67 Curr Neurobiol 2019 Volume 10 Issue 2

Curr Neurobiol 2019; 10(2): 67-72 ISSN 0975-9042

Association of non-infectious isolated internal carotid arteritis with the de novo appearance of a saccular aneurysm of the anterior communicating arteryFrancisco Revilla-Pacheco1, Arantxa Anton-Alonso1, Laura Sanchez-Garcia2, Pamela Rodríguez-Salgado1, Salvador Manrique-Guzman1, Alonso Turrent-Carriles3, Johnatan Rubalcava-Ortega2 and Tenoch Herrada-Pineda1

1Neurological Center, The American British Cowdray Medical Center, IAP. Mexico City, Mexico2Image Department, The American British Cowdray Medical Center, IAP. Mexico City, Mexico3Rheumatology and Internal Medicine Department, The American British Cowdray Medical Center, IAP. Mexico City, Mexico

AbstractA condition named isolated internal carotid arteritis has been recently described in the literature. This new concept after studying a patient with atypical arteritis circumscribed to the internal carotid arteries, who did not fulfill the diagnostic criteria associated with contemporary classified vasculitides. We present the case of a 43-year-old male patient, previously healthy, who arrived to the Emergency Department with sudden apparition of dysphasia and right hemiparesis. Initial magnetic resonance image (MRI) and magnetic resonance angiography (angio MRI) showed isolated areas of leukoaraiosis in both frontal lobes and decreased flow of the petrous segment of the left internal carotid, with decrease in caliber of the same segment; as well as increased thickness of the left internal carotid’s wall in the cervical, petrous and lacerum segments, with a circumferential pattern, and severe stenosis. Two months later an aneurysm of the anterior communicating artery was diagnosed.

IntroductionVasculitides can be grossly divided for their study in two

major groups: infectious vasculitis, caused by the direct invasion of a pathogenic organism that causes an inflammatory response in the blood vessel’s wall; and non-infectious vasculitis, in which it is known that the phenomenon is not secondary to the invasion of an infectious agent [1].

Non-infectious vasculitis can be defined as a blood vessel´s inflammatory process, which can affect vessels of any size. Contemporary classification is based on many characteristics: etiology, pathogenic mechanism, clinical and laboratory parameters, size of the affected vessels, inflammatory components at histological or molecular level, affected organ or territory [2].

Examples and description of patients or small group of patients, with the diagnosis of vasculitis which affects organs or isolated systems can be found in the specialized literature, such as thoracic aorta [3], gastrointestinal tract [4], spinal cord [5], urinary bladder [6], isolated muscular groups [7], the orbit [8], or central nervous system (brain, spinal cord, meninges) [9].

Fukuma et al. [1] recently described the case of a patient with isolated vasculitis of the internal carotid arteries; they considered that the characteristics the patient presented differed from those described in the contemporary criteria of vasculitis, such as Takayasu’s arteritis, giant cell arteritis, granulomatosis with polyangiitis, and Behçet’s disease; so they proposed a novel entity called “isolated internal carotid arteritis”.

We present the case of a 43-year-old male patient, with no history of previous relevant medical conditions, whom suddenly developed neurological signs and symptoms secondary to isolated internal carotid arteritis, and two months later, the de novo appearance of a saccular aneurysm in the anterior communicating artery.

Medical History and Clinical PresentationWe present a male patient, 43 years old at the time of

diagnosis. He had no history of surgical interventions or chronic diseases. He was not taking any medication. He is not consumer of tobacco, alcohol or drugs. There was no history of recent infections, and he was considered healthy until his admission to hospital.

Keywords: Arteritis, Non-infectious vasculitis, Internal carotid artery, Intracranial saccular aneurysm, De novo formation

Curr Neurobiol 2019 Volume 10 Issue 2

Association of non-infectious isolated internal carotid arteritis with the de novo appearance of a saccular aneurysm of the anterior communicating artery

