Incidence, Epidemiology, and Natural History

Ischemia of the posterior (vertebrobasilar [VB]) circulation may manifest as a wide range of clinical entities, from the subtle and vague symptoms of VB insufficiency to the devastating locked-in syndrome. The most common causes of posterior circulation ischemia are cardioembolism, large-vessel (i.e., vertebral and basilar arteries) atherosclerosis, and small-vessel (i.e., brainstem perforating arteries) disease. ¹ Strokes of the posterior circulation account for approximately 20% of all ischemic strokes and may be caused by atherosclerosis (of both large and small vessels), cardioembolism, subclavian steal, arterial dissection, VB dolichoectasia (VBD), or hemodynamic compromise.

An understanding of the anatomy of the posterior circulation is critical to endovascular intervention for ischemic pathology. The normal diameter of the vertebral artery (VA) is 3 to 5 mm, ² whereas the mean diameter of the basilar artery (BA) is 3 mm at the level of the pons. Anatomical variations of the posterior circulation are not uncommon, but the affected patients often do not have symptoms attributable to these variations. Asymmetric VAs may occur in up to two-thirds of the population with true unilateral hypoplasia identified in up to 12% of the population. ³ Although persistent carotid–VB anastomoses may predispose to posterior circulation aneurysm formation, they are infrequently associated with ischemia. A fetal posterior cerebral artery (PCA) is a common anatomical variant that occurs in up to 30% of the general population. Recognition of this variant is critical to the appropriate work-up of posterior circulation territory strokes occurring in these cases. Evaluation of the anterior circulation is essential, because the PCA territory is supplied by the carotid artery rather than the BA. When a fetal PCA is present, even carotid stenosis may lead to an occipital stroke. Another anatomical variant of clinical significance to posterior fossa ischemia is the artery of Percheron. This single thalamic perforating artery arises from the proximal P1 PCA segment and supplies the rostral mesencephalon and paramedian bilateral thalami. Though bilateral thalamic infarcts may also be caused by venous thrombosis and basilar apex occlusion, there should be high suspicion for embolism to this vessel when bilateral thalamic infarcts are present.

Atherosclerosis most commonly affects the VA at its origin or in its distal segments. Intracranial atherosclerosis of the vertebral or basilar arteries is most frequently seen in African, African-American, and East Asian populations, whereas extra-cranial VB atherosclerotic disease is more common in whites and is associated with peripheral vascular disease. ⁴ Atherosclerotic disease may result in thromboembolism to the downstream vessels or hemodynamic compromise. Large-vessel atherosclerosis has been associated with 35% of posterior circulation strokes, whereas small-vessel disease has been associated with 13%. ⁵

Posterior circulation lacunar infarcts result from diseases of the small penetrating arteries of the intracranial VAs, BAs, and PCAs. Lipohyalinosis of these small vessels can result in lacunar infarction, which is most common among individuals with chronic hypertension.

In the New England Medical Center Posterior Circulation Registry, which included 407 consecutive patients with posterior circulation stroke, arterial embolism was determined to be the most common etiology, accounting for 40% of strokes. ⁶ Cardiac origin was the likely source in 24% of these cases and resulted in primarily infarcts in distal territory (i.e., rostral to the superior cerebellar artery); patients with PCA, superior cerebellar artery, or basilar apex infarcts had a high likelihood of having a cardiac source.

VBD is an uncommon but ominous cause of both hemorrhagic and ischemic posterior circulation strokes. Although VBD is often diagnosed incidentally, patients may present with signs or symptoms of posterior circulation ischemia. The natural history of VBD includes a 10.1% risk of posterior circulation transient ischemic attacks (TIAs). ³ The etiology of ischemia in VBD may be multifactorial, including distal emboli, hemodynamic compromise, and occlusion of small vessels due to progressive anatomical derangement.

Although the aforementioned most common causes of VB ischemia are associated with chronic diseases and therefore most often manifest in older adults, VA dissection is an important cause of posterior circulation stroke in young adults. Dissections of the VA most commonly occur in the V2 or V3 segments of that artery, ⁷ extending intracranially in 10% of cases. ⁸ The posterior inferior cerebellar artery territory is the most common site of ischemia associated with VA dissection. ³ However, isolated neck pain without ischemic symptoms has been observed in up to 12% of patients. Given their location within the foramen transversarium, the VAs are particularly vulnerable to neck manipulation and trauma in which the head violently moves. Therefore, the presence of stroke associated with a history of trauma or neck manipulation should raise clinical suspicion for VA dissection. Compared with patients with anterior circulation dissections, those with VA dissections tend to be younger and more commonly have neck pain and associated subarachnoid hemorrhage; making the diagnosis tended to take longer, likely because the symptoms are often not well recognized. ⁹ Rarely, spontaneous dissections can occur, particularly in patients with underlying connective tissue disorders (such as Marfan syndrome).

