Role of Head and Neck Imaging Preview in Patient With Trigeminal Neuralgia / Orthodontic Courses by Indian Dental Academy

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Role Of Head & Neck Imaging

Preview In Patients With Trigeminal
Neuralgia

INDIAN DENTAL ACADEMY

Leader in continuing dental education
www.indiandentalacademy.com

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Contents
Course of Trigeminal nerve
Trigeminal neuralgia
History
Clinical features
Causes
Diagn criteria
Diff modalities of investigations
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Trigeminal Nerve
INFECTION & NEOPLASIA commonly
Involve PERIPHERAL divisions (AJR 176,Jan 2001)
4 www.indiandentalacademy.com
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Opthalmic branch
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Maxillary Nerve
During its course- gives
branches in 4 regions:
1. Middle cranial fossa
Middle Meningeal Nerve
2. Pterygopalatine fossa
Ganglionic
Zygomatic
PSA
3. Infraorbital groove & canal
MSA and ASA
4. On face
Inferior Palpebral
Lat/ Ext Nasal
Superior labial
Trigeminal N
Maxillary
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Mandibular Nerve
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Subarachnoid Spaces/ Cisterns
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Trigeminal Neuralgia
Also called tic douloureax
Distributed along 5
th
cranial nerve
As described by IHS:
A painful, unilateral affliction of the face ,
characterized by brief electric shock lightening-like
(lancinating) pain limited to distr. one or more div. of
trigeminal nerve
4 per 1,00,000 population
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Trigeminal Neuralgia
>50 yrs
> Women
< Right side of face
Pain is unilateral, most often in V2 & V3
Often misdiagnosed as dental pathology due to acute
bouts of severe pain in the lower face evoked by
perioral triggers,

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Bilateral Cases-3%
Division of involvement Max - 66%

- Mand - 49%

- Opthal 16%

- Both Max & Mand 19%

- All 3 Divisions- 1%

(Katusic et al -1990)

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History
Aretaeus of cappadocia at the end of 1
st
century -
1
st
clinical description of TN

J ohn Locke in 1677 (american physician &
philosopher) accurately identified clin features

Nicolaus Andre in 1756 tic douloureux (painful
jerking)

J ohn fothergill in 1773- full & accurate description
of TN
{OOO medical management update, Vol. 100, No. 5 Nov 2005}
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Etiopathogenesis
Focal demyelination at the site of compression may also allow
electrical spread of excitation betwn. adjacent sensory axons
(ephaptic transmission).
An ephaptic short-circuit of this type within the trigeminal
nerve might explain the sudden electric jolts of pain that
characterize the disorder.
{OOO 2005}

Central myelin replaced by - peripheral myelin.
Continued pulsatile pressure of the trigeminal nerve at the
REZ may result in disordered conduction and short-
circuiting of impulses, producing trigeminal neuralgia
{Robert et al, TN: MRI Features, Radiology 1989;172:767-70}
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Sweet in 1967, diagnostic criteria for TN
1. The pain is paroxysmal.
2. The pain may be provoked by light touch to the face (trigger
zones).
3. The pain is confined to the trigeminal distribution.
4. The pain is unilateral.
5. The clinical sensory examination is normal.
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ICHD Criteria for Classical TN
Classical Trigeminal Neuralgia:
A. Paroxysmal attacks of pain lasting from a fraction of a
second to 2 minutes, affecting one or more divisions of the
trigeminal nerve and fulfilling criteria B and C:

B. Pain has at least one of the following characteristics:
1. intense, sharp, superficial or stabbing
2. Precipitated from trigger areas or by trigger factors

C. Attacks are stereotyped in the individual patient.

D. There is no clinically evident neurological deficit.

E. Not attributed to another disorder.
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ICHD Criteria for Classical TN
Symptomatic trigeminal neuralgia:
A causative lesion, other than vascular compression, has been
demonstrated by special investigations and/or posterior fossa
exploration.

Symptomatic TN has the same key features of TN but results
from another disease process (such as multiple sclerosis or a
cerebellopontine angle tumor).
Symptomatic TN is defined by IHS as:
Pain indistinguishable from classic TN but caused by a
demonstrable structural lesion other than vascular
compression.
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Clinical evaluation
Diagnosis is of TN is based on a
Clinical history of pain attacks that fit accepted
diagnostic criteria supplemented by
Physical exam findings and
Cranial imaging studies.