68

He presented motor dysphasia, which was also noted by his wife, but initially refused to seek medical help. After 12 hours of evolution, dysphasia worsened, and right sided hemiparesis appeared. He arrived at the Emergency Department, alert, blood pressure was 122/80 mmHg, temperature 36.5°C, and heart rate 74 bpm. Dysphasia was severe, he had also right sided hemiparesis 3/5, right sided Hoffman’s and Babinski’s signs positive; National institute of Health Stroke Scale (NIHHS) punctuation was 9. His physical examination did not show tenderness in the scalp and temple areas, there was not any thoracic or neck murmur, no respiratory distress. The patient was cooperative, reactive, and willing to answer questions, but unable to do so because of the dysphasia. Comprehension was not altered. He answered questions by nodding or shaking his head. He had adequate eyelid opening and closing, and he could hold the fingers of the examiner with his left hand. His exam showed normal conjugate eye movement and orthophoria. No deficit was noticed in the visual fields. He presented discrete facial asymmetry, with moderate weakness of the right orbicularis oris muscle. He was able to perform movement of the right upper and lower extremity with difficulty to overcome gravity. Movement and strength were normal in his left extremities. Motor coordination and sensitivity was normal in the left side of the body; only moderate superficial hypoesthesia was found on the right side of the body. Hyperactive reflexes were found in right limbs.

Initial MRI showed isolated areas of leukoaraiosis in both frontal lobes and decrease in flow of the petrous segment of the left internal carotid, with a decrease in the caliber of the same segment. Angio MRI showed an increased thickness of the left internal carotid’s wall in the cervical, petrous and lacerum segments with a circumferential pattern and severe stenosis. No alterations were observed on the right carotid artery, no abnormalities were appreciated in the intracranial arteries, and no intracranial aneurysms were found (Figure 1).

He was not considered eligible to receive alteplase or undergo mechanical thrombectomy. An extensive investigation on inflammatory and procoagulant conditions was performed, and treatment with heparin and methylprednisolone was initiated.

The neurological deficit did not progress. The next day, a new MRI showed multiple areas with restricted diffusion, due to an acute infarction in the territory of the left middle cerebral artery (Figure 2). He was hospitalized in the Neurological Intensive Care Unit (NICU), and remained stable, with no new neurological deficit.

When he was admitted to the hospital, he presented leukocytosis, elevated globular sedimentation rate, and elevated complement level. Glycemic levels, international normalized ratio, activated partial thromboplastin time, platelet count, and troponin levels were normal; immunoglobulin levels were normal; hepatitis antigens, rheumatoid factor, tumor markers, and anti-cardiolipin antibodies were negative, anti-C1q antibodies

serum IgG4 levels were normal, anti-neutrophil cytoplasmic antibodies (ANCAs, MPO-ANCA, and PR3-ANCA) negative; vitamin levels, amino acids, and alpha-galactosidase were in normal range.

Vast laboratorial analysis and complementary studies were performed. There was no evident infectious process before or during his hospitalization; no cardiac disease was found, Mucocutaneous lymph node syndrome search was negative, no evidence of glomerulonephritis, arteriolar, venular, or capillary vasculitis was found. No superior or inferior respiratory tract, ocular, auditory or vestibular disease was found; there were no oral or genital ulcers; there were no nasal polyps, no myocardial, mediastinal, retroperitoneal, digestive, testicular, hepatic, pancreatic or cutaneous disease was found; there were no clinical or laboratory data of arthritis of any kind. No salivary gland, thyroid or aortic illness was found. There was no evidence of neoplastic disease, lymphoproliferative or myelodysplastic disorders. A 48-hour Holter did not show heart arrhythmias.

He remained stable the next 7 days in the NICU. In his fourth day of hospitalization, a cranial, neck, thoracic and abdominal computed tomography angiography (angio-CT) was performed (Figure 3). No disorders were found in the aorta, supra-aortic branch arteries, abdominal and retroperitoneal aortic branches, or in both common carotid arteries. Left internal carotid artery presented a concentric wall thickening starting in the

Figure 1. A and B. Diffusion sequence and ACD map without restriction areas. C. Decreased caliber of the petrous and lacerum segment of the left internal carotid artery in angioresonance sequence. D. Decreased signal of the left internal carotid artery and its branches in 3D TOF sequence.

Figure 2. A. Frontal strokes in diffusion sequence which are confirmed in ACD map. Angioresonance persists with decreased signal in the cervical, petrous, and lacerum segments of the left internal carotid artery. B. Angiotomography with usual origin and adequate caliber of supra-aortic vessels, pseudoaneurysm in the petrous segment of the left internal carotid artery.

69 Curr Neurobiol 2019 Volume 10 Issue 2

Revilla-Pacheco F, Anton-Alonso A, Sanchez-Garcia L,

doses of methylprednisolone, and was discharged 4 weeks after his admission, 3 weeks after the stents placement, with discrete dysphasia and right hemiparesis, to continue medical and rehabilitation treatment as an external patient. Methylprednisolone was replaced with prednisone, which he continued for 1 month after he was discharged, and clopidogrel 75mg OD was added and maintained.