Clinical Presentation

As with any vascular disorder, the symptoms of VB ischemia are attributable to dysfunction of the regions supplied by these arteries—the brainstem, cerebellum, inferior temporal lobe, occipital lobe, and thalamus. As is typical of anterior circulation stroke, the symptoms of posterior circulation stroke are maximal at onset. Symptoms of posterior circulation ischemia range from relatively benign, transient symptoms of dizziness to devastating, widespread paresis (locked-in syndrome).

In the New England Medical Center Posterior Circulation Registry, the most frequent symptoms were dizziness (47%), unilateral limb weakness (41%), dysarthria (31%), headache (28%), and nausea or vomiting (27%). ¹⁰ The signs of posterior circulation ischemia were found to be similarly vague and included gait ataxia (31%), limb ataxia (30%), dysarthria (28%), and nystagmus (24%). Logistic regression analysis revealed some correlation between clinical symptoms and infarct location ( Table 23.1 ¹⁰ ). The presence of any of these symptoms in combination with neck pain (especially in young patients) should prompt suspicion for VA dissection. ^{11 , 12}

A VB TIA may precede a posterior circulation stroke in up to 25% of cases. ³ This fact, combined with the frequency of many symptoms of posterior circulation ischemia (e.g., dizziness, headache, nausea), emphasizes the need to achieve an accurate diagnosis and initiate appropriate treatment. Some clinicians consider the presence of diplopia, vertically oriented binocular visual field loss, vertigo, ataxia, impaired sensorium, or crossed-findings (ipsilateral cranial nerve deficit with contralateral long-tract signs) to be localizing signs requiring prompt evaluation of posterior circulation patency. ³ However, clinical evaluation alone is insufficient. Flossmann et al ¹³ evaluated the reliability of clinical diagnosis of patients with symptoms of VB TIA or minor stroke by having three independent clinicians, blinded to brain imaging, predict the most likely affected vascular territory. The sensitivity of correct identification of VB territory involvement ranged from 54.2% to 70.8%, whereas the specificity ranged from 84.4% to 91.7%. Those authors found only the presence of visual symptoms to improve the accuracy of diagnosis.

Periprocedural Evaluation

Maintenance of a high level of suspicion for posterior circulation ischemia is critical to the proper evaluation of these patients. Contrast-enhanced magnetic resonance imaging (MRI) remains the most sensitive imaging modality for the detection of acute ischemia. This holds particularly true for ischemia of the posterior circulation, where the skull base creates artifact that may obscure subtle early ischemic changes on computed tomography (CT). ¹⁴

Given the vague localizing signs and symptoms of posterior fossa ischemic disease, it is essential to image the entire posterior circulation, from the aortic arch and VA origin through the intracranial circulation. Duplex ultrasound imaging has been a mainstay of evaluation and monitoring of the extracranial carotid arteries. It is utilized much less commonly for evaluation of the posterior circulation. However, recent studies have demonstrated its utility. ^{15 , 16} Doppler studies are noninvasive, inexpensive, and easily obtained. They can be used to identify reversed flow, which is characteristic of subclavian steal syndrome, as well as turbulence and waveform dampening, as seen in stenosis ( Fig. 23.1 ). ¹⁷ Peak systolic velocity has been shown to be a reliable indicator of stenosis, with a range of velocities of >108 to 140 cm/s indicative of > 50% stenosis. ¹⁵ The sensitivity and specificity of Doppler studies for the detection of 50 to 99% VA stenosis are 70.2% and 93.4%, respectively. ¹⁸ For the detection of complete VA occlusion, the sensitivity is 98.8% and the specificity is 90.8%.

Limitations of ultrasound examination of the VAs include the inability to visualize the entire artery and in fact that it is highly operator dependent. The features of more sophisticated machines, including the addition of color imaging, have improved the identification of VA dissections. Although these dissections sometimes can be visualized, the VA ostia may be difficult to directly examine with ultrasound, and surrogates (e.g., damped distal waveforms) may be necessary to identify disease at this location. Disease of the intracranial VAs is also not visualized with ultrasound. Despite these limitations, Doppler examination of the VAs can be used as a screening tool and as a means to routinely monitor patients with VA stenosis, both before and after treatment.

