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Table of Contents    
Year : 2017  |  Volume : 65  |  Issue : 2  |  Page : 405-407

A case of infectious intracranial dissecting aneurysm

1 Department of Neurology, Third Xiangya Hospital, Central South University, Changsha, Hunan, China
2 Department of Pharmacy, College of Medicine, Hunan Normal University, Changsha, Hunan, China

Date of Web Publication10-Mar-2017

Correspondence Address:
Dr. Xuejun Fan
Department of Neurology, Third Xiangya Hospital, Central South University, Tongzipo Road 138, Yuelu District, Changsha, Hunan - 410013
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Source of Support: None, Conflict of Interest: None

DOI: 10.4103/neuroindia.NI_1223_15

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How to cite this article:
Zhong X, Li X, Shao S, Yang X, Fan X. A case of infectious intracranial dissecting aneurysm. Neurol India 2017;65:405-7

How to cite this URL:
Zhong X, Li X, Shao S, Yang X, Fan X. A case of infectious intracranial dissecting aneurysm. Neurol India [serial online] 2017 [cited 2023 Jan 28];65:405-7. Available from: https://www.neurologyindia.com/text.asp?2017/65/2/405/201829


We report a case of a 17-year-old male patient who presented to our hospital with headache and fever. Following investigations, he was diagnosed with bacterial endocarditis and secondary meningitis, for which he received antibiotics. During his admission, he developed left sided ptosis. Imaging revealed the presence of an infected dissecting intracranial aneurysm (IIA) in the cavernous sinus segment of the left internal carotid artery. The aneurysm was stented, the ptosis resolved, and the patient was discharged without complications. Here, we review the pathogenesis and management of IIA.

A 17-year-old man initially presented for investigation of his headache and fever. His only significant past medical history included intermittent sinus arrhythmia. Echocardiography revealed aortic valve vegetation, and blood cultures demonstrated the growth of Staphylococcus aureus, confirming the presence of bacterial endocarditis.

Investigation for his headache and fever also included a work-up for meningitis. The cerebrospinal fluid (CSF) pressure during lumbar puncture was 218 mm H2O. CSF protein, glucose, and chloride were 741 mg/L, 2.10 mmol/L, and 114.8 mmol/L, respectively. CSF white blood cell and total cell counts were 340 × 106/L and 400 × 106/L, respectively, and the lymphocyte and neutrophil percentages were 60% and 40%, respectively. The computed tomographic (CT) scan of the brain was negative for an intracranial hemorrhage or an intracranial aneurysm. Enhanced magnetic resonance imaging (MRI) showed an abnormal meningeal enhancement [Figure 1]d and [Figure 1]e. The investigations, therefore, revealed bacterial endocarditis with meningeal involvement. The patient was started on a 2-week course of levofloxacin and cefoperazone-sulbactam based on his culture and sensitivity study. The echocardiography following treatment confirmed that the aortic valve vegetation had resolved.
Figure 1: MRI at the initial presentation: (a) T2-weighted MRI images of the brain showing a low-density lesion in the left cavernous sinus (arrow). (b) T1-weighted MRI of the brain showing a mixed density focus in the left cavernous sinus (arrow). (c) T1-weighted MRI of the brain showing low-density lesion in the left cavernous sinus (arrow). (d and e) Contrast-enhanced MRI of the brain, demonstrating multiple meningeal lesions 12 days after the initial presentation

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On the tenth day after the initial presentation, the patient developed acute ptosis of the left upper eyelid. Brain MRI revealed a suspicious aneurysm in the left cavernous sinus [Figure 1]a, [Figure 1]b, [Figure 1]c. CT angiogram demonstrated a fusiform aneurysm in the cavernous segment of the left internal carotid artery [Figure 2]f, arrow]. Digital subtraction angiography (DSA) showed a dissecting aneurysm of the cavernous segment of the internal carotid artery, measuring 12 × 7.5 mm [Figure 2], arrow], with an intimal tear located within the anterior and posterior arterial wall. Given the progression of symptoms, location, volume, and thin wall of the aneurysm, we estimated that the aneurysm was likely to rupture with severe consequences.
Figure 2: Preoperative intracranial vascular imaging. (a-d) Preoperative left internal carotid artery digital subtraction angiography (lateral view) demonstrating the development of fusiform dilatation of the left internal carotid artery cavernous segment (arrow). The outline of the vascular superior wall is continuous; however, the inferior wall blurs with iodinated contrast media retention, indicating that the tear is located in the anterior and posterior segment of the wall. (e) Preoperative left internal carotid artery digital subtraction angiography (frontal view) showing a dissecting aneurysm with iodinated contrast media retention in the aneurysm (arrow). (f) CT angiography of the head on initial presentation demonstrating fusiform dilatation toward the anterior and posterior direction at the cavernous segment of the left internal carotid artery (arrow)

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The patient underwent a stent-assisted aneurysm tamponade of the intracavernous internal carotid artery and was continued on antibiotics. Postoperative DSA confirmed the occlusion of the IIA [Figure 3], arrow]. The patient's symptoms improved and he was discharged from the hospital shortly afterwards without any complications.
Figure 3: Postoperative intracranial vascular imaging. (a) Postoperative left internal carotid artery digital subtraction angiography (lateral view) showing the intervention process (arrow). (b, c) Postoperative left internal carotid artery digital subtraction angiography showing successful obliteration of the left internal carotid artery cavernous segment infectious aneurysm with the preserved parent artery (arrow)

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IIA rupture rates have been reported to be less than 2%, with an 80% rupture-related mortality.[1] However, regardless of their propensity to rupture, IIAs are difficult to detect. By the time most patients present to hospital, IIAs have already ruptured or are about to rupture.

