patients.This association
has led to a concept that BMS may be a defect in
sensory peripheral neural mechanisms.
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29. Clinical Features
• Women experience symptoms of BMS seven times more
frequently than men.
• 10 to 15% of postmenopausal women are found to have
a history of oral burning sensations, and these
symptoms are most prevalent 3 to 12 years after
menopause.
• Tongue is the most common site of involvement, but the
lips and palate are also frequently involved.
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30. • The burning can be either intermittent or constant,
but eating, drinking, or placing candy or chewing gum in
the mouth characteristically relieves the symptoms.
• This contrasts with the increased oral burning noted
during eating that occurs in patients with lesions or
neuralgias affecting the oral mucosa.
• Patients presenting with BMS are often apprehensive
and admit to being generally anxious or “high-strung.”
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31. Treatment of burning mouth syndrome
• Eliminating the possibility of detectable lesions or
underlying medical disorders
• Counseling and reassurance may be adequate
management for individuals with mild burning
sensations, but patients with symptoms that are more
severe often require drug therapy.
• The drug therapies that have been found to be the most
helpful are low doses of TCAs, such as amitriptyline and
doxepin, or clonazepam (a benzodiazepine Derivative).
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33. Therapeutic options of Superficial
Somatic Cutaneous or Mucogingival Pain
• Analgesics for palliative relief
• Cause related therapy
-Elimination of all oral irritants
-Restriction of oral functions within reasonable
limits
-Antibiotics and Antimicrobials, topical and systemic
-Antivirals
-For Xerostomia-Paraffin or gum to stimulate
saliva,saliva substitutes
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35. Deep Somatic Pain
1.The pain has a dull, depressing quality.
2. Subjective localization of the pain is variable and
somewhat diffuse.
3. The site of pain may or may not identify the correct
location of its true source.
4. Response to provocation at the site of pain is fairly
faithful in incidence and intensity but not in location.
5. Accompanying secondary central excitatory effects are
frequently displayed.www.indiandentalacademy.com
36. There are two distinct types of deep somatic pain
• Musculoskeletal pain
• Visceral pain.
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37. Musculoskeletal Pain
1.The pain is intimately related to biomechanical function.
2. The response to provocation is a gradient that is
proportionate to the stimulus.
Visceral Pain
1. The pain is irrelevant to biomechanical function.
2. The pain is nonresponsive to provocation until a
threshold is reached.
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40. PAINS OF DENTAL ORIGIN
It may be -
1)Dental pain of pulpal origin(visceral)
2)Dental pain of Periodontal origin(musculoskeletal)
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41. Classification of Toothaches
• Pulpal disease
– Reversible pulpitis (brief, stimulated pain)
– Irreversible pulpitis (prolonged, stimulated or spontaneous pain)
– Necrotic pulp (asymptomatic, no response to pulp testing)
• Periapical disease
– Acute apical periodontitis (sensitivity to percussion)
– Acute apical abscess (sensitivity to percussion, swelling, pus)
– Chronic apical abscess (often asymptomatic, periapical
radiolucency)
• Heterotopic pain
– Projected pain (pain in adjacent teeth)
– Referred pain (pain in teeth in opposing arch)
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42. Characteristics of Pulpal &
Periapical Pain
Pulpal Pain
(Deep, Somatic,
Visceral)
Periapical Pain
(Deep, somatic,
Musculoskeletal)
Masticatory function
(Biomechanical
stimulation)
Not stimulated by
biting, chewing, or
percussion
Stimulated by biting,
chewing, or percussion
Localization Frequently difficult to
localize specifically
Usually can localize
precisely
Sequence Usually precedes
periapical pain
Usually follows pulpal
pain (unless periodontitis,
hyperocclusion, bruxism)
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43. Nonodontogenic Toothaches
Most toothaches will be of odontogenic origin.
However, if there is no identifiable cause or source (e.g.
caries) for the pain,
or
the history and clinical findings are inconsistent with
odontogenic pain,
then
a nonodontogenic source should be considered.
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44. Heterotopic Pain
• Pain felt in an area other than its true site of
origin (associated with deep, somatic pain).
– Projected pain: perceived in the anatomic distribution
of the same nerve that mediates the primary pain
(painful adjacent teeth).
– Referred pain: felt in an area innervated by a different
nerve from the one that mediates the primary pain
(teeth in opposing arch, face, head, neck).
• Does not cross the midline.
• Convergence of afferent neurons.
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45. Toothache of Maxillary Sinus/Nasal
Mucosa Origin
Origin
Infection of the maxillary sinus or inflammation of nasal
mucosa.
Clinical
Characteristic
s
Constant dull ache or pressure; sensitivity to cold,
percussion, chewing; pain in multiple teeth; pain
increased by bending body forward; sinus tender to
palpation; Water’s may show air-fluid level.
Local
Anesthesia
Topical anesthesia of nasal mucosa relieves pain in
anterior teeth; infiltration anesthesia of posterior teeth
relieves pain.
Treatment Antibiotics, antihistamine with a decongestant,
analgesic.
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46. Toothache of Myofascial Origin
Origin
Referral of pain from myofascial trigger points in
muscles of mastication – primarily masseter,
temporalis, anterior digastric.
Clinical
Characteristic
s
Nonpulsatile; constant, aching; variable and cyclic;
pain increases with stress and use of offending
muscles.