Both CT angiography (CTA) and magnetic resonance angiography (MRA) are used to examine the entire VB system, including the VA ostia and intracranial vasculature. CTA requires the injection of iodinated contrast material and may be prohibited in patients with contrast allergies or renal insufficiency. In one study, CTA was found to have a sensitivity of 100% and a specificity of 95.2% for detection of 50 to 99% stenosis of the VA origin. ¹⁹ However, a more recent comparison of ultrasound, CTA, and MRA for the diagnosis of VA stenosis found the sensitivity and specificity of CTA for the diagnosis of > 50% stenosis to be 68% and 92%, respectively. ¹⁸ These rates improved to 80% and 99%, respectively, for the diagnosis of higher-grade stenosis (e.g., > 70%).

MRA can be performed with or without contrast enhancement (e.g., time-of-flight technique). The sensitivity and specificity of time-of-flight MRA for the diagnosis of 50 to 99% stenosis are reported to be 71.4% and 95.1%, respectively. ^{18 , 20 , 21} The addition of contrast material improves these rates to 93.9% and 94.8%, respectively. ^{18 , 22 , 23 , 24} In a blinded evaluation by three radiologists comparing ultrasound, CTA, and MRA, MRA was found to have the highest sensitivity and specificity for the detection of 50 to 99% VA stenosis. ²⁵ However, CTA and MRA were found to be equivalent for the diagnosis of VA origin stenosis.

Although noninvasive imaging techniques (e.g., ultrasound, CT/CTA, and MR/MRA) continue to improve, cerebral digital subtraction angiography (i.e., catheter-based angiography) remains the gold standard for imaging disease of the VB system. Imaging of the entire VB circulation with this modality allows various pathologic conditions responsible for posterior circulation ischemia (including atherosclerosis and dissection) to easily be distinguished. In addition, dynamic imaging can be obtained easily. This technique is particularly valuable for the evaluation of patients noting symptoms associated with specific positions (e.g., bow hunter’s syndrome, which is a rotational occlusion of the VA). However, given the invasive nature of digital subtraction angiography, the risk of iatrogenic stroke or vessel injury is higher than that of noninvasive methods.

The symptoms of posterior circulation ischemia may be vague and nonlocalizing. Therefore, it may be difficult to determine whether a patient is truly symptomatic from VB stenosis. Radio-graphic evaluation for ischemia may aid in the decision-making and treatment algorithms. Demonstration of high-grade steno-sis, particularly with identification of associated restricted diffusion (e.g., evidence of acute stroke) or signs of previous infarct, suggests that the patient is symptomatic and therefore requires treatment.

Treatment Options

Endovascular options are available for most causes of posterior circulation ischemia. Indications and endovascular options for treatment are presented according to the most common sites of disease.

Subclavian Artery Steal or Stenosis

Subclavian steal results in retrograde blood flow down the ipsilateral VA due to proximal subclavian artery steno-sis ( Fig. 23.2 ). Few patients with subclavian steal are symptomatic and require treatment. In their series, Labropoulos et al ²⁶ reported that only 1.4% of 7,881 patients required treatment and that an elevated arm pressure differential (> 40 mm Hg) was more commonly associated with symptoms and the need for intervention. Open surgical techniques for subclavian steal syndrome include carotid-subclavian bypass. This technique has been demonstrated to be safe and effective, with patency rates of 95% at 10 years and very low rates of surgical morbidity. ²⁷ The development of endovascular techniques has changed the management of this disease, maintaining similar technical and clinical results with minimal risk and without the need for general anesthesia.

Endovascular treatment for subclavian artery stenosis includes angioplasty with or without stenting. In 2005, de Vries et al ²⁸ reported their 10-year experience comprising 110 patients treated with angioplasty alone. They noted technical success in 93%, with permanent morbidity in 1%. Patency at 5 years was observed in 89% of patients, and recurrent stenosis was successfully treated with repeat angioplasty in 7% of patients. More recently, Wang et al ²⁹ reported their experience with stenting of proximal subclavian artery obstructions in 61 patients. Technical success was achieved in 95%, with 6.5% procedure-related morbidity. Stent patency was found to be 98% at 1 year, 93% at 2 years, and 82% at 5 years.

Data surrounding angioplasty alone versus angioplasty with stenting for subclavian artery stenosis are limited to retrospective reviews and observational studies. A recent systematic review found stenting to be superior to angioplasty alone with higher patency at 1 year. ³⁰ However, because of the lack of randomized control trials, both a 2011 Cochrane review and its 2014 update found insufficient evidence to favor one treatment over another. ