4 Acute Basilar Artery Occlusion
Abstract
Acute basilar artery occlusion is usually not compatible with life in most of the cases. The initial clinical presentation is very variable, delaying clinical suspicions and diagnosis. Despite the overall high mortality, the outcome can be good if it is diagnosed and treated promptly. Poor neurological exam or high National Institutes of Health Stroke Scale (NIHSS) score should not be an exclusion criterion. If no contraindications, patient should receive tissue plasminogen activator. Expeditious endovascular therapy is recommended if patients have a NIHSS greater than 6. Plane computed tomography (CT) and CT angiography (CTA) of the head and neck are necessary for diagnosis. If patients present within longer than 6 hours after onset of symptoms, CT perfusion or magnetic resonance imaging (MRI) should be obtained rapidly to assess brainstem ischemia. If possible, collateral flow from posterior communicating arteries should be assessed on CTA or during cerebral angiogram. CT angiogram of the neck should be analyzed carefully looking for dominant vertebral artery (VA), dissection or stenosis of the VA, and VA tortuosity. If significant VA or subclavian artery tortuosity is observed, interventionists should consider radial or brachial artery approach. Endovascular mechanical thrombectomy can be achieved by different techniques, including a direct aspiration first pass technique (ADAPT), stent retriever, or combination of both (Solumbra technique). Similar to anterior circulation, symptomatic intracerebral hemorrhage is the most dangerous complication. Adequate patient selection and appropriate endovascular knowledge and experience are the two most important factors necessary to prevent this potential catastrophic complication.
Introduction
Acute ischemic stroke (AIS) caused by basilar artery occlusion (BAO) are less common, representing 6 to 10% of all large vessel ischemic strokes annually. Presentation may include vertigo, gait imbalance, nausea/vomiting, cranial nerve dysfunction, acute onset of coma, decerebrate rigidity, and small nonreactive “pontine” pupils. The natural history of BAO can be extremely morbid, but timely intervention can greatly improve morbidity and mortality. Initial management involves the standard approach for managing AIS, usually by stroke neurologists. Neurosurgeons or neurointerventionists are often consulted after initial management.
Despite its overall high mortality rate, the outcome from presentation of BAO can vary greatly. There are many confounding factors, such as site of occlusion, clot load, collateral flow, and use of intravenous thrombolysis (IVT) and intra-arterial thrombolysis (IAT). We do not recommend endovascular therapy in patients who present with a National Institutes of Health Stroke Scale (NIHSS) score less than 6.
Endovascular intervention for BAO is an important therapy with some history of strong evidence dating back to 1997. In their series, Wijdicks et al demonstrated that local fibrinolysis of BAO reduces mortality and improves long-term outcome. In fact, patients with BAO and an initially poor clinical exam were shown to have an uncharacteristically good outcome with prompt management.
Since then, technology originally focused on and studied in anterior circulation strokes has been used for treatment of BAO. Treatments have progressed from indirect (e.g., IVT) to more directed therapies, such as local IAT and mechanical thrombectomy.
The most recently updated American Heart Association/American Stroke Association guidelines for the management of patients with AIS state that, although uncertain (Class IIb, Level of Evidence C), thrombectomy may be reasonable when initiated within the first 6 hours of stroke onset in carefully selected patients with posterior circulation strokes.
Major controversies in decision making addressed in this chapter include:
Whether or not treatment is indicated.
Safety and efficacy of endovascular treatment of acute BAO.
Timing of intervention.
Outcome severity.
Whether to Treat
Treatment should be offered within a reasonable time window from onset of symptoms. No studies have established a definitive time window, but various authors have considered cutoffs as short as 6 hours and as long as 24 hours from onset. Poor neurological exam or high NIHSS should not be an exclusion criterion. Patients should receive IV tissue plasminogen activator (tPA) if they are within the appropriate time window to receive it ( 1 in algorithm ). Those who are not IV tPA candidates but still present in less than 6 hours should be considered for endovascular therapy ( 2 in algorithm ). We recommend proceeding expeditiously to endovascular therapy if the patient has a significant stroke burden (NIHSS ≥6) ( 5 in algorithm ). In patients with milder stroke burden (NIHSS <6), risks of endovascular therapy may exceed the potential benefits; medical management is appropriate for these patients. In patients presenting with longer than 6 hours after onset of symptoms, we recommend rapid magnetic resonance imaging (MRI) of the brain to assess for brainstem ischemia ( 3 in algorithm ). Computed tomography (CT) perfusion imaging, as used in the EXTEND-IA trial, is useful for assessing salvageable penumbra in the cerebrum, but assessment of the brainstem is insufficient. MRI should be completed rapidly and can be abbreviated to fluid attenuation inversion recovery (FLAIR), diffusion-weighted imaging (DWI), and apparent diffusion coefficient (ADC) sequences. Conservative management may be considered reasonable if extensive brainstem ischemic core is present ( 4 in algorithm ).