Local
Anesthetics
Anesthetic block of tooth does not alter pain;
anesthetic injection of trigger point relieves pain.
Treatment Treatment and elimination of trigger points by spray
and stretch, injection, or physical therapy.
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48. Toothache of Neuropathic Origin
(Trigeminal Neuralgia)
Origin
Abnormal function of nerves that innervate teeth
(mandibular and maxillary branch of the trigeminal
nerves).
Clinical
Characteristic
s
Unilateral, severe, paroxysmal bursts of electric-like
shocks stimulated by minor superficial provocation;
may be felt in teeth; asymptomatic between
episodes.
Local
Anesthetics
Topical anesthetic of mucosal or skin “trigger” blocks
pain; anesthetic block of nerve root blocks pain.
Treatment Referral to neurologist or neurosurgeon.
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49. Toothache of Neuropathic Origin
[Atypical Odontalgia (Phantom Pain)]
Origin Not definitely known; most probably a deafferentation
pain after trauma.
Clinical
Characteristic
s
Constant pain with no obvious pathology; burning,
aching pain in molar/premolar area longer than 4
months; local provocation not reliably effect pain.
Local
Anesthetics
Equivocal response
Treatment Tricyclic antidepressants, gabapentin
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50. Toothache of Neurovascular Origin
(Tooth migraine)
Origin Neurogenic inflamation in the trigeminovascular
system
Clinical
Characteristic
s
Maxillary canines/premolars; no dental cause;
throbbing, episodic, persistent, recurrent pain; dental
treatment may provide temporary relief; may become
widespread.
Local
Anesthetics
Effects are unpredictable.
Treatment Same as for migraine headache; NSAIDs, beta
blockers, ergotamines.
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51. Toothache of Cardiac Origin
Origin Myocardial ischemia with regional referral of pain.
Clinical
Characteristic
s
Periodic dull pressure of aching in the mandible or
teeth; may accompany pain in chest or arm; history of
angina; pain precipitated by exercise, stress, or
physical activity.
Local
Anesthetics
Anesthesia of teeth not effective.
Treatment Refer to medical physician
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52. Toothache of Psychogenic Origin
Origin Psychogenic origin.
Clinical
Characteristic
s
Bizarre behavior; history of psychiatric treatment;
migratory pain in multiple teeth, frequently bilateral;
unexpected or inappropriate response to treatment.
Local
Anesthetics
Equivocal effects.
Treatment Refer to psychiatrist.
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53. Non-Odontogenic Toothaches Warning
Symptoms- Summary
1. Spontaneous multiple toothaches
2. Inadequate local dental cause for the pain
3. Stimulating, burning, non-pulsatile toothaches
4. Constant, unremitting, non-variable toothaches
5. Persistent, recurrent toothaches
6. Local anesthetic blocking of the offending tooth does not
eliminate the pain
7. Failure of the toothache to respond to reasonable dental
therapy
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54. Differential diagnosis of Primary deep
somatic pain of dental origin
• Heterotopic referred pains and secondary hyperalgesias
as secondary effects of deep pain originating in the
following somatic structures: musculoskeletal, vascular,
cardiac , or sinus mucosa
• Neuropathic pains
• Somatoform pain disorders
• Heterotopic pains of central origin
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57. Ocular pain
Ophthalmic pain results from stimulation of pain fibers relating either
directly or indirectly to the orbit and can be classified as ocular, orbital,
or referred.
Ocular pain:
• Corneal irritation or damage is associated with local pain,
photophobia, and lacrimation.
• Anterior scleritis presents with severe ocular pain, while posterior
scleritis is characterized by less well-defined orbital pain.
• Either may be associated with a systemic collagen vascular
disease.
• A triad of red eye, increased intra-ocular pressure, and mid-dilated
pupil is pathognomonic of acute angle glaucoma.
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58. Orbital pain:
• Orbital cellulitis presents acutely with pain exacerbated by palpation
and movement.
• Orbital pseudotumor is an inflammatory process of unknown etiology
that presents with pain, chemosis, diplopia, and red eye.
Referred pain:
• Occasionally, pain from the area of the greater occipital nerve may
radiate to the eye and face, due to convergence and communication
between the cervical nerves, and the trigeminal sensory complex.
• Migraine, cluster headache, sinusitis, otitis, mastoiditis, temporal giant
cell arteritis, and dental pain can be referred to the eye.
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59. Auricular
• Otitis media presents with dull aching or sudden exquisite pain,
with or without aural discharge, inflamed tympanic membrane, and
systemic evidence of infection.
• Otitis externa can be exquisitely painful and is generally an acute
process.
• Mastoiditis and otitis pain may be referred to the eye, pharynx,
and neck due to involvement of multiple cranial and cervical
nerves, and convergence into the trigeminal sensory complex.
• A common cause of otalgia that is frequently overlooked
is referred myofascial pain from muscles of the neck,pharynx, and face
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60. Salivary Gland Disorders
• The salivary glands can be affected by many diseases,
including ductal obstruction,infection, inflammation,
cystic degeneration, and tumor growth.
• Pain and tenderness are typically found in association
with ductal obstruction, inflammation,or infection.
• Etiology. The most common causes are mumps and
acute parotitis in children and blockage of salivary flow
by a mucus plug or a sialolith in adults.
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61. • Salivary gland pain is typically localized to the gland
itself, and the gland is tender to palpation.
• Precipitating and aggravating factors to the pain are
salivary production prior to meals, eating, and
swallowing.
• Mouth opening may aggravate the pain because of
pressure on the gland from the posterior border of the
mandible during this movement.
• Associated symptoms include salivary gland swelling
and, occasionally, fever and malaise. Salivary flow from
the affected gland may be minimal or nonexistent.
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64. Sinus and Paranasal Pain
The most common extraoral source of dental pain arises
from the maxillary sinus and associated pain-sensitive
nasal mucosa.
Symptoms.
• Infection and inflammation of the sinuses rarely cause
facial pain or headache.
• Chronic sinusitis may cause symptoms of fullness or
pressure but rarely pain.
• A history of increased pain at altitude
• Patients may also complain of a “stuffy nose,” blood- or
pus-tinged mucus, postnasal drip, fever, and malaise.
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65. • Frequently, pain is exacerbated by leaning the head
forward.
• Medial orbital pain with radiation to the temple is a
feature of ethmoid sinusitis.
• Frontal sinusitis features forehead pain and headache
• Maxillary sinusitis is suggested by pain over the upper
teeth or orbit.
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66. • The teeth feel elongated and tender
• The maxillary teeth are hypersensitive to cold fluids.
• Occasionally, all of the maxillary teeth on the involved
side, to the midline, feel uncomfortable and elongated.
• The pain is mild but deep and nonpulsating, radiates out
of this area onto the face, upward toward the temple,
and forward toward the nose.
• Cutaneous hyperalgesia along the side of the face and
scalp may also be present.
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67. • The diagnosis of maxillary sinusitis may be confirmed
by spraying 4% lidocaine anesthetic from a spray bottle
into the nostril on the affected side. This will anesthetize
the sensitive area around the ostium.
• The pain from the congested nasal mucosa and
accompanying maxillary sinusitis should be substantially
reduced within a minute or two.
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68. Treatment
• Complete diagnosis and treatment of maxillary sinusitis
are left to the ENT specialist.
• Treatment usually consists of the use of decongestants
and analgesics.
• If there is persistent purulent discharge, cultures should
be taken and appropriate antibiotics prescribed.
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70. Vascular Pain
Temporal Arteritis
• Burning, temporal, throbbing, sharp, intermittent, then
continuous.
• May be associated with loss of visual acuity.
• Polymyalgia Rheumatica. Associated fever, weight loss.
• Teatment: Prednisolone 60 mg/day. Reducing doses
after 5 days.
• Rheumatology referral mandatory.
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71. Carotidynia
• Carotid Artery stimulation of various parts of the carotid
artery in the region of the bifurcation has been shown to
cause pain in the ipsilateral jaw, maxilla, teeth, gums,
scalp, eyes, or nose.
• In the absence of other demonstrable pathology,
unilateral dull, aching, sometimes throbbing pain in the
jaws, temple, and neck may be attributable to a carotid
system arteritis, also known as carotidynia (carotid pain).
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72. • The patient with carotidynia will most likely complain of
constant or intermittent dull, aching, rarely pulsing jaw
and neck pain, with intermittent sore throat or swollen
glands.
• The pain may also involve the temple and TMJ region
and Radiate forward into the masseter muscle with
occasional Concomitant tenderness and fullness.
• Aggravating factors may include chewing, swallowing,
bending over, or straining.
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73. Treatment.
• Medications used in the treatment and prevention of
migraine headaches have been shown to be effective in
controlling the symptoms of carotidynia.
• Steroids and NSAIDs.
• Concomitant treatment of any myofascial TrPs will
ameliorate the symptoms to some extent.
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76. Muscle co-contraction
• Protective co-contraction is a CNS response to injury or
threat of injury
• In the presence of an injury or threat of injury, normal
sequencing of muscle activity seems to be altered to
protect the threatened part from further injury.
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77. • The etiology of protective co-contraction can be any
change in sensory or proprioceptive input from
associated structures.
• Protective co-contraction can also be caused by any
source of deep pain input or an increase in emotional
stress
• The key to identifying co-contraction is that it
immediately follows an event and therefore the history is
very important. Protective co-contraction only lasts a few
days. If it is not resolved, an acute myalgic disorder is
likely to follow.
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78. Myositis
• Myositis is an inflammation of the muscle due to a local
cause such as trauma, strain, or infection. Symptoms
include swelling, tenderness to palpation, and pain with
function .
Muscle spasm
• Muscle spasm is a sudden, involuntary contraction of a
muscle or group of muscles, accompanied by pain,
limited vertical opening of the mandible, and tenderness
to palpation.
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79. Myofascial pain
• Myofascial pain, a common chronic muscular pain
disorder is a regional aching pain associated with
localized tenderness in firm bands of muscle and
tendons called trigger points (TrPs).
• Myofascial TrPs can develop in masticatory and
associated head and neck muscles secondary to
prolonged muscle tension, protracted muscle spasm,
forward head posture, parafunctional activity,and trauma.
• Factors such as sleep disturbances, joint problems, viral
diseases, and metabolic disturbances that weaken a
muscle often predispose a weakened muscle to the
development of TrPs.
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80. • The key to diagnosing myofascial pain is to identify a
TrP. When palpated, active TrPs cause referred pain in
predictable patterns to a known reference zone and are
often associated with secondary excitatory effects.
