This document provides an overview of orofacial pain and discusses trigeminal neuralgia in particular. It begins by defining pain and noting that orofacial pain can result from diseases of the orofacial structures, musculoskeletal issues, peripheral or central nervous system diseases, or psychological abnormalities. It then discusses the cranial nerves involved in orofacial sensation before focusing on the trigeminal nerve and its distribution. The document explains that trigeminal neuralgia is the most common facial pain disorder resulting from trigeminal nerve involvement and describes its potential causes and clinical features such as paroxysmal episodes of intense, electric shock-like pain precipitated by light touch of trigger zones.
2. Pain
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“An unpleasant sensory
and emotional experience
associated with actual or
potential tissue damage,
or described in terms of
such damage.”
3. Orofacial pain (OFP) is the presenting
symptom of a broad spectrum of diseases
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Disease of the
oro-facial
structures
Generalized
musculoskeletal or
rheumatic disease
Peripheral or
CNS disease
Psychological
abnormality
As a symptom, it may be due to
The pain may be referred
from other sources
(eg. cervical muscles or
intracranial pathology).
or
OFP may also occur in the absence
of detectable physical, imaging, or
laboratory abnormalities
4. Cranial nerves responsible for orofacial pain
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Trigeminal nerve,(CN V) is the dominant
nerve that relays sensory impulses from the
orofacial area to the central nervous system.
Facial (CN VII),
Glossopharyngeal (CN IX),
Vagus (CN X) nerves
5. Trigeminal nerve
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Skin of face,
Forehead and scalp
The top of the head
Conjunctiva and bulb of the eye
Oral and nasal mucosa
External aspect of the tympanic membrane
Teeth
Anterior two-thirds of tongue
Masticatory muscles
TMJ
Meninges of anterior and middle cranial fossae
6. The most common facial pain disorder resulted
from involvement of trigeminal nerve is
Trigeminal neuralgia
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▪ One disease affecting the
trigeminal nerve is trigeminal
neuralgia.
▪ A person experiencing
trigeminal neuralgia may suffer
an episode of facial pain that can
last as long as two minutes.
▪ The cause of this disease is
not currently known, but it may
have to do with blood vessels
putting pressure on the trigeminal
nerve as it leaves the brain
stem.
trigeminal neuralgia
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•Bell’s palsy is a weakness or
paralysis of the muscles on one
side of the face.
•The facial nerve is often
damaged by inflammation and
causes one side of the face to
droop.
•Other symptoms of Bell’s palsy
may be pain in or behind the
ear, drooping, excessive tearing
or dry eyes, numbness on one
side of the face, or increased
sensitivity to sound.
Bell’s Palsy
11. Glossopharyngeal (CN IX)
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Mucosa of the pharynx;
Palatine tonsils;
Posterior one-third of the
tongue;
Internal surface of the
tympanic membrane;
Skin of the external ear
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Glossopharyngeal Neuralgia
Glossopharyngeal
neuralgia is a condition
believed to be caused by
irritation of the 9th
cranial nerve.
In which there are
repeated episodes of
severe pain in the
tongue, throat, ear, and
tonsils, which can last
from a few seconds to a
few minutes.
14. vagus (CN X)
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Skin at the back of
the ear;
Posterior wall and floor
of external auditory
meatus.
Tympanic membrane.
Meninges of posterior
cranial fossa.
Pharynx.
Larynx.
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The vagus nerve is one of the largest nerve
systems in the body.
The name vagus is Latin for "wandering,"
which describes the long and complicated
path this nerve takes through the body and
all of the different systems it comes in
contact with.
In some cases this nerve is linked to medical
conditions such as low blood pressure, and in
other cases doctors will stimulate this nerve
to help treat disorders such as epilepsy.
