Imaging neurovascular conflict: what a radiologist need to know and to report?

Transcription

1 Imaging neurovascular conflict: what a radiologist need to know and to report? Poster No.: C-1933 Congress: ECR 2012 Type: Educational Exhibit Authors: E. LOZUPONE, G. Di lella, S. Gaudino, A. Pedicelli, R Colantonio, M. Martucci, M. Pileggi, L. Bonomo, C. Colosimo ; ROME/IT, Rome/IT, ROMA (RM)/IT, rome/it, Roma/IT Keywords: Inflammation, Imaging sequences, MR, Neuroradiology brain DOI: /ecr2012/C-1933 Any information contained in this pdf file is automatically generated from digital material submitted to EPOS by third parties in the form of scientific presentations. References to any names, marks, products, or services of third parties or hypertext links to thirdparty sites or information are provided solely as a convenience to you and do not in any way constitute or imply ECR's endorsement, sponsorship or recommendation of the third party, information, product or service. ECR is not responsible for the content of these pages and does not make any representations regarding the content or accuracy of material in this file. As per copyright regulations, any unauthorised use of the material or parts thereof as well as commercial reproduction or multiple distribution by any traditional or electronically based reproduction/publication method ist strictly prohibited. You agree to defend, indemnify, and hold ECR harmless from and against any and all claims, damages, costs, and expenses, including attorneys' fees, arising from or related to your use of these pages. Please note: Links to movies, ppt slideshows and any other multimedia files are not available in the pdf version of presentations. Page 1 of 36

2 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. Page 2 of 36

3 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. Page 3 of 36

4 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. Page 4 of 36

5 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 Page 5 of 36

6 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. Page 6 of 36

7 Fig. 5: Treatment References: E. LOZUPONE; RADIOLOGY, ROME, ITALY Images for this section: Page 7 of 36

8 Fig. 1: Root Entry Zone Page 8 of 36

9 Fig. 2: Pathophysiology of neurovascular conflict Page 9 of 36

10 Fig. 3: Pathophysiology of neurovascular conflict Fig. 4: Differential diagnosis Page 10 of 36

11 Fig. 5: Treatment Page 11 of 36

12 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 T2weighted 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 vertebrobasilar 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. Page 12 of 36

13 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 postgadolinium 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: Page 13 of 36

14 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 Page 14 of 36

15 Fig. 8: Neurovascular conflict of the trigeminal nerve References: E. LOZUPONE; RADIOLOGY, ROME, ITALY Page 15 of 36

16 Fig. 9: Neurovascular conflict of the trigeminal nerve References: E. LOZUPONE; RADIOLOGY, ROME, ITALY Page 16 of 36

17 Fig. 10: Neurovascular conflict of the trigeminal nerve References: E. LOZUPONE; RADIOLOGY, ROME, ITALY Page 17 of 36

18 Fig. 11: Neurovascular conflict of the trigeminal nerve References: E. LOZUPONE; RADIOLOGY, ROME, ITALY Page 18 of 36

19 Fig. 12: Neurovascular conflict of the facial nerve References: E. LOZUPONE; RADIOLOGY, ROME, ITALY Page 19 of 36

20 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. Page 20 of 36

21 Fig. 14: Asymptomatic neurovascular "contact" References: E. LOZUPONE; RADIOLOGY, ROME, ITALY Page 21 of 36

22 Fig. 15: Differential diagnosis References: E. LOZUPONE; RADIOLOGY, ROME, ITALY Page 22 of 36

23 Fig. 16: Differential diagnosis References: E. LOZUPONE; RADIOLOGY, ROME, ITALY Images for this section: Page 23 of 36

24 Fig. 6: MR imaging protocol Page 24 of 36

25 Fig. 7: Key imaging findings Page 25 of 36

26 Fig. 8: Neurovascular conflict of the trigeminal nerve Page 26 of 36

27 Fig. 9: Neurovascular conflict of the trigeminal nerve Page 27 of 36

28 Fig. 10: Neurovascular conflict of the trigeminal nerve Page 28 of 36

29 Fig. 11: Neurovascular conflict of the trigeminal nerve Page 29 of 36

30 Fig. 12: Neurovascular conflict of the facial nerve Page 30 of 36

31 Fig. 13: Neurovascular conflict of the glossopharyngeal nerve Page 31 of 36

32 Fig. 14: Asymptomatic neurovascular "contact" Page 32 of 36

33 Fig. 15: Differential diagnosis Page 33 of 36

34 Fig. 16: Differential diagnosis Page 34 of 36

35 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 emilio.lozupone@live.it References Love S, Coakham HB. Trigeminal neuralgia: pathology and pathogenesis. Brain Dec;124(Pt 12): 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 ;71(15): Page 35 of 36

36 Casselman J, Mermuys K, Delanote J, Ghekiere J, Coenegrachts K. MRI of the cranial nerves - more than meets the eye: technical considerations and advanced anatomy. Neuroimaging Clin N Am May;18(2): Borges A, Casselman J. Imaging the cranial nerves: Part I: Methodology, infectious and inflammatory, traumatic and congenital lesions. Eur Radiol (2007) 17: Borges A., Casselman J. Imaging the cranial nerves: part II: primary and secondary neoplastic conditions and neurovascular conflicts. Eur Radiol (2007) 17: 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 caused by neurovascular compression. AJR Am J Roentgenol Aug;191(2): Page 36 of 36