A follow-up angio MRI was performed 1 month after he was discharged from hospital; there were no new arterial abnormalities, and no evidence of activity of the vasculitis process. For the first time since the beginning of his condition, the presence of a 3mm saccular aneurysm on the anterior communicating artery was documented (Figure 7).

Two subsequent angio MRI were performed, at two and four months, which did not show size or shape changes of the

Figure 3. New left frontal and parietal ischemic lesions, angioresonance with decreased signal in the petrous and lacerum segment of the left internal carotid artery.

cranial base transition, in the petrous, lacerum, and cavernous segments, with mural enhancement, and partial recovery of its caliber beginning in the clinoid segment. The abnormalities found did not show significant changes from those found in his admission’s angio MRI.

In his eighth day of hospitalization, in a follow-up MRI, brain infarct appeared like multiple areas of restricted diffusion in the left frontal lobe and left internal capsule, without hemorrhagic transformation. However, two lesions with similar characteristics appeared in the right cerebral hemisphere, the largest was adjacent to the anterior horn of the lateral ventricle (Figure 4).

Surprisingly, in the angio MRI, the right internal carotid had an important decrease of its arterial lumen and a concentric wall thickening with mural enhancement, in the petrous, lacerum and cavernous segments, with recovery of its caliber in the clinoid segment (Figure 5). In spite of this, his neurological condition was stable and there were no clinical data that could make us suspect the evident vascular anatomy deterioration.

We decided to perform urgent endovascular treatment; digital subtraction angiography showed severe stenosis of the left internal carotid artery with a pseudoaneurysm, severe stenosis of the right internal carotid starting at cervical bifurcation; there was no evidence of Moyamoya disease, fibromuscular dysplasia, arterial dissection, or central nervous system arteritis. A stent was deployed in the right carotid, and balloon angioplasty was performed in the left carotid artery (Figure 6). The procedure concluded without complications; the patient continued receiving descendent

Figure 4. Thorax and abdomen angiotomography with adequate caliber and pathway of the aorta and its principal branches, two right renal polar arteries can be seen as anatomical variants.

Figure 5. Angioresonance with absent signal of the cervical and petrous segment of the right internal carotid artery.

Figure 6. A and B. Ectasia in the petrous and lacerum segment of the left internal carotid artery and decreased caliber of the lacerum segment. C. Balloon angioplasty. D. Adequate flow in the distal branches. E. Right internal carotid with stenosis in the cervical and petrous proximal segment with adequate caliber of the distal segment. Metallic stent placement. F. Recovery of the caliber. G. opacification of distal branches.

Curr Neurobiol 2019 Volume 10 Issue 2

Association of non-infectious isolated internal carotid arteritis with the de novo appearance of a saccular aneurysm of the anterior communicating artery

70

aneurysm. Surgical treatment was decided. A left pterional craniotomy with clipping of a small saccular aneurysm on the anterior communicating artery was performed without complications (Figure 8); biopsy was obtained from the left superficial temporal artery and from the left inferior frontal gyrus. The postsurgical evolution was uneventful, and no neurological deficit appeared. Both biopsies were analyzed, no abnormalities were found.

The patient has been followed-up for 2 years. His speech has recovered completely. He has presented a slow improvement of the right hemiparesis; he can walk and look after himself. No new signs or symptoms have appeared. An angio MRI has been performed every 6 months, no new abnormalities have arisen. A second angio-CT scan performed 1 year after his hospital discharge resulted negative for aorta, supra aortic branches, abdominal and retroperitoneal aortic branches disorders. Both internal carotid arteries remain with stable with postsurgical changes.

Since no systemic or active vasculitis has been documented, the consideration to expand his treatment to cyclophosphamide, Rituximab, mycophenolate mofetil, chlorambucil, or plasmapheresis has been carefully analyzed, but not recommended.

DiscussionMain diagnostic considerations in a young man, who

presents with an acute ischemic stroke concomitant to vasculitis without evidence of concomitant infectious process, are Takayasu’s arteritis and giant cell arteritis. The absence of evidence for systemic vasculitis reduces enormously the diagnostic possibilities [10,11].

Documentation of arterial wall inflammation, an element that all forms of vasculitis share even when temporarily in the course of the disease, is mandatory for vasculitis diagnosis [2], arterial wall inflammation can be documented with image studies or serological markers [12]; digital subtraction angiography is not a useful study to demonstrate early changes due to vasculitis, and therefore it is not considered a valuable study in the early phases of suspected vasculitis; the most common finding in the digital subtraction angiography is stenosis, sometimes associated to occlusion, aneurysms or pseudoaneurysms in the affected arteries can occasionally be observed [13]. Angio-CT can show aortic and big vessels vasculitic changes, and can adequately evaluate artery’s wall and lumen [14] it can inconstantly show artery´s wall enhancement [15,16]. MRI can show vasculitis’s wall thickening and contrast enhancement in T1-weighted sequence [17], and arterial wall edema in T2-weighted sequence, as early signs of inflammation [18]. Color doppler ultrasound can detect early inflammatory changes in the arterial wall in vasculitis processes [19,20]. Positron emission tomography can be more sensible to detect early stages vasculitis than magnetic resonance image [21,22].

Serological markers can be either unspecific [23-25], as acute phase reactants, or specific for certain types of conditions as rheumatoid factor or anti-cardiolipin antibodies [26-30].

Once vasculitis is diagnosed, classification should be intended, the process, however, could be complex and challenging because in most cases, the etiology is unknown [31-34]; for this reason, contemporary nomenclature classifies vasculitides depending on various categories, which includes etiology, type of affected artery, affected organs, clinical characteristics, association with genetic factors, among others [2].

Early classification allows establishing prognostic factors, predicting specific patterns of organ involvement, defining association with other conditions, and establishing treatment preferences [31,32,35]. In most cases, because of the lack of randomized controlled clinical trials, the level of evidence to choose the best medical treatment and its duration is low [31,32,36].

In 2016 Kazuki Fukuma et al. [1] published the case of a 38-year-old woman with a clinical picture catalogued as “atypical arteritis in internal carotid arteries”, she underwent an extensive, scrupulous study, in which no other arterial illness was documented and, “ characteristics were not in accordance with existing diagnostic criteria of vasculitis, such as Takayasu’s

Figure 7. A. In Angioresonance sequence, adequate caliber of the arterial polygon. B. Ectasia in the petrous segment of the left internal carotid artery. C. Encephalomalacia and peripheral gliosis as sequels of previous strokes. D. Artifact in right internal carotid artery due to the presence of a stent. E. Saccular aneurysm in the anterior communicating artery.

Figure 8. Angiographic control study aneurysmal clipping. Left pterional craniotomy, metallic clip adjacent to the anterior communicating artery without residual aneurysm.

71 Curr Neurobiol 2019 Volume 10 Issue 2

Revilla-Pacheco F, Anton-Alonso A, Sanchez-Garcia L,

arteritis, giant cell arteritis, granulomatosis with polyangiitis, and Behçet’s disease”, therefore they suggested the concept of “isolated internal carotid arteritis”.

We present a similar case, in which we propose the same denomination: a 43-year-old man, with a left front parietal stroke, in whom bilateral isolated internal carotid arteritis was documented, his clinical, serological and image characteristics were not in accordance with the contemporary criteria of Takayasu’s disease, giant cell arteritis, primary angiitis of the central nervous system, and other forms of arteritis. The progression of his condition diminished and apparently stopped in association with the use of steroids in high-dose and with the placement of two carotid stents. He has been stable for two years, with no MRI or CT scan evidence of a relapse or the appearance of other vascular lesions that could let us associate his condition with known vasculitis diagnoses; he, however, developed the de novo appearance of a saccular aneurysm of the anterior communicating artery, that was not documented on the initial imaging studies, and that was diagnosed and surgically treated during his follow-up.

The cause of the development of saccular intracranial aneurysms is unknown [37]; current conceptualization highlights the association between mechanical properties of the arterial wall, and multiple hemodynamic factors in their formation, growth, and rupture, because of their well-known preferred localization on curves and bifurcations [38]. Recently, it has come to consideration the emergence of inflammatory processes as central mediators in the formation of intracranial saccular aneurysms [39]. The association of arteritis, angiitis, and vasculitis with the development or growth of intracranial saccular aneurysms is scarcely reported in the literature [40] and remains as a wide opportunity area for research.

References1. Fukuma K, Kowa H, Nakayasu H, Nakashima K. Atypical arteritis

in internal carotid arteries: a novel concept of isolated internal carotid arteritis. Yonago Acta Med. 2016; 59: 248-254.