16. Classification of the pain
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I- According to location
II- According to origin
17. I- According to location
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1- Neuritis
Inflammation of nerve ending induced by chemical,
microbial or toxic agents …..Burning sensation
II- Neuralgia
Paroxysmal pain along the course of the nerve
III-Psychogenic
No anatomical distribution, no clinical cause, not
interfere with eating or sleeping
18. II- According to origin
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1. Somatic pain
2. Neurogenous pain
3. Psychogenic pain
4. Referred pain
5. Vascular pain & headache.
20. Somatic pain
It resulting from stimulation of normal neural
structures that innervates body tissue
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Origin: Skin & MM
Nature: Burning or pricking in nature
Character: Localized
Pts can identify its site
For Example:
Thermal pain: Pizza, hot instrument
Chemical pin: aspirin burn
Mechanical: traumatic ulcer
Superfacial ulceration due to systemic
disease eg; leukemia
Superficial
Deep
21. Deep pain
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joint
Muscle
Bone
Collection of
infected fluid in
bone as in
abscess
OVER
stretching or
Contraction
Rupture
of some fibers
TMJ
22. Character of deep somatic pain
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1- Bone pain will be throbbing in nature
2- May be referred involve area supplied with
the same sensory nerve
3- Muscle and joint pain: dull aching in nature.
4- Patient can hardly identify the source of the
pain.
23. II- According to origin
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1. Somatic pain
2. Neurogenous pain
3. Psychogenic pain
4. Referred pain
5. Vascular pain & headache.
31. Referred pain
Is pain that perceived at a location other than the site
of the painful stimulus.
An example is the case of angina pectoris brought on
by a myocardial infarction, where pain is often felt in
the neck, shoulders, and back rather than in the
thorax (chest), the site of the injury
Referred pain is not felt at the site of disease but felt
at distance site
Radiating pain is the extension of pain from original site
to another site with persistance of pain at original site
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32. II- According to origin
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1. Somatic pain
2. Neurogenous pain
3. Psychogenic pain
4. Referred pain
5. Vascular pain & headache.
35. Tension headache
A tension headache is the most common type
of headache.
It can cause mild, moderate, or intense pain
behind your eyes and in your head and neck.
Some people say that a tension headache feels
like a tight band around their forehead.
Most people who experience tension
headaches have episodic headaches
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36. Migraine
Migraine is a neurological condition that can
cause multiple symptoms.
It's frequently characterized by intense,
debilitating headaches.
Symptoms may include nausea, vomiting,
difficulty speaking, numbness or tingling,
and sensitivity to light and sound.
Migraines often run in families and affect
all ages
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37. Cluster headache
Cluster headache (CH) is a neurological
disorder characterized by recurrent
severe headaches on one side of the head,
typically around the eye.
There is often accompanying eye watering,
nasal congestion, or swelling around the eye
on the affected side.
These symptoms typically last 15 minutes to
3 hours
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39. Cranial arteritis.
Or Temporal arteritis is a form of vasculitis
(inflammation of the blood vessels) in
temporal arteries.
Also known as giant cell arteritis or Horton's
arteritis
Frequently it causes headaches, scalp
tenderness, jaw pain and vision problems.
Untreated, it can lead to blindness.
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42. Facial Neuralgias
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The classic neuralgias that affect the craniofacial
region are a unique group of neurologic disorders
involving the cranial nerves and are characterized by
II.Neurogenous pain
Brief episodes of
shooting, often
electric shock–
like pain along
the course of
the affected
nerve branch.
pain-free periods
between attacks
and refractory
periods
immediately
after an attack,
during which a
new episode
cannot be
triggered
trigger zones on
the skin or
mucosa that
precipitate
painful attacks
when touched.
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These clinical characteristics differ from
neuropathic pain, which tends to be
- constant
- has a burning quality
- without the presence of trigger zones.
II.Neurogenous pain
44. Facial Neuralgias resulting in Neurogenous pain
1-Trigeminal neuralgia
2-Glossopharyngeal n. Paroxysmal
4- Post herpetic neuralgia
5- Post traumatic pain
6- Atypical odontalgia Non paroxysmal
7- Bell’s palsy
8- Frey’s auriculo-temporal syndrome
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45. TRIGEMINAL NEURALGIA
tic douloureux
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II.Neurogenous pain
People with this pain often twitch, which is where trigeminal
neuralgia gets its French nickname 'tic douloureux’,
meaning "painful twitch”.
46. TRIGEMINAL NEURALGIA
tic douloureux
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It is a sharp sever paroxysmal pain along the course of
trigeminal nerve with un-definitive etiology
It is the most common of the cranial neuralgias
• Chiefly affects individuals older than 50 years of age.
