Trigeminal nerve friday presentation

Trigeminal Nerve
Dr Mahammad Samim Mondal
Unit Presentation
N-2
Chairperson: Prof. S R Chandra
NIMHANS

To Be Discussed:
•Introduction
•Anatomy
•Embryology
•Physiology
•Clinical Correlates
•Radiology
•Surgical and NeuroRehab
2Dr. M. M. Samim Trigeminal Nerve

Introduction

TriGeminal Nerve
1. 3 divisions- Trigeminal ("trigeminal" = tri-, or three, and - geminus, or
twin: thrice-twinned) derives from the fact that each of the two nerves
(one on each side of the pons)
2. Herbert Mayo & Charles Bell described functions of TN
3. Dentist Nerve
4. Mixed Cranial Nerve
5. Fifth Cranial & Largest Cranial Nerve

Indigenous Description Of Trigeminal Nerve
Aacharya Charak described 5 types of Shiroroga (Vataja,
Pittaja, Kaphaja, Sannipataja, Krimija) in
Kiyantashirahsiyam Adhyaya and 4 types of Shirorogas
(Ardhavbhedak, Suryavart, Anantvata, Shankhak) in
Trimarmiya Siddhi Adhyaya.
Acharya Sushruta and Vagbhatta have described 11
types & 10 types of Shiroroga respectively.
Among them Vataja Shirahshoola, Ardhavbhedak,
Anantvata, Raktaja Shirahshoola are much similar to TN
Anjali V. Makodiya1 Akanksha Sharma2 Dr. Sweety Ruparel 3 Dr. Ram Shukla4- IAMJ5Dr. M. M. Samim Trigeminal Nerve

Anatomy

Template of Cranial Nerve
• Supranuclear
• Nuclear
• Intraaxial Fascicular
• Extra-axial Cavernous
• Soft Tissue

Trigeminal Nerve Nuclei
The trigeminal nerve has four nuclei:
(1) The main sensory nucleus,
(2) The spinal nucleus,
(3) The mesencephalic nucleus, and
(4) The motor nucleus.
Gray's 41th Edition

Snell's Neuroanatomy 7th Edition
Main Sensory Nucleus
The main sensory nucleus lies in the posterior part of the pons, lateral to the
motor nucleus . It is continuous below with the spinal nucleus.
Spinal Nucleus
The spinal nucleus is continuous superiorly with the main sensory nucleus in the
pons and extends inferiorly through the whole length of the medulla oblongata
and into the upper part of the spinal cord as far as the second cervical segment .

Mesencephalic Nucleus
The mesencephalic nucleus is composed of a column of unipolar
nerve cells situated in the lateral part of the gray matter around the
cerebral aqueduct. It extends inferiorly into the pons as far as the
main sensory nucleus .
Motor Nucleus
The motor nucleus is situated in the pons medial to the
main sensory nucleus .

Motor Component of the Trigeminal Nerve
• The motor nucleus receives corticonuclear fibers from both cerebral
hemispheres .
• It also receives fibers from the reticular formation, the red nucleus,
the tectum, and the medial longitudinal fasciculus.
• In addition, it receives fibers from the mesencephalic nucleus,
thereby forming a monosynaptic reflex arc.
• The cells of the motor nucleus give rise to the axons that form the
motor root.
• The motor nucleus supplies the muscles of mastication, the tensor
tympani, the tensor veli palatini, and the mylohyoid and the
anterior belly of the digastric muscle.

The fifth nerve is a mixed sensory and motor nerve.
It conducts sensory impulses from the greater part of the face and head; from the mucous
membranes of the nose, mouth, and paranasal sinuses; and from the cornea and
conjunctiva.
It also provides the sensory innervation of the dura in the anterior and middle cranial fossae.
The cell bodies of the sensory part of the nerve lie in the gasserian, or semilunar, ganglion.
This, the largest sensory ganglion in humans, lies in the inferomedial part of the middle
cranial fossa in a recess called Meckel's cave (a dural cavity overlying the apex of the petrous
bone).
The central axons of the ganglion cells form the sensory root of the nerve.
These fibers, on entering the lateral mid pons, divide into short ascending and long
descending branches.
The former are concerned mainly with tactile and light pressure sensation and synapse with
second-order neurons in the principal sensory nucleus.

Proprioceptive afferents from facial muscles and the masseter also ascend to
terminate in the mesencephalic nucleus.
The fibers that mediate pain and temperature sensation do not end in these
nuclei but form long descending branches of the spinal trigeminal tract.
This pathway, which contains both facilitatory and inhibitory fibers, together
with its adjacent nucleus, extends from the junction of the pons and medulla
to the uppermost segments (C2 or C3) of the spinal cord (as evidenced by the
relief of facial pain after medullary trigeminal tractotomy).
Proprioceptive impulses from the muscles of mastication and from the facial
and extraocular muscles are carried by fibers in the sensory root of the
trigeminal nerve that have bypassed the semilunar or trigeminal ganglion.
Snell's Neuroanatomy 7th Edition18Dr. M. M. Samim Trigeminal Nerve

The axons of the neurons in the main sensory and spinal
nuclei and the central processes of the cells in the
mesencephalic nucleus cross the median plane and ascend
as the trigeminal lemniscus to terminate on the nerve cells
of the ventral posteromedial nucleus of the thalamus.The
axons of these cells now travel through the internal capsule
to the postcentral gyrus (areas 3, 1, and 2) of the cerebral
cortex.