2. Jennette JC, Falk R, Bacon P, Basu N, Cid M, Ferrario F, et al. 2012 revised international chapel hill consensus conference nomenclature of vasculitides. Arthritis Rheum. 2013; 65:1-11.

3. Stone JR. Aortitis, periaortitis, and retroperitoneal fibrosis, as manifestations of IgG4-related systemic disease. Curr Opin Rheumatol. 2011; 23: 88-94.

4. Louie CY, DiMaio MA, Charville GW, Berry GJ, Longacre TA. Gastrointestinal tract vasculopathy: clinicopathology and description of a possible “new entity” with protean features. Am J Surg Pathol. 2018; 42: 866-876.

5. Fisher A, Rahman H, Farrell M, Hennessy M. Progressive fatal myelopathy secondary to isolated spinal cord vasculitis. Front Neurol. 2017; 8: 705.

6. Fall M, Hoper L, Kabjorn-Gustafsson C, Trysberg E. Isolated vasculitis of the urinary bladder: a note on diagnosis and prognosis. Scand J Urol. 2018; 52: 230-231.

7. Tripoli A, Barsotti S, Pollina LE, Della Rossa A, Neri R, d’Ascanio A, et al. Muscular vasculitis confined to lower limbs: description of two case reports and a review of the literature. Rheumatol Int. 2017; 37: 2115-2121.

8. Park J-H, Park K-A, Cha J, Kim ST, Chung C-S, Lee MJ. A case report of isolated orbital vasculitis mimicking retinal migraine: A potential cause of recurrent transient monocular blindness and ipsilateral headache. Cephalalgia. 2018.

9. Mandal J, Chung SA. Primary angiitis of the central nervous system. Rheum Dis Clin North Am. 2017; 43: 503-518.

10. Masood QF, Naeem A, Tariq SM, Asad A, Habib S. Takayasu Arteritis: A diagnosis made using a multidisciplinary approach. Cureus. 2018; 10: e2781.

11. Van Rooij JL, Rutgers DR, Spliet WG, Frijns CJ. Vessel wall enhancement on MRI in the diagnosis of primary central nervous system vasculitis. Int J Stroke. 2018; 13: NP24-NP27.

12. Pipitone N, Versari A, Salvarani C. Role of imaging studies in the diagnosis and follow-up of large-vessel vasculitis: an update. Rheumatology (Oxford, England). 2008; 47: 403-408.

13. Vanoli M, Daina E, Salvarani C, Sabbadini MG, Rossi C, et al. Takayasu’s arteritis: A study of 104 Italian patients. Arthritis Rheum. 2005; 53: 100-107.

14. Gotway MB, Araoz PA, Macedo TA, Stanson AW, Higgins CB, et al. Imaging findings in Takayasu’s arteritis. Am J Roentgen. 2005; 184: 1945-1950.

15. Yoshida S, Akiba H, Tamakawa M, Yama N, Takeda M, et al. The spectrum of findings in supra-aortic Takayasu’s arteritis as seen on spiral CT angiography and digital subtraction angiography. Cardiovasc Intervent Radiol. 2001; 24: 117-121.

16. Park JH, Chung JW, Im J-G, Kim SK, Park YB, Han MC. Takayasu arteritis: evaluation of mural changes in the aorta and pulmonary artery with CT angiography. Radiology. 1995; 196: 89-93.

17. Choe YH, Lee WR. Magnetic resonance imaging diagnosis of Takayasu arteritis1. Int J Cardiol. 1998; 66: S175-S9.

18. Choe YH, Kim DK, Koh EM, Do YS, Lee WR. Takayasu arteritis: diagnosis with MR imaging and MR angiography in acute and chronic active stages. J Magn Reson Imaging. 1999; 10: 751-757.

19. Kissin EY, Merkel PA. Diagnostic imaging in Takayasu arteritis. Curr Opin Rheumatol. 2004; 16: 31-37.

20. Romera-Villegas A, Vila-Coll R, Poca-Dias V, Cairols-Castellote MA. The role of color duplex sonography in the diagnosis of giant cell arteritis. J Ultrasound Med. 2004; 23: 1493-1498.

21. Belhocine T, Blockmans D, Hustinx R, Vandevivere J, Mortelmans L. Imaging of large vessel vasculitis with 18 FDG PET: illusion or reality? A critical review of the literature data. Eur J Nucl Med Mol Imaging. 2003; 30: 1305-1313.