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Clinical examination
Head and neck examination.
The sensory examination: careful search for cutaneous or
intraoral trigger zones in addition to areas of focal sensory
loss.
In majority - sensory examination will be normal,
In some patients - mild tactile sensory deficit (hypesthesia)
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Clinical examination
Because the facial (VII) and auditory (VIII) nerves lie adjacent
to the trigeminal nerve in the cerebellopontine angle (CPA),
they also deserve particular attention during the examination.

A patient with symptomatic TN resulting from a CPA mass will
often also show subtle facial weakness and hearing loss on
that side.
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Physical examination
Physical examination findings are normal;
In fact, a normal neurologic examination is part of the
definition of idiopathic TN.
Perform a careful examination of the cranial nerves, including
the corneal reflex.
Abnormality suggests that the pain syndrome is secondary to
another process
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History
In the past, clinical symptoms & signs accurate means

Assessment of the patient consisted of Computed tomography
(CT) and Angiography.

CT: has limited value in the evaluation of Posterior fossa &
the Trigeminal nerve
Normal T. Nerve - not typically visualized.
Abnormalities along the expected course of the nerve.
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History
Angiography: more successful in predicting - causative vessel
Invasive & fails to show exact relationship bet Vess & N
{Robert et al, TN: MRI Features, Radiology:1989;172:767-70}
Conventional biplane angiography
Intraarterial Digital substraction angiography (DSA)
(quicker & requires smaller amounts of contrast medium
Venous abnormalities - detected more easily- better contrast in
the venous phase) {Radiology 1986;158:721-27}
AP Towns
DSA DSA
Towns
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MRI
Directly depicts the course of the cisternal portion of T. nerve.
All portions of the nerve from the REZ to the cavernous sinus
can be more easily evaluated with MR imaging than with
traditional modalities.
The possible impingement of neighboring vascular structures
is also readily suggested.
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MRI
Provides accurate information on
the anatomical location &
course of ectatic vessel in CPA &
the caused mass effect on the brainstem
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MRA
MRA- a more recent imaging technique, allows visualization
of the vascular anatomy of the relevant region without the use
of contrast media.
{Shahrokh C et al, J ADA, Vol 135, 2004}

Allows evaluation of:
Vessel Anatomy & Blood flow rates

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Subarachnoid Spaces/ Cisterns
Sagittal T2W MRI
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PONS
Axial T1W MRI

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Causes
I . Typical/ Classical/ I diopathic and Essential TN.
Sec. to a vascular loop that compresses the
trigeminal nerve a few mm proximal to the pons.
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Causes of TN
I I . SECONDARY/ SYMPTOMATI C forms:
Tumor (Acoustic neurinoma, pontine glioma, epidermoid
chondroma, metastases, lymphoma)
Amyloidoma of Meckels Cave: A Rare Cause of Trigeminal
Neuralgia, Eugene Yu ,University of Toronto Canada, AJ R:182,
J une 2004
Vascular (pontine infarcts, Aneurysms of Arteries, Veins,
AV malform)
Vertebrobasilar ectasia rare cause of TN (MRI of vertebrobasilar
ectasia in TN, Kirsch et al, April 2005)

Inflammatory (MS, sarcoidosis)
Paraneoplastic
{Marc E. et al, trig neuralgia, march 2006}

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Vascular loops
The main cause of trigeminal neuralgia is neurovascular
compression (NVC) in the root entry zone (REZ) of the
trigeminal nerve in the CPA cistern
{Norio Yoshino, et al, Radiology 2003}

Sup Cereb A > Ant inf Cerebellar A > smaller pontine arteries
> petrosal veins
{Lawrence et al, 1990}

Superior cerebellar artery (SCA)> the ant infer cerebellar A.
(AICA)> the basilar artery, or the vertebral antery.
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BASILAR ARTERY
39
Axial T2W MRI
SCA (arrow) Compressing PGS of
V (open arrow)
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Images of a 64-year-old man with left-sided V2 and V3 distribution of
facial pain.
a. Coronal T1W MR: Focal area of signal void (white arrow)
deforming the left fifth nerve (black arrow) at REZ.
b. AP Angiogram: Ectatic distal vertebral artery.
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Vascular loops
Magnetic resonance angiography has been reported to be
effective in the detection of NVC in trigeminal neuralgia

Norio Y. et al, Radiology 2003;
Three-dimensional MR imaging with constructive interference
in steady-state (3D CISS) sequence images provided more
sufficient information than did MR angiography

Nerve & Arteries- identified by both (MRA & 3D CISS)
But Veins- on 3D CISS images
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MR angiography,
Artery - fast blood flow - high signal intensity &
Nerve - intermediate signal intensity,
Contrast between the artery & nerve good
Contrast resolution betn CSF & nerve is somewhat unclear
Depiction of the vein is impossible cause of slow blood flow.

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`
3D CI SS images
Provide high spatial resolution & excellent contrast resolution
betn CSF & nerve
Clearly depict the veins
3D CISS imaging offers high spatial resolution & excellent
contrast resolution & depicts both artery & vein responsible
for the NVC.
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3D CISS MR images
Superior cerebellar artery (short arrow) has compressed the REZ
of the right trigeminal nerve (long arrow) at the medial site.
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MR angiographic images
Superior cerebellar artery (short arrow) has compressed the
right trigeminal nerve (long arrow) at the medial site.
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(a) Transverse 3D CISS MR image: both vein (curved arrow) &
ant inf cerebellar artery (short straight arrow) have compressed
left trigeminal nerve (long straight arrow) at the REZ.
(b) Transverse MR angiographic image does not depict the vein,
although it shows the ant inf cerebellar artery (short arrow)- has
compressed the REZ of the left trigeminal nerve (long arrow).
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Cisternal portion of V compressed by:
1. Extra axial diseases:
Schwannomas
Meningiomas
Epidermoids
Lipoma
Metastasis
Inflam parocesses
2. Intra axial diseases:
MS
Infarct
Metastasis
Primary tumors
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Basilar Artery Aneurysm.
Postcontrast axial CT.
Angiographic confirmation
Tubular-shaped area of enhancement in left cerebellopontine angle (arrows)
typical for fusiform basilar artery aneurysm.
Left-to-right shift of fourth ventricle.
David et al, AJ R 135:93- 95 1980
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Multiple sclerosis
Prevalance: 1-8% in TN
Common cause of symptomatic TN,
Probably resulting from a demyelination plaque at the level of
REZ
Frequently goes undiagnosed in patients who have relatively
mild or infrequent MS exacerbations.
Should be considered in any person with TN symptoms,
in younger TN patients or with bilateral TN.
A TN evaluation can be the first opportunity for the clinician
to diagnose MS.
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Multiple sclerosis
Neurologic symptoms seen in MS:
Unexplained episodes of monocular blindness,
Diplopia,
Vertigo,
Unusual clumsiness (ataxia),
Weakness.

Routine brain CT scan - adequate to screen CPA tumor,

MRI scan - better demonstrates MS plaques & anatomic
relationships of trigeminal root.
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Multiple sclerosis
Axial T2W MRI
Plaques along intrapontine segments of both trig nerves
Transient enhancement resolution of enhancement occurs in 2 months in
contrast to neoplastic disease {Radiographics, Charles et al 1995}
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Acoustic Schwannoma
Approx. 10 % of all intracranial tumors
80% -90% of all CPA tumors
< 21 yrs
Becomes symptomatic before 25 yrs
Mostly arises within IAC
If widening is >2mm consider presence of tumour
Clinical findings:
Tinnitus,
Hearing loss
Signs of cerebellar dysfunction
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Acoustic Schwannoma
Mass within the right IAC with extension into the CPA cistern
T1W MRI
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Trigeminal schwannoma
0.2% of all intracranial tumors
Majority develop in gasserian ganglion
Clinical findings:
Sensory disturbance of T Nerve:
Numbness
Diminished/ absent corneal reflex
Hypesthesia
Hypalgesia
Weakness of muscles of mastication
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The pressure exerted by the tumor leads to erosion of the
underlying bone & enlargement of the foramen ovale, foramen
rotundum, or the superior orbital fissure.

Small tumors are homogeneous;
Large tumors can have heterogeneous signal intensity due to
degenerative changes, including cyst formation and fatty
degeneration
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CE TI W
Smoothly marginated tumors, Large, dumbbell- shaped enhancing
tumor (arrows) in the left middle cranial fossa that follows the
course of the trigeminal nerve and extends into the
pterygopalatine and posterior fossae.
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Most common Location: Gasserian ganglion
T1W MRI
Smooth margins, low signal intesity

T2W MRI
High heterogeous signal intesity

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Meningioma
2
nd
most freq tumors occuring in CPA,
10- 15 % of all tumors
Distinct female prediliction (2:1 to 4:1)
Middle age

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Meningioma
Signal intensity similar to acoustic schwannomas
Charac feature: Broad based attachment to adj dura matter
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Epidermoid Cyst
Rare - 0.2% to 1% of all intracranial tumors
Most common location: CPA
5 9% of all CPA masses.
4
th
5
th
decade of life
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Epidermoid Cyst
HP: composed of int layer of squam epith. covered by an ext
fibrous capsule
These cysts grow by desquamation of epithelial cells that
break down into keratin and cholesterol within the tumor
capsule.
Grows slowly & is soft & very pliable

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Epidermoid Cyst

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Epidermoid Cyst
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Trigeminal Epidermoid
Axial T1W
TE of Trig N & Meckels cave
Low signal intensity
Axial T2W
Moderately high heterogeneous signal intensity
LOBULATED margins
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Pontine Glioma
95% of neoplasms in brainstem are Astrocytomas
In children betwn 5- 14 yrs
M > F
May be totally solid,
Solid with cystic, necrotic or hemorrhagic component
T1W: Isointense or hypointense
If cystic: Hypointense
T2W: Hyperintense in both solid & cystic component
After Gd adminstration: solid comp - enhancement
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Astrocytomas

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Astrocytomas

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Pontine Infarct
Pontine ischemia- due to bilateral ventral pontine infarction
Burning orofacial pain- early symptom
Locked in Syndrome- pt. is able to understand what is being
said & happening, is imprisoned by inability to speak or move
anything apart from eyes

Small infarcts invisible in CT
Evident in MRI
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Metastasis
Met. lesions involving CPA:
0.2% - 2%
Note obliteration of CSF in
right Meckels cave by mass
(large arrow)
Note expansion of convex
dural margin by mass
Note normal cisternal
portions of V bilaterally
(small arrow)
T2W MRI
Neoplastic lesions most commonly involve the extracranial branches
Spread by PNS
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Conclusion
Diagnostic brain imaging should be part of the initial
screening of all patient with TN symptoms - cause a significant
% of patients have symptomatic TN

If TN identifiable cause, such as a tumor or mass compressing
the nerve, the neurologist - elimination of the pathology or
decompression of the nerve.

In cases of idiopathic TN, clinicians consider medical and
surgical options.

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MRI useful in identification of MS or masses
Gross Vascular changes: eg. Basilar A. dolichoectasia
Magnetic resonance angiography- effective in NVC
3D CISS MR Imaging offers high spatial resolution &
excellent contrast resolution & depicts both artery & vein
responsible for the NVC.

Coronal MRI: PGS
Sagittal & Axial detection of intraparenchymal lesions (MS)

AV malformation Angiography

{Lawrence et al, TN: MRI Assessment, Radiology1990}
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Treatment
Medical
Carbamazepine
+ Baclofen / Clonezepam
Phenytoin
Gabapentin
Valproate
Surgical
MV Decompression
Peripheral injections
Peripheral neurectomy
Cryotherapy (Nitrous oxide cryo probe is used)
Thermocoagulation (65)
Gasserian ganglion procedures
Intracranial procedures
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2. Pre-Trigeminal Neuralgia
Days to years before the first attack of TN pain, some sufferers
experience odd sensations in the trigeminal distributions
destined to become affected by TN.
These odd sensations of pain, (such as a toothache) or
discomfort (like "pins and needles", parasthesia), may be
symptoms of pre-trigeminal neuralgia.
Pre-TN is most effectively treated with medical therapy used for
typical TN
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Trigger zones may result from ephaptic coupling between
partially damaged trigeminal axons that allows abnormal
spread of excitation, facilitating a synchronous discharge of
hyperexcitable trigeminal afferents that produce a pain attack.

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Pulsation of vessels do not visibly damage the nerve.
Irritation from repeated pulsations may lead to changes of nerve function,
& deliver abnormal signals to the trigeminal nerve nucleus.
Causes hyperactivity of the trigeminal nerve nucleus, resulting in the generation
of TN pain
82
TN trigger zone is an area of facial skin or oral mucosa
where low-intensity mechanical stimulation (such as light
touch, an air puff, or even hair-bending) can elicit a typical
pain attack.

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