Cavernous Internal Carotid Artery Aneurysm: Visual Disturbance due to a Large Cavernous Aneurysm Presumably Causing Recurrent Retinal Ischemia; Coil Occlusion of the Aneurysm Together with the Parent Artery; Resolution of the Visual Disturbance and Clinical Recovery During Long-term Follow-up

  • Frances ColganEmail author
  • Marta Aguilar Pérez
  • Hansjörg Bäzner
  • Hans Henkes
Living reference work entry


A 44-year-old male patient presented with recurrent episodes of visual disturbance. CT, MRI/MRA, followed by DSA, demonstrated a large aneurysm of the cavernous segment of the left internal carotid artery (ICA). The left A1 segment was absent and a large caliber left posterior communicating artery (PcomA) with a patent P1 segment was present. The left anterior cerebral artery (ACA) was exclusively supplied by the right ICA via the anterior communicating artery (AcomA). A balloon test occlusion of the left ICA was tolerated without any neurological deficit. The aneurysm was treated endovascularly with coil occlusion of both the aneurysm and the parent artery (parent vessel occlusion, PVO). The episodes of visual disturbance did not recur and the PVO of the left ICA was tolerated without neurological deficit. During the following 6 years, the patient complained of dizziness, memory disturbance, and episodes of amnestic aphasia. Further examinations during this time failed to demonstrate any impairment of the cerebral perfusion. The treatment of large cavernous ICA aneurysms by PVO is the main topic of this chapter.


Cavernous internal carotid artery Saccular aneurysm Retinal ischemia Balloon test occlusion Parent vessel occlusion Collateral supply 


A 44-year-old male patient presenting with recurrent episodes of visual disturbance in the left eye. The medical history of the patient was otherwise unremarkable.

Diagnostic Imaging

Diagnostic CT, MRI/MRA, and DSA examinations in September 2011 demonstrated a large aneurysm of the cavernous segment of the left ICA. The left A1 segment was not demonstrated on angiography. Collateral supply to the left middle cerebral artery (MCA) was visible via the left P1 segment and the left posterior communicating artery (PcomA) (Fig. 1).
Fig. 1

Diagnostic imaging of a large left cavernous ICA aneurysm. CT (a) and CTA (b, c) demonstrate the aneurysm at the left cavernous sinus (arrows). Due to the slow flow within the aneurysm, the signal intensity on TOF MRA (d) is low (arrow), with a high signal intensity on contrast enhanced T1WI (arrow, (e)). TOF MRA demonstrated the absent A1 segment on the left (arrow, (f) and the large caliber left PcomA (arrow, (g)). DSA confirming these findings. Contrast injection of the left ICA shows the dilution of the contrast medium distal to the aneurysm through nonopacified blood from the PcomA (posterior-anterior projection, (h)), the origin of the ophthalmic artery distal to the aneurysm (lateral view, arrow (i), the supply of the left ACA via the AcomA from the right ICA (posterior-anterior view, (j)), and the spontaneous supply of the left MCA via the left P1/PcomA (lateral view, arrow (k))

Treatment Strategy

The aim of the treatment was to prevent recurrent emboli from the aneurysm to the ipsilateral retinal circulation or the dependent cerebral vasculature and to avoid further growth of the aneurysm with the risk of cranial nerve compression. The risk of intracranial hemorrhage was considered to be very low due to the extradural location of the aneurysm. The location made the aneurysm unsuitable for microsurgical clipping. Attempted endosaccular coil occlusion with a view to preservation of the parent vessel was considered unpredictable since the lumen of the left cavernous ICA at the level of the aneurysm was no longer visible. Stent-assisted coiling was also considered, as was flow diverter stent (FDS) insertion, but PVO was the treatment of choice in this case. The advantages of PVO were the instantaneous occlusion of the aneurysm and also avoiding the need for antiplatelet medication. In 2011, which was early in our flow diversion experience, the reconstruction of the ICA with a Pipeline Embolization Device (PED) would have been our second choice had carotid balloon test occlusion (BTO) not been tolerated.


Procedure #1, 27.09.2011: BTO of the left ICA

Anesthesia: local anesthesia, 1× 5000 IU non-fractionated heparin (Heparin Natrium, B. Braun) IV

Premedication: none

Access: right common femoral artery, 6F sheath (Terumo); left common femoral artery, 4F sheath (Terumo); guide catheter: 6F Guider Softip (Boston Scientific); diagnostic catheter: 4F Tempo4 vertebral (Cordis); microguidewire: SilverSpeed 14 (Medtronic)

Compliant balloon catheter: Ascent 4/10 (Micrus), inflated for 20 min

Course of treatment: A 6F guide catheter was inserted into the left ICA. A compliant balloon catheter was then inserted to the petrous segment of the left ICA and inflated under fluoroscopy until occlusion was achieved. From the left groin access, the right ICA was catheterized and angiography demonstrated opacification of the left ACA from the right ICA via the AcomA. The left A1 segment was not opacified. Contrast injection from the left vertebral artery (VA) showed collateral supply of the left MCA through the left P1 segment and the left PcomA (Fig. 2).
Fig. 2

Balloon test occlusion in a left cavernous ICA aneurysm in preparation for the potential PVO. A compliant balloon is inflated in the petrous segment of the left ICA (posterior-anterior view, arrow (a)). Injection of the left VA with left ICA occlusion shows the collateral supply of the left MCA via the left PcomA (posterior-anterior projection, arrow (b); lateral projection, arrow (c)). Contrast injection of the right ICA, also with balloon occlusion, demonstrates perfusion of the left ACA via the AcomA but no leptomeningeal collaterals to the left MCA territory (posterior-anterior view, arrow (d)). The BTO was tolerated without any neurological symptoms for 20 min at a systemic blood pressure of 120/75 mmHg. A hypotensive challenge was not considered necessary

Duration: 1st–6th run: 31 min; fluoroscopy time: 6 min

Complications: none

Postmedication: none

The result of this examination was discussed with the patient the following day and he consented to the proposed aneurysm treatment with PVO.

Procedure #2, 29.09.2011: parent vessel occlusion of an aneurysm of the cavernous segment of the left ICA together with the parent artery

Anesthesia: general anesthesia, 1× 3000 IU nonfractionated heparin IV

Premedication: none

Access: right common femoral artery, 6F sheath (Terumo); guide catheter: 6F Guider Softip; microcatheter: Echelon14 45° (Medtronic); microguidewire: Traxcess 14 (MicroVention)

Implants: 22 coils: 1× Morpheus 3D 9/28, 1× Morpheus 3D 9/18, 1× Helix Standard 5/20, 19× Helix Standard Fiber 3/10 (ev3)

Course of treatment: Via a 6F guide catheter positioned in the left ICA, the cavernous aneurysm was catheterized with an Echelon14 microcatheter. Using two long 3D coils, a mesh was created in the aneurysm sac in order to avoid an inadvertent distal migration of the small fibered coils used during this procedure to densely obliterate the ICA proximal to the aneurysm. An occlusion distal to the aneurysm sac was avoided since compromise of the ophthalmic artery or the PcomA origins might have resulted. The fibered coils, which are no longer available, were used because their enhanced thrombogenicity allowed a faster parent vessel occlusion with fewer coils. Detachable balloons were no longer used by us owing to the potential risk of distal embolization from balloon deflation or shrinkage. Alternative implants to achieve complete vessel occlusion today would include the Amplatzer Vascular Plug (St. Jude Medical/Abbott) and the UNO (Medtronic). Once the left ICA was considered occluded, the left VA was injected to confirm collateral supply via the left PcomA (Fig. 3).
Fig. 3

Endovascular coil occlusion of a wide-necked cavernous ICA aneurysm and the parent artery. Contrast injection from the left ICA demonstrates the 20 mm diameter cavernous aneurysm (posterior-anterior view, (a); lateral view, (b)). Under roadmap conditions, the aneurysm is catheterized (lateral view, (c)). Aneurysm and ICA are occluded with coils (lateral view, (d)). Despite the thrombogenic fibered coils used in this patient, several centimeters of the artery have to be filled with coils in order to interrupt the flow. The final DSA run shows the collateral supply of the left MCA via the left PcomA (lateral projection with contrast injection from the left VA, arrow (e)). Since the left ICA is proximally occluded, the left ophthalmic artery now shows retrograde flow with supply through the left external carotid artery (arrows (f))

Duration: 1st–8th run: 106 min; fluoroscopy time: 32 min

Complications: none

Post medication: 100 mg ASS PO daily for 1 year, 2× 8000 U Certoparin (Mono-Embolex, Novartis, Pharma) SC daily for 3 days, during the following 3 days the patient was continuously monitored on the intensive care unit with a target systolic blood pressure > 140 mmHg

Clinical Outcome

The patient tolerated PVO of the left ICA well. The patient was discharged home 6 days later without any new neurological deficit. In the following year, he presented to another hospital with dizziness, memory disturbance, and episodes of amnestic aphasia, requesting a bypass procedure. Perfusion CT (CTP) and transcranial Doppler investigation (TCD) failed to show any compromise of the anterior circulation.