• Continuous, dull pain and localized tenderness in one or
more muscles are characteristics of myofascial pain, but
the severity of pain may range from mild to agonizing,
excruciating, or incapacitating.
• In early stages, the pain may be more localized, but with
chronicity, the TrP can refer pain to more distant sites .
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82. DIAGNOSTIC FEATURES OF THE
MPD PATIENT
Unilateral, dull, aching facial pain that is poorly localized
Moderate to severe limitation of mouth opening
No TMJ tenderness
Muscle tenderness (masticatory and cervical)
No radiographic TMJ changes
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83. GENERAL CHARACTERISTICS OF
MPD PATIENTS
Predominately females
20–40 year age group
Frequent history of other psychophysiologic diseases
Often suffer from chronic depression
Seek multiple care providers
Have difficulty accepting a psychophysiologic etiology for their
problem
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84. HOME THERAPY
Check for clenching habits
Limitation of jaw movement
Soft non-chewy diet
Moist heat and massage of the jaw muscles
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85. Physical therapy
• Massage/myofascial release/muscle energy
• Manipulation techniques
• Spray and stretch
• Heat/cold treatments
• Surface stimulation techniques: TENS etc.
• Relaxation/biofeedback techniques
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90. 1.Ligamentous pain
CLASSIFICATION OF INTERNAL DERANGEMENTS
Anteriorly displaced disc that returns to normal position
during mouth opening (clicking)
Anteriorly displaced disc that does not return to normal
position during mouth opening (locking)
Adhesion of the disc to the joint socket (locking)
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94. MEDICAL MANAGEMENT OF
PAINFUL TMJ CLICKING
Medications for relief of pain
Soft, nonchewy diet
Use of a bite appliance to prevent chronic tooth
clenching and grinding
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95. SURGICAL TREATMENT OF
PAINFUL TMJ CLICKING
Arthroscopic surgery
Discoplasty (surgical repositioning of the disc)
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96. TREATMENT OF TMJ LOCKING
Arthrocentesis
Surgical treatment of TMJ locking
Arthroscopic surgery
Discoplasty (surgical repositioning of the disc)
Discotomy (surgical removal of the disc)
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97. 2.Retrodiscal Pain
• If condylar encroachment occurs on the retrodiscal
tissues then inflammation may occur
• Acute retrodiscitis- may occur due to trauma to mandible
• An insidious chronic form of retrodiscitis may occur as a
result of functional encroachment of the condyle on the
retrodiscal tissues due orthopedic instability that
displaces the condyle posteriorly when the teeth are
clenched firmly in maximum intercuspation.
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98. Clinical symptoms of retrodiscal pain
• The pain is accentuated by clenching the teeth in maximum
intercuspation.
• Such pain is decreased by biting against a separator that prevents
intercuspation of the teeth.
• The pain is accentuated by forced ipsilateral excursive movement of
the mandible.
• Pain is not induced by resisted protrusion of the mandible.
• Dysfunction may be displayed as acute malocclusion in the resting
occluded position.
• Secondary central excitatory effects may be displayed.
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99. 3.Capsular pain
• Capsular pain results from inflammation of the synovial
and fibrous capsules, which is referred to as synovitis
and capsulitis, respectively.
• Synovitis may result from localized trauma, abusive use,
toxemias, specific infection, or as an allergic response. It
frequently occurs as a manifestation of arthritis.
• Capsulitis may result from acute trauma or from intrinsic
strains that injure the capsular ligament
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100. Capsular pain - Clinical Features
• Palpable tenderness directly over the condyle.
• Occasional palpable fluctuant swelling over the joint proper.
• The pain is accentuated by translatory movements that stretch the
capsule.
• There is no increase in pain by clenching the teeth, nor is there any
alteration in pain by biting against a separator.
• Dysfunction occurs in the form of restricted mandibular movement,
especially in extended ranges. Most restriction is due to the
inhibitory influence of pain. Joint stiffness and strange joint sounds
may occur during the first few movements following periods of
inactivity. Acute malocclusion may occur as the result of increased
intracapsular fluid.
• Secondary central excitatory effects may be displayed.
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102. Arthritic Pain
The following are clinical symptoms by which arthritic pain
can be recognized:
• There is usually some degree of capsular pain as well as
other symptoms of synovitis/capsulitis.
• The pain is accentuated by biting pressure, fast
movements, and forced movements.
• The pain is decreased by biting against a separator on
the ipsilateral side
• The pain is increased by biting against a separator on
the contralateral side.www.indiandentalacademy.com
103. • Dysfunction is expressed as restricted movement,
interference during movements, and acute malocclusion.
Restricted movement may be due to inflammatory
swelling, capsular inflammation, altered synovial fluid
function,and the inhibitory influence of pain(muscle co-
contraction). Interference during movement results from
damaged articular surfaces or condyle-disc complex
impairment. Acute malocclusion may be due to
increased intracapsular fluid or osseous change.
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105. OTHER MUSCULOSKELETAL PAINS
Osseous and periosteal pain
• The other musculoskeletal pains of the face and mouth
include osseous pains, periosteal pains, and soft
connective tissue pains .
• Since osseous structures and soft connective tissue are
less intimately related to biomechanical function, they
are less well-innervated proprioceptively and therefore
are less localizable subjectively.
• Also, pains emanating from such structures are less
likely to induce muscle effects.