The sensations of touch and pressure are conveyed by
nerve fibers that terminate in the main sensory nucleus.
The sensations of pain and temperature pass to the
spinal nucleus .
The sensory fibers from the ophthalmic division
of the trigeminal nerve terminate in the inferior
part of the spinal nucleus; fibers from the
maxillary division terminate in the middle of the
spinal nucleus; and fibers from
the mandibular division end in the superior part
of the spinal nucleus.
Proprioceptive impulses goes to mesencephalic nucleus.

On entering the pons, the fibres of the sensory root of the
trigeminal nerve run dorsomedially towards the principal
sensory nucleus, which is situated at this level. Before
reaching the nucleus, approximately 50% of the fibres
divide into ascending and descending branches; the others
ascend or descend without division. The descending fibres,
of which 90% are less than 4 μm in diameter, form the
spinal tract of the trigeminal nerve, which embraces the
spinal nucleus of the trigeminal nerve and reaches the
upper cervical spinal cord ). There is a precise somatotopic
organization within the tract .
Fibres from the ophthalmic division of the
trigeminal nerve lie ventrally,
those from the mandibular division lie
dorsally, and
those from the maxillary division lie
between.
The tract is completed on its dorsal rim by fibres from the
sensory roots of the facial, glossopharyngeal
and vagus nerves. All of these fibres synapse in the pars
caudalis of the spinal nucleus of the trigeminal nerve.
Somatotopic Arrangement Gray's 41th Edition

Ophthalmic fibres are ventral and descend to the lower limit of the first cervical spinal segment,
Maxillary fibres are central and do not extend below the medulla oblongata, whilst
Mandibular fibres are dorsal and do not extend much below the mid-medullary level.
More recently, it has been proposed that fibres are arranged dorsoventrally within
the spinal tract. There appear to be sound anatomicophysiological and clinical
reasons for believing that all divisions terminate throughout the whole nucleus,
although the ophthalmic division may not project fibres as far caudally as the
maxillary and mandibular divisions. Fibres from the posterior face (adjacent to C2)
terminate in the lower (caudal) part, whilst those from the upper lip, mouth and
nasal tip terminate at a higher level. This can give rise to a segmental (cross-
divisional) sensory loss in syringobulbia. Tractotomy of the spinal tract, if carried
out at a lower level, can spare the perioral region, a finding that would accord with
the ‘onion-skin’ pattern of loss of pain sensation. However, in clinical practice, the
progression of anaesthesia on the face is commonly ‘divisional’ rather than strictly
‘onion-skin’ in distribution Gray's 41th Edition

Fibres of the glossopharyngeal, vagus and facial nerves subserving common sensation
(general somatic afferent) enter the dorsal region of the spinal tract of the trigeminal nerve
and synapse with cells in the caudal part of the spinal nucleus.
Consequently, operative section of the dorsal part of the spinal tract results in analgesia
that extends to the mucosa of the tonsillar sinus, the posterior third of the tongue and
adjoining parts of the pharyngeal wall (supplied by the glossopharyngeal nerve), and the
cutaneous areas of the ear.
Other afferents that reach the spinal nucleus are from the dorsal roots of the upper cervical
nerves and from the sensory–motor cortex.
Gray's 41th Edition

The spinal nucleus of the trigeminal nerve consists of three parts:
the pars oralis (which adjoins the principal sensory nucleus);
the pars interpolaris; and
the pars caudalis (which is continuous with the dorsal horn of the spinal cord).
The pars caudalis is different from the other parts because it has a structure analogous to
that of the dorsal horn of
the spinal cord, with a similar arrangement of cell laminae (subnuclei zonalis, gelatinosus
and magnocellularis), and is involved in trigeminal pain perception.
Cutaneous nociceptive afferents and small-diameter muscle afferents terminate in layers I,
II, V and VI of the pars caudalis
(see Fig. 21.1). Low-threshold mechanosensitive afferents of Aβ neurones terminate in
layers III and IV of the pars caudalis and in the rostral (interpolaris, oralis, principal sensory)
nuclei.
Gray's 41th Edition

Nucleus raphe magnus and associated reticular formation. The nucleus raphe magnus
projects directly to the pars caudalis, probably via enkephalin, noradrenaline
(norepinephrine) and 5-HT (5-hydroxytryptamine, serotonin)-containing terminals.
These fibres directly, or indirectly through local interneurones, influence pain perception.
Stimulation of periaqueductal grey matter or nucleus raphe magnus inhibits the jaw-opening
reflex to nociception, and may induce primary afferent depolarization in tooth-pulp afferents
and other nociceptive facial afferents.
Neurones in the pars caudalis can be suppressed by stimuli applied outside their receptive
field, particularly by noxious stimuli. The pars caudalis is an important site for relay of
nociceptive input and functions as part of the pain ‘gate control’.
However, rostral nuclei may also have a nociceptive role. Tooth-pulp afferents via
widedynamic-range and nociceptive-specific neurones may terminate in rostral nuclei, which
all project to the subnucleus caudalis.
Gray's 41th Edition

• Most fibres arising in the trigeminal sensory nuclei cross the midline and
ascend as trigeminothalamic fibres (trigeminal lemniscus).
• They end in the contralateral ventral posteromedial thalamic nucleus, from
which third-order neurones project to the cortical postcentral gyrus (areas 3,
1, 2).
• However, some trigeminal nuclear efferents ascend to the ipsilateral ventral
posteromedial nucleus.
• Fibres from the pars caudalis, especially from laminae I, V and VI, also project
to the rostral trigeminal nuclei, cerebellum, periaqueductal grey of the
midbrain, arabrachial area of the pons, the brainstem reticular formation and
the spinal cord.
• Fibres from lamina I project to the subnucleus medius of the medial
thalamus.
Gray's 41th Edition

Gray's 41th Edition

Trigeminal Nerve and Branches
• Three large areas of the face can be mapped out to indicate the peripheral nerve
fields associated with the three divisions of the trigeminal nerve.
• The fields are not horizontal but curve upwards , apparently because the facial
skin moves upwards with growth of the brain and skull.
• Embryologically, each division of the trigeminal nerve is associated with a
developing facial process that gives rise to a specific area of the adult face:
• the ophthalmic nerve is associated with the frontonasal process,
• the maxillary nerve with the maxillary process, and
• the mandibular nerve with the mandibular process.

