Cerebral and cervical artery dissection: Treatment and prognosis

INTRODUCTION — Arterial dissections are a common cause of stroke in the young but may occur at any age. Dissection occurs when structural integrity of the arterial wall is compromised, allowing blood to collect between layers as an intramural hematoma. Dissections that occur without overt trauma are often labeled as "spontaneous" even though there is often a triggering event or underlying predisposition contributing to the pathogenesis. The optimal treatment of dissection remains a challenge due to limitations in rapidly establishing a definitive diagnosis, the overall low incidence, low recurrence rate, and marked variation in patient characteristics [1].

This topic will review the treatment and prognosis of cerebral and cervical artery dissection. Other aspects of this disorder are reviewed separately. (See "Cerebral and cervical artery dissection: Clinical features and diagnosis".)

ACUTE ISCHEMIC STROKE OR TIA DUE TO DISSECTION

General management — For patients with cervicocephalic dissection who present with transient ischemic attack (TIA) or acute ischemic stroke, standard approaches to management should be rigorously followed including blood pressure regulation, fluid administration, control of hyperglycemia and other metabolic derangements, and airway management. These issues are discussed in detail separately. (See "Initial assessment and management of acute stroke" and "Ischemic stroke in children: Clinical presentation, evaluation, and diagnosis" and "Initial evaluation and management of transient ischemic attack and minor ischemic stroke".)

All patients with acute ischemic stroke should be evaluated to determine eligibility for reperfusion therapy with intravenous thrombolysis and/or mechanical thrombectomy (see 'Reperfusion therapy for eligible patients' below).

Reperfusion therapy for eligible patients — The immediate goal of reperfusion therapy for acute ischemic stroke is to restore blood flow to the regions of brain that are ischemic but not yet infarcted. The long-term goal is to improve outcome by reducing stroke-related disability and mortality. Options for reperfusion therapy that are proven effective include intravenous thrombolysis with alteplase or tenecteplase, and mechanical thrombectomy. Since the ischemic stroke mechanism is often unknown or unconfirmed at the time of decision-making for intravenous thrombolysis, and since cervical or cerebral artery dissection is not a contraindication, patients with suspected cervical or intracranial dissection should receive intravenous thrombolysis if otherwise eligible.

●Intravenous thrombolysis – Intravenous thrombolysis with alteplase (tPA) or tenecteplase is indicated for eligible patients (table 1) with acute ischemic stroke, including those with isolated extracranial or intracranial cervical artery dissection. Extension of aortic dissection, however, is a known complication of thrombolysis. (See "Approach to reperfusion therapy for acute ischemic stroke" and "Intravenous thrombolytic therapy for acute ischemic stroke: Therapeutic use".)

The major randomized trials of intravenous thrombolysis for acute ischemic stroke did not exclude patients with cervicocephalic arterial dissection. While thrombolysis in the setting of dissection may theoretically cause enlargement of the intramural hematoma, accumulating evidence suggests that the effectiveness and safety of thrombolysis for patients with ischemic stroke related to cervical artery dissection are similar to its effectiveness and safety for patients with ischemic stroke from other causes [2-7]. Perhaps the strongest evidence, although indirect, comes from a 2011 meta-analysis of individual patient data from 14 retrospective series and 22 case reports involving 180 patients with cervical artery dissection who were treated with thrombolysis and followed for a median of three months [4]. When these patients were compared with matched historic controls from the observational SITS-ISTR registry of patients treated with intravenous alteplase for acute ischemic stroke, there were no major differences between groups for rates of symptomatic intracranial hemorrhage, mortality, excellent outcome, or favorable outcome.

There is controversy regarding the use of thrombolysis for ischemic symptoms in patients with isolated intracranial dissection alone or intracranial extension of extracranial dissection because of a presumed increased risk of subarachnoid or symptomatic intracranial hemorrhage. Limited observational data suggest this risk is minimal, but efficacy and safety are still uncertain [8].

●Mechanical thrombectomy – For select patients with acute ischemic stroke caused by a proximal intracranial arterial occlusion in the anterior circulation, early treatment with mechanical thrombectomy is indicated when performed at stroke centers with appropriate expertise, whether or not the patient received treatment with intravenous thrombolysis. This includes patients with extracranial carotid dissection who have a tandem proximal intracranial artery occlusion amenable to mechanical thrombectomy [9-13]. The efficacy of mechanical thrombectomy for vertebral and basilar artery occlusions is unproven. (See "Mechanical thrombectomy for acute ischemic stroke".)