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106. Osseous Pains
• Pains that emanate from the bony structures of the
mouth and face exclusive of the periodontal structures
and the temporomandibular joints constitute another
subdivision of musculoskeletal pain.
• Pains from this source are predominantly inflammatory
as a result of injury, infection, or surgical intervention.
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107. • There is minimal dysfunction other than that due to the
inhibitory influence of pain. Secondary factors, however,
such as muscle co-contraction, local muscle soreness,
myospasm, or cellulitis may contribute to some
dysfunction.
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108. Dry-Socket Pain
• A frequent osteitic involvement of the mouth is
dry-socket that follows tooth extraction.
• This condition is the result of inflammation of
remnants of the periodontal ligament and
cortical bone of the alveolus.
• Being components of a fibrous joint, these
structures are richly innervated with both
mechanoreceptors and nociceptors.
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109. • They therefore have the propensity to initiate reactive
muscle effects and considerably more nociceptive
response than do other osseous structures.
• Protective muscle co-contraction as well as secondary
central excitatory effects are frequent complications.
• Referred pain involving many teeth, spots of touchy
gingiva or skin, areas of deep palpable tenderness, and
secondary masticatory muscle soreness may be
displayed.
• Dry-socket pain may also initiate a myofascial trigger
point pain mechanism especially affecting the masseter
and temporalis muscles.
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110. Periosteal Pains
• The periosteum, in contrast to bone, is richly innervated
with sensory receptors.
• It is particularly sensitive to pressure and impact stress.
• The mechanoreceptors in periosteal tissue supply
proprioceptive input for underlying bony structures.
• Noxious stimulation of the periosteum therefore has a
high potential for reactive muscle effects and
nociception.
• The pain that emanates from the periosteum is
disproportionately greater than the initiating noxious
stimulus.
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112. Soft Connective Tissue Pains
• Pain that emanates from the soft connective tissue
structures of the mouth and face constitutes a major
subdivision of musculoskeletal pain.
• Pains from these structures are predominantly
inflammatory and relate to other signs of inflammation by
which the source of pain may be identified.
• The pain is considerably more constant than muscle pain
and it usually follows an inflammatory time frame.
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113. • Acute cellulitis is usually evident from the swelling and
pain, and no diagnostic problem occurs as long as the
inflammation is located in accessible regions
• Subacute and chronic cellulitis is less dramatic and may
present diagnostic problems of differentiation from cysts
and tumors.
• The history and clinical course plus manual palpation
and surgical aspiration are the usual means of
establishing the diagnosis.
• Pain of cellulitic origin should be differentiated from
muscle pain, vascular pain, and glandular pain. Other
conditions that may initiate soft connective tissue pain
are cysts and tumors, both benign and malignant.
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114. Therapeutic Options
For the management of primary deep somatic
musculoskeletal pains that emanate from osseous,periosteal,
and soft connective tissue structures, the following
therapeutic options are available
• Analgesics for palliative relief
• Reduction of functional demands
• counseling
• Cause-related therapy consisting of the identification and
treatment of causative factors and contributing conditions,
and general medical and surgical supportive care including
antibiotics, antiinflammatory agents, and deep heat
therapy
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116. Neuropathic Pain
1.Burning-type pains that are spontaneous, triggered, or
ongoing and unremitting.
2. The pain occurs disproportionate to the stimulus.
3. The pain is accompanied by other neurologic signs.
4. The pain may be initiated, accentuated, or maintained by
sympathetic activity.
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118. Episodic Neuropathic Pain
1.Quick, sharp, electrical-like pain (paroxysmal).
2. Very intense debilitating pain.
3. Duration is momentary (seconds).
4. Very little to no pain between episodes.
5. The pain follows the distribution of the affected nerve.
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119. Neuralgias
• Trigeminal
– Primary (idiopathic)
– Secondary (symptomatic)
• Acute herpetic and Post herpetic
• Geniculate (Ramsay Hunt)
• Glossopharyngeal
• Superior laryngeal
• Occipital
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120. Trigeminal neuralgia
• Trigeminal neuralgia is characterized by sudden, stabbing, and
severe unilateral facial pain in ≥1 of the 3 divisions of the trigeminal
nerve, most frequently the second.
• Onset is frequently triggered by mechanical stimulation such as
talking, chewing, or touch.
• Attacks can last from seconds to a few minutes. Periods of attacks
can last weeks or months, followed by periods of remission for
months or years.
• Incidence increases with age, with the average onset at age 50
years; it more commonly presents in women.
• Limited information is available about the etiology of trigeminal
neuralgia other than the possible compression of the trigeminal root
by a vessel or tumor.
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121. Treatment
• Carbamazepine is the drug of first choice for treatment,
with an initial beneficial response in >75% of patients.
• Baclofen potentiates the action of carbamazepine and
can be a useful adjunct.
• Gabapentin is a safe and well-tolerated adjunct to
• Carbamazepine or may be used as sole treatment. Other
less frequently used agents include oxcarbazepine,
lamotrigine, clonazepam, and sodium valproate.
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122. • Some of the surgical approaches to the treatment of
trigeminal neuralgia include
• microvascular decompression
• radiofrequency rhizothomy
• gamma knife surgery.
Microvascular decompression of the trigeminal nerve
provides immediate and long-term pain relief in >70% of
patients.
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123. GLOSSOPHARYNGEAL NEURALGIA
• Paroxysmal pain that is similar to, though less intense
than, the pain of TN.
• The location of the trigger zone and pain sensation
follows the distribution of the glossopharyngeal nerve,
namely, the pharynx, posterior tongue, ear, and
infraauricular retromandibular area.
• Pain is triggered by stimulating the pharyngeal mucosa
during chewing, talking, and swallowing.
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124. • May be associated with vagal symptoms, such as
syncope and arrhythmia, owing to the close anatomic
proximity of the two nerves.
• The application of a topical anesthetic to the pharyngeal
mucosa eliminates glossopharyngeal nerve pain and can
aid in distinguishing it from the pain of other neuralgias.
• The most common causes of glossopharyngeal
neuralgia are intracranial or extracranial tumors and
vascular abnormalities that compress CN IX.
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125. • Treatment is similar to that for TN,with a good response
to carbamazepine and baclofen.
• Refractory cases are treated surgically by intracranial or
extracranial section of CN IX, microvascular
decompression in the posterior cranial fossa, or (more
recently) by percutaneous radiofrequency
thermocoagulation of the nerve at the jugular foramen.
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126. NERVOUS INTERMEDIUS (GENICULATE)
NEURALGIA
• Nervous intermedius (geniculate) neuralgia is an uncommon
paroxysmal neuralgia of CN VII, characterized by pain in the
ear and (less frequently) the anterior tongue or soft palate.
• Pain is not as sharp or intense as in TN, and there is often
some degree of facial paralysis,indicating the simultaneous
involvement of the motor root.
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127. • Geniculate neuralgia commonly results from herpes
zoster of the geniculate ganglion and nervus intermedius
of CN VII, a condition referred to as Ramsay Hunt
syndrome.
• Viral vesicles may be observed in the ear canal or on the
tympanic membrane.
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128. Treatment
• A short course (2 to 3 weeks) of high-dose steroid
therapy
• Acyclovir
• Carbamazepine and antidepressants.
• Patients who do not respond to these medications may
undergo surgery to section the nervus intermedius
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129. OCCIPITAL NEURALGIA
• Occipital neuralgia is a rare neuralgia in the distribution
of the sensory branches of the cervical plexus (most
Commonly unilateral in the neck and occipital region).
• The most common causes (in descending order of
frequency) are trauma, neoplasms, infections, and
aneurysms involving the affected nerve(s).
• Palpation below the superior nuchal line may reveal an
exquisitely tender spot.
• Treatment has included corticosteroids, neurolysis,
avulsion, and blocking the nerve with a local anesthetic
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130. Superior Laryngeal neuralgia
• Superior Laryngeal nerve is a branch of vagus and
innervates the cricothyroid muscle of the larynx.
• Periodic ,unilateral submandibular pain radiating
through the ear, eye or shoulder.
• Pain is paroxysmal, lasting momenterily and may be
provoked by swallowing,straining the voice,turning the
head,coughing,sneezing or blowing the nose.
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133. Migraine headaches
The pathogenesis of migraine headaches is controversial,
but current research has implicated a neurogenic etiology
(neurogenic inflammation) possibly causing secondary
cerebrovascular changes.
• Triggering factors
Diet, stress, sleep disturbances, and menstruation.
• The forms of migraine
Migraine with aura
Migraine without aura
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134. • No laboratory or radiological tests exists for migraine and diagnosis
is made on the basis of clinical features.
• Both forms of migraine have a hereditary predisposition,
• Begins at a young age
• Primarily affect women
• Typical attacks may last from 4–72 hours
• Usually unilateral
• Pulsating pain with moderate to severe intensity.
• Sometimes the pain may be bilateral, especially in children, and
non-pulsatile.
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135. • Associated with symptoms of nausea and/or vomiting,
photophobia, and phonophobia.
• Often begin immediately after awakening or soon thereafter.
• Patients typically are unable to function and just wish to lie
down in a dark room.
• Migraine with aura is characterized by visual disturbances,
such as flashing lights and colors, zigzag patterns, or blind
spots and, on occasion, numbness and tingling more on one
side of the face and arm .
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136. Cluster headaches
• Although cluster headaches are relatively uncommon, it
is one of the most severe forms of headache and facial
pain, and has been referred to as a "suicide headache"
• Male-to-female ratio of 5:1.
• It is of two types:
-An episodic type, where the attacks of pain occur during
a time of susceptibility, known as the cluster period,
which may last for weeks or months
-Chronic form, where there is an absence of pain-free
remission periods .
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137. • A cluster attack may last from 15 minutes to 3 hours, and
can occur from once every other day to as often as 8 times
per day.
• Frequently, the patient is awakened from sleep by the
attack.
• Cluster pain is excruciating and has a boring, sharp, or
Burning quality. unilateral in location, involving the
periorbital area, often with radiation to the ipsilateral temple
and maxilla, including the teeth.
• And is associated with autonomic symptoms such as
lacrimation from the eye on the affected side, nasal
congestion, rhinorrhea, forehead and facial sweating, ptosis,
and eyelid edema. www.indiandentalacademy.com
138. Tension-type headache
Tension-type headache is divided into two major
categories:
• Episodic-The episodic tension-type headache lasts for
30 minutes to one week
• Chronic- form occurs with a frequency of at least 15
days a month for at least 6 months.
• Pain is usually described as a steady, dull, aching
sensation of mild to moderate intensity, but throbbing
pain may occasionally be present.
• The headaches occur primarily in the bifrontal occipito-
nuchal and bitemporal areas, and are often associated
with stiffness and tenderness of the neck.
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139. • Photophobia or phonophobia may also be part of the
headache complaint in some patients.
• Unlike migraine, physical activity does not worsen the
pain, and nausea is usually absent.
• The chronic type may evolve from the episodic type and
shares similar clinical features.
• Tension-type headaches must be differentiated from
migraine without aura, referred pain from myofascial
trigger points, cranial arteritis, and TMD, especially when
bitemporal pain is a chief complaint.
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140. Chronic paroxysmal hemicrania
• Is short-lasting (2 to 45 minutes)
• Frequently occurring attacks of pain (five per day for
more than half of the time).
• The quality of pain is throbbing or pounding,with an
intensity that parallels that of cluster headaches, the
patient often choosing to pace the floor during an attack.
• Pain location is predominantly oculotemporal and frontal,
always on the same side, and can spread to involve the
entire side of the head and the neck, shoulder, and arm.
Cases involving CPH presenting as intermittent
toothache have been reported.
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141. • Turning or bending the head forward may precipitate
an attack in some cases.
• Associated symptoms include unilateral lacrimation,
nasal stuffiness, and conjunctival injection.
• Nausea and vomiting are usually absent, as are visual or
somatosensory auras.
• In contrast to cluster headache, CPH is seen
predominantly in women.
• Age at onset appears to be 20 years,
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142. Chronic Paroxysmal Hemicrania-
Treatment
• Indomethacin is the medication of choice for CPH.
• If the pain does not resolve with this medication, it is
unlikely to be CPH.
• Aspirin and naproxen have a partial effect, but the relief
is not as dramatic as with indomethacin.
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143. Continuous Neuropathic Pain
1.Quality is often dull, yet burning-type pain.
2. The pain is ongoing and unremitting, yet the intensity
can show patterns of fluctuation.
3. The pain is accompanied by other neurologic signs.
(anesthesia, paresthesia, hypoesthesia, hyperesthesia)
4. There is normally no evidence of any tissue (somatic)
changes or disease.
5. The pain may be initiated, accentuated, or maintained
by sympathetic activity.www.indiandentalacademy.com
146. Neuropathic Toothache: Continuous
1. Neuritis
• Inflammatory condition in the peripheral
distribution of the nerve due to trauma,
chemical, viral or bacterial causes
– Arises in the maxillary or mandibular division of the
trigeminal nerve along with other neurological
symptoms
– Neuritis of the superior dental plexus due to extension
from maxillary sinusitis may cause a toothache in
and around one or more of the maxillary teeth
– Neuritis of the inferior alveolar nerve in the
mandibular teeth from direct trauma, dental infection
or surgery
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148. Herpes Zoster
• It is an acute neuritis of viral source that presents with
severe pain in the exact distribution of the involved
nerve.
• Tiny vesicles appear usually 4-5 days after the onset of
the pain and burst open to produce surface lesions.
• Unilateral presentation
• Ophthalmic division of trigeminal nerve is most
commonly affected.
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149. Post-Herpetic Neuralgia
• Patients with PHN experience persistent pain,
paresthesia, hyperesthesia, and allodynia months to
years after the zoster lesions have healed.
• The pain is often accompanied by a sensory deficit, and
there is a correlation between the degree of sensory
deficit and the severity of pain.
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150. • The best therapy for PHN is prevention. The use of
antiviral drugs, particularly famciclovir, along with a short
course of systemic corticosteroids during the acute
phase of the disease may decrease the incidence and
severity of PHN.
• Topical therapy includes the use of topical anesthetic
agents, such as lidocaine, or analgesics, particularly
capsaicin.
• Tricyclic antidepressants- amitriptyline,nortriptyline,
doxepin, and desiprimine
• Gabapentin
• Anticonvulsant drugs, such as carbamazepine or
phenytoin. www.indiandentalacademy.com
151. • When medical therapy has been ineffective in managing
intractable pain, nerve blocks or surgery at the level of
the peripheral nerve or dorsal root have been effective
for some patients.
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152. Peripheral Neuritis
• It is a painful condition that relates to the entire
peripheral nerve trunk,not just the nerve endings and
terminal branches.
• Sensory ,motor and autonomic symptoms may be
present,depending on the fibre content of the affected
nerve.
• The pain is described as burning, bright, or stimulating,
and is usually accompanied by a feeling of paresthesia
or anesthesia in the distribution of the affected nerve.
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153. • Trigeminal neuritis is due to inflammation of the peripheral branches of a
nerve trunk as a result of trauma, bacterial or viral infection, or toxic
causes.
• An example of neuritis affecting the facial nerve is Bell’s palsy, which
usually results from compression of the nerve inside the facial canal or
Stylomastoid foramen.
• It should be noted that the sympathetic nervous system, specifically
sympathetic efferent activity, may be involved in various deafferentation
pain disorders as well as other neuropathies related to trauma.
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155. Neuropathic Pain: Continuous
2. Deafferentation
• Crushing or cutting of a peripheral nerve
(Traumatic Neuralgia)
– May follow an injury such as external trauma,
pulp extirpation, extraction or major oral
surgery
– Often mistaken for a post-traumatic or
postoperative complication
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156. • When a peripheral nerve is partially or completely
severed as a result of trauma injury, it attempts to repair
the damage by regenerating.
