Demystifying Trigeminal Neuralgia Classic vs Symptomatic

23 Pages·2015·2.33 MB·English

by  Glastonbury, Christine

22/04/2015
• The graphics in this presentation were created
by Amirsys.
• DrGlastonbury has received royalties from
Amirsysand Elsevier
• Unilateral recurrent episodic intense facial pain
• Also known as Trigeminal Neuralgia Type 2 (TN2)
–“electric-shock”, “stabbing”, “lancinating”,
• Constant, aching, burning pain
“shooting”, “burning”, “excruciating”
–of lowerintensitythan TN1
–Abrupt onset following physical
stimulation of ipsilateral ‘trigger zone’
• Typically assoc’dwith cramping • Bilateral TN -simultaneous involvement of
of facial muscles
both sides of face is rare
–“Tic Douloureux” = painful twitch
• The “Suicide disease”
• Empirical evidence suggests 95% TN due to • Routine MR sequences
neurovascular compression –Normal brain
? Wearing away of myelin sheath (both de-& • High resolution T2 MR (CISS/FIESTA):
dys-myelination have been shown) –Vascular loop (artery) @ CN5 REZ
→ Impaired nociceptive system –±CN5 nerve atrophy
→ Ephaticcrosstalk / Ignition hypothesis • MRA
• 5% MS plaque / brainstem infarct, CPA mass, –Source images most helpful for vascular
perineuralprocess loop @ REZ
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• Most often arterial
– Superior cerebellar
– Anterior inferior (AICA) &
posterior inferior (PICA)
cerebellar
• Sometimes venous
– Superior petrosalvein &
its tributaries
• 13-60%asymptomaticvascular contact with • Be carefulthat trigeminal symptoms are
CN5 at surgery;up to 78% MRI frequently all called “TN”!
• 3-17% of TN decompressive surgeries find no • Always consider other causes of facial pain:
vascular compression –TMJ, dental or sinus disease
• CN9-12 often in contact with vertebral @ –Multitude of trigeminal nerve pathologies
–Rarely have syndromes other than CN9 may manifest with pain / dysesthesias
• Three twins: CN5¹, CN5²& CN5³(V1/V2/V3)
• Sensory -face, conjunctiva, sinuses, teeth,
tongue, external aspect of TM
– PLUS anterior + middle fossa meninges
• Motor to most of jaw muscles
• Complex brainstemnuclei
• Largest cisternalcranial nerve
• Complex extracranialbranches
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Motor nucleus
Sensory nuclei
Mesencephalic
Primary sensory
proprioceptive
Chief sensory
Facial touch
Spinal tract
Pain & temperature
5¹: Ophthalmic -
Nasociliary, frontal
lacrimal
5²: Maxillary -
Leptomeningeal
PPF, zygomatic,
infraorbital, MS, Infarct, Infection, Perineural,
inflammation, tumor or process
palatine Lyme disease tumor Inflammation
5³: Mandibular & CPA masses
Masticator,
mylohyoid, 4 SYMPTOMATIC TRIGEMINAL NEURALGIA
sensory nerves
• TN is specific neurologic disorder
–TN1: Unilateral, CN5² / CN5³ intense episodic pain • Sensory changes
–Specific triggers may be identified • Deafness or inner ear balance issues
–Tends to worsen in frequency/severity over time • Poor response to medical therapy
• TN2 = atypical TN = constant aching pain • Prior skin or oral neoplasm
• Classic= No established etiology • Isolated to CN5¹ or bilateral TN
–Vascular compression at CN5 REZ implicated • Optic neuritis, family history of MS
–SCA most often, AICA, PICA, sup petrosalvein • Onset <40 years age
• Symptomatic= Lesion / mass / tumor etc
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•TanrikuluL et al. Preoperative MRI in neurovascular compression syndromes and its
role for microsurgical considerations.ClinNeurolNeurosurg. 2015 Feb;129:17-20.
•MaarbjergS et al. Significance of neurovascular contact in classical trigeminal
• Look for vascular loop @ REZ (T2 & MRA) neuralgia. Brain. 2015 Feb;138(Pt2):311-9.
•Suzuki M et al. Trigeminal neuralgia: differences in magnetic resonance imaging
characteristics of neurovascular compression between symptomatic and asymptomatic
nerves. Oral SurgOral Med Oral PatholOral Radiol. 2015 Jan;119(1):113-8.
• Not until afteryou have evaluated the entire •AntoniniG et al. Magnetic resonance imaging contribution for diagnosing
symptomatic neurovascular contact in classical trigeminal neuralgia: a blinded case-
course of CN5 brainstem nuclei to deep face control study and meta-analysis.Pain. 2014 Aug;155(8):1464-71.
•Thomas KL, VilenskyJA. The anatomy of vascular compression in trigeminal neuralgia.
Exclude Symptomatic TN (brainstem lesion / ClinAnat. 2014 Jan;27(1):89-93.
•ZakrzewskaJM, LinskeyME. Trigeminal neuralgia. BMJ. 2015 Mar 12;350:h1238.
CN5 mass / perineuralprocess) first! •Prasad S, GalettaS. Trigeminal neuralgia: historical notes and current concepts.
Neurologist.2009 Mar;15(2):87-94.
You must know your CN5 nerve anatomy! •DevorM et al. Pathophysiology of trigeminal neuralgia: the ignition hypothesis. ClinJ
Pain. 2002 Jan-Feb;18(1):4-13.
•DevorM et al. Mechanism of trigeminal neuralgia: an ultrastructuralanalysis of
trigeminal root specimens obtained during microvascular decompression surgery. J
Neurosurg. 2002 Mar;96(3):532-43.
[email protected]
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22/04/2015
Disclosures
Imaging for Hemifacial
• None
Spasm (HFS)
Sugoto Mukherjee, MD
Assistant Professor
University of Virginia Health System
OBJECTIVES 1893 by Edouard Brissaud
• Understand HFS, the • “A case of a 35-year-old
work up and treatment woman with clonic
options
contractions (secousses
• Review relevant facial cloniques) in the right face. All
nerve anatomy
the facial muscles were
• Characterize the involved, including the
imaging appearance of frontalis, the orbicularis oculi,
vascular compression of
the zygomaticus, and the
the facial nerve in
platysma”.
patients with HFS
What is Hemifacial Spasm? Hemifacial Spasm
• Hemifacialspasm is a • HFS is most commonly
neuromuscular caused by vascular
disorder characterized compression of the
by frequent facial nerve.
involuntary • Other etiologies
contractions (spasms)
–Intracranial masses
of the muscles on one
–Facial nerve injury
side (hemi-) of the
–Brain stem infarct
face (facial).
–Demyelinating plaque
The Many Faces of HemifacialSpasm: Differential Diagnosis of Unilateral
Facial Spasms
Toby C. Yaltho, MD1 and Joseph Jankovic, MD*
Parkinson’s Disease Center and Movement Disorders Clinic, Department of
Neurology, Baylor College of Medicine, Houston, Texas, USA
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Hemifacial Spasm Vascular Cause
• HFS is most commonly Vessels
caused by vascular
• Vertebrobasilarartery
compression of the
• Posterior inferior cerebellar
facial nerve. artery (PICA)
• Other etiologies • Anterior inferior cerebellar
–Intracranial masses artery (AICA)
–Facial nerve injury
–Brain stem infarct
–Demyelinating plaque
Variations in vascular compression HFS work up – 3 step
• 1 vessel –multiple • Clinical history &
contacts Neurological examination
• Mutiplevessel with • Electromyography (EMG) to
distinguish from other
contacts
abnormal facial movement
• Adhesions and other disorders such as
variations blepharospasm, tics, partial
motor seizures, synkinesis,
Meige’ssyndrome, and
neuromyotonia
• MRI
HemifacialSpasm, A Neurosurgical Perspective
Park et al, JKNS, 2007 “Lateral spread”
Role of MRI - Confusion Protocol features
• Ability to detect • Advances in imaging • Ax T1, T2 FS, T1 FS
vascular techniques allows for post, T2
compression of the determination of SPACE/CISS/ SSFP
facial nerve with
culprit vessel in • CorT1, STIR, T1 FS
MRIANDalso the
almost all patients post
significance of
vascular • Exclude other • WB: Ax FLAIR
compression by structural causes and • MRA TOF COW
MRI confounding
diagnosis
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Protocol – Sample Coverage 3D SSFP sequences
• Superior: top of CC
Axial
• Inferior: bottom of
mandible
• Anterior: tip of nose
• Posterior: back of CC Coronal
Sagittal
HFS – Treatment Options HFS – Treatment Options
Botulinuminj MVD
• Local botulinumtoxin • Only microvascular
injection into the orbicularis decompression offers the
oculi or lower facial potential for cure of HFS
muscles is a nonsurgical with success rates
palliative option that can exceeding 90%......
reduce the severity of HFS.
Dannenbaum, M., et al. "Microvasculardecompression for hemifacialspasm: long-
term results from 114 operations performed without neurophysiological
monitoring."Journal of neurosurgery109.3 (2008): 410.
