16.1.1 Clinical Presentation

A 66-year-old male presented to the hospital in the early morning, with fluctuating right-sided weakness, right gaze preference and right facial droop, bilateral legs ataxia, slurred speech, and drowsiness. National Institute of Health Stroke Scale (NIHSS) score was 13. His wife recalled that the patient was talking somewhat slowly the night before. They slept in different rooms and, in the morning, she found him on the ground.

16.1.2 Imaging Workup and Investigations

On noncontrast CT, there was no evidence of established infarctions. A CT angiography (CTA) demonstrated a basilar artery (BA) filling defect extending in bilateral posterior cerebral arteries (PCAs). CT perfusion demonstrated a significant cerebral blood flow (CBF)/time to peak (TTP) mismatch in the territory of the BA and to a lesser extent of the PCAs bilaterally (Fig. 16.1a).

16.1.3 Diagnosis and Treatment

Acute basilar artery occlusion (BAO). Intravenous tissue plasminogen activator (IV-tPA) was not given due to the long time since last known well. The patient was brought to the angiography suite for endovascular treatment (EVT).

16.1.4 Technique

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  Right common femoral artery puncture with placement of an 8-Fr short vascular access sheath into the common femoral artery.

  
  
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  A 6-Fr guide catheter placed in the left vertebral artery, which was of sufficient caliber to allocate a large catheter. A digital subtraction angiography run demonstrated the known distal BAO (Fig. 16.1b).

  
  
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  A large-bore aspiration catheter was advanced into the right vertebral artery over a 1.8-Fr microcatheter and a 0.014-in microwire.

  
  
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  The aspiration catheter was parked with the tip adjacent to the proximal end of the thrombus, and the microcatheter was removed.

  
  
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  The aspiration catheter was connected to the suction device and aspiration was carried out for 5 minutes.

  
  
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  After 5 minutes, the aspiration catheter was pulled under continuous aspiration and manual sucrion from the guiding catheter.

  
  
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  A postaspiration angiographic run demonstrated complete recanalization with a modified treatment in cerebral ischemia (mTICI) score of 3 (Fig. 16.1c). Time from puncture to recanalization was 23 minutes.

16.1.5 Postprocedural Care and Outcome

The patient was transferred to the stroke unit. Postoperative investigations identified a previously undiagnosed atrial fibrillation, for which treatment was initiated.

The patient had full recovery of his motor, cognitive, and speech function, with a residual deficit in short-term memory, and was discharged after 10 days. An MRI a few days after treatment demonstrated bilateral, left-greater-than-right hippocampal infarctions (Fig. 16.1d). At the 4-month clinic follow-up, the patient still had remarkable short-term memory deficits, which caused him significant anxiety and depression.

16.2.1 Clinical Presentation

Shortly after midnight, a 57-year-old male was emergently brought by ambulance to the emergency department after suffering a syncopal event while drinking with some friends at a bar. On arrival he was pale and diaphoretic and had multiple episodes of vomiting. His NIHSS score was 13, with right-sided weakness and facial droop, right-sided neglect, and aphasia.

16.2.2 Imaging Workup and Investigations

On noncontrast CT, there was no evidence of established infarctions. A CTA demonstrated a nonocclusive thrombus in the proximal BA (Fig. 16.2a). CT perfusion demonstrated a significant CBF/TTP mismatch in the cerebellum. Neck images demonstrated significant tortuosity of the aortic arch (type 3) and of bilateral vertebral arteries.

16.2.3 Diagnosis and Treatment

Acute basilar artery subocclusion. IV-tPA was given and the patient was referred for EVT.

16.2.4 Technique

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  Right common femoral artery puncture with placement of an 8-Fr short vascular access sheath into the common femoral artery.

  
  
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  A 6-Fr guide catheter placed in the left subclavian artery and the left vertebral artery was catheterized with an aspiration catheter and a microcatheter. A run confirmed subocclusion of the BA. An extremely tight bend in the V2 segment made impossible the navigation of the devices; therefore, this approach was aborted (Fig. 16.2b).

  
  
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  The extreme tortuosity of the arch made impossible the catheterization of the right vertebral artery, despite multiple attempts with Simmons 2 and 3 catheters and normal and shapeable glidewires.

  
  
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  A 6-Fr dedicated sheath was inserted in the right radial artery and a 0.071-in catheter was advanced into the right vertebral artery until another sharp turn (Fig. 16.2c).

  
  
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  The turn was negotiated with a soft-tipped 5-Fr distal access catheter and a 0.18-in microcatheter over a 0.014-in microwire (Fig. 16.1c).

  
  
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  The distal access catheter was parked at the V2–V3 junction and the microcatheter was navigated through the occlusion and positioned in the right PCA.

  
  
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  A 4 × 30 mm stent retriever was deployed over the thrombus and left in place for 5 minutes, after which it was removed under aspiration from the distal access catheter.

  
  
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  A postaspiration angiographic run demonstrated complete recanalization with an mTICI score of 3. There was an underlying stenosis of the proximal BA of 50%, which was not treated given its noncritical features (Fig. 16.2d). Puncture to reperfusion time was 90 minutes.

16.2.5 Postprocedural Care and Outcome

The patient was transferred to the stroke unit. Postoperative echocardiography identified a patent foramen ovale.

The patient had complete recovery of his motor, cognitive, and speech function, with residual homonymous hemianopia and imbalance. An MRI prior to discharge demonstrated bilateral cerebellar and occipital lobe infarctions. At the 4-month clinic follow-up, the patient was completely independent and only endorsed minimal visual symptoms.

16.2.6 Background

Posterior circulation strokes are less frequent than their anterior counterparts, and account for approximately 15 to 20% of the total ischemic strokes. BAO is an even rarer event and represents 1 to 4% of all strokes. ¹

Due to the particular anatomical and physiological characteristics of the BA, its occlusion can be difficult to diagnose clinically. The condition carries an extremely high mortality, with multiple large cohort studies quoting rates between 85 and 95% if left untreated. ^{2 ,​ 3 ,​ 4}

The BA originates at the pontomedullary junction from the union of the vertebral arteries. The vessel measures an average diameter of 3.74 mm, ⁵ courses along the anterior surface of the brainstem, and eventually divides in the bilateral PCAs at its tip. The vessel gives the anterior inferior cerebellar arteries (AICAs), the superior cerebellar arteries (SCAs), multiple brainstem and thalamic perforators and has been schematically divided in proximal, middle, and distal segments. The proximal segment goes from the vertebrobasilar junction to the origin of the AICAs, the middle from the AICAs to the SCAs, and the distal from the SCAs to the basilar tip. Besides supplying a large portion of the cerebellum, the BA is the main feeder for some of the most critical areas of the brainstem. The proximal and middle segments and their branches supply the pons, while the distal segment and its branches, including the PCAs, supply the midbrain, thalami, and hippocampi. The basilar tip gives multiple critical perforators to the thalamus and midbrain. ¹

Clinically, the manifestations of BAOs are manifold, depending on multiple factors such as location and extent of the thrombus, collateral circulation (including anastomoses between perforators), and etiology of the occlusion. ⁶ In general, reduced consciousness is a clinical hallmark of BAO. ⁷ Symptoms include the following: (1) various degrees of motor deficits, from facial or bland hemiparesis to tetraplegia; (2) dysarthria; (3) headache; (4) visual impairment; (5) vertigo, nausea, and vomiting; and (6) loss of consciousness and coma. Symptom onset is as well variable, going from vague, nonspecific prodromal symptoms like vertigo or nausea to sudden loss of consciousness and coma. Especially if the emergence of symptoms is insidious, the syndrome can mimic a nonstroke condition, thus delaying a referral to neurology and a timely diagnosis and appropriate treatment. This is particularly evident in patients with a preexisting atherosclerotic stenosis of the BA, which, by virtue of having developed rich collateral network, can develop a BAO and show only small ischemic lesions on imaging or very mild clinical manifestations. Once a pontine infarct is established, secondary to a middle segment occlusion, depending on the extent, the patient can present with hemi- or tetraplegia, altered consciousness, and cranial nerve palsies. Extensive pontine infarction is also the most common cause of locked-in syndrome. Distal segment and basilar tip occlusions can result in nuclear and supranuclear symptoms, tetraparesis/plegia, and thalamic syndromes with or without amnesia and behavioral abnormalities. Depending on the conformation of the circle of Willis, symptoms can involve one or both PCAs, with possible visual symptoms and hippocampal infarctions, as shown in the first case.

The most common causes of posterior circulation occlusion are cardiac and large-artery embolism, arterial dissection, and atherosclerotic stenotic disease. In general, patients with atherosclerotic BA occlusions are in the sixth or seventh decade, while those with embolic stroke are younger. ⁶ Underlying intracranial atherosclerosis with significant stenosis (>70%) has been reported in as high as 24% of patients with BAO. ⁴

After having ruled out a hemorrhage with a plain head CT, CTA, or MRI angiography, provide the final diagnosis of BAO. The hyperdense BA sign on noncontrast CT, although relatively specific in cases with high pretest probability of BAO, is seen only in 50 to 70% of patients. ⁸

Similar to what has been developed in anterior circulation strokes, a 10-point posterior circulation Acute Stroke Prognosis Early CT (pc-ASPECTS) score was developed and validated to quantify early ischemia. This score is reportedly most effective if calculated on source images of a CTA. ⁹

While, in general, DWI sequences are the gold standard for the detection of acute infarction, it has been shown that 6 to 10% of all strokes are initially DWI negative—this rate being higher in the posterior circulation, particularly in the early period after occlusion. ¹⁰

EVT in BAO can be carried out by stent retrieval, aspiration, or by a combination thereof. Given the relatively small caliber of the vertebral arteries, a large bore guiding catheter cannot be placed in this vessel most of the times and needs to be left in the subclavian artery. An intermediate, aspiration-capable distal access catheter can be then navigated in the vertebral artery over a microcatheter and J-tipped microwire. Depending on the technique of choice, the aspiration catheter can be positioned at the proximal end of the thrombus/embolus or the microcatheter can be used to gently pass the occlusion and advanced until the tip is in one of the PCAs prior to deployment of a stent retriever. The technique for EVT of BAO does not differ from that used in anterior circulation occlusions. As shown in the second case described earlier, particularly tortuous anatomies can require a radial access. In this instance, given the maximum radial sheath diameter of 6 Fr, smaller guide and aspiration catheters need to be used. In cases with an underlying atherosclerotic stenosis, angioplasty with or without stenting might be necessary to consolidate the results of the procedure. The technical aspects of these procedures are described in other sections of the book. Deployment of a stent in the acute setting will require emergent institution of dual-antiplatelet therapy to avoid acute thrombosis. At our institution, we use a loading dose of 325 mg of aspirin associated with 300 mg of clopidogrel or 180 mg of ticagrelor. We also routinely use a weight-based continuous IV drip of eptifibatide as a bridging therapy, to be stopped 6 hours after administration of the oral dual-antiplatelet agents.