• When this attempt is unsuccessful, a disorganized,
intertwined mass of nervous tissue can result.
• Neuromas are characterized by deep, aching, burning
pain induced by compression or stretching at the site of
injury.
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157. Neuropathic Pain: Continuous
Atypical Odontalgia (Phantom Toothache)
• Pain is felt in a tooth or tooth site (maxillary canine and
premolar are most common)
• Pain is continuous or almost continuous
• Pain persists more than four months
• No sign of local or referred pain
• Local anesthetic of the painful tooth provides equivocal
results
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159. Sympathetically Maintained Pains
Deafferentation tooth pains may be influenced by the
efferent activity of the sympathetic nervous system
• Normal sympathetic activity (sympathetic tone) can be
responsible for maintaining the pain
• An increase in sympathetic activity could increase the
pain condition
• Increased levels of emotional stress could aggravate
this condition
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160. Atypical Facial Pain
• Diagnosis of exclusion
• Psychogenic facial pain
• Location and description inconsistent
• Women, 30 – 50 years old
• Usually accompanies psychiatric diagnosis
• Treat with antidepressantswww.indiandentalacademy.com
161. Axis II Categories (Psychologic
Conditions)
• Psychologic conditions influence all pains. These
conditions have their greatest effects on chronic pains.
The longer a patient suffers, the greater the influence of
these factors.
• Psychological intensification of pain may proceed until
the suffering is wholly disproportionate to the peripheral
nociceptive input.
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162. • Although the original pain complaint may have displayed
the usual clinical characteristics of somatic or
neuropathic pain, as psychological intensification
converts it into a chronic pain disorder, the clinical
symptoms take on identifying features.
• Such pain lacks an adequate source of input that is
anatomically related to the site of pain.
• It may be felt in multiple and sometimes changeable
locations.
• Pain bilaterally may become evident in the absence of
bilateral sources of noxious input.
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163. • The complaint may display unusual or unexpected
responses to therapy. It may respond too quickly or too
slowly. It may respond in an exaggerated way or with
unusual side effects or complications.
• The response may be followed by a relapse without
organic justification, or the condition may remain
refractory in spite of otherwise effective therapy.
• Pains that are greatly influenced by psychologic factors
may display changeableness in location, intensity, or
temporal behavior without a reasonable, identifiable
organic cause.
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164. Although there are numerous disorders, the following
common mental disorders can greatly influence the
individual's pain experience:
• 1) Mood Disorders
• 2) Anxiety Disorders
• 3) Somatoform Disorders
• 4) an Other category that includes many other mental
conditions or psychologic factors that affect the outcome
of a medical condition.
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165. Mood disorders are subdivided into
• Depressive disorders,
• Bipolar disorders
• Mood disorder is due to a medical condition.
Anxiety disorders are subdivided into
• Generalized anxiety disorders
• Posttraumatic stress disorders,
• Anxiety disorders that are due to a medical condition.
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166. Somatoform Disorders are a group of disorders that are
characterized by physical symptoms suggesting a physical
disorder for which there are no demonstrable organic
findings of known physiologic mechanisms.
The somatoform disorders are subdivided into
• Undifferentiated somatoform disorders
• Conversion disorders
• Pain disorders
• Hypochondriasis.
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167. The last category is a broad group of mental
disorders that may be related to pain conditions.
This category includes –
• Malingering
• Psychological factors affecting a medical condition
-personality traits or coping styles
-maladaptive health behavior
-stress-related physiological responses.
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168. CONCLUSION
An organized approach is necessary to assess and
diagnose orofacial pain, since multiple medical and dental
specialties are involved in the management of patients. The
clinician must be able to correctly diagnose and treat the
patient accordingly, or refer the patient to the appropriate
specialist.
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169. REFERENCES
• Jeffrey P Okeson,Bell’s Orofacial Pains,5th
edition,Quintessence Publishing Co,1995
• Burket’s,Oral Medicine,11th
edition,BC decker Inc 2008
• Burket’s,Oral Medicine-Diagnosis and Treatment,9th
edition, Lippencott –Raven Publishers 1997.
• O. P. Tandon, V. Malhotra, S. Tandon and I.
D’silva,Review Article Neurophysiology of pain : Insight
to orofacial pain, Indian J Physiol Pharmacol 2003; 47
(3) : 247–69
www.indiandentalacademy.com
170. • Ingle and Bakland, Endodontics,5th
edition, Chapter 8,
Nonodontogenic toothache and chronic head and neck pains ,page
no. 287-356, Published by PMPH-USA, 2002
• David J. Alvarez, Pamela G. Rockwell, Trigger Points: Diagnosis
and Management,Am Fam Physician 2002;65:653-60
• Jean Schoenen, Differential diagnosis of facial pain ,Acta neurol.
belg., 2001, 101, 6-9
• Richard A. PERTES, Differential diagnosis of orofacial
pain,october/november 1998 number 5 & 6 volume 65:348–354
www.indiandentalacademy.com
171. • Melis M, Secci S. Diagnosis and Treatment of Atypical
Odontalgia: A Review of the Literature and two Case
Reports. J Contemp Dent Pract 2007 March;(8)3:081-
089.
• Sujay A. Mehta, Joel B. Epstein, Charles Greene,
Headache Recognition and Management of Headache,J
Can Dent Assoc 2006; 72(9):835–9
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