Spontaneous thrombosis of giant cavernous internal carotid artery (ICA) aneurysm with parent artery occlusion is rare. We present the history of a 28-year-old female who presented with a large hemispheric infarct secondary to a ICA dissection, the dissection simultaneously inducing thrombosis of an incidental pre-existing giant cavernous ICA aneurysm.
A 28-year-old female presented with sudden onset altered sensorium, dysphasia and right hemiplegia. Emergency magnetic resonance imaging (MRI) done under stroke protocol revealed a large left middle cerebral artery (MCA) infarct with mass effect and midline shift [Figure 1]. The MRI also revealed the presence of a giant cavernous segment aneurysm probably thrombosed [Figure 2]. The cavernous lesion measured 2.6 cm × 2.7 cm × 2.7 cm and was seen extending from the superior orbital fissure till the petrous apex suggestive of a cavernous carotid aneurysm. As the patients' neurological condition was rapidly deteriorating, she underwent an emergency decompressive craniectomy on the left side. Following few days of intensive care, she improved but had a residual aphasia and right hemiplegia. Plain computerised tomography scan done in the post-operative period revealed adequate decompression as well as a hyperdense lesion in the left paracavernous region [Figure 3]. She subsequently underwent a digital subtraction angiography which revealed total cutoff of ICA just distal to the carotid artery bifurcation with a flame-shaped occlusion suggestive of dissection [Figure 4]. The cavernous aneurysm and the entire ICA were seen occluded on the left side. The right ICA injection showed moderate cross circulation with partial filling of the left hemisphere through the anterior communicating artery [Figure 5]. The vertebral angiogram picked up an additional top of the basilar fusifosaccular aneurysm [Figure 6].
She had a good recovery in the postoperative period and underwent an autologous cranioplasty at 6 weeks following surgery. Her speech and right-sided weakness also showed significant improvement and at 6 months' follow-up she was nearly independent. The basilar aneurysm was later managed by an interventional neuroradiologist.
Management of giant cavernous carotid aneurysms (CCA) is challenging. The primary dilemma is in deciding on the need for intervention as many of these lesions remain asymptomatic for long and are often detected incidentally. Moreover, spontaneous thrombosis of a giant intracranial aneurysm is also known and can occur in 13%–20% of cases providing a natural cure. The factors that precipitate thrombosis are related to the ratio of aneurysm volume to orifice size, the age of the aneurysm and haemodynamics within the parent artery.
Spontaneous thrombosis of a giant aneurysm can at times be associated with concomitant thrombosis of the parent vessel. Spontaneous occlusion of the parent artery can result in also catastrophic ischemic deficits even in patients with good collaterals as happened in our patient who developed a MCA infarct despite having a reasonable good cross circulation through anterior communicating artery. This raises the question whether all incidental giant CCAs should be investigated in detail and offered intervention in view of the potential risk of spontaneous occlusion and ischaemic deficits.
Several mechanisms have been proposed for this phenomenon of spontaneous thrombosis of aneurysm with parent vessel occlusion. One postulate is a reverse mechanism, i.e., progression from aneurysm thrombosis to parent vessel occlusion. This probably happens due to-distortion, stretching and compression of the parent artery with the growth of aneurysm or due to compression of the surrounding structure by aneurysm. It can also happen due to sudden expansion of the aneurysm causing compression and slow flow in the parent artery causing retrograde thrombus formation originating from the aneurysm into the parent vessel. Dissection as a precipitating factor for upstream thrombosis of giant cavernous ICA aneurysm has also been reported.
Our patient had a giant cavernous aneurysm which remained incidental. The initial event in our patient was probably dissection of her left carotid artery at the cervical segment which led to total occlusion of the ICA distal to the dissected site with acute cessation of forward blood flow. This resulted in acute total thrombosis of the pre-existing giant cavernous ICA aneurysm and infarction of the left middle cerebral territory. We believe that dissection of the parent artery would have initiated the thrombus formation was evidenced by 'flame' and 'string sign' on angiogram. The anterior cerebral artery territory was spared due to cross circulation from the opposite side. The relatively rapid recovery also could be attributed to the cross circulation and the presence of collaterals which developed later. The presence of another co-existing basilar aneurysm in a relatively young patient also suggests the possibility of some co-existing connective tissue disorder which could account for both – aneurysm formation and spontaneous thrombosis.
Arterial dissection can simultaneously result in both favourable (spontaneous thrombosis of a giant aneurysm) and unfavourable consequences (vessel occlusion with ischemic infarct). The etiopathogenesis of aneurysm formation, spontaneous thrombosis and dissection still remains a mystery.
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The authors certify that they have obtained all appropriate patient consent forms. In the form the patient(s) has/have given his/her/their consent for his/her/their images and other clinical information to be reported in the journal. The patients understand that their names and initials will not be published and due efforts will be made to conceal their identity, but anonymity cannot be guaranteed.
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