Conservative Management
Conservative management is usually of little benefit for patients with BAO. It does not differ from the typical management for all ischemic strokes, other than the additional critical care that these patients may require. IVT should be given if within the appropriate time window, followed by measures for secondary stroke prevention. Workup for the etiology of the stroke should be sought, including vascular imaging to rule out dissection and identify the site of occlusion. For patients with BAO who do not receive thrombolytic therapy, the mortality rate can be as high as 80 to 90%.
Anatomical Considerations
The basilar artery (BA) is the most important artery in the posterior circulation and supplies the majority of the brainstem. It arises at the pontomedullary junction as the bilateral vertebral arteries (VAs) coalesce. As it terminates, it gives rise to the bilateral posterior cerebral arteries (PCAs). The other important branches of the basilar artery include the superior cerebellar artery (SCA), anterior inferior cerebellar artery (AICA), and several paramedian and circumferential branches to the midbrain and pons. These branches irrigate a large territory, ranging rostrally from the superior parietal lobule and caudally down to the middle cerebellar peduncle.
The anatomy of the BA proper should be considered along with the collateral flow provided to the bilateral PCAs via the posterior communicating arteries (PCoAs), dominance of flow, and anatomical variants. In addition to the directed therapy, a complete diagnostic angiogram helps delineate this.
Depending on the amount of collateral flow mediated by the PCoAs, the PCA distribution may be involved by BAO; this includes supratentorial structures such as the inferior temporal gyrus, occipital lobe, superior parietal lobule, thalamus, and choroid plexus.
Workup
Clinical Evaluation
Given the richness of collaterals from the BA, BA thrombosis can range in presentation from mild transient symptoms to devastating strokes. As the predominant vessel in the posterior circulation, it supplies the brainstem, portions of the occipital and temporal lobes, cerebellum, and thalami. Clinical symptoms and signs depend on the location of occlusion and the corresponding affected anatomical regions. Maximal time of appearance of symptoms seems to range between 1 and 2 days.
▶ Table 4.1 delineates common symptoms based on the general locations associated with BAO.
Common etiologies of BAO include severe atherosclerosis, thromboembolic occlusions, and VA dissections. Often, spontaneous recanalization of the occluded artery may occur, and presentations may include transient loss of consciousness without localizing factors. The most common premonitory symptoms are vertigo and nausea. There should be a low threshold for intervention in the presence of decreased consciousness, cranial nerve (CN) palsy, and long tract signs, frequently contralateral. Long tract signs indicate involvement of the corticospinal tracts and sensory fibers. Most common presentations will involve occurrence of CN IV, VI, VII palsies followed by ataxia and dysdiadochokinesia. In addition, “crossed signs” (e.g., sudden onset of right facial weakness with left extremity weakness) may signal a likely basilar thrombosis.
Imaging
Initial evaluation of patients presenting with stroke-like symptoms will include CT without contrast, which may or may not show a hypodense area consistent with infarction. If clinical signs are suspicious for acute BAO, vascular imaging should also be included. Depending on the institution, vascular imaging may include CT angiography (CTA), CT perfusion (CTP), MR angiography (MRA), or digital subtraction angiography (DSA; ▶ Fig. 4.1 ). We recommend proceeding with intervention only after confirmatory vascular imaging.
Imaging can be used to assess the length of the clot and even predict treatment outcome with IVT or procedural success for thrombectomy. Even at long clot lengths (>30 mm), as many as 30% of patients with BAO can be recanalized; however, those with delayed recanalization may have poor outcomes.
Differential Diagnosis
Many basilar thrombosis mimics do exist. Extensor jerking and decerebrate posturing are frequently mistaken for seizure-like activity with a post-ictal state. Acute headaches may initially raise concern for subarachnoid hemorrhage, and supratentorial lesions with herniation falsely produce upper brainstem-localizing symptoms as well.
Treatment
Choice of Treatment
Endovascular therapy for BAO has been practiced widely since 1997, following the report by Wijdicks et al. However, much of the current evidence and experience are based on the use of local IA thrombolysis; fewer centers have published extensive experience with suction thrombectomy, and fewer still with stent retrievers.
Treatment options thus include antiplatelet/anticoagulants as “conservative management,” IVT, IAT, nonstent retriever (including suction) thrombectomy, and stent retriever thrombectomy.
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