Ophthalmic nerve
The cutaneous branches of the ophthalmic nerve supply the conjunctiva, skin over the forehead, upper
eyelid and much of the external surface of the nose.
Supratrochlear nerve
Supraorbital nerve
Lacrimal nerve
Infratrochlear nerve
External nasal nerve
Maxillary nerve The maxillary nerve passes through the orbit to supply the skin of the lower eyelid, the prominence of the
cheek, the alar part of the nose, part of the temple, and the upper lip.
Zygomaticotemporal nerve
Zygomaticofacial nerve
Infraorbital nerve
Mandibular nerve The mandibular nerve supplies skin over the mandible, the lower lip, the fleshy part of the cheek, part of the
auricle of the ear and part of the temple via the buccal, mental and auriculotemporal nerves.
Buccal nerve
Mental nerve
Auriculotemporal nerve

Embryology

CN V Trigeminal week 5 Stage and week 16
In the embryo, the trigeminal ganglia is first visible in week 4 , initially developing from neural crest cells before
neural fold fusion, and after fusion receive contributions from the neural tube roof plate.
In the adult, cavum trigeminale (Meckel's cave) is an arachnoidal pouch containing cerebrospinal fluid.
Though the dura and arachnoid layers end at the trigeminal ganglion and do not extend to cover the three branches
of the trigeminal nerve.

Physiology

Trigeminal Reflexes
•Blink Reflex
•Lacrimal Reflex
•Jaw Jerk
•Occulocardiac Reflex

Corneal and blink reflexes
• Touching the cornea of one eye elicits reflex closure of both eyes via the corneal reflex.
• The afferent limb of the pathway involves mainly nasociliary branches of the ophthalmic
division of the trigeminal nerve, with cell bodies in the trigeminal ganglion and central
processes synapsing on second-order neurones in the ipsilateral spinal tract and chief sensory
nuclei of the trigeminal nerve.
• These neurones drive a polysynaptic chain of interneurones in the lateral reticular formation
in the pons and medulla, which, in turn, activate neurones innervating the palpebral
components of orbicularis oculi in both ipsilateral and contralateral facial motor nuclei; the
stimulated muscles contract to produce a bilateral blink. The sweep of the eyelids carries
lacrimal secretions across the eye, helping to remove any irritating particles.
• Shining a bright light into one eye elicits a similar reflex closure of both eyes via the blink
reflex; the afferent limb of this reflex involves stimulation of the retina and optic pathway.

Anatomy
Blink reflex

Blink Reflex

An explanation of reflex blink hyperexcitability in Parkinson’s disease
• The basal ganglia can regulate reflex blink excitability by altering the inhibitory
drive from the SNr to the SC.
• In turn, the level of SC activation modulates the activity of NRM neurons that
tonically inhibit spinal trigeminal nucleus responsiveness, the afferent limb of
the reflex blink .
• The dopamine depletion of Parkinson’s disease leads to an increase in SNr
activity. This increased inhibitory output decreases the activity of lateral and
rostral SC neurons.
• The loss of the SC excitatory drive on continuously active NRM neurons
removes some of the tonic inhibition of trigeminal neuronal responsiveness,
which leads to reflex blink hyperexcitability.
• Conversely, Huntington’s disease, which causes a decrease in SNr inhibition of
the SC, leads to reflex blink hypoexcitability. Thus, the tonic level of BG output
modulates trigeminal reflex blink excitability.Michele A. Basso and Craig Evinger
Journal of Neuroscience 15 November 1996, 16 (22) 7318-7330; DOI: https://doi.org/10.1523/JNEUROSCI.16-22-07318.1996

Michele A. Basso and Craig Evinger
Journal of Neuroscience 15 November 1996, 16 (22) 7318-7330; DOI: https://doi.org/10.1523/JNEUROSCI.16-22-07318.1996

Blink Reflex Tracing
Recorded potentials:
A two-channel recording is performed:
R1: muscle action potential from the facial nerve (ipsilateral to stimulated side)
R2: reflex response from trigeminal nerve input ipsilateral side and facial nerve
output bilaterally.

Dr. Chandra's Hypothesis
Increased latency between
R waves can be used as poor
prognostic marker in
overlap dementias.
Sadanandavalli Retnaswami Chandra

• Rapid stretching of the muscles that close the jaw (masseter, temporalis,medial
pterygoid) activates muscle spindle afferents, which travel via the mandibular division of
the trigeminal nerve to the brain stem.
• The cell bodies of these primary afferent neurones are located in the mesencephalic
trigeminal nucleus.
• Collaterals project monosynaptically to the motor nucleus of the trigeminal nerve in the
pons.
• Motor axons arising in the nucleus travel via the mandibular nerve to innervate the
muscles that act on the temporomandibular joint and close the jaw.
• Most fibres that arise in the trigeminal sensory nuclei cross the midline and ascend in the
trigeminal lemniscus.
• They end in the contralateral ventral posteromedial thalamic nucleus, from which thirdorder
neurones project to the postcentral gyrus (areas 3, 1, 2).
• Some trigeminal nuclear efferents ascend to the ventral posteromedial nucleus of the
thalamus.
Jaw jerk reflex

