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Imaging neurovascular conflict: what a radiologist need to

know and to report?

Poster No.: C-1933


Congress: ECR 2012
Type: Educational Exhibit
Authors: 1 2 1
E. LOZUPONE , G. Di lella , S. Gaudino , A. Pedicelli , R.
3

2 4 2 2 5
Colantonio , M. Martucci , M. Pileggi , L. Bonomo , C. Colosimo ;
1 2 3 4 5
ROME/IT, Rome/IT, ROMA (RM)/IT, rome/IT, Roma/IT
Keywords: Inflammation, Imaging sequences, MR, Neuroradiology brain
DOI: 10.1594/ecr2012/C-1933

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Learning objectives

• To determine the best MR imaging protocol in the assessment of


neurovascular conflict
• To provide a systematic approach in order to detect a neurovascular conflict
and present the key MR imaging features

Background

Several syndromes involving hyperactivity and abnormal spread of activity within the
distribution of innervations of cranial nerves V-IX are now known to be associated, in
several patients, with vascular compression of the cranial nerve roots. Redundant arterial
loops may cause compression of nerve's root entry zone (REZ) in the cerebellopontine
cistern, producing hyperactive dysfunction of cranial nerve. Trigeminal neuralgia,
hemifacial spasm, glossopharyngeal neuralgia, some cases of tinnitus and positional
vertigo represent the clinical spectrum of long-term compression on V, VII, IX, VIII nerve.

PATHOPHYSIOLGY

Neurovascular conflict (NVC) is defined as an "abnormal" contact between an artery and


the REZ of a cranial nerve.

REZ is the cisternal part of the nerve close to the entrance into the pons (or the exit from).
It represents a transition zone between the peripheral myelin, derived from Schwann
cells, and central myelin, derived from oligodendroglia. According to this anatomical
organization, this junctional zone is thinner and more vulnerable to vascular compression
than the other nerve's segments.

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Fig. 1: Root Entry Zone
References: E. LOZUPONE; RADIOLOGY, ROME, ITALY

The existing literature suggests that the vascular compression exerted on the nerve at
the level of the REZ, leads to increased excitability, at least in some of the nerve fibers,
and consequently to the dysfunction syndrome. In the long term, pulsations of vessel
on the nerve's REZ cause fibers' demyelination with axons juxtaposition and absence
of intervening glial process. This anatomical arrangement favors the ectopic generation
of spontaneous impulses and their ephaptic conduction to adjacent fibers, leading to a
rapid buildup of electrical activity, either spontaneously or in response to external stimuli.
This results in a rapid and paroxysmal explosion of symptoms. Furthermore, a functional
reorganization of the nucleus could play a role in the genesis and recurrences of the
paroxysm.

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Fig. 2: Pathophysiology of neurovascular conflict
References: E. LOZUPONE; RADIOLOGY, ROME, ITALY

Vascular compression of REZ could be depicted as a "cross-compression", a contact


with variable angle between the two structures, or as a "sandwich compression" in which
the nerve is entrapped between two different vessels. Commonly the offending vessel
implicated is an artery of the vertebro-basilar system while is still debated, and highly
unlikely, the role of veins in NVC.

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Fig. 3: Pathophysiology of neurovascular conflict
References: H. Ric Harnsberger, Anne G. Osborn, Jeff Ross, Andre Macdonald.
Diagnostic and surgical imaging anatomy: Brain, Head and Neck, Spine. First edition
(2006). AMIRSYS

CLINICAL ASPECTS

Clinical aspects of NVC of the most involved nerves are listed below.

• Trigeminal neuralgia represents the most common dysfunction syndrome.


It is characterized by recurrent episodes of intense, lancinating pain
localized to small areas of the face. The episodes are often precipitated by
mild sensory stimulation of a trigger zone, which may be located everywhere
within the territory of the affected trigeminal nerve; typical antecedent stimuli
include light touching, draught of wind, eating, drinking, washing, shaving
and applying make-up.
• Hemifacial spasm is characterized by frequent, involuntary rapid onset of
muscle contractions (often tics or spasms of the orbicularis oculi muscle),
that gradually progress in severity and frequency , and spreads downward to
include all the muscles of facial expression. It usually affects only one side of

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the face, but in severe cases, tics may occur on both sides. Fatigue, anxiety,
or reading may precipitate the movements.
• Glossopharyngeal neuralgia presents as a severe paroxysmal pain of
sudden onset in the oropharynx, in the tonsillar fossa, at the base of the
tongue and in the ear's region; it is often precipitated by trigger activities
such as swallowing, chewing, or coughing.

Nowadays vascular compression is known to be involved in a great majority (80-90%)


of dysfunction syndromes, but in a small percentage of cases could be caused by other
pathologies. Lesions that could secondarily affect the REZ include neoplasms, vascular
lesions, infections and inflammatory diseases.

Fig. 4: Differential diagnosis


References: E. LOZUPONE; RADIOLOGY, ROME, ITALY

TREATMENT

Nowadays different therapies are available in the treatment of spasmodic hyperfunction


generated by neurovascular conflict.

Drugs represent generally the first approach; anti-epileptics may relief symptoms in
cranial neuralgias but it usually results curative only in a small number of cases.
Intramuscular injection of botulinum toxin can reduce the facial contraction and has
proven useful in many cases of hemifacial spasm. In those patients refractory to
medical treatment, the surgical approach is mandatory. In the last decades several
different surgical techniques have been used in the treatment of cranial neuralgia but
microvascular decompression, proposed by Jannetta, has shown the best results; the
procedure consists in decompressing the nerve's REZ by the interposition of a small
piece of teflon between the nerve and the offending vessels.

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Fig. 5: Treatment
References: E. LOZUPONE; RADIOLOGY, ROME, ITALY

Images for this section:

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Fig. 1: Root Entry Zone

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Fig. 2: Pathophysiology of neurovascular conflict

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Fig. 3: Pathophysiology of neurovascular conflict

Fig. 4: Differential diagnosis

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Fig. 5: Treatment

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Imaging findings OR Procedure details

A correct clinical evaluation is fundamental for the Patient's management: moreover, the
identification of the physiopathological process underlying the condition is of paramount
importance because it may lead to the appropriate therapy. Role of imaging is essential to
exclude secondary causes of dysfunction syndrome and can confirm the clinical suspect
of NVC. Currently the NVC imaging relies predominantly on magnetic resonance imaging,
while CT and angiographic techniques maintain an ancillary role in specific issues.

MR IMAGING PROTOCOL

MRI imaging protocol is essentially based on two sequences: a 3D steady state sequence
and an angiographic sequence.

The 3D steady state sequences (CISS, FIESTA, DRIVE) are high-resolution heavily T2-
weighted techniques and allow very good delineation of vascular structures and nerves
in the CSF spaces. The anatomic course and complex vascular relationships of nerve's
cisternal segment can be visualized successfully by these sequences. They provide very
good CSF-nerve contrast and very thin submillimetric slices (0.7 mmevery0.35 mm),
allowing for multiplanar studies and virtual, eventually, endoscopic views. The alignment
of the slices to the course of the nerve could hep to obtain a detailed visualization of
cranial nerve's anatomy.

High-resolution 3D MRA (TOF-MRA) and/or contrast-enhanced MRA (CE-MRA), with


careful analysis of MIP (maximum intensity projection), multiplanar reconstructions and
source images, is the method of choice to evaluate the vascular anatomy of vertebro-
basilar system. These sequences depict the vessels as hyperintense structures within
the hypointense CSF and nerves as linear structures of intermediate signal intensity.

Furthermore it is important to underline that the time needed for the acquisition of a 3D
steady-state and an angiographic sequence is about 12 minutes.

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Fig. 6: MR imaging protocol
References: E. LOZUPONE; RADIOLOGY, ROME, ITALY

Patients evaluated for suspect NVC, should be studied also using the brain morphological
sequences (FLAIR, T1 and T2 FSE, GRE and DWI) to exclude other causes that could
mimic the symptoms: acquisition of high-resolution T1 pre- and fat-suppressed post-
gadolinium sequences could provide also additional information on the studied nerves
(i.e. nerve sheath tumors).

MR KEY IMAGING FINDINGS OF NEUROVASCULAR CONFLICT

The finding of an asymmetrical vessel with serpiginous shape at the ponto-cerebellar


angle is of paramount importance, indicating the artery presumably responsible of the
abnormal contact with the cranial nerve under investigation. An accurate assessment of
the implicated nerve's REZ and the offending vessels should be undertaken to obtain a
correct diagnosis of neurovascular conflict.

Therefore the following criteria have to be carefully considered:

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• The offending vessel should be an artery
• The vessel must cross the nerve, at the REZ , perpendicularly
• At least one of nerve's abnormalities stated below should be found:
• • Deformations and angulations of nerve's course ("bending")
• Footprints on the surface of the nerve ("grooving")
• Partial nerve shearing by an arterial loop generating a deep
indentation on the nerve surface ("stretching")

Multiplanar reconstructions from 3D steady state sequences generally help to define the
diagnosis of NVC in suspected cases.

Fig. 7: Key imaging findings


References: E. LOZUPONE; RADIOLOGY, ROME, ITALY

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Fig. 8: Neurovascular conflict of the trigeminal nerve
References: E. LOZUPONE; RADIOLOGY, ROME, ITALY

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Fig. 9: Neurovascular conflict of the trigeminal nerve
References: E. LOZUPONE; RADIOLOGY, ROME, ITALY

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Fig. 10: Neurovascular conflict of the trigeminal nerve
References: E. LOZUPONE; RADIOLOGY, ROME, ITALY

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Fig. 11: Neurovascular conflict of the trigeminal nerve
References: E. LOZUPONE; RADIOLOGY, ROME, ITALY

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Fig. 12: Neurovascular conflict of the facial nerve
References: E. LOZUPONE; RADIOLOGY, ROME, ITALY

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Fig. 13: Neurovascular conflict of the glossopharyngeal nerve
References: E. LOZUPONE; RADIOLOGY, ROME, ITALY

Identify a contact between a vessel and a nerve in patients both asymptomatic or with
shaded symptoms, is not an infrequent occurrence. Therefore the careful application of
these criteria is essential to reach a correct diagnosis of neurovascular conflict and to
avoid to misinterpret a simple contact between an artery and a nerve.

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Fig. 14: Asymptomatic neurovascular "contact"
References: E. LOZUPONE; RADIOLOGY, ROME, ITALY

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Fig. 15: Differential diagnosis
References: E. LOZUPONE; RADIOLOGY, ROME, ITALY

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Fig. 16: Differential diagnosis
References: E. LOZUPONE; RADIOLOGY, ROME, ITALY

Images for this section:

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Fig. 6: MR imaging protocol

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Fig. 7: Key imaging findings

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Fig. 8: Neurovascular conflict of the trigeminal nerve

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Fig. 9: Neurovascular conflict of the trigeminal nerve

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Fig. 10: Neurovascular conflict of the trigeminal nerve

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Fig. 11: Neurovascular conflict of the trigeminal nerve

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Fig. 12: Neurovascular conflict of the facial nerve

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Fig. 13: Neurovascular conflict of the glossopharyngeal nerve

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Fig. 14: Asymptomatic neurovascular "contact"

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Fig. 15: Differential diagnosis

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Fig. 16: Differential diagnosis

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Conclusion

Neurovascular conflict represents a nosological entity that can deeply impact on the
life quality of a patient, up to nearly debilitating forms of chronic and irrepressible pain.
Therefore a correct clinical and diagnostic assessment is fundamental.

Imaging of neurovascular conflict requires a thorough understanding of the


neuroanatomy, neurophysiology and main clinical aspect of cranial nerve dysfunction
syndrome.

3D steady state and angiographic MR sequences represent nowadays the most


sensitive tools available to radiologists, allowing an optimal identification of the vascular
compression of the cranial nerve's REZ.

A systematic approach and the accurate application of the suggested criteria represent
essential requisites for Radiologists, in order to increase the diagnostic accuracy in the
assessment of neurovascular conflict, therefore reducing the false negative and false
positive rate.

Personal Information

E. Lozupone, G. Di Lella, S. Gaudino, A. Pedicelli, R. Colantonio, M. Martucci, M. Pileggi,


L. Bonomo, C. Colosimo.

Department of Radiology, Università cattolica del sacro cuore, Policlinico "A. Gemelli",
Rome, Italy

E-mail: emilio.lozupone@live.it

References

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Brain. 2001 Dec;124(Pt 12):2347-60
• Gronseth G, Cruccu G, Alksne J, Argoff C, Brainin M, Burchiel K, et al.
Practice parameter: the diagnostic evaluation and treatment of trigeminal
neuralgia (an evidence-based review): report of the Quality Standards
Subcommittee of the American Academy of Neurology and the European
Federation of Neurological Societies. Neurology. Oct 7 2008;71(15):1183-90

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• Casselman J, Mermuys K, Delanote J, Ghekiere J, Coenegrachts
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(2007) 17: 2112-2125
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secondary neoplastic conditions and neurovascular conflicts. Eur Radiol
(2007) 17: 2332-2344
• Yoshino N et al.Trigeminal neuralgia: Evaluation of neuralgic
manifestations and site of neurovascular compression with 3D CISS MR
imaging and MR angiography. Radiology 228:539-45,2003
• Satoh T, Onoda K, Date I. Fusion imaging of three-dimensional magnetic
resonance cisternograms and angiograms for the assessment of
microvascular decompression in patients with hemifacial spasms. J
Neurosurg 2007; 106:82- 89
• Hiwatashi A, Matsushima T, Yoshiura T, Tanaka A, Noguchi T,
Togao O, Yamashita K, Honda H. MRI of glossopharyngeal neuralgia
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