When younger individuals are involved, suspicion of a
detectable underlying lesion such as a tumor, an
aneurysm, or multiple sclerosis must be increased.
II.Neurogenous pain
47. Etiology and Pathogenesis.
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The cause of the majority of cases of TN remains
controversial, but approximately 10% of cases have
detectable underlying pathology such as:
1- Tumor of the cerebellar pontine angle,
2- Multiple sclerosis, MS
3- A vascular malformation.
The remainder of cases of TN (90%) are classified as
idiopathic.
Several theories exist regarding the etiology of TN.
II.Neurogenous pain
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The most widely accepted theory
is that a majority of cases of
TN are caused by an
atherosclerotic blood vessel
(usually the superior cerebellar
artery) pressing on and grooving
the root of the trigeminal nerve.
This pressure results in focal
demyelinization and
hyperexcitability of nerve fibers,
which will then fire in response
to light touch, resulting in brief
episodes of intense pain.
II.Neurogenous pain
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Evidence for this theory includes the
observation that neurosurgery that removes
the pressure of the vessel from the nerve root
by use of a microvascular decompression
procedure eliminates the pain in a majority of
cases.
II.Neurogenous pain
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Additional evidence for this theory was obtained
from a study using tomographic magnetic
resonance imaging (MRI), which showed that
contact between a blood vessel and the
trigeminal nerve root was much greater on the
affected side.
54. Clinical Features
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The majority of patients with TN present with
characteristic clinical features, which include episodes
of intense shooting stabbing pain that lasts for a few
seconds and then completely disappears.
The pain has an electric shock–like quality and is
unilateral except in a small percentage of cases.
The maxillary branch is the branch that is most
commonly affected, followed by the mandibular branch
and (rarely) the ophthalmic branch. Involvement of
more than one branch occurs in some cases.
II.Neurogenous pain
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Pain in TN is precipitated by light touch on a
“trigger zone” present on the skin or mucosa within
the distribution of the involved nerve branch.
Common sites for trigger zones include the nasolabial
fold and the corner of the lip.
II.Neurogenous pain
56. TRIGGER FACTORS
Touching Washing of
face Shaving
Teeth
cleaning Cold breeze Eating
Talking
Application
of lotions and
cosmetics
patients often protect the trigger zone with their hand or
an article of clothing.
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Intraoral trigger zones can confuse the
diagnosis by suggesting a dental disorder,
and TN patients often first consult a dentist
for evaluation.
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Just after an attack,
there is a refractory
period when touching
the trigger zone will
not precipitate pain.
The number of attacks
may vary from one or
two per day to several
per minute.
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Half an inch finger sign: The patient points
to the trigger area with his finger away by
half an inch to avoid touching it.
II.Neurogenous pain
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Diagnosis.
The diagnosis is based on the history of
shooting pain along a branch of the trigeminal
nerve, precipitated by touching a trigger
zone, and possibly examination that
demonstrates the shooting pain.
A routine cranial nerve examination will be
normal in patients with idiopathic TN, but
sensory and/or motor changes may be evident
in patients with underlying tumors or other
CNS pathology.
II.Neurogenous pain
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Local anesthetic blocks, which temporarily
eliminate the trigger zone, may also be
helpful in diagnosis.
Since approximately 10% of TN cases are
caused by detectable underlying pathology,
enhanced MRI of the brain is indicated to
rule out tumors, multiple sclerosis, and
vascular malformations.
66. Mechanism of action of anticonvulsants,
antiepileptic or antiseizure drugs)
Anticonvulsants suppress the excessive
rapid firing of neurons during seizures.
Anticonvulsants also prevent the spread
of the seizure within the brain.
Conventional antiepileptic drugs may block
sodium channels or enhance γ-
aminobutyric acid (GABA) function.
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67. Several antiepileptic drugs have multiple or
uncertain mechanisms of action.
Next to the voltage-gated sodium channels
and components of the GABA system, their
targets include GABAA receptors, the GAT-1
GABA transporter, and GABA transaminase.
Additional targets include voltage-
gated calcium channels, SV2A, and α2δ.
By blocking sodium or calcium channels,
antiepileptic drugs reduce the release of
excitatory glutamate, whose release is
considered to be elevated in epilepsy, but also
that of GABA. 5/18/2021
68. This is probably a side effect or even the
actual mechanism of action for some
antiepileptic drugs, since GABA can itself,
directly or indirectly, act proconvulsively.
Another potential target of antiepileptic
drugs is the peroxisome proliferator-
activated receptor alpha.
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Since TN may have temporary or
permanent spontaneous remissions, drug
therapy should be slowly withdrawn if a
patient remains pain free for 3 months.
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Clinicians treating TN must be aware that
drug therapy often becomes less effective
over time and that progressively higher
doses may be required for pain control.
In cases in which drug therapy is
ineffective or in which the patient is unable
to tolerate the side effects of drugs after
trials of several agents, surgical therapy is
indicated.
II.Neurogenous pain
2. Surgical
71. SURGICAL
1. Injection of phenol or alcohol into
a trigeminal ganglion
2. Radiofrequency coagulation of a
branch
3. Sectioning of sensory root of
trigeminal ganglion inside the
cranium
4. Microvascular decompression
72. PREVENTION
While the condition itself can't be prevented, there are
a number of things patients can do to
avoid triggering attacks:
Wash with cotton pads and warm water over the
face
Rinse the mouth with water after eating, if tooth-
brushing triggers pain
Eat and drink food and beverages at room temperature
Chew on the unaffected side
Eat soft foods, if eating is becoming a problem
74. POSTHERPETIC NEURALGIA
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Etiology and Pathogenesis.
Herpes zoster, is caused by the reactivation of latent
varicella-zoster virus that results in both pain and
vesicular lesions along the course of the affected
nerve.
Approximately 15 to 20% of cases of herpes zoster
involve the trigeminal nerve although the majority of
these cases affect the ophthalmic division of the fifth
nerve, resulting in pain and lesions in the region of the
eyes and forehead.
II.Neurogenous pain
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Herpes zoster of the maxillary and mandibular
divisions is a cause of facial and oral pain as
well as of lesions.
In a majority of cases, the pain of herpes
zoster resolves within a month after the lesions
heal.
Pain that persists longer than a month is
classified as postherpetic neuralgia (PHN)
although some authors do not make the
diagnosis of PHN until the pain has persisted
for longer than 3 or even 6 months.
II.Neurogenous pain
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PHN may occur at
any age, but the
major risk factor
is increasing age.
Elderly patients
also have an
increased risk of
experiencing severe
pain for an
extended period of
time.
II.Neurogenous pain
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Clinical Manifestations.
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.
II.Neurogenous pain
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Management.
Many treatment options are available for
the management of PHN, and the method
chosen should depend on the severity of
the symptoms as well as the general
medical status of the patient.
Treatment includes topical and systemic,
drug therapy and surgery.
II.Neurogenous pain
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Topical therapy includes the use of topical
anesthetic agents, such as lidocaine, or analgesics,
particularly capsaicin.
Lidocaine used either topically or injected gives
short-term relief from severe pain.
Capsaicin, an extract of hot chili peppers that
depletes the neurotransmitter substance when used
topically, has been shown to be helpful in reducing
the pain of PHN, but the side effect of a burning
sensation at the site of application limits its
usefulness for many patients.
II.Neurogenous pain
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The use of tricyclic antidepressants is a well-
established method of reducing the chronic
burning pain that is characteristic of PHN.
Because a significant number of elderly
patients cannot tolerate the sedative or
cardiovascular side effects associated with
tricyclic antidepressants, the use of other
drugs, particularly gabapentin, has been
advocated.
II.Neurogenous pain
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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.
The best therapy for PHN is prevention.
There is evidence that 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
II.Neurogenous pain
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Glossopharyngeal Neuralgia
Glossopharyngeal
neuralgia is a condition
believed to be caused by
irritation of the 9th
cranial nerve.
In which there are
repeated episodes of
severe pain in the
tongue, throat, ear, and
tonsils, which can last
from a few seconds to a
few minutes.
87. POST-TRAUMATIC NEUROPATHIC PAIN
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Etiology and Pathogenesis.