●Emergency stenting – In addition to mechanical thrombectomy, angioplasty and stenting of arterial dissection may be treatment options for acute stroke at expert centers [14-17].

Choosing between antiplatelet and anticoagulation therapy — Antithrombotic therapy is often used for the prevention of new or recurrent ischemic symptoms caused by arterial dissection, but the approach may differ for extracranial versus intracranial dissection.

Extracranial dissection — For patients with extracranial carotid or vertebral artery dissection, antithrombotic treatment using either antiplatelet or anticoagulation therapy is generally recommended [18-24]. However, there is no clear consensus about which of these is optimal. Some experts, including the author, prefer anticoagulation rather than antiplatelet therapy [25], while other experts advise antiplatelet therapy rather than anticoagulation. The choice between antiplatelet and anticoagulant therapy should be guided by the clinical experience of the treating physician and by shared decision making that incorporates patient values and preferences, comorbid conditions, and tolerance of these agents.

The limited available evidence suggests, but does not establish, that there is no difference in efficacy between anticoagulation and antiplatelet treatment for preventing ischemic stroke in patients with extracranial dissection.

●In an open-label, assessor-blind pilot trial (CADISS), 250 subjects with extracranial carotid and vertebral dissection were randomly assigned to antiplatelet or anticoagulant treatment for three months [26]. At the end of this period, there was no significant difference between the two treatment groups; ipsilateral ischemic stroke occurred in 3 of 126 (2 percent) in the antiplatelet group and 1 of 124 (1 percent) in the anticoagulant group (odds ratio 0.34, 95% CI 0.01-4.23). There were no deaths in either group. There was one major bleeding event, a subarachnoid hemorrhage, in a patient assigned to the anticoagulation group who had a vertebral artery dissection with intracranial extension. At 12 months of follow-up, the rate of recurrent stroke remained low (approximately 2.5 percent) in both treatment groups with no difference between groups for any outcome, including no difference in the angiographic recanalization rate among patients with confirmed dissection [27].

Because of the low stroke rate and rarity of outcome events, the CADISS trial was unable to establish which treatment is superior or safer when used to treat cervical artery dissection [1]. The investigators estimated that a definitive trial would require approximately 10,000 participants, making such a trial unfeasible given the slow enrollment rate of the CADISS trial. However, it is highly likely that anticoagulation is associated with a higher risk of hemorrhagic events, since anticoagulation is a known risk factor for bleeding. (See "Risks and prevention of bleeding with oral anticoagulants".)

●The subsequent TREAT-CAD trial was an open-label, assessor-blind trial that enrolled 194 adult patients who presented with symptomatic extracranial dissection within two weeks of enrollment and were randomly assigned to aspirin monotherapy (300 mg daily) or to anticoagulation with a vitamin K antagonist (target INR 2.0 to 3.0) for 90 days [28]. The trial was designed to test the noninferiority of aspirin compared with vitamin K antagonist anticoagulants. The trialists chose a composite primary endpoint of clinical events (stroke, major hemorrhage, or death) and magnetic resonance imaging findings (new silent ischemic or hemorrhagic brain lesions) in order to achieve sufficient power, and performed a per-protocol analysis of 173 patients who received the allocated treatment and completed the assessment period. The composite endpoint occurred more often in the aspirin group compared with the vitamin K antagonist group (23 versus 15 percent, absolute difference 8 percent, 95% CI -4 to 21 percent); while the difference was not statistically significant, aspirin failed to meet noninferiority criteria because the upper limit of the 95% CI (21 percent) exceeded the predefined noninferiority margin of 12 percent. Ischemic stroke was also more frequent in the aspirin group (8 versus 0 percent), and all ischemic stroke occurred within seven days of trial enrollment. There were no deaths in either group. There was one major extracranial hemorrhage (a gastrointestinal bleed) in a patient from the vitamin K antagonist group and none in the aspirin group.

The risk of ischemic stroke in the TREAT-CAD aspirin group (8 percent) was greater than that in the CADISS antiplatelet group (2 percent); one possible explanation for the difference is that TREAT-CAD used aspirin monotherapy, whereas CADISS permitted the use of other antiplatelet agents and dual antiplatelet therapy [29]. However, this is speculative, as indirect cross-trial comparisons may be confounded by various issues and lead to erroneous conclusions.

●A 2012 meta-analysis of nonrandomized studies with over 1600 patients with cervical artery dissection reported no significant difference in recurrent stroke risk or mortality comparing anticoagulation with antiplatelet agents [30]. Similarly, a 2015 meta-analysis of nonrandomized studies with over 1300 patients who had acute carotid artery dissection found no differences in outcome or complication rates comparing anticoagulation with antiplatelet therapy [31].

Intracranial dissection — For patients who have ischemic neurologic symptoms caused by intracranial arterial dissection, we suggest antiplatelet therapy rather than anticoagulation [24]. Anticoagulation is generally avoided in the setting of intracranial dissection due to the risk of subarachnoid hemorrhage, although limited evidence suggests that anticoagulation can be used safely for some patients who have intracranial dissection without subarachnoid hemorrhage [32].

Starting antiplatelet therapy — For patients selected for antiplatelet therapy (rather than anticoagulation), initiation should be delayed for 24 hours after infusion of intravenous thrombolytic therapy. Otherwise, antiplatelet agents should be started as soon as possible after the diagnosis of TIA or ischemic stroke is confirmed, even before the evaluation for ischemic mechanism is complete. (See "Early antithrombotic treatment of acute ischemic stroke and transient ischemic attack", section on 'Treatment on presentation'.)

●For patients with a low-risk TIA, defined by an ABCD² score <4 (table 2), or moderate to major ischemic stroke, defined by a National Institutes of Health Stroke Scale (NIHSS) score >5 (table 3), we start treatment with aspirin (162 to 325 mg daily) alone.

●For patients with a high-risk TIA, defined by an ABCD² score ≥4 (table 2), or minor ischemic stroke, defined by a NIHSS score ≤5 (table 3), we begin with dual antiplatelet therapy (DAPT) for 21 days using aspirin (160 to 325 mg loading dose, followed by 50 to 100 mg daily) plus clopidogrel (300 to 600 mg loading dose, followed by 75 mg daily) rather than aspirin alone. (See "Early antithrombotic treatment of acute ischemic stroke and transient ischemic attack", section on 'Efficacy of DAPT'.)

Most reports of antiplatelet therapy for acute cervical artery dissection have employed daily aspirin at various doses; there are few data regarding other antiplatelet agents such as clopidogrel, dipyridamole, or combinations of these agents.

Starting anticoagulation therapy — For patients selected for anticoagulation rather than antiplatelet therapy, the initiation of therapy is affected by a number of factors. For medically stable patients with a small- or moderate-sized infarct, anticoagulation using heparin or low molecular weight heparin (as a bridge to warfarin) can be started as soon as 24 hours after symptom onset, or at least 24 hours after infusion of thrombolytic therapy, with minimal risk of transformation to hemorrhagic stroke; anticoagulation with a direct oral anticoagulant (DOAC) can be started as soon as 48 hours after stroke onset, as DOACs have a more rapid anticoagulant effect. However, the role of DOACs for treating dissection is uncertain and data are limited [21].

For patients with large infarctions, symptomatic hemorrhagic transformation, or poorly controlled hypertension, withholding oral anticoagulation for one to two weeks is generally recommended. In such cases, we start aspirin if there are no significant bleeding complications; anticoagulation can be started (and aspirin stopped) after one to two weeks if the patient is stable. (See "Early antithrombotic treatment of acute ischemic stroke and transient ischemic attack", section on 'Timing of long-term anticoagulation'.)

Anticoagulation can be started immediately for patients with a TIA due to dissection.

Acute anticoagulation may be achieved with either subcutaneous low molecular weight heparin such as enoxaparin (1 mg/kg twice daily) or dalteparin (100 units/kg twice daily) or with intravenous unfractionated heparin (dose-adjusted to achieve a goal activated partial thromboplastin time of 1.5 to 2 times control). Transition to warfarin (dose adjusted for a goal international normalized ratio [INR] of 2.5 with an acceptable range of 2 to 3) can be pursued in the subacute period for clinically stable patients.

Vessel monitoring and repeat imaging — After three to six months from symptom onset or diagnosis of dissection, repeat neurovascular imaging is suggested to assess the status of artery or arteries affected by dissection and guide the need for ongoing treatment, particularly if the patient is being treated with anticoagulation. We use transcranial Doppler, carotid duplex, computed tomography angiography (CTA), and/or magnetic resonance angiography (MRA) to help us decide the status of the arterial system prior to discontinuing anticoagulation therapy. Further treatment is tailored to imaging findings. (See 'Duration of antithrombotic therapy' below.)

In most cases, arteries with stenosis or luminal irregularities caused by dissection undergo recanalization and healing in the first months after the initial event. In a report of 61 patients with acute vertebral artery dissection who presented with symptoms of vertebrobasilar territory ischemia, complete recanalization of the vertebral artery was observed at six months in 62 percent [33]. In another study that followed 76 patients with cervical artery dissection involving 105 vessels with a mean follow-up of 58 months, complete recanalization was noted in 51 percent of vessels, nearly all occurring within the first nine months, and hemodynamically significant recanalization in 20 percent [34].

Data from the prospective CADISS study suggest that dissecting aneurysms are inconstant and can either resolve or develop for the first time in the months following the clinical diagnosis of extracranial cervical artery dissection [35].

Residual headache may indicate persistent vascular abnormalities [36].

Duration of antithrombotic therapy — For patients treated with anticoagulation in the acute phase, it is reasonable to stop warfarin and start long-term antiplatelet therapy after six months of anticoagulation, as long as symptoms are not recurrent and the arterial lesion is thrombosed or healed on repeat imaging at three to six months. For patients with persistent vascular luminal stenosis, irregularity, or dissecting aneurysm, it is reasonable to continue anticoagulation.

For patients treated with antiplatelet therapy in the acute phase, long-term antiplatelet therapy is recommended using aspirin, clopidogrel, aspirin-extended-release dipyridamole, or cilostazol for secondary prevention of stroke.

However, there are no concrete data regarding optimal duration of antithrombotic therapy. The time course of healing of the vessel wall or resolution of vascular abnormalities may be used to guide duration of initial treatment. Most arterial abnormalities stabilize in appearance or resolve by three months, and vessels that fail to reconstitute a normal lumen by six months are highly unlikely to recover at later time points [37].

Recurrent ischemia — Recurrence of TIA or ischemic stroke may be due to dissection or another stroke mechanism (eg, large artery atherosclerosis, cardiac embolism, small vessel disease, or other determined etiology) and should be thoroughly evaluated for all causes with a history and examination, brain and vessel imaging, and cardiac and laboratory testing. (See "Initial assessment and management of acute stroke" and "Initial evaluation and management of transient ischemic attack and minor ischemic stroke" and "Neuroimaging of acute stroke".)

●Due to dissection – In various reports, the rate of recurrent ischemic symptoms (stroke and transient ischemic attack) after dissection ranges from 0 to 13 percent [38,39], but it is likely that the actual rate of recurrent ischemic stroke caused by dissection is at the lower end of this range. The prospective CADISS trial found that the rate of recurrent ischemic stroke at three months was approximately 2 percent, and all recurrences were within 10 days of randomization, suggesting that the risk beyond the first two weeks is extremely low [26]. Prospective data from the CADISS study also suggest that extracranial cervical dissecting aneurysms have a benign prognosis, with a low rate (1 of 48, or approximately 2 percent) of ischemic stroke during 12 months of follow-up, similar to the rate observed in dissections without aneurysm formation [35].

Another study evaluated 432 surviving patients with carotid or vertebral dissection who were followed for a mean time of 31 months [40]. Recurrent ischemic stroke due to initial or recurrent dissection was observed in four patients (0.9 percent), giving an annual incidence of 0.3 percent. Transient ischemic attack was observed in eight patients (1.8 percent), for an annual incidence of 0.6 percent.

●Endovascular and surgical repair for dissection – Endovascular techniques or surgical repair have been used to treat dissection, mainly for patients who have recurrent ischemia despite antithrombotic therapy [23].

Endovascular techniques for the treatment of dissection and dissecting aneurysm include angioplasty, stent placement, embolization with various materials, and combinations of such approaches [23,41]. Angioplasty and stenting may occlude the false lumen and restore true arterial lumen patency. However, data regarding endovascular treatment of dissection is limited to case reports and case series [41-48]. There are no randomized trial data comparing endovascular techniques with medical therapies, and the long-term safety and durability of these methods are unknown.

In isolated cases, accessible lesions may be treated by surgical vessel reconstruction or bypass around a dissecting aneurysm [49,50]. Other surgical revascularization procedures include extracranial-intracranial bypass, endarterectomy, thrombectomy, and proximal vessel ligation.

SUBARACHNOID HEMORRHAGE DUE TO INTRACRANIAL DISSECTION — Subarachnoid hemorrhage is an uncommon complication of intracranial dissection. (See "Nonaneurysmal subarachnoid hemorrhage", section on 'Intracranial arterial dissection'.)

It is managed according to the same principles as subarachnoid hemorrhage caused by rupture of a saccular aneurysm (see "Aneurysmal subarachnoid hemorrhage: Treatment and prognosis"), with the exception that the surgical or endovascular treatment of dissecting aneurysm itself may differ from that of a saccular aneurysm because of morphologic differences between the two types of aneurysms. The risk of rebleeding from an intracranial dissecting aneurysm is as high as 40 percent in the first week or so after the event [51-54]. Thus, early repair is typically recommended [51].

The morphology of most dissecting aneurysms limits standard surgical clipping. Management is individualized according to location and other anatomic features, and can include proximal occlusion of the artery, trapping or wrapping of the pseudoaneurysm, bypass, embolization, or stenting [52,54]. These are complicated procedures that can incur additional morbidity.

NONISCHEMIC LOCAL SYMPTOMS — For patients with nonischemic symptoms caused by extracranial or intracranial carotid or vertebral artery dissection, we suggest antiplatelet therapy for prevention of ischemic stroke.

Headache and neck pain associated with dissection can usually be managed with simple analgesics such as acetaminophen. Anecdotally, gabapentin may be helpful. Nonsteroidal antiinflammatory drugs (NSAIDs; eg, naproxen sodium, ibuprofen) are generally avoided in patients receiving anticoagulation because of the increased risk of bleeding.

There is no specific treatment for other local symptoms of dissection such as Horner syndrome, lower cranial nerve palsy, audible bruit, or tinnitus, but these may improve with time and vessel healing.

MEASURES TO REDUCE RISK OF DISSECTION — There are no proven methods that reduce the risk of recurrent cervicocephalic arterial dissection. Nevertheless, some experts suggest that patients with dissection should avoid contact sports, chiropractic neck manipulation, and any activity that involves abrupt rotation and flexion-extension of the neck [55,56]. In addition, estrogen-containing compounds should be discontinued, as estrogen may induce proliferation of intimal and fibromuscular arterial tissue. All vascular risk factors including hypertension should be addressed. (See "Overview of secondary prevention of ischemic stroke".)

PROGNOSIS

Neurologic outcome — The prognosis of cerebral and cervical artery dissection is related primarily to the severity of associated ischemic stroke or subarachnoid hemorrhage. Morbidity and mortality of acute cervicocephalic arterial dissection varies according to the specific arteries involved and location of the lesion.

In the CADISP study of 982 patients with extracranial cervical artery dissection, an unfavorable outcome at three months among patients with ischemic stroke, defined as a modified Rankin Scale (table 4) score >2, was more likely with stroke due to internal carotid artery dissection compared with stroke due to vertebral artery dissection (25 versus 8 percent) [57]. This result was largely driven by stroke severity at onset, which was greater for patients with internal carotid dissection compared with those who had vertebral dissection by mean National Institutes of Health Stroke Scale (NIHSS) score on admission (8 versus 3).

Only limited systematic data are available regarding long-term outcomes of dissection. Complete or excellent recovery occurs in 70 to 85 percent of patients with extracranial dissection, with major disabling deficits in 10 to 25 percent, and death in 5 to 10 percent of cases [38,58].

In observational studies, factors associated with poor functional outcome after cervical artery dissection include a high NIHSS score at onset, arterial occlusion, and older age [58-61]. Quality of life may be impaired in almost half of long-term survivors after dissection [62].

Recurrence of dissection — The recurrence rate of cervical and intracranial artery dissection, with or without symptoms, is uncertain, and available data are inconsistent. In the CADISP study, which retrospectively and prospectively recruited 982 patients with cervical artery dissection, the recurrence rate for extracranial cervical dissection at three months was 2 percent [57]. Even higher rates were reported by a single-center study of 232 patients with cervical artery dissection who were followed clinically and with serial imaging for at least one year. Over the course of the study, there were 46 new dissections affecting 39 patients (16 percent). Recurrent dissection was detected within one month of the initial event in 9 percent, and beyond one month until up to eight years after the initial event in another 7 percent [63]. Most initial dissections were linked to ischemic stroke, but the majority of recurrent dissections were either asymptomatic or associated with purely local symptoms.

