27 Intracranial Dissection
27.1 Case Description
27.1.1 Clinical Presentation
A 26-year-old woman with no significant medical history developed right-side weakness in association with headache and deviation of the eyes to the left. She arrived at a peripheral hospital 105 minutes after the onset of the symptoms, with National Institutes of Health Stroke Scale (NIHSS) and Glasgow Coma Scale (GCS) scores of 9 and 10, respectively. She immediately underwent plain CT that demonstrated diffuse subarachnoid hemorrhage (SAH) and left frontal intraparenchymal hematoma (Fig. 27.1). CT angiography (CTA) showed complete occlusion of the left internal carotid artery (ICA) at the level of the supraclinoid segment. The patient was promptly transferred to the main hospital; during the transportation, one episode of generalized seizure occurred. On arrival, her neurological status worsened (GCS 8) and she was intubated.
27.1.2 Imaging Workup and Investigations
Noncontrast CT was performed at 120 minutes. This did not demonstrate hypodensity, but diffuse SAH and left frontal hematoma (Fig. 27.1).
CTA revealed a left ICA occlusion at the ophthalmic segment.
Digital subtraction angiography (DSA; performed at 170 minutes from the onset) confirmed the complete occlusion of the left ICA and excellent collaterals via anterior communicating artery with no significant venous delay (< 2 seconds; Fig. 27.2).
Intracranial dissection of the left ICA (ophthalmic segment).
Given the chance of spontaneous recanalization of the dissected segment and consequent second bleeding, considering the excellent collaterals via anterior communicating artery, we decided to coil the ICA proximal to the dissection. An Envoy 6 Fr was parked in the cervical segment of the left ICA, and we catheterized the ICA with an Echelon 10 microcatheter in conjunction with a Traxcess .014 microwire. Ten coils were detached and the complete occlusion of the artery was ensured.
27.1.5 Posttreatment Management
After treatment, the patient was transferred to the neurological intensive care unit (ICU) to maintain the stability of the vital parameters. A plain CT performed at 24 hours did not show evidence of rebleeding or ischemic signs; also, paroxysmal eye movement (PEM) and electroencephalography (EEG) had no abnormalities. When sedation was reduced for a neurological evaluation, the patient’s GCS score was 7.
The patient remained stable for the following 4 days, then the transcranial Doppler (TCD) was suspicious for vasospasm, and CT/CTA/CT perfusion (CTP) were performed (Fig. 27.3). No evidence of ischemic signs or vasospasm was found, but there was a diffuse increase of mean transit time (MTT) on CTP with no ischemic core.
On day 6, a significant increase of IP was noted along with abnormal TCD findings; the decision to skip CT and go directly to the angiography suite was taken the same day. The images showed severe vasospasm of the left anterior cerebral artery (ACA) and middle cerebral artery (MCA), and selective injection of nimodipine was carried out through the anterior communicating artery (Fig. 27.4). Despite this treatment, the patient developed a large ischemic stroke due to vasospasm and died on day 12 after a decompressive craniotomy was performed (Fig. 27.5).
A surgical superficial temporary artery–MCA bypass should have probably been considered when patient was still asymptomatic for vasospasm. There is no doubt that an attempt of recanalization of the ICA would have led to massive bleeding, and coiling the ICA to ensure the arterial occlusion was the right therapeutic option.
Intracranial arterial dissections (IAD) are a rare cause of acute ischemic stroke and SAH. Epidemiological studies suggest that the incidence of IAD is higher in Asian populations than in European populations. Depending on the study, the mean age of patients presenting with IAD ranges from 45 to 60 years old. 1 Interestingly, men are two times more likely to suffer from IAD than women. To date, there are no systematic epidemiologic studies examining the risk factors contributing to IAD. Trauma has anecdotally been associated with this disease as have connective tissue diseases such as Loeys-Dietz, polycystic kidney disease, and segmental arterial mediolysis. The role of hypertension in IAD is still unclear. 1 Overall, it is generally assumed that there is a genetic component involved due to the ethnic differences in disease prevalence.
IADs differ substantially from cervical arterial dissections (CADs) in a number of ways. The presentation of CAD is typically neck pain, headache and acute ischemic stroke, while IAD typically presents with SAH or acute ischemic stroke. In addition, IAD is much more likely to occur in the posterior circulation, while cervical artery dissection is more likely to occur in the anterior circulation. 2 The higher rates of bleeding associated with IAD can be explained by the structural differences in the cervical versus intradural arteries. Intradural arteries have a robust internal elastic lamina; when compared to the cervical arteries, they are lacking in elastic fibers in the tunica media and external elastic lamina and have little adventitial tissue. Thus, the intradural arteries are more prone to subadventitial dissection and SAH. 1 Two mechanisms have been proposed for IADs. IADs presenting with ischemia are thought to result from dissection between the internal elastic lamina and the media, with pushing of the internal elastic lamina toward the vessel lumen resulting in vessel occlusion or narrowing. Meanwhile, dissection, resulting in SAH, is believed to occur due to dissection within the tunica media or adventitia with disruption of the vessel wall. 3 , 4
The natural history and outcomes of IAD depend heavily on the presentation. Patients who present with SAH have high mortality rates when left untreated (20–50%), 5 while those who present with stroke or headache have early mortality rates (0–5%). 5 Patients who present with SAH have rebleeding rates of up to 50%, generally within the first week of the initial event. At the same time, patients who present with acute ischemic stroke experience recurrent stroke rates of about 10%, generally within the first 2 to 3 years following the initial event. 5 In general, patients with posterior circulation dissections show a poorer prognosis compared to those with anterior circulation dissections. 6 Among patients who present without stroke or SAH (i.e., asymptomatic or headache), clinical deterioration rates are exceedingly low ranging from 2 to 3%. 7
On imaging, IAD has a wide range of manifestations including aneurysmal dilatation, focal stenosis, and occlusion. 8 In general, it is thought that fusiform aneurysmal dilatations and pearl-and-string lesions are associated with SAH, while a focal narrowing or occlusion is associated with stroke. A focal stenosis or occlusion in the setting of SAH can be suggestive of an IAD, 8 , 9 like in the case presented. Studies on the serial imaging of untreated IADs have shown that these lesions heal in multiple ways, including focal aneurysmal dilatation, persistent stenosis or occlusion, or recanalization and normalization of vessel caliber. 10 The exact time course for these structural changes is unknown.
Treatment of IADs depends on the clinical presentation of the lesion. IADs which present without SAH are treated medically unless they are associated with mass effect. 11 There are a few case reports on the use of intra-arterial and intravenous thrombolysis in patients with IAD-related stroke; however, the safety and efficacy of these treatments in this setting have yet to be systematically studied. 12 , 13 Patients with cerebral ischemia are typically treated with anticoagulation or antiplatelet therapy, but this has yet to be studied in a clinical trial. 11 Studies on treatment of CAD have demonstrated no difference in anticoagulation and antiplatelet therapy. 11 , 14 Some caution against the use of anticoagulation in IAD is because of the potential risk for SAH. 15 As IAD without stroke or SAH is known to have a benign course, conservative management without antiplatelet or antithrombotic therapy has been advocated. 7
Currently, the most favored method of treatment of ruptured dissecting aneurysms is endovascular therapy. Endovascular techniques for treating ruptured dissecting aneurysms can be divided into deconstructive and reconstructive techniques. Deconstructive techniques involve sacrifice of the parent vessel through occlusion and trapping of the aneurysm. With the advent of stents and flow diverters, reconstructive techniques, allowing for parent artery preservation, have been increasingly used. To date, there are no randomized clinical trials studying the efficacy and safety of deconstructive and reconstructive techniques. However, one recently published meta-analysis on the topic found that deconstructive techniques were associated with higher rates of long-term complete occlusion (88 vs. 81%). 16 While this meta-analysis found that deconstructive techniques were associated with higher rates of perioperative morbidity, long-term good neurological outcome rates were similar, about 90% for both groups. 16 One of the major limitations of endovascular techniques is in the treatment of posterior inferior cerebellar artery (PICA)-involving lesions. Deconstructive techniques are associated with high rates of stroke and subsequent mass effect in the treatment of PICA lesions. In a series of 72 patients treated with deconstructive techniques, Kashiwazaki et al found two cases of spinal cord infarction and seven cases of Wallenberg syndrome, secondary to occlusion of PICA dissecting aneurysms. 17 However, reconstruction of PICA-involving lesions requires the aneurysm sac to be left partially open to ensure adequate PICA flow, thus placing the patient at a higher risk of recanalization and hemorrhage. Thus, for these types of lesions, bypass surgery has traditionally been advocated. 18