Trigeminal nerve injuries may result from
facial trauma or
surgical procedures, such as the removal of impacted
third molars, the placement of dental implants, the
removal of cysts or tumors of the jaws, or osteotomies.
In some individuals, nerve injury results only in
numbness whereas others experience pain that may be
either spontaneous or triggered by a stimulus.
The pain associated with nerve injury often has a burning
quality.
II.Neurogenous pain
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Total nerve section (neurotmesis)
Frequently causes permanent nerve damage, resulting in
anesthesia and/or dysesthesia.
Nerve injuries
Minor nerve injuries (neurapraxia)
Do not result in axonal degeneration but may cause
temporary symptoms of parasthesia for a few hours or days.
Serious nerve damage (axonotmesis)
Results in the degeneration of neural fibers although the
nerve trunk remains intact.
It cause symptoms for several months but have a good
prognosis for recovery after axonal regeneration is
complete.
90. Manifestation
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Patients with nerve damage may experience
persistent burning pain arising from trauma plus:
II.Neurogenous pain
Anesthesia=loss of sensation
Paraesthesia=feeling of pins and needles
Allodynia=Pain by non painful stimuli
Hyperalgesia=Exaggerated response to
mild painful stimuli
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It is peripheral facial weakness of
unknown etiology affecting any age group
of either sex.
How did Bell’s palsy get its name?
Sir Charles Bell was a Scottish surgeon
who described the nerve supply to the
facial muscles over 200 years ago.
Bell’s palsy
II.Neurogenous pain
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Bell’s palsy is recognized as a unilateral
paralysis of the facial nerve.
The dysfunction has been attributed to an
inflammatory reaction involving the facial
nerve.
A relationship has been demonstrated between
Bell’s palsy and the isolation of herpes simplex
virus 1 from nerve tissues.
Bell’s palsy must be differentiated from
other causes of facial nerve paralysis, such as
herpes zoster of the geniculate ganglion
(Ramsay Hunt syndrome).
95. Pathogenesis of Bell’s palsy
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Geneculate ganglion
Stylomastoid foramen
Facial nerve
Petrosal artery Stylomastoid artery
Fibrous C T
Middle meningeal External carotid
Inflammation of Facial
nerve inside the canal
demyelination & edema
loss blood supply
II.Neurogenous pain
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Its etiology is unknown and there is no local
or systemic causes can be identified.
It may be immunologically mediated or
associated with infection especially viral
infection
II.Neurogenous pain
98. Clinically
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Very rapid onset, patient may wake up with facial paralysis
Bell’s palsy begins with slight pain around one ear and along the
mandibular angle, followed by an abrupt paralysis of the muscles on
that side of the face.
The eye on the affected side stays open, the corner of the mouth
drops.
As a result of masseter weakness, food is retained in both the upper
and lower buccal and labial folds.
The facial expression changes remarkably.
Due to impaired blinking, corneal ulcerations from foreign bodies can
occur.
Involvement of the chorda tympani nerve leads to loss of taste
sensation on the anterior two-thirds of the tongue and reduced
salivary secretion.
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Eyelid drooping and difficulty closing one (or
both) upper eyelids are classic findings in Belle’s
palsy.
101. Asymmetric or
incomplete
smiles, decrease
in forehead
wrinkling, nasal
stuffiness, and
mild difficulty
with speaking are
also common
signs.
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102. Frequent early
symptoms include
abrupt onset of dry
eye and tingling
around the mouth,
with progression to
more complete
facial palsy
occurring within one
to several days.
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103. Treatment
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Systemic corticosteroids within the first few days
after the onset of paralysis.
Combining steroids with antiherpetic drugs such as
acyclovir may decrease the severity and length of
paralysis.
It is also helpful to protect the eye with lubricating
drops or ointment and a patch if eye closure is not
possible.
In chronic condition, surgical decompression of the
nerve in the stylomastoid canal is effective
Disease of Nervous system
105. Frey’s auriculo-temporal
syndrome
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Disease of Nervous system
In this condition there is
flushing and sweating of the skin
of the face innervated by the
auriculotemporal nerve whenever
salivation is stimulated
(gustatory sweating).