Recurrent dissection may affect several vessels at once, even when preceded by initial dissection isolated to one artery [63,64].

Although data are limited, rare patients with familial dissection tend to be young (mean age 36 years) and are probably at high risk for recurrent or multiple dissection [65].

SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Stroke in adults" and "Society guideline links: Stroke in children".)

SUMMARY AND RECOMMENDATIONS

●Acute management of TIA or ischemic stroke – For patients with cervicocephalic dissection who present with transient ischemic attack (TIA) or acute ischemic stroke, standard approaches to stroke management should be rigorously followed. All patients with acute ischemic stroke should be evaluated to determine eligibility for reperfusion therapy with intravenous thrombolysis and/or mechanical thrombectomy. (See 'General management' above and 'Reperfusion therapy for eligible patients' above and "Approach to reperfusion therapy for acute ischemic stroke".)

●Choice of antithrombotic therapy for secondary ischemic stroke prevention – Beyond the hyperacute period of acute stroke, antithrombotic therapy with either anticoagulation or antiplatelet drugs is accepted treatment for prevention of new or recurrent ischemic symptoms due to extracranial artery dissection, although there is controversy regarding the choice between the two. (See 'Choosing between antiplatelet and anticoagulation therapy' above.)

•Ischemia due to extracranial dissection – For patients with acute ischemic stroke or TIA caused by extracranial carotid or vertebral artery dissection, antithrombotic treatment using either antiplatelet or anticoagulation therapy is generally recommended. Some experts, including the author, prefer anticoagulation rather than antiplatelet therapy, while other experts advise antiplatelet therapy rather than anticoagulation. The choice between antiplatelet and anticoagulant therapy should be guided by the clinical experience of the treating physician and by patient values and preferences, comorbid conditions, and tolerance of these agents. The limited available evidence suggests (but does not establish) that there no difference in efficacy between anticoagulation and antiplatelet treatment for preventing ischemic stroke in patients with extracranial dissection, although it is likely that anticoagulation is associated with a higher risk of hemorrhagic events. (See 'Extracranial dissection' above.)

•Nonischemic local symptoms due to extracranial dissection – For patients with nonischemic local symptoms caused by extracranial cervical dissection, we suggest antiplatelet therapy for prevention of ischemic stroke (Grade 2C). (See 'Nonischemic local symptoms' above.)

•Ischemia due to intracranial dissection – For patients who have ischemic stroke or TIA caused by intracranial dissection, we suggest antiplatelet therapy rather than anticoagulation (Grade 2C). (See 'Intracranial dissection' above.)

•Initiating therapy – The timing and suggested dosing for starting antiplatelet or anticoagulant therapy is detailed in the sections above. (See 'Starting antiplatelet therapy' above and 'Starting anticoagulation therapy' above.)

●Vessel monitoring and duration of antithrombotic therapy – Repeat neurovascular imaging is suggested after three to six months from symptom onset or diagnosis of dissection to assess the status of the artery or arteries affected by dissection. For patients treated with anticoagulation in the acute phase, it is reasonable to stop warfarin and start long-term antiplatelet therapy after six months of anticoagulation, as long as symptoms are not recurrent and the arterial lesion is thrombosed or healed. (See 'Vessel monitoring and repeat imaging' above and 'Duration of antithrombotic therapy' above.)

●Recurrent ischemia requires evaluation for all causes – Recurrence of TIA or ischemic stroke may be due to dissection or another stroke mechanism (eg, large artery atherosclerosis, cardiac embolism, small vessel disease, or other determined etiology) and should be thoroughly evaluated for all causes. (See 'Recurrent ischemia' above.)

●Subarachnoid hemorrhage due to intracranial dissection – Subarachnoid hemorrhage is an uncommon complication of intracranial dissection and has a high risk of early rebleeding. Early repair is typically recommended. (See 'Subarachnoid hemorrhage due to intracranial dissection' above.)

ACKNOWLEDGMENT — The UpToDate editorial staff acknowledges Jeffrey Saver, MD, who contributed to earlier versions of this topic review.