The trochlear nerve controls eye movement through innervation of the superior oblique muscle. It has the longest intracranial course of the cranial nerves and is responsible for intorsion and depression of the eye. Damage can result in hypertropia and excyclotorsion of the affected eye. The abducens nerve controls lateral gaze through innervation of the lateral rectus muscle. Isolated 6th nerve palsy is commonly due to vascular causes like diabetes or hypertension and results in esotropia and diplopia worse on lateral gaze to the affected side.

2. TROCHLEAR NERVE

3. • The trochlear nerve is the fourth paired cranial nerve.
• It is the smallest cranial nerve (by number of axons), yet has the longest intracranial course.
• It has a purely somatic motor function.
• One of the ocular motor nerves that controls eye movement.
• The trochlear nerve, while the smallest of the cranial nerves, has the longest intracranial course as it is the only nerve
to have a dorsal exit from the brainstem.
• It originates in the midbrain and extends laterally and anteriorly to the superior oblique muscle
INTRODUCTION

4. • Trochlea is Latin for pulley, which
appropriately describes the sling of
connective tissue that houses the
tendon of the superior oblique.
• Moreover, the trochlear nerve is a
somatic efferent (motor) nerve, and
along with oculomotor (III) and
abducens (VI) nuclei, it is responsible for
eye movement.
• Through its innervation of the superior
oblique, the trochlear nerve controls
the abduction and intorsion of the eye
STRUCTURE AND FUNCTION

5. • The trochlear nerve, as well as the abducens (VI), hypoglossal (XII), and
oculomotor (III) nerves, is a homolog of the ventral roots of the spinal
nerves.
• The somatic efferent columns of the brainstem give rise to these cranial
nerves.
• The muscles that they innervate are derived from the cranial (preoptic
and occipital) myotomes in early skeletal muscle development.
• During the fourth week of development, the neural tube is composed
of three primary vesicles, the prosencephalon, mesencephalon, and
rhombencephalon.
• The mesencephalon goes on to develop into the midbrain.
• It is from the posterior part of the midbrain that the trochlear nerve
originates.
• From here the nerve passes ventrally to innervate the superior oblique
muscle
EMBRYOLOGY

6. NUCLEUS
• MIDBRAIN – ventromedial part of central gray
matter at the level of inferior colliculus.
• Caudal to and continuous with 3rd nerve
nucleus complex.
• Belongs to somatic efferent column of nuclei
and closely related to medial longitudinal
bundle.
FUNCTIONAL COMPONENTS
• SOMATIC EFFERENT – movements of the
eyeball through superior oblique muscle.
• GENERAL SOMATIC AFFERENT –
proprioceptive impulses from superior
oblique relayed in mesencephalic
nucleus of trigeminal nerve.

8. COURSE AND ITS DISTRIBUTIONS
PARTS
1. Fascicular part
2. Precavernous part
3. Intracavernous part
4. Intraorbital part

9. FASCICULAR PART
Nucleus efferent fibres posteriorly around the aqueductal
gray matter anterior medullary velum decussate completely.

10. PRECAVERNOUS PART
Superior medullar vellum frenum veli dorsal aspect of midbrain
just above pons winds around cerebral peduncle between posterior
cerebellar and superior cerebellar arteries lateral to cerebral peduncle
posterior corner of roof of cavernous sinus.

11. INTRACAVERNOUS PART
Cavernous sinus lateral wall below oculomotor + above 1st
division of trigeminal nerve anterior part crosses over 3rd nerve
lateral part of superior orbital fissure.

12. INFRAORBITAL PART
• Superior orbital fissure above the origin of LPS orbital surface of superior oblique
• Extra fibres in intraorbital part carry proprioceptive impulses join ophthalmic division
of 5th nerve in cavernous sinus relay in mesencephalic nucleus of 5th nerve.

13. SUPERIOR OBLIQUE MUSCLE
 PRIMARY POSITION OF GAZE
 GLOBE 51’’ ADDUCTED
 GLOBE 39’’ ABDUCTED
• Primary action – INTORSION (along A-P axis)
• Secondary action – DEPRESSION (along
horizontal axis)
• Tertiary action – ABDUCTION (along vertical
axis )
• Axis of muscle rotation coincides with
optical axis.
• DEPREESION only
• Optical axis and line of pull of muscle
meet at an angle of 90’
• INTORSION only.

14. 4th NERVE PARALYSIS
• Idiopathic: Most idiopathic cases are believed to be congenital, with presentation occurring in adult
life.
• Trauma: Trauma (moderate frontal head trauma) is a frequent cause of bilateral trochlear nerve
palsy.
• Vascular
• Others
• Often, the cause of 4th cranial nerve palsy cannot be identified.
• The most common identified cause is A head injury often due to a motorcycle accident but
sometimes even relatively minor head trauma.
• Occasionally, diabetes causes this palsy by damaging small blood vessels that carry blood to the
nerve.
• Rarely, the cause is a tumor, a bulge (aneurysm) in an artery in the skull, or multiple sclerosis
CAUSES

15. CLINICAL FEATURES
Signs
Ipsilateral hypertropia and excyclotorsion are frequently seen due to the superior oblique’s function of intorsion
and depression the eye. Patients can also develop a compensatory head tilt in the direction away from the
affected muscle.
Symptoms
Patients can present with binocular, vertical or torsional diplopia. The superior oblique causes eye depression in
adducted gaze. This can explain the worsening of a patient’s diplopia when they attempt to visualize objects in
primary position, especially in down-gaze. Patients with mild or long-standing disease may have blurred vision,
difficulty focusing and dizziness instead of diplopia

16. The trochlear nerve has the longest intracranial course of all of the cranial nerves. There are four anatomic regions
which can be responsible for non-isolated CN IV palsies
Midbrain (nuclear/fasicular)
• Hemisensory loss, ataxia, internuclear ophthalmoplegia, hemiparesis, central Horner syndrome, cranial nerve III
palsy
• Frequently due to infarction or hemorrhage
• Presence of an ipsilateral or contralateral rAPD without loss of visual acuity, color vision, or peripheral vision in an
apparently isolated CN IV palsy suggests superior colliculus brachium involvement. This suggests a central CN IV
palsy.
Subarachnoid Space
• Fever, headache, neck stiffness may be associated with meningitis.
• Aneurysms may manifest as an isolated CN IV palsy
Cavernous Sinus
Signs and symptoms associated with CN III, V, VI and Horner’s syndrome (e.g. ptosis,miosis, etc.)
Orbit
• Signs and symptoms associated with CN II,III, V, VI and II.
• Proptosis, chemosis, and orbital edema may also be seen.
LOCALIZED CLINICAL FEATURES

18. SYNDROMES
1.NUCLEAR - FASCICULAR
• Diffuse to distinguish nuclear and
fasicular lesions due to short course of
fascicles within midbrain.
• Fascicular lesions may get contralateral
Horner’s syndrome ; and trauma (
especially near anterior medullary
velum ) may cause bilateral CN IV
palsies.
1. Haemorrhage
2. Infraction
3. Demyelination
4. Trauma

19. 2.SUBARACHNOID SPACE:
• Closed head trauma
• Meningitis
• Neoplasms like – pinealomas , tentorial meningiomas
• Aneurysms

20. Table 1: Causes and clinical features of cavernous sinus syndrome
Cause Clinical Features
Tumor[5]
Meningioma, chordoma, neuroma, pituitary
adenoma, metastases, lymphoma,
nasopharyngeal carcinoma, chondrosarcoma,
hemangioma, neuroblastoma
Inflammatory Disease[5] Tolosa-Hunt syndrome, sarcoidosis
Trauma[4] Basal skull fracture, operative trauma to
cavernous sinus after skull base surgery
Vascular[5] Intracavernous aneurysm, carotid-cavernous
fistula, cavernous sinus thrombosis
Infection[6] Mucormycosis, aspergillosis, actinomycosis,
nocardiosis, mycobacterium, herpes zoster
3.CAVERNOUS SINUS SYNDROME
Cavernous sinus syndrome (CSS) is a condition caused by any pathology involving the cavernous sinus
which may present as a combination of unilateral ophthalmoplegia (cranial nerve (CN) III, IV, VI),
autonomic dysfunction (Horner syndrome) or sensory CN V1- CN V2 loss

21. 4. ORBITAL SYNDROME
Orbital Apex Syndrome (also known as Jacod
syndrome)
Disease
Orbital apex syndrome (OAS) involves cranial
neuropathies in association with optic nerve
dysfunction. Orbital apex syndrome is
symptomatically related to superior orbital
fissure syndrome and cavernous sinus syndrome
with similar etiologies. The distinction is the
precise anatomic involvement of the disease
process.

22. Signs/Symptoms
•The most common initial manifestation of OAS is visual loss
and ophthalmoplegia involving multiple cranial nerves
• Visual loss is due to CNII involvement. Optic disc edema
or subsequent optic atrophy may develop within weeks
to months.
• Ophthalmoplegia with variable diplopia, mydriasis, and
ptosis due to CNIII, IV, VI involvement
•Absence of corneal sensations and corneal reflex
•Pupillary abnormalities: Relative Afferent Pupillary Defect
(RAPD)
•Choroidal folds
•Periorbital/facial pain and hypoesthesia of the forehead due to
CNV involvement.
•Proptosis with or without orbital congestion
•Chemosis and/or conjunctival injection

23. 5.ISOLATED SUPERIOR OBLIQUE PALSY
Most commonly etiologies are congenital
and traumatic
1.CONGENITAL – large vertical fusion
amplitude (10 – 15 prism diopters )
FAT – Family Album Tomography Scan
2.ACQUIRED – In ischemic conditions –
diabetes , herpes zoster.

24. Differential Diagnosis
1.Oculomotor palsy
2.Guillain Barre Syndrome
3.Orbital Pseudotumor
4.Brown Superior Oblique Tendon Sheath
Syndrome
5.Fisher Syndrome
6.Botulism
7.Chronic Progressive External
Ophthalmoplegia (CPEO)
8.Vertical one-and-a-half syndrome
9.Monocular Supranuclear Gaze Palsy
10.Myasthenia Gravis
11.Ocular Tilt Reaction/Skew Deviation
12.Thyroid Eye Disease

25. Management
• The management of a trochlear nerve palsy depends on the etiology
of the palsy.
• Patients with traumatic or congenital fourth nerve palsies may be
considered for patch, prism, or surgical treatment, especially if they
are symptomatic in primary gaze.
• Patients with an acquired trochlear nerve palsy may respond to
treatment of the underlying disease. Microvascular causes may
spontaneously resolve over the course of weeks or months. When
these palsies persist, they are typically responsive to prism treatment
as they tend to cause comitant deviations.
• Prism therapy is a reasonable treatment option for patients amenable
to therapy.
• Strabismus surgery can be used in patients who do not respond or
tolerate prisms.
• Patching is also an acceptable alternative for patients who defer
prisms or surgery.

26. ABDUCEN NERVE

28. COURSE
Passes upwards and anterolaterally in subarachnoid space of posterior cranial fossa.
Pierces the arachnoid and dura lateral to dorsum sellae (part of the sphenoid bone).
Arises between the layers of dura on posterior surface of petrous bone near its
apex.
Turns anteriorly to transverse the cavernous sinus.
Enters the orbit through the superior orbital fissure within the annular tendon to
supply the lateral rectus muscle.

29. 6TH CRANIAL
NERVE
FACIAL
COLLICULUS
GENICULUM OF
NERVE

30. ANATOMICAL LANDMARKS
POSTERIOR CRANIAL FOSSA
SUPERFICIAL EMERGENCE
MIDDLE CRANIAL FOSSA
CAVERNOUS SINUS
SUPERIOR ORBITAL FISSURE
ORBIT

31. BLOOD SUPPLY
1. Anterior inferior cerebellar artery
2. Posterior inferior cerebellar artery
3. The internal auditory artery
4. The anterolateral artery
5. The pontomedullary artery
6. The inferolateral pontine artery
7. The anterolateral artery – the
majority of the abduces nerves are
supplied by this artery.