106. Frey’s auriculo-temporal syndrome
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Mandibular nerve
Auriculo-temporal
Disease of Nervous system
Paroted
glands
Sweat
glands
Periauricular &
temporal region
Sympathetic fibers
107. Etiology
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Surgery
Neoplasm
Inflammation
Damage of
auriculotemporal
nerve
In Parotid
Innervations of sweat
glands by the
parasympathetic
salivary fibers
108. Clinically
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During eating:
Flushing, sweating and paroxysmal pain in
periauricular & temporal region
Between attacks
Hyperesthesia or anesthesia of periauricular &
temporal region
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Diagnosis:
Nerve block of auriculotemporal will relieve
symptoms.
Treatment:
Sectioning of auriculotemporal nerve
112. Burning Mouth Syndrome
(Glossodynia)
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The patient suffering from burning sensation
of mucosa without definitive causes
Pain dose not follow anatomical pathway
No lab. Findings
No neurological findings
Psychogenic pain
113. Etiology
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The cause of BMS is unknown, but a number
of factors have been suspected such as:
1- Hormonal imbalance (postmenopausal)
2- Allergic reaction
3- Dry mouth
4- Chronic rubbing of mucosa
5- Psychogenic
114. CLINICAL MANIFESTATIONS
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Women experience symptoms of BMS seven
times more frequently than men.
Mainly complain at tongue, lips and cheek
Burning intermittent or constant pain
Diffuse pain, patient can not identify the site
of the pain
Pain is relieved by eating drinking or chewing
Normal oral mucosa or mild atrophic
Depression symptoms, lack of appetite,
insomnia,
115. Diagnosis
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1- Exclusion of possibility of any oral or
dental lesions
2-Careful clinical examination & lab
investigation to detect undiagnosed anemia
3- If it unilateral, exam the cranial nerves.
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•MPD, or masticatory myalgia, is a
psychophysiologic disease that primarily
involves
the muscles of mastication and not the TMJ.
•Women are affected more frequently than
men.
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•MPD frequently is confused with painful conditions
affecting the TMJ, such as degenerative arthritis
or internal derangements,
•because patients with primary MPD can develop
these diseases secondarily, and patients with
primary joint disease can develop secondary MPD.
•Better understanding of the causes and
pathogenesis of this condition now makes its
diagnosis easier, however, and its treatment more
effective.
119. Myo-fascial pain dysfunction syndrome
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It is a chronic disorder characterized by
Clicking
Trismus
Pain
+ Absence of pathologic abnormality of TMJ
Psychogenic causes
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Stress seems to be an important factor in the
development of MPD.
It is hypothesized that centrally induced
increases in muscle activity, frequently combined
with the presence of parafunctional habits such
as clenching or grinding of the teeth, result in
the associated muscle fatigue, pain, and
dysfunction.
Similar symptoms also occasionally can result,
however, from muscle overextension, muscle
overcontraction, or trauma
122. Etiology
5/18/2021 9:03 PM Oelshall
Muscle over
Extension Or Contraction
intermaxillary space over closure of mouth
Muscle fatigue
Oral habits due to psychic factors
Grinding clenching bruxism
123. 5/18/2021 9:03 PM Oelshall
Altered chewing pattern
Chewing on one
side
Deviation of
bite to avoid
painful tooth
Malerupted
tooth
Muscle over
extension, over
contraction or
spasm
Sertonin,
histamin, kinin,
PG release
Inflammation
& pain
124. Clinically
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1-Unilateral pain
Pain over ear or periauricular area
Pain dull, sharp, pressure, burning as described by
the pts
Pain intensity: mild to sever
Pain may described as a vague pain affecting the
whole side of the face
Pain may radiate to forehead, occipital, temporal,
cervical region or the mandibular angel
Pain increased with tension, fatigue or chewing
125. 5/18/2021 9:03 PM Oelshall
2-Active trigger point
Area of muscle that is tender on palpation
It include temporalis, masseter, digastric,
ptrygoid, sternomastoid
3-Deviation
Deviation of the jaw towards the affected
side on opening
126. Late clinical manifestations
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Limitation of the jaw function
The patient cannot open his mouth widely
except with gentle pressure on lower jaw
Clicking
detected by palpation