Aschner reflex or trigeminovagal reflex (TVR)
Occulocardiac Reflex
Defined by a decrease in heart rate by greater than 20% following globe
pressure or traction of the extraocular muscles.
The incidence of the oculocardiac reflex is reported to be anywhere from 14% to 90% and decreases with age,
meaning pediatric patients are most at risk.
• The trigeminal nerve, otherwise known as the fifth cranial nerve, serves as the sensory afferent limb.
• The vagus nerve, also known as cranial nerve ten, comprises the efferent limb of the OCR.
• The pathway is initiated by activation of stretch receptors in the ocular and periorbital tissues.
• The short and long ciliary nerves conduct impulses that carry the sensory message to the ciliary ganglion.
From there the impulses are transported by way of the ophthalmic division of the trigeminal nerve to the
Gasserian ganglion, followed by the trigeminal nucleus, where the afferent limb will terminate in the central
nervous system (CNS).
• The CNS will then process this sensory information, and internuclear communication will occur between the
trigeminal sensory nucleus and the visceral motor nucleus of the vagus nerve.
• This stimulates the efferent limb, causing impulses to exit the brainstem and transmit to the myocardium to
synapse as the sinoatrial node and activate the vagal motor response.
• The resultant effects include negative chronotropy, leading to bradycardia.

Occulocardiac Reflex

Tensor tympani and stapedius reflex
• Loud sound elicits reflex contraction of tensor tympani and
stapedius, which attenuates movement of the tympanic
membrane and middle ear ossicles.
• Afferent impulses travel in the cochlear nerve to the cochlear
nuclei in the brainstem.
• Efferent fibres to tensor tympani arise in the motor nucleus of the
trigeminal nerve and travel in the mandibular division of the
nerve.
• Efferent fibres to stapedius originate in the facial nucleus and
travel in the facial nerve. 53Dr. M. M. Samim Trigeminal Nerve

The Sternutatory (Nasal, Sneeze) Reflex
• Stimulation of the nasal mucous membrane with cotton, a spear of tissue, or
similar object causes wrinkling of the nose, eye closure and often a forceful
exhalation resembling a feeble sneeze, as the nose tries to rid itself of the
foreign object.
• The ophthalmic, division of the trigeminal innervates the nasal septum and the
anterior nasal passages.
• The afferent limb of the reflex arc is carried over CN V1, the efferent limb over
CNs V, VII, IX, X, and the motor nerves of the cervical and thoracic spinal cord.
The reflex center is in the brainstem and upper spinal cord. The nasal mucosa
may also be stimulated by irritating inhalants; this is a nasal reflex which
should not be confused with olfaction .
• The primary clinical use of the sternutatory reflex is as a crosscheck on the
corneal reflex. 57Dr. M. M. Samim Trigeminal Nerve

 Stimulation of the trigeminal ganglion in cats or monkeys leads to a decrease in carotid
resistance, with increased flow and facial temperature, predominantly through a reflex
mechanism.
 The afferent limb of this are is the trigeminal nerve, and the efferent is the
facial/greater superficial petrosal nerve (parasympathetic) dilator pathway.
 About 20% of the dilatation remains after facial-nerve section and is probably
mediated by antidromic activation of the trigeminal system directly.
 The portion running through the parasympathetic outflow traverses the
sphenopalatine (pterygopalatine) and otic ganglia and uses vasoactive intestinal
polypeptide as its transmitter.
 The cells of origin for the cranial parasympathetic autonomic vasodilator pathway are
in the superior salivatory nucleus in the pons, which can be activated with stimulation
of a trigeminovascular nociceptive input, such as that from the superior sagittal sinus.
 This vasodilator reflex is the trigeminoparasympathetic or trigeminal-autonomic
reflex,which is a normal physiological reflex.
Trigeminal-autonomic reflex

Clinical Correlates

Supranuclear
A higher central lesion (eg. cerebral or thalamic) will have to be
contralateral to the clinical findings.
A hemispheric infarct of the MCA territory may produce sensory
loss in the trigeminal distribution on the same side as the
hemiparesis.
With hemispheric lesions, masseter strength is usually preserved.
The supranuclear control of trigeminal nerve motor functions is
bilateral, so a hemispheric infarct is never going to produce a
unilateral lesion (although voluntary control of the masseter will be
lost).

Supranuclear lesions, particularly of the parietal lobe or sensory radiations, may
raise the sensory threshold of the contralateral face,
A thalamic lesion may cause facial hypesthesia with hyperpathia or allodynia

Trigeminal Nucleus
• The extension of the trigeminal nuclear complex throughout the entire brainstem
renders it susceptible to involvement from any pathological brainstem process.
• Trigeminal lesions are particularly common with demyelinating disease, may involve
either the nuclei or sensory root, and may be clinically silent or symptomatic (Bischof
and Sprenger, 2014; Kremer et al., 2013; Mills et al., 2010).
• Ischemia, hemorrhage, infectious and noninfectious inflammation, and neoplasm are
other causes of trigeminal brainstem involvement (Kim et al., 2013).
• Additional brainstem signs are frequently present.
• Wallenberg syndrome from lateral medullary ischemia typically causes ipsilateral facial
numbness and impaired pinprick sensation secondary to descending spinal tract and
nucleus involvement .

Brainstem lesions would be ipsilateral.
• Pontine stroke (lateral rostral pons or above) - with ipsilateral
body sensory loss
• Medullary stroke (lateral medulla) - with contralateral body
sensory loss
• Mid-pontine stroke (ipsilateral pons) - if only the face is
affected
• Isolated masticatory motor failure suggests that the lesion is
actually limited to a small area of the mid-pons.
• Raised intracranial pressure (a "false localising sign")
• Pontine tumours

Trigeminal neuralgia (Fothergill’s disease)
Writings of Galen, Aretaeus of Cappadocia (born circa AD 81), and in the 11th century by
Avicenna (“tortura oris”)
Nicolas André invented the term tic douloureuxin 1756 in a book,bservations
pratiques sur les maladies de l’urethre et sur plusiers faits convulsifs.
Description:
A disorder characterized by recurrent unilateral brief electric shock-like pains,
abrupt in onset and termination, limited to the distribution of one or more
divisions of the trigeminal nerve and triggered by innocuous stimuli. It may
develop without apparent cause or be a result of another diagnosed disorder.
Additionally, there may be concomitant continuous pain of moderate intensity
within the distribution(s) of the affected nerve division(s).

1. Trigeminal convergence/projection
This theory proposes that nociceptive entries recurrent from head and neck converge to the
trigeminal spinal nucleus (caudal sub-nucleus), leading to the release of neurotransmitters and
vasoactive substances.
These mediators decrease second order neurons activation threshold, which also receive
impulses from non-nociceptive fibers, generating increased flow of information transmitted to
upper centers which interpret pain.
2. The bioresonance theorystates that vibration frequency of structures
involving the trigeminal nerve may injury nervous fibers, leading to abnormal transmission of
impulses and generating facial pain.
3. Ignition suggests that injuries in trigeminal afferents of the root or of the trigeminal
ganglion generate hyperexcitability of the axon and/or cell body, originating pain paroxysms as a
function of exacerbated neuronal activity.
Lets analize the algia...

Pathology:
Vacuolated neurons, segmental demyelination, vascular changes, and other abnormalities
were more common in gasserian ganglia from patients with a history of trigeminal
neuralgia than in control specimens. Focal demyelination of the axons in the main sensory
root may be associated with compression by vascular loops.
Pathogenesis and Etiology: The cause of trigeminal neuralgia is probably
multifactorial. Multiple sclerosis, cerebellopontine angle tumors, schwannomas, and other
local lesions account for a very small proportion of cases, and most cases have long been
called idiopathic. Dandy’s vascular loop-nerve compression theory,
proposed in 1932, was revitalized by the work of Jannetta. Modern surgical series have
reported vascular compression of the posterior root in the vast majority of cases. Vascular
compression is believed to increase with age and cause changes in the trigeminal sensory
root and root entry zone that result in prolongation of electrical impulses within the nerve
and re-excitement of the axons, leading to repetitive neuronal discharges.

Diagnostic criteria:
 Recurrent paroxysms of unilateral facial pain in the
distribution(s) of one or more divisions of the trigeminal nerve,
with no radiation beyond1, and fulfilling criteria B and C
A. Pain has all of the following characteristics:
1. lasting from a fraction of a second to 2 minutes
2. severe intensity
3. electric shock-like, shooting, stabbing or sharp in quality
B. Precipitated by innocuous stimuli within the affected trigeminal
distribution,
C. Not better accounted for by another ICHD-3 diagnosis.

When trigeminal neuralgia occurs bilaterally, it is
often due to multiple sclerosis or other structural
lesions.
Trigeminal neuropathy is a more accurate term
when one finds trigeminal dysfunction such as
sensory loss.

13. Painful lesions of the cranial nerves and other facial pain
13.1 Pain attributed to a lesion or disease of the trigeminal nerve
13.1.1 Trigeminal neuralgia
13.1.1.1 Classical trigeminal neuralgia
13.1.1.1.1 Classical trigeminal neuralgia, purely paroxysmal
13.1.1.1.2 Classical trigeminal neuralgia with concomitant continuous pain
13.1.1.2 Secondary trigeminal neuralgia
13.1.1.2.1 Trigeminal neuralgia attributed to multiple sclerosis
13.1.1.2.2 Trigeminal neuralgia attributed to space-occupying lesion
13.1.1.2.3 Trigeminal neuralgia attributed to other cause
13.1.1.3 Idiopathic trigeminal neuralgia
13.1.1.3.1 Idiopathic trigeminal neuralgia, purely paroxysmal
13.1.1.3.2 Idiopathic trigeminal neuralgia with concomitant continuous pain
13.1.2 Painful trigeminal neuropathy
13.1.2.1 Painful trigeminal neuropathy attributed to herpes zoster
13.1.2.2 Trigeminal post-herpetic neuralgia
13.1.2.3 Painful post-traumatic trigeminal neuropathy
13.1.2.4 Painful trigeminal neuropathy attributed to other disorder
13.1.2.5 Idiopathic painful trigeminal neuropathy
3

Treatment of trigeminal neuralgia due to a focal lesion compressing the sensory
root of the trigeminal nerve is surgical exploration and decompression of the
nerve.
Management of primary trigeminal neuralgia can be either medical or surgical.
Treatment
Carbamazepineis the drug of choice for treatment of trigeminal neuralgia,
with a highly favorable response in approximately 75% of patients.
• Initiated with small doses of 50 to 100 mg and increased slowly as tolerated.
Vertigo, drowsiness, and ataxia are common side effects if the preparation is
introduced too quickly, especially in elderly patients.
• Therapeutic doses generally range from 600 to 1200 mg/day in divided
dosing. The appropriate dose is the lowest dose needed to control the pain.
• Once the pain is controlled completely, the dose can be tapered every few
weeks to determine whether a remission has developed. 75Dr. M. M. Samim Trigeminal Nerve

Second-line options
Gabapentin,
Pregabalin,
Phenytoin and baclofen.
Other drugs that have been used include lamotrigine, oxcarbazepine, valproate, clonazepam,
and topiramate (Cheshire, 2007). Second-line drugs should be considered for trial, alone or in
combination, when carbamazepine is either unhelpful or not tolerated.
Given the beneficial effects of gabapentin in other neuropathic conditions and its benign side-
effect profile, an initial trial with this drug may be an alternative option to carbamazepine.
Vixotrigine
Vixotrigine , formerly known as raxatrigine, is an analgesic which
is under development by Convergence Pharmaceuticals for the treatment of
lumbosacral radiculopathy (sciatica) and trigeminal neuralgia (TGN).

On occasion, one may encounter a patient in the midst
of a severe attack.
A useful technique in this situation is the administration
of IV fosphenytoin at a dose of 15 to 20 g/kg body
weight.
Anesthetizing the ipsilateral conjunctival sac with the
local ophthalmic anesthetic, proparacaine, has also
proved effective in providing relief from pain for several
hours to days.
Acute Attack of Trigeminal Neuralgia

Non-medical & Surgical Treatments
• Microvascular decompression
• Percutaneous glycerol rhizotomy
• Percutaneous stereotactic rhizotomy
• Percutaneous balloon compression
• Gamma Knife, Cyberknife, LINAC

 The Numb Chin Syndrome
 Hypesthesia and sometimes paresthesias involving the lower lip and chin,
approximately in the distribution of the mental nerve.
 The numb chin syndrome is often due to a neoplastic process, with metastasis
either to the mental foramen of the mandible or to the intracranial meninges
or skull base, often from carcinoma of the breast or lung.
 The predilection for involvement of the CN V3 distribution may reflect the
relatively protected position of the other trigeminal divisions in the cavernous
sinus, with greater exposure of the third division to neoplastic processes
involving the meninges and base of the skull.

 The numb cheek syndrome is similar but usually due to a
lesion involving the infraorbital nerve.
The numb chin or cheek syndrome can be the presenting
manifestation of cancer.
 The numb cheek-limp lower lid syndrome includes
weakness involving the distal branches of the facial nerve
due to carcinoma infiltrating the infraorbital and facial
nerves.

Congenital ocular aberrant innervation syndromes are
a complex
group of disorders involving abnormal miswiring of the extraocular muscles.
The Marcus Gunn phenomenon, or jaw-winking, occurs in patients with
congenital ptosis; opening the mouth, chewing or lateral jaw movements
cause an exaggerated reflex elevation of the ptotic lid .
The phenomenon may be the result of proprioceptive impulses from the
pterygoid muscles being misdirected to the oculomotor nucleus.

Trigeminoabducens synkinesis is due to abnormal communications
between CN V and CN VI. Involuntary closure of one eye on mouth
opening (reversed Gunn phenomenon, inverse jaw winking, or
Marin Amat sign) is a synkinesia due to aberrant regeneration of the
facial nerve; it occurs most often following Bell's palsy.
The auriculotemporal (Frey's) syndrome produces flushing,
warmness, and excessive perspiration over the cheek and pinna on
one side following ingestion of spicy food. This syndrome is due to
misdirection of the secretory fibers to the parotid gland to the
sweat glands and vasodilator endings in the Auriculotemporal nerve
distribution; it usually follows trauma or infection of the parotid
gland or local nerve injury.

Neck tongue syndrome
• Is a rare disorder involving the trigeminal and upper cervical nerves.
• Pain and numbness in the distribution of the lingual nerve and C2 root are
provoked by sudden head turning.
• Afferent fibers from the lingual nerve are thought to join the hypoglossal nerve
and send filaments to the upper cervical nerves. The symptoms are allegedly
caused by minor subluxation of the C2 articulatory process tweaking these
nearby structures.
• The condition is benign. In the absence of any structural
abnormality, management is conservative and may include anti-
inflammatory agents and temporary immobilization of the neck in a
cervical collar. 83Dr. M. M. Samim Trigeminal Nerve

Congenital trigeminal anaesthesia (CTA) is an unusual paediatric
disorder.
CTA is a rare paediatric condition which usually presents with painless
keratopathy in a young child and may be mistaken for herpes
simplex keratitis.
Most children present in infancy or early childhood. One child was diagnosed at
14, but it seems likely that he had been experiencing symptoms for some time
before the diagnosis was made.
Cases appear to be mostly sporadic, but they can have an autosomal dominant
inheritance pattern as two families have been reported with at least two
generations of family members affected. However, no specific genetic mutations
have been identified in this diverse group of conditions.

Rosenberg’s classification of CTA reflects the embryology of the trigeminal nerve
• The sensory component of the trigeminal nerve originates from the
neural crest.
• The motor root of the trigeminal nerve arises from the ventral part
of the developing neural tube and is separate from the sensory
nerve.
• Therefore, the motor function of the trigeminal nerve is intact in this
disorder. The neural crest also gives rise to the mesoderm and some
of the ectoderm of the first branchial arch.
• This explains the association of trigeminal anaesthesia with
mesodermal and ectodermal abnormalities of the ear, skull and
vertebral spine.