32. CLINICAL ASPECTS

33. 1. AT THE LEVEL OF NUCLEUS
• Ipsilateral weakness of
abduction
• Failure of horizontal gaze
towards the side of lesion
• Ipsilateral facial nerve palsy (
lower motor neuron) leads to
involvement of facial fasciculus.
• AN ISOLATED 6TH NERVE PALSY I[
THERFORE NEVER NUCLEAR IN
ORIGIN.
• In adults , the most likely
etiology of isolated sixth nerve
palsy is ischemic
mononeuropathy that may be
due to diabetes mellitus,
arteriosclerosis, hypertension,
temporal arteritis or anemia.

34. 2. PONTINE SYNDROMES – AT THE LEVEL OF FASCICULUS
M
• MILLARD GUBLER SYNDROME
R
• RAYMOND CESTON
SYNDROME
F
• FOVILLE SYNDROME

35. A. MILLARD – GUBLER SYNDROME
• Involves fasciculus as it passes through the pyramidal tract.
• Ipsilateral 6th nerve palsy.
• Contralateral hemiplegia (paralysis)

36. B. RAYMOND – CESTON SYNDROME
• Due to tumour of
cerebral peduncle.
• Red nucleus – speech
and gait disorder.
• Paralysis of lateral
conjugate gaze
• Ipsilateral 6th nerve
palsy.
• 5th nerve – facial
anaesthesia.
• Contralateral
hemiparesis.

37. C. FOVILLE SYNDROME
• Involves fasciculus as it passes through PPRF.
• 5TH nerve – facial anaesthesia
• 6th nerve + gaze palsy
• 7th nerve – facial weakness
• 8th nerve – deafness
• Central horner syndrome.

38. 3. AT THE PONTOMEDULLARY JUNCTION
ACOUSTIC NEUROMA :
• May damage the 6th nerve at pontomedullary junction.
• 1st symptom – hearing loss
• 1st sign – decrease corneal sensitivity.
• It is very important to test hearing and corneal sensation in all patients with 6th nerve palsy.

39. 4. IN THE BASILAR COURSE
A. RAISED INTRACRANIAL TENSION:
• Downward displacement of brainstem
• Stretching of 6th nerve over petrous tip
• Bilateral localizing sign.
B. NASOPHARYNGEAL TUMOURS:  invade skull and its foramen
.
C. BASE OF SKULL FRACTURES : both unilateral and bilateral.
D. GRADENIGO’S SYNDROME :
• Mastoiditis / acute petrositis
• Damage to 6th nerve at the petrous tip
• Facial weakness
• Pain
• Hearing difficulties.

40. 5. INTRACAVERNOUS PART
• Situated close to the internal carotid artery.
• More likely to damage than other cranial nerves.
• Intra cavernous 6th nerve palsy is accompanied by a postganglionic HORNER’S syndrome .

41. • Esotropia
• Head – turn
• Binocular diplopia (worse at
distance)
• Vision loss
• Pain
• Hearing loss
• Symptoms of vasculitis,
particularly giant cell arteries
• trauma
CLINICAL PRESENTATION

42. :
•Vasculopathy: Hypertension, Diabetes mellitus, aneurysm
•Congenital: Duane retraction syndrome (Types 1 and 3), congenital esotropia,
•Infectious/Inflammatory: Sphenoiditis, lateral rectus myositis.
•Autoimmune/Inflammatory: Myasthenia gravis, Miller-Fisher syndrome, thyroid eye disease
•Neoplastic
•Traumatic: Blowout fracture with entrapment of the medial rectus
•Other: Spasm of the near reflex, longstanding esotropia with medial rectus contracture, ocular
neuromyotonia
• Duane syndrome may be differentiated from an abducens nerve palsy by the presence of narrowing of the
lid fissure in adduction, which may be seen in Duane syndrome but not in an abducens nerve palsy.
• Thyroid eye disease, although more commonly bilateral, may present with unilateral symptoms including
proptosis and symptoms of inflammation upon awakening.[11]
• Diplopia in myasthenia gravis fluctuates and is fatigable and with or without generalized fatigability,
shortness of breath and hoarseness
DIFFERENTIAL DIAGNOSIS