In the present case, the patient presented with typical symptoms of headache and fever. Subsequently, we observed ptosis of the left upper eyelid. We believe that this sign resulted from an impingement on the oculomotor nerve by the infected aneurysm. Our successful treatment in this case highlights the importance of an early detection and diagnosis, precise risk evaluation, and appropriate and timely intervention before rupture.

The most common infected aneurysms are intracranial. IIAs are typically heralded by the onset of headache and fever; however, they can rapidly rupture and result in intracranial hemorrhage.[2] Considering that infectious endocarditis is the most common cause of IIA and that most infection-associated carotid aneurysms are caused by bacterial pathogens, investigations such as echocardiography, blood culture, erythrocyte sedimentation rate, and C-reactive protein, should be pursued. Differentiation of IIAs from systemic arteritis or a noninflammatory aneurysm is needed because each entails completely different treatment strategies.

IIAs are not common and are potentially dangerous. Koffie et al.,[1] highlighted the need for neurovascular specialists to be vigilant in the management of patients with IIA—including an accurate measurement of the aneurysm size—that could warrant an earlier neurosurgical or endovascular intervention. Patients with infectious endocarditis should undergo regular CT angiography or DSA surveillance to detect the presence of an aneurysm and monitor its stability.[3],[4] Cervical artery dissection may rupture spontaneously or from trauma. This can be confirmed pathologically by the presence of a hematoma in the vessel wall. Infection is a major risk factor for an intracranial aneurysm dissection. Other risk factors also include minor cervical trauma, migraine, and hypertension. Obesity or hypercholesterolemia has an inverse association with cervical artery dissection.[5] No confirmed factors indicating their genetic susceptibility have been identified.[6]. The most likely mechanism for the rupture of the aneurysm is destruction of the vessel wall through interaction of the pathogens and the host's inflammatory response.[7]

For IIA patients, antibiotics are typically the standard treatment regardless of neurosurgical or endovascular intervention, and should follow antimicrobial susceptibility testing. Control of systemic blood pressure should be considered, and serial imaging to monitor the progress is also warranted. According to a previous report,[8] medical therapy alone can eliminate small intracranial aneurysms without recurrence. The precise intervention for IIA depends on several factors, including the location, size, expertise of the clinical team, and whether the IIA has ruptured or is expanding. If the aneurysm has ruptured, the patient is symptomatic or the aneurysm is growing, neurosurgical or endovascular intervention should be immediately undertaken. Endovascular intervention is a feasible and efficacious option, which is minimally invasive, contains less risk of postoperative wound bleeding induced by anticoagulation and wound infection, and ensures a quick patient recovery. Endovascular intervention should be recommended as the first line treatment for appropriate IIA patients, especially in the presence of cardiovascular instability. Ultimately, medical, surgical, or endovascular treatment should be appropriately selected for the management of IIAs to achieve satisfactory results.

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Conflicts of interest

There are no conflicts of interest.

 » References Top

Koffie RM, Stapleton CJ, Torok CM, Yoo AJ, Leslie-Mazwi TM, Codd PJ. Rapid growth of an infectious intracranial aneurysm with catastrophic intracranial hemorrhage. Clin Neurosci 2015;22:603-5.  Back to cited text no. 1
Kannoth S, Iyer R, Thomas SV, Furtado SV, Rajesh BJ, Kesavadas C, et al. Intracranial infectious aneurysm: Presentation, management and outcome. J Neurol Sci 2007;256:3-9.  Back to cited text no. 2
Kojima Y, Saito A, Kim I. The role of serial angiography in the management of bacterial and fungal intracranial aneurysms–report of two cases and review of the literature. Neurol Med Chir 1989;29:202-16.  Back to cited text no. 3
Ahmadi J, Tung H, Giannotta SL, Destian S. Monitoring of infectious intracranial aneurysms by sequential computed tomographic/magnetic resonance imaging studies. Neurosurgery 1993;32:45-9.  Back to cited text no. 4
Debette S, Metso T, Pezzini A, Abboud S, Metso A, Leys D, et al. Association of vascular risk factors with cervical artery dissection and ischemic stroke in young adults. Circulation 2011;123:1537-44.  Back to cited text no. 5
Debette S, Markus HS. The genetics of cervical artery dissection: A systematic review. Stroke 2009;40:e459-66.  Back to cited text no. 6
Tilson MD. Pathogenesis of mycotic aneurysms. Cardiovasc Surg 1999;7:1-2.  Back to cited text no. 7
Noriaki M, Shigeru M, Takashi I, Takashi Y, Takumi A, Keisuke O, et al. Results and current trends of multimodality treatment for infectious intracranial aneurysms. Neurol Med Chir 2015;55:155-62.  Back to cited text no. 8


  [Figure 1], [Figure 2], [Figure 3]

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