Autosomal Compelling Helio-Ophthalmic Outburst (ACHOO) syndrome
Autosomal Dominant Compelling Helioopthalmic Outburst (ACHOO) Syndrome is
characterized by uncontrollable sneezing in response to the sudden exposure to
bright light, typically intense sunlight . This type of sneezing is also known as
photic sneezing. About one in four individuals who already have a prickling
sensation in their nose will sneeze in response to sunlight, but “pure” photic
sneezing is far less common.
Sneezing is usually triggered by contact with infectious agents or after inhaling
irritants, but the cause of photic sneezing is not fully understood. It may involve
an over-excitability of the visual cortex in response to light, leading to a stronger
activation of the secondary somatosensory areas.
Laura Dean, MD

TRIGEMINAL AUTONOMIC CEPHALGIAS
 The trigeminovascular system consists of the neurons
innervating the cerebral vessels and dura mater that have
cell bodies located in the trigeminal ganglion.
 The ganglion contains bipolar cells—the peripheral fibre
makes a synaptic connection with the vessel and other
cranial structures, particularly the pain-producing large
cranial vessels and dura mater, and the centrally
projecting fibre synapses in the caudal brainstem or high
cervical cord.
 Some projections involve both cerebral (middle cerebral
artery) and extracerebral (middle meningeal artery)
vessels.
 Activation of afferents in both the large venous sinuses
and intracranial arteries leads to Fos production in
neurons with the same anatomical distribution,
trigeminal nucleus caudalis and dorsal horns of C1 and
C2, the trigeminocervical complex. 87Dr. M. M. Samim Trigeminal Nerve

Elements of a neurobiologically based explanation for cluster headache.
 Pain afferents from the trigeminovascular system traverse the ophthalmic division of
the trigeminal nerve, taking signals from the cranial vessels and dura mater.
These synapse in the trigeminocervical complex, trigeminal nucleus caudalis (TNC), and
dorsal horns ofC1 and C2, and then project to the thalamus and lead to activation in
cortical areas, including frontal cortex, insulae, and cingulate cortex, resulting in pain.
There is reflex activation of the parasympathetic outflow from the superior salivatory
nucleus (SSN) via the facial (VIIth cranial) nerve, predominantly through the
pterygopalatine (sphenopalatine) ganglion, which acts as a positive feedback system to
dilate the vessels and imitate trigeminal endings further.
This autonomic activation leads to lacrimation, reddening of the eye, and nasal
congestion, and a local third-order sympatheticnerve lesion due to carotid swelling31
results in a partial Homer's syndrome.
The key site in the CNS for triggering the pain and controlling the cycling aspects is in the
posterior hypothalamic grey matter region 88Dr. M. M. Samim Trigeminal Nerve

 Pain afferents from the trigeminovascular system traverse the ophthalmic division of the trigeminal nerve, taking signals from the cranial vessels and dura mater.
 These synapse in the trigeminocervical complex, trigeminal nucleus caudalis (TNC), and dorsal horns ofC1 and C2, and then project to the thalamus and lead to activation in cortical areas,
including frontal cortex, insulae, and cingulate cortex, resulting in pain.
 There is reflex activation of the parasympathetic outflow from the superior salivatory nucleus (SSN) via the facial (VIIth cranial) nerve, predominantly through the pterygopalatine
(sphenopalatine) ganglion, which acts as a positive feedback system to dilate the vessels and imitate trigeminal endings further.
 This autonomic activation leads to lacrimation, reddening of the eye, and nasal congestion, and a local third-order sympatheticnerve lesion due to carotid swelling31 results in a partial
Homer's syndrome.
 The key site in the CNS for triggering the pain and controlling the cycling aspects is in the posterior hypothalamic grey matter region

3. Trigeminal autonomic cephalalgias (TACs)
3.1 Cluster headache
3.1.1 Episodic cluster headache
3.1.2 Chronic cluster headache
3.2 Paroxysmal hemicrania
3.2.1 Episodic paroxysmal hemicrania
3.2.2 Chronic paroxysmal hemicrania
3.3 Short-lasting unilateral neuralgiform headache attacks
3.3.1 Short-lasting unilateral neuralgiform headache attacks with conjunctival injection and tearing (SUNCT)
3.3.1.1 Episodic SUNCT
3.3.1.2 Chronic SUNCT
3.3.2 Short-lasting unilateral neuralgiform headache attacks with cranial autonomic symptoms (SUNA)
3.3.2.1 Episodic SUNA
3.3.2.2 Chronic SUNA
3.4 Hemicrania continua
3.4.1 Hemicrania continua, remitting subtype
3.4.2 Hemicrania continua, unremitting subtype
3.5 Probable trigeminal autonomic cephalalgia
3.5.1 Probable cluster headache
3.5.2 Probable paroxysmal hemicrania
3.5.3 Probable short-lasting unilateral neuralgiform headache attacks
3.5.4 Probable hemicrania continua
3

Gasser's ganglion or Gasserian ganglion
This historic terminology was given by Antonius Hirsh who
described the ganglion in 1765 and then named the ganglion
in the honour of his teacher, Johann Lorenz Gasser (1723-
1765) an Austrian anatomist.

Radiology

42-year-old woman with lateral medullary syndrome caused by spontaneous vertebral artery dissection.
Localized high signal intensity caused by area of infarction on right side of medulla oblongata (arrow) on T2-
weighted spin-echo MR image. Note absence of flow void in right vertebral artery. 95Dr. M. M. Samim Trigeminal Nerve

45-year-old man with diagnosis of multiple sclerosis. Oblong plaque of high signal intensity (arrow) involving
right trigeminal sensory nucleus on T2-weighted spin-echo MR image. Note small area of high signal intensity
adjacent to fourth ventricle and high signal intensity in white matter of temporal lobes. 96Dr. M. M. Samim Trigeminal Nerve

28-year-old man with diagnosis of neurosarcoidosis. Coronal T1-weighted spin-echo MR image shows bilateral
asymmetric thickening and enhancement of trigeminal (solid straight arrow) and occulomotor (curved arrow)
nerves and hypothalamus (open straight arrow). Lateral ventricles are dilated.