43. General treatment
• Treatment of abducens nerve palsy depends on the underlying etiology.
• systemic conditions are treated primarily.
• Most patients recover within 3-6 months.
• Treatment for the diplopia managed with prisms, occlusion, botulinum toxin, or surgery.
• Occlusion using a Bangerter filter or patch can eliminate diplopia and confusion, prevent amblyopia or
suppression in children, and decrease the possibility of ipsilateral medial rectus contracture.
• Base-out Fresnel prisms can be used to help the patient maintain binocular single vision.
• Botulinum toxin injections into the medial rectus of the affected eye.
MANGEMENT

44. • Strabismus surgery can be performed for persistent abducens nerve palsies that demonstrate stable measurements over
a 6-month period.
• Forced duction test is performed
• If there is residual lateral rectus muscle function: often, a resection of the affected lateral rectus and recession of the
ipsilateral medial rectus (recess/resect or “R and R” procedure) is performed. Alternatively, a resection of the affected
lateral rectus with a recession of the contralateral medial rectus may be performed.
• If there is no lateral rectus muscle function: various forms of transposition surgeries can be considered (e.g., full tendon
transposition, Jensen, Hummelsheim, Augmented Hummelsheim with resections +/- Foster modifications, Knapp's
procedure).
• Superior rectus transposition combined with medial rectus recession has been shown to improve esotropia, head
position, and abduction in patients with abducens palsy.
• Botulinum toxin injections to the medial rectus of the affected eye can also be used as a temporizing treatment.
• Surgical follow up
• Patients may be managed closely postoperatively, and any residual diplopia can be managed with prisms
SURGICAL PROCEDURES

46. TRIGEMINAL NERVE

47. INTRODUCTION
1. IT IS THE FIFTH CRANIAL NERVE AND THE LARGEST NERVE.
2. IT COMPRISES OF THREE COMPONENTS :
 OPHTHALMIC NERVE
 MAXILLARY NERVE
 MANDIBULAR NERVE
1. IT IS THE NERVE OF FIRST BRACHIAL ARCH.
2. THE FIRST TWO BRANCHES ARE PURELY SENSORY AND THE THIRD BRANCH IS MIXED NERVE.

49. • The spinal trigeminal nucleus is one of
three nuclei in the sensory trigeminal nerve
pathway.
• The spinal trigeminal nucleus further
subdivides into the pars (subnucleus)
caudalis, pars (subnucleus) oralis, and pars
(subnucleus) interporalis.
• Each nucleus serves its own purpose.
• The pars oralis, one portion of the primary
sensory nucleus of the trigeminal nerve, as
well as the pars interpolaris are responsible
for transmission of discriminative tactile
sense from the face.
• The pars caudalis is responsible for the
transmission of pain and temperature from
the ipsilateral face

50. PATHWAY OF TRIGEMINAL NERVE

51. BRANCHES OF TRIGEMINAL NERVE

52. ANATOMICAL COURSE
The trigeminal nerve originates from three sensory nuclei (mesencephalic, principal sensory, spinal
nuclei of trigeminal nerve) and one motor nucleus (motor nucleus of the trigeminal nerve) extending
from the midbrain to the medulla.
At the level of the pons, the sensory nuclei merge to form a sensory root. The motor nucleus
continues to form a motor root. These roots are analogous to the dorsal and ventral roots of the spinal
cord.

53. ANATOMICAL COURSE
In the middle cranial fossa the sensory root expands into the trigeminal ganglion which is located in the
trigeminal cave.
The peripheral aspect of the trigeminal nerve gives rise to the three divisions.
Motor root passes inferiorly to the sensory root along the floor of the trigeminal cave . its fibres are distributed
to the mandibular division .
1. opthalmic nerve exits through superior orbital fissure
2. Maxillary nerve exits through foramen rotundum
3. Mandibular nerve exits through foramen ovule

54. OPHTHALMIC NERVE
IT GIVES RISE TO THREE BRANCHES :
1. FRONTAL
2. LACRIMAL
3. NASOCILIARY

55. Ophthalmic
nerve

56. OPHTHALMIC NERVE
It innervate the skin and mucous membrane derivatives of the frontonasal prominence:
A.Forehead and scalp
B.Frontal and ethmoidal sinus
C.Upper eyelid and its conjuntiva
D.Cornea
E.Dorsum of the nose
It provides parasympathetic innervation to the lacrimal gland.