Follow-up Examinations

Follow-up MRI/MRA, DSA, and CTP examinations were carried out after the left ICA PVO. Both aneurysm and parent vessel remained occluded. Despite nonspecific complaints and the perception of reduced cerebral perfusion by the patient, perfusion abnormality in the left anterior circulation was not confirmed (Fig. 4).
Fig. 4

MRI/MRA 5 days after left ICA PVO. No ischemic lesion is visible and the left PcomA now supplies the left MCA (DWI, (a); T2WI, (b); ToF MRA, (c)). DSA 5 months (d) and 6 years (e) after left ICA PVO. The ophthalmic artery is not visible after injection of the vertebral arteries due to the retrograde flow in this artery. A comparison of the caliber of the left PcomA immediately after PVO (f) and 6 years later (g) shows a slight increase in the vessel diameter (arrows). T2WI MRI 6 years after treatment did not show any parenchymal lesions (h). The ventricular asymmetry was longstanding. CTP did not show any perfusion abnormality or asymmetry (i)


Aneurysms of the cavernous portion of the internal carotid artery have a varied etiology and comprise approximately 2% of all intracranial aneurysms and up to 6% of all ICA aneurysms (International Study of Unruptured Intracranial Aneurysms Investigators 1998). On account of their extradural location, the most common presentation is not of rupture, as for many other intracranial aneurysms, but more usually from the compressive effects of the aneurysm on surrounding structures. Patients most frequently present with symptoms of distal embolization or adjacent cranial nerve compression, including visual symptoms (diplopia, retro-orbital pain, and visual disturbance) and headaches (Hahn et al. 2000). Clinical examination may reveal visual deficits, ophthalmoplegia, and trigeminal neuropathy. In the event of aneurysm rupture, usually only occurring after the aneurysm has achieved a significant size, carotid-cavernous sinus fistula (CCF), subdural hemorrhage, subarachnoid hemorrhage (SAH), and epistaxis can also occur (Starke et al. 2014; Wiebers et al. 2003). As the use of diagnostic imaging is increasing, a significant proportion of cavernous carotid aneurysms, like many other intracranial aneurysms, are now detected incidentally, and agreement regarding the optimum management of these incidentally detected lesions has not been reached.

The skull base location of the cavernous ICA makes microsurgical clipping techniques difficult and most operative interventions in this area are associated with significant perioperative risks of cerebral ischemia and cranial nerve damage (Abe et al. 2011; Sriamornrattanakul et al. 2017). In cavernous ICA aneurysms presenting without CCF, surgical treatment of the aneurysm might include proximal ICA occlusion with or without the creation of an extra-intracranial bypass. Surgical intervention for cavernous ICA aneurysm presenting with CCF aims to obliterate the fistula and may require aneurysm trapping, again, with or without bypass. To allow safe ICA ligation and aneurysm trapping without surgical bypass, the presence of sufficient collateral supply to the cerebral parenchyma should be proven, usually via carotid occlusion testing (Koebbe et al. 2006). Delayed complications of the surgical management of these aneurysms include late aneurysm reperfusion, with the recurrent risk of rupture and distal embolization (Abe et al. 2011; Sriamornrattanakul et al. 2017).

The advent of interventional neurovascular techniques has enabled aneurysms in these locations to be treated with a higher success and lower complication rates (Koebbe et al. 2006). Strategies can broadly be divided into aneurysm obliteration with preservation of the parent vessel lumen and parent vessel occlusion (PVO) with or without prior surgical bypass, and more recently, flow-diverter stenting (van Rooij and Sluzewski 2009). Many operators report preferring coiling techniques in smaller aneurysms and PVO in large or giant cavernous ICA aneurysms, owing to the smaller perceived risks of significant periprocedural cerebral ischemia (Labeyrie et al. 2015; Morita et al. 2011).