22. Meller J, Grabbe E, Becker W, Vosshenrich R. Value of F-18 FDG hybrid camera PET and MRI in early Takayasu aortitis. Eur Radiol. 2003; 13: 400-405.

23. Amezcua-Guerra LM, Springall R, Arrieta-Alvarado AA, Rodríguez V, Rivera-Martinez E, et al. C-reactive protein and complement components but not other acute-phase reactants discriminate between clinical subsets and organ damage in systemic lupus erythematosus. Clin Lab. 2011; 57: 607-613.

Curr Neurobiol 2019 Volume 10 Issue 2

Association of non-infectious isolated internal carotid arteritis with the de novo appearance of a saccular aneurysm of the anterior communicating artery

72

24. Huang MY, Gupta-Malhotra M, Huang JJ, Syu FK, Huang TY. Acute-phase reactants and a supplemental diagnostic aid for Kawasaki disease. Pediatric Cardiol. 2010; 31: 1209-1213.

25. Ramirez G, Maugeri N, Sabbadini M, Rovere‐Querini P, Manfredi A. Intravascular immunity as a key to systemic vasculitis: a work in progress, gaining momentum. Clin Exp Immunol. 2014; 175: 150-166.

26. Radic M, Kaliterna DM, Radic J. Overview of vasculitis and vasculopathy in rheumatoid arthritis—something to think about. Clin Rheumatol. 2013; 32: 937-942.

27. Bhagat M, Sehra ST, Shahane A, Kwan M. Utility of immunologic testing in suspected rheumatologic disease. Curr Allergy Asthma Rep. 2014; 14: 405.

28. Ashida A, Murata H, Ohashi A, Ogawa E, Uhara H, et al. A case of hypocomplementaemic urticarial vasculitis with a high serum level of rheumatoid factor. Australas J Dermatol. 2013; 54: e62-e3.

29. Kuret T, Lakota K, Hočevar A, Burja B, Čučnik S, et al. Evaluating the utility of autoantibodies for disease activity and relapse in giant cell arteritis. J Biol Regul Homeost Agents. 2018; 32: 313-319.

30. Hočevar A, Rotar Ž, Žigon P, Čučnik S, Ostrovršnik J, et al. Antiphospholipid antibodies in adult IgA vasculitis: observational study. Clin Rheumatol. 2019; 38: 347-351.

31. Elefante E, Bond M, Monti S, Lepri G, Cavallaro E, et al. One year in review 2018: systemic vasculitis. Clin Exp Rheumatol. 2018; 36: S12-S32.

32. Scott DG, Watts RA. Epidemiology and clinical features of systemic vasculitis. Clin Exp Nephrol. 2013; 17: 607-610.

33. Terrades-Garcia N, Cid MC. Pathogenesis of giant-cell arteritis: how targeted therapies are influencing our understanding of the mechanisms involved. Rheumatol. 2018; 57: ii51-ii62.

34. Berteau F, Rouviere B, Delluc A, Nau A, Le Berre R, et al. Autosomic dominant familial Behçet disease and haploinsufficiency A20: A review of the literature. Autoimmun Rev. 2018; 17: 809-815.

35. Yoshida M, Watanabe R, Ishii T, Machiyama T, Akita K, et al. Retrospective analysis of 95 patients with large vessel vasculitis: a single center experience. Int J Rheum Dis. 2016; 19: 87-94.

36. Keser G, Direskeneli H, Aksu K. Management of Takayasu arteritis: a systematic review. Rheumatol. 2013; 53: 793-801.

37. Toth G, Cerejo R. Intracranial aneurysms: Review of current science and management. Vasc Med. 2018; 23: 276-288.

38. Brisman JL, Song JK, Newell DW. Cerebral aneurysms. N Engl J Med. 2006; 355: 928-939.

39. Turjman AS, Turjman F, Edelman ER. Role of fluid dynamics and inflammation in intracranial aneurysm formation. Circulation. 2014; 129: 373-382.

40. Santos JM, Kaderali Z, Spears J, Rubin LA, Marotta TR. Flow diversion in vasculitic intracranial aneurysms? Repair of giant complex cavernous carotid aneurysm in polyarteritis nodosa using Pipeline embolization devices: first reported case. J Neurointerv Surg. 2016; 8: e28.

Correspondence to:Francisco Revilla-PachecoNeurological CenterThe American British Cowdray Medical CenterIAP, Mexico CityMexicoE-mail: frevilla@neurociencias.net