57. MAXILLARY NERVE
 Middle meningeal nerve
 Zygomaticotemporal nerve
 Zygomaticofacial nerve
 Nasopalatine nerve
 Greater palatine nerve
 Lesser palatine nerve
 Anterior superior alveolar nerve
 Middle superior alveolar nerve
 Posterior superior alveolar nerve
 Inferior palpebral branches
 External nasal branches
 Superior labial branches

58. MAXILLARY NERVE

59. MAXILLARY NERVE
IT INNERVATES THE SKIN, MUCOUS MEMBRANE AND SINUSES OF DERIVATIVES OF THE
MAXILLARY PROMINENCE OF THE 1ST PHARYNGEAL ARCH.
1.LOWER EYELID AND ITS CONJUNCTIVA
2.CHEEKS AND MAXILLARY SINUS
3.NASAL CAVITY AND LATERAL NOSE
4.UPPER LIP
5.UPPER MOLAR,INCISOR AND CANINE THE AND THE ASSOCIATED GINGIVA
6.SUPERIOR PALATE
IT PROVIDES PARASYMPATHETIC SUPPLY TO LACRIMAL AND NASAL GLAND

60. MANDIBULAR
NERVE
THE TERMINAL BRANCES AREA:
BUCCAL NERVE
INFERIOR ALVEOLAR NERVE
AURICULOTEMPORAL NERVE
LINGUAL NERVE

62. MANDIBULAR NERVE
ANTERIOR DIVISION
(motor innervation-muscle of mastication)
Masseteric nerve
masseter
Medial pterygoid nerve
medial pterygoid
tensor tympani
Tensor veli palatine nerve
tensor veli palatine

63. •NERVOUS SPINOUS(SENSORY) FROM FORAMEN SPINOSUM
• lateral pterygoid nerve
Lateral pterygoid
 Deep temporal nerve
temporalis
(sensory innervation)
 Buccal nerve
inside of the cheek
MANDIBULAR NERVE

64. POSTN
Lingual split
(sensory innervation)
 Anterior 2/3 of tongue (mucous membrane
inferior alveolar split)
(motor innervation)
mylohyoid
Digastric(anterior belly)
Sensory innervation
Teeth and mucoperiosteum of mandibular teeth
Chin and lower lip
Auriculotemporal split
Scalp(auricle/temporal region)

65. CLINICAL FEATURES OF TRIGEMINAL NERVE:
TRIGEMINAL NEURALGIA
It is a chronic pain disorder that affect the trigeminal nerve
TYPES
1.Typical
2.Atypical
SYMPTOMS
1.Typical
Episodes of severe ,sudden ,electric shock like pain in one side of the face that lost for
seconds to minutes .
2.Atypical
constant burning sensation that is less severe

66. TRIGEMINAL NEURALGIA

67. TRIGEMINAL GANGLIA
Covering - contained in a Dural pouch known as
cavum trigeminale ( meckel’s cave).
Dural extend forward as a ballooning of meningeal
layer of Dura mater from posterior cranial to
middle cranial fossa below attached margin of
tentorium cerebelli
Cavum-
ROOF - formed by two meningeal layer
FLOOR- one meningeal and one endosteal
layer

68. DEFINITION
Trigeminal neuralgia is defined as sudden, usually unilateral,
shock like pain, severe, brief, stabbing, laminating, paroxysmal,
recurring pain in the distribution of one or more branches of fifth cranial nerve.

69. TYPES

70. ETIOLOGY
The cause of this disease is unknown. It is usually
idiopathic.
The probable etiologic factors are
1. VASCULAR FACTORS.
Transient ischemia and autoimmune
hypersensitivity responses have been proposed as
causes of the demyelination of the nerve
2. MECHANICAL FACTORS
It also been postulated such as the pressure of
aneurysms of the intrapetrous portion of the
internal carotid artery that may erode through the
floor of the intracranial fossa to exert a pulsatile
irritation on the ventral side of the trigeminal
ganglion.

73. Pathophysiology
Atherosclerotic blood vessel pressing on the root of trigeminal nerve
Focal demyelination
Hyperexcitability of nerve fibres.
Episode of intense pain

74. GENERAL CHARACTERISTICS
INCIDENCE : It is a rare affliction, seen in about 4 in 1,00,000 persons.
AGE OF OCCURRENCE: 5th or 6th decade
SEX PREDILECTIONS: with female predispositions 58%
AFFLICTION FOR SIDES : Predilections for right side is noted 60%
DIVISION OF TRIGEMINAL NERVE INVOLVEMENT : V3 is more commonly involved than V2
division. Very rarely V1 ophthalmic division is involved in about 5% of cases (only sensory
division is affected)

75. CLINICAL CHARECTERISTICS
1. Trigeminal neuralgia typically manifests as a sudden,
unilateral,intermittent,paroxysmal,sharp,shooting,lancinating,shock like by slight
touching superficial “trigger points “which radiates from that point, across the
distribution of one or more branches of the trigeminal nerve.
2. During an attack, the patient grimaces with pain, clutches his hands over the
affected side of the face, stopping all the activities and holds or runs his face, which
may redden or the eyes water until the attack subsides.

76. Presence of an intraoral or extra oral trigger points provacable by obvious stimuli is seen
in TN.
The location of the trigger points depends on which division of trigeminal nerve is
involved.
In V2 – points are located on the skin of the upper lip,ala nasi or cheek or on the upper
gums
In V3 – this is the most frequently involved branch. Trigger points are seen over the lower
lip,teeth or gums of the lower jaw.Tongue is rarely involved.
In V1 – the trigger zone usually lies over the supra orbital ridge of the affected side

77. Signs
•Corneal reflex
•Sensory examination- 25% have abnormalities ( lewi & grant 1938)
•Motor examination -asymmentrical jaw motion
•Ipsilateral nasolabial fold hypesthesia
•other deficits symptomatic TGN

78. SYMPTOMS
Sudden burning or shock like facial pain
episodes can be 5 seconds to 2 minutes
multiple occurence per day are possible
no pain between attacks
talking, eating, brushing teeth, or even cool air on the face
Flurries of episodes can occur from weeks to months then stop abruptly for a month or yar at a time
there is no loss of taste ir hearing in someone suffering from tic doulerex

79. TRIGGER FACTORS
Hair brushing and cleaning of teeth
tilting head and shaving
Stress and tiredness
Cold and hot weather
Chewing and swallowing
Touching and washing face
Light breeze and wind on face

80. DIAGNOSIS
SWEET DIAGNOSTIC DIAGNOSTIC 5 MAJOR CRITERIA FOR TN(TRIGEMINAL NEUROLOGY)
1. The pain paroxysmal
2. The pain may be provoked by light touch to the face(trigger zones)
3. The pain is confident to trigeminal distribution
4. The pain is unilateral
5. The clinical sensory examination is normal.

81. Differential diagnosis
• Dental pathology.
• Temporomandibular joint dysfunction.
• Migraine.
• Giant cell arteritis (temporal arteritis)
• Cluster headaches.
• Multiple sclerosis and other disorders of myelin. Overlying aneurysm of a blood vessel.
• Tumour in the posterior fossa eg, meningiomas. Arachnoid cyst at the cerebellopontine angle.
• Postherpetic neuralgia after shingles.

82. SURGICAL
PROCEDURES
ABLATIVE
PERIPHERAL
Cryotherapy
radiofrequency
Neurectomy
Alcohol injection
Peripheral
neurectomy
GASSERIAN
GANGLION
Partial sensory
thermocoagulation
Glycerol rizholysis
Balloon compression
POSTERIOR
FOSSA
Rhizotomy
Gamma knife
radiosurgery
NONABLATIVE
MICROVASCULAR
DECOMPRESSI
ON

83. Investigations
MRI scan of the brain is indicated to rule out other potential causes of pain if the diagnosis is uncertain or if
red flags are present. Mit may be used to identify Sinusitis, Extracranial masses along the course of the
trigeminal nerve.
Pathological enhancement of the trigeminal nerve that could indicate perineural spread of malignancy
Cavernous sinus masses, Demyelination plaques that might indicate multiple sclerosis,
Intrinsic brain lesions in the thalamus or trigeminal brain stem pathways such ac lacunar infarctions.
Cerebelloponine angle mass lesions such as tumour. epidermoid, dermoid, or arachnoid cyst,

84. PHARMACOLOGICAL MANAGEMENT
FIRST LINE OF APPROACH
Carbamazepine 100, 200mg..
SECOND LINE OF APPROACH
Phenytoin 100mg
Baclofen 5-80 mgiday
Lamotrigine 25 mgiday
THIRD LINE OF APPROACH
Clonazepam 4-ing
Valproic acid 250-500 mg

85. SURGICAL MANAGEMENT
Those patients who do not respond to medications and are physically fit can go
for invasive procedures.
Peripheral Injections
Longer acting anesthetic agents
Agents like bupivacaine without adrenaline but with or without corticosteroids
are injected to the peripheral nerve end.

86. Alcohol injections Glycerol injection in
the gasserian ganglion
• 0.5-2ml of 95% absolute alcohol is used
for injection.
• Injected behind the ganglion and
destroy both small and large
nerve fibers.

87. MICROVASCULAR DECOMPRESSION
It is the only medical or surgical intervention that directly addresses the presumed underling
pathology of classic TGN.
Jannetta procedure
Relatively minimal loss of facial sensation or numbness
Opening is made in the skull and teflon pillow is placed between the nerve and the artery to
relieve pressure.
95% immediate relief success rate

88. • Put to sleep with GA
• Positioned on their
back, head turned
on their side
• Straight incision-
2finger breadths
behind the ear about
length of ear
• A portion of skull
30mm<dia> is
removed
• Exposing dura—
cerebellum---
brainstem
• Arachnoid
membrane is
dissected , 5th,7th,8th
nerve is visualized

89. • Offending loop of blood vessel is then mobilized
• Once the vessel is mobilized, sponge is placed between nerve and
offending vessel to prevent vessel from returning to its native position
• After the decompression is complete, the wound is flushed clean with
saline
• Dura is sewn closed
• Skull is closed

91. GLYCEROL RHIZOLYSIS(GR)
 Rapid, safe, reliable, and relatively inexpensive approach
 Test dose – 0.1-0.15ml
 0.05-0.1ml at 3-5 min. intervals
 Total dose -0.1-0.4ml
 Sensory changes; pain, burning or paresthesia

92. PERCUTANEOUS BALLOON COMPRESSION
• 0.5-1ml of contrast
• Pear shaped balloon
• Compression time 1-7 min

93. RADIOFREQUENCY THERMOCOAGULATION
 Selectively injures/destroys the unmyelinated or poorly myelinated noninceptive nerve fibres and
spares the myelinated fibres which serve touch, proprioception, and motor function
 A permanent lesion in the retrogasserian TN is made by beginning at 10V and aprox 60mA for 30-
40sec and increasing to 20V and 100mA

95. GAMMA KNIFE RADIOSURGERY
 Focused array of 201 intercepting beams of gamma radiation, produced by separate cobalt
sources
 the dose is 70-90gy
 Pain relief is not usually immediate
 The mean time to pain relief in two series was approx 1 month

96. Peripheral Neurectomy
Oldest and most effective method.
Mostly performed on the infraorbital nerve, inferior alveolar nerve, mental nerve and rarely
lingual nerve.

97. Cryotherapy
Direct application of cryoprobe (temperature -60°) intraorally to the affected nerve producing
wallerian degeneration of the affected nerve.
In this, the nerve is not sectioned but destroyed.