Facial nerve nucleus-Motor Proximal Facial Nerve Anatomy
• Muscles of facial
expression
• Ventral pons
• Fibers loop around
abducensnuclei FFFNNN---MMMoootttooorrr NNNuuucccllleeeuuusss
causing facial FFFNNN---SSSSSSNNN
colliculus AAAbbbddduuuccceeennnsssnnnuuucccllleeeuuusss
• Exit in CP cistern at FFFNNN---NNNTTTSSS
pontomedullary
junction
FFFaaaccciiiaaalll cccooolllllliiicccuuullliii
Campos-Benitez M, Kaufmann AM. Neurovascular
compression findings in hemifacialspasm. J
Raghavanet al, Imaging of Facial Nerve, NICNA Neurosurg2008;109: 416 –20
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Proximal Facial Nerve Anatomy MR Images
Campos-Benitez M, Kaufmann AM. Neurovascular
compression findings in hemifacialspasm. J
Neurosurg2008;109: 416 –20
Step by step approach Case 1
• Confirm laterality
• Exclude other structural causes
• Identify facial nerve
• Identify the offending vessel (almost always an
artery –Vertebrobasilar, PICA or AICA)
• Point of contact -Proximal/ Middle/ Distal
• If proximal –delineate it more precisely
• Single or multiple vessels/ point of contact
• Define contact: contact +/-displacement
Case 2 Case 3
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Case 3 Case 4
Future directions Further Reading
• TomiiM, OnoueH, Yasue M, et al. Microscopic
measurement of the facial nerve root exit zone from central
glial myelin to peripheral Schwann cell myelin. J Neurosurg
2003;99: 121–24
• Hughes, M. A., et al. "MRI Findings in Patients with a
History of Failed Prior MicrovascularDecompression for
HemifacialSpasm: How to Image and Where to
Look."AJNR. American journal of neuroradiology(2014).
• Tu, Y., et al. "Altered spontaneous brain activity in patients
with hemifacialspasm: a resting-state functional MRI
study." PloSone 10.1 (2015): e0116849.
Tu, Y., et al. "Altered spontaneous brain activity in patients with hemifacialspasm: a
resting-state functional MRI study." PloSone 10.1 (2015): e0116849.
THANKS
[email protected]
5
Imaging for Facial Reanimation
Loss of facial nerve function can be devastating to patients. The field of facial plastics has developed
many methods of improving the appearance and function of the face in patients with facial paresis, and
in this session we will discuss imaging evaluation in preparation for one of these methods – gracillis
muscle transfer.
The most common cause of facial paresis is Bell’s palsy. Typically patients with Bells experience a rapid
onset and resolve spontaneously. A small percentage will be left with persistent Bells palsy and the first
and most important role of the radiologist in patients with facial paresis is distinguishing those patients
with more ominous causes of facial paresis from patients with persistent Bells. Features which suggest
mass lesions as a cause of facial paresis include recurrent or progressive course of weakness, history of
prior parotid or skin cancer, mass lesion in the parotid, multiple cranial neuropathies and ipsilateral
adenopathy. Patients with any of these features must have high quality imaging through the entire
course of the facial nerve in order to evaluate it fully for the presence of perineural tumor spread,
vascular lesion, or benign tumor such as facial nerve schwannoma.
An additional role of the radiologist in the patient with mass lesion as the cause of facial palsy is
identification of the extent of disease. In a patient with parotid cancer and perineural tumor spread,
accurate delineation of the extent of disease is required for pre-operative planning. In particular it is
important for the surgeon to know whether temporal bone drilling will be required to achieve a clean
margin. This can also be helpful for pre-operative planning of cable grafts to bridge any defects in the
facial nerve.
A variety of surgical approaches can improve the appearance and quality of life for patients with facial
paresis. Lid weights (made of gold or platinum) can reduce corneal exposure. Fascial lata slings may
improve facial tone and elevate the corner of the mouth and nasolabial fold. Gracillis muscle grafts can
significantly improve the voluntary smile of patients and radiologists can be very helpful in their
placement.
The gracillis graft features a gracillis muscle from the thigh, which comes with an artery, two veins and
an obturator nerve. It is placed in the face, extending from the temple region to the corner of the
mouth. The obturator nerve is anastamosed to either a cross face nerve graft (brought over during a
prior surgery) or to a branch of the ipsilateral trigeminal nerve. Unlike most other head and neck flaps,
there is no skin brought with the gracillis graft, and it is buried deep to the skin of the face. For this
reason, features such as skin turgor and capillary refill cannot be used to monitor the integrity of the
venous and arterial anastomosis. Bedside Doppler can be used for the arterial pedicle, but gives no
information on the venous pedicle.
We do ultrasound on these grafts, the morning after the procedure. We identify the site of venous
anastomosis by identifying the venous coupler. We evaluate the artery and vein both above and below
the venous coupler and ensure that there is good color flow, Doppler signal and compressibility of the
vein.