Parent vessel occlusion techniques prevent flow to the aneurysm and facilitate thrombosis of the aneurysm sac. This approach has the advantage of instantaneous aneurysm occlusion and subsequent reduction in the local mass effect exerted by the aneurysm sac as the thrombus within it starts to resorb. Lower aneurysm reperfusion rates occur than with coiling, meaning fewer secondary re-interventions (Labeyrie et al. 2015; Morita et al. 2011). If performed after satisfactory carotid occlusion testing or after successful extracranial-intracranial bypass surgery, significant ischemic complications occur rarely. There exists some debate, however, as to the interpretation of satisfactory and unsatisfactory carotid occlusion test results.

In this case, aneurysm coiling without ICA stenting was not possible owing to the aneurysm configuration, and while stent-assisted coiling may have been possible, it would not have achieved instantaneous aneurysm occlusion. Flow diverter stent (FDS) insertion was also considered, having the advantage of preserving the parent vessel lumen, but the disadvantage of delayed aneurysm occlusion. This case occurred before the widespread use of FDS, and at this time PVO was chosen for its advantage of immediate isolation of the aneurysm from the circulation.

Several longitudinal studies report good results from PVO in the treatment of giant cavernous ICA aneurysms, but owing to the low incidence of this condition, case numbers are relatively small. A large meta-analysis compared procedural success and clinical outcomes of 509 patients with 515 large or giant cavernous aneurysms across 20 retrospective series (Turfe et al. 2015). In this series, 77% of the treated patients presented with cranial nerve symptoms and approximately 7% each with SAH and CCF. A total of 176 aneurysms were treated with PVO without bypass and 339 with aneurysm coiling and preservation of the parent vessel lumen. The meta-analysis demonstrated a higher rate of persistent aneurysm occlusion at 3 months in the PVO group (93% vs. 67% in the coiling group) as well as a lower rate of reintervention (6% vs. 18% in the coiling group). However, a higher incidence of peri-operative morbidity (ischemia or hemorrhage) was demonstrated in the PVO group (7% vs. 3% in the coiling group).

A large single-center series demonstrated good results with low complication and reintervention rates after treatment of 86 CCA aneurysms in 85 patients with both endosaccular coiling (in smaller lesions) and PVO in large and giant aneurysms (van Rooij 2012). The authors describe a treatment preference for coiling in asymptomatic aneurysms and PVO in those lesions presenting with cranial neuropathies owing to the differential effect on aneurysm mass effect.

PVO has the advantages of effective aneurysm exclusion and a low rate of aneurysm reperfusion, over endosaccular coiling. It also offers some advantage over the newer FDS technology as it does not require ongoing treatment with dual antiplatelet therapy (Raper et al. 2017; Starke et al. 2014).

Shimizu et al. (2017) report low morbidity and mortality in their series of 28 patients with cavernous carotid aneurysms treated with PVO, after judicious use of surgical bypass depending on the results of the BTO. The most frequently occurring complications in this series were perioperative ischemic complications and cranial nerve palsies. Perioperative ischemia was observed more frequently in patients with preexisting cardiovascular risk factors and a venous phase delay of 1–2 s on BTO and the authors attribute this phenomenon to coverage of the perforating arteries. Temporary cranial nerve palsies occurred in four patients, all of which resolved completely. Similar findings have been reported in other case series (Labeyrie et al. 2015; Ganesh Kumar et al. 2017).

In conclusion, owing to the low incidence of this condition, robust data on the safety and efficacy of PVO in the treatment of ICA aneurysms compared with other treatment options are not available. If competent collateral supply is confirmed or created through bypass-surgery, PVO is thought to be a safe and effective strategy in the management of a symptomatic nonruptured cavernous ICA aneurysm with low periprocedural morbidity and unlike treatment with FDS, does not require treatment with dual antiplatelet medication.



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Copyright information

© Springer Nature Switzerland AG 2019

Authors and Affiliations

  • Frances Colgan
    • 1
    Email author
  • Marta Aguilar Pérez
    • 2
  • Hansjörg Bäzner
    • 3
  • Hans Henkes
    • 2
  1. 1.Department of RadiologyUniversity of Otago, Christchurch HospitalChristchurchNew Zealand
  2. 2.Neuroradiologische KlinikNeurozentrum, Klinikum StuttgartStuttgartGermany
  3. 3.Neurologische KlinikNeurozentrum, Klinikum StuttgartStuttgartGermany

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