Transient ischaemic attack secondary to extracranial carotid artery aneurysm

Dear Editor:

Extracranial carotid artery aneurysms present a low incidence (1.3%), making it more difficult to study their aetiology, natural course, and response to treatment.^1–6

We present the case of a 32-year-old woman, a former smoker taking oral contraceptives. The patient presented a 15-minute self-limited episode of dysarthria and loss of strength in the right arm, followed by spontaneous full recovery. Results from the neurological examination were normal and no alterations were found in the blood test, electrocardiogram, chest radiography, or head CT. Clinical signs were compatible with transient ischaemic attack (TIA) in the left hemisphere. We requested tumour markers, serology tests, immunology tests, and a hypercoagulation study, which only revealed a homozygous MTHFR C667T mutation. We performed a transthoracic echocardiogram that showed no alterations. An echo Doppler study of the supra-aortic trunks (SAT) and a CT-angiography of SAT, circle of Willis (CW) and thoracoabdominal aorta revealed a patent saccular aneurysm in the distal cervical portion of both internal carotid arteries (IC), with a maximum diameter of 19 mm on the RIC and 16 mm on the LIC (Fig. 1). After evaluating the case and ruling out surgical intervention because carotid artery aneurysms were inaccessible, we decided to perform endoluminal repair. Firstly, the symptomatic aneurysm on the LIC was repaired by placing 3 intraaneurysmal Matrix^® coils and a Silk^® stent (4 mm × 30 mm). Total thrombosis of the aneurysm, adequate permeability of the distal portion of the LIC and intracranial circulation were achieved (Fig. 2). Secondly, the asymptomatic aneurysm on the RIC was repaired by placing 3 intraaneurysmal GDC^® coils and a Silk^® stent (4 mm × 30 mm). Total thrombosis of the aneurysm, adequate permeability of the distal portion of DIC and intracranial circulation were achieved (Fig. 2). The patient was asymptomatic upon discharge and treated with dual anti-platelet therapy for 2 months, followed by single anti-platelet therapy to be continued for indefinitely. After 2 years of follow-up, she remains asymptomatic and the results of the endoluminal repair appear to be good.

Figure 1.

CT-angiography of SAT: patent saccular aneurysm in the distal portion of both ICs (19 mm on the RIC and 16 mm on the LIC).

Figure 2.

Embolisation of aneurysm on the RIC and LIC.

Extracranial carotid artery aneurysms are usually located in the carotid bifurcation, followed by the IC and the external carotid artery as the next most frequent locations.^1,2,4 As in our case and according to some series, they may be bilateral, and/or associated with aneurysms in other locations.¹ They may be fusiform or saccular in shape^1,2 and their aetiologies vary.^1–5 Their main cause in the past was infection, but it is currently atherosclerosis (55%), followed by fibromuscular dysplasia of the arteries, trauma, dissection, and surgical procedures. Other less frequent causes are cystic medial necrosis, Marfan syndrome, Takayasu arteritis and idiopathic medial aortopathy.^1–4 Up to 60% of extracranial carotid artery aneurysms are symptomatic and their clinical manifestations vary according to their location, size, and aetiology. Patients may present symptoms compatible with TIA or stroke (40-45%)^1–4 as in our case, retro-orbital compression, pulsating headache, dysphagia, relapsing facial pain, deafness, hoarseness, tinnitus, Horner syndrome, and Raeder paratrigeminal syndrome. Physical examination usually reveals a pulsating mass on the neck or pharynx, often painful, and associated in some cases with deficits and/or focal neurological signs.^1–3 Differential diagnosis should examine carotid artery kinking or elongation, carotid body tumour, adenopathies, peritonsillar abscess, branchial cleft cyst, and cystic hygroma.^1,2 Echo Doppler and especially CT-angiography or MRI-angiography of SAT and CW are necessary to determine the diagnosis, but today's gold standard for assessing anatomical details and choosing the optimal treatment is arteriography of SAT and CW.^1–3 Treatment indications depend on the aneurysm's clinical manifestations, size, location, and aetiology, as well as the patient's surgical risk.^1–3,5,6 The aim of treatment is to prevent severe neurological complications and associated secondary mortality.^1,2,5 Extracranial carotid artery aneurysms show a mortality rate of 71% due to thrombosis, embolism, or rupture. In patients undergoing surgical or endoluminal repair, this rate decreases to 30%.^1–4 Today's treatment alternatives are surgical procedures involving aneurysm exclusion and arterial suture, or bypass graft (prosthetic or autologous). Techniques are associated with neurological morbidity (peripheral and central) ranging between 6% and 20%, depending on the series, and a mortality rate of about 2%.^1–5 Another alternative is endoluminal treatment with aneurysm embolisation and placement of endoprosthesis; this is useful when the aneurysms are surgically inaccessible, as in our case, or in patients with a high surgical risk. This last alternative is on the rise, but no randomised studies that analyse long-term results are available at present.^1–3 To conclude, we highlight that while this entity is infrequent, it should be considered among the possible causes of TIA or stroke.¹