53-year-old man with histologic diagnosis of epidermoid cyst. (Courtesy of McKinstry CS, Belfast, United
Kingdom) T2-weighted spin-echo MR image shows spread of slow-growing smooth mass of high signal intensity
from cerebellopontine cistern to prepontine cistern across root entry zone of trigeminal nerve. Note septa and
focal areas of high signal intensity within mass. Associated brainstem compression is causing hydrocephalus.98Dr. M. M. Samim Trigeminal Nerve

48-year-old man with pial arteriovenous malformation. Tangle of dilated blood vessels
(arrow) at root entry zone of right trigeminal nerve on T2-weighted spin-echo MR image.99Dr. M. M. Samim Trigeminal Nerve

15-year-old girl with known diagnosis of leukemia. Coronal T1-weighted spin-echo MR image after IV contrast
injection shows bilateral Meckel's cavity enhancement (arrows), particularly of left side, as result of leukemic
deposits. 100Dr. M. M. Samim Trigeminal Nerve

15-year-old girl with known diagnosis of leukemia. Expansion and reduction of normal high
signal intensity in Meckel's cavity (arrows) on T2-weighted spin-echo MR image. Note signal
void from internal carotid artery medial to Meckel's cave. 101Dr. M. M. Samim Trigeminal Nerve

72-year-old man with nasopharyngeal carcinoma. Coronal contrast-enhanced T1-weighted spin-echo MR image with fat
suppression shows enhancement and thickening of mandibular nerve extending into trigeminal ganglion (arrow). Note
widening of foramen ovale basis cranii and enhancing soft-tissue mass causing destruction of right side of sphenoid bone.102Dr. M. M. Samim Trigeminal Nerve

33-year-old woman with herpes zoster. Axial contrast-enhanced T1-weighted spin-echo MR image shows
enhancement along pontine course of trigeminal nerve and low signal intensity at site of main trigeminal sensory
nucleus (arrow). 103Dr. M. M. Samim Trigeminal Nerve

Surgical and NeuroRehab

Gasserian ganglion block

Classic approach
• The patient is placed in a supine position with the head in a neutral position and the eyes
staring straight ahead. The key anatomic landmark—a point 2-3 cm lateral to the angle of the
mouth on the side to be blocked—is marked.
• The skin over the cheek on the involved site is prepared with iodophor or povidone-iodine
and draped. A skin wheal is raised with a local anesthetic. A 22-gauge 10-cm long spinal
needle is inserted here and advanced upward toward the mandibular condyle. This plane
should be in line with the pupil as the patient’s eyes stare ahead, and the trajectory should
be cephalad toward the external auditory meatus.
• At a depth of 4-6 cm, the greater wing of the sphenoid at the base of the skull is contacted.
The needle is withdrawn and redirected more posteriorly so as to enter the foramen ovale. It
is then advanced 1-1.5 cm. Paresthesia at the mandible is elicited, followed by paresthesia in
the maxilla and orbit.

Foramen ovale is a surgically important aperture of the skull since it allows
approach to and manipulation of the trigeminal ganglion as it lies in the
Meckel’s cave. This transfacial approach, Hartel’s approach.
Hartel’s approach
The three landmarks of the Hartel's route on the right hemiface:
The first corresponds to location of the skin puncture: 2.5 cm lateral to the
angle lip.
The second is on the inferior edge of the zygomatic arch, 3 cm anterior to
the external auditory canal.
The third is on the line joining the first point to the pupil on the inferior
edge of the orbit

Percutaneous Procedure
• Hartel anatomic landmarks3 for percutaneous
procedures were used. The head was positioned
supine and slightly rotated away from the side of the
puncture.
• The entry point was 2.5 cm lateral to the angle of the
mouth. An 18-gauge needle cannula was inserted
medial to the coronoid process of the mandible and
aimed toward the plane intersecting a point 30 mm
anterior to the external acoustic meatus along the
zygomatic arch and the medial aspect of the pupil.
• A free-hand technique was then used to direct the
needle toward the foramen ovale with a finger inside
the oral cavity to prevent perforation of the ipsilateral
buccal mucosa and to ensure that the needle
traveled medial to the mandible.

Supraorbital Rim Syndrome
Compression of the peripheral nerves of the supraorbital rim (SON, STN, and
ZTN) can have varying underlying etiologies. Decompression of these nerves by
addressing muscle, fascia, bone, or vessel can result in significant improvement
in headache pain. Decompression of the SON at the supraorbital rim with
positive results on patients with frontal pain syndromes has been reported by
Sjaastad et al24 in 1999. Sjaastad et al. correctly identified a “fascial band or
bony extension” at the supraorbital notch, which they removed in 5 patients.

Deafferentation Pain:
• Sometimes, lesioning procedures can result in too much injury to
the trigeminal nerve, such that the nerve does not recover and
the face becomes permanently numb with a different, more
difficult to treat type of pain, called deafferentation pain.
• In these situations, another surgical procedure can be done, that
includes placement of one or more electrodes underneath the
skull over the covering of the brain, or sometimes directly on the
brain, to deliver electrical stimulation to the part of the brain
responsible for sensation of the face.
• This procedure is called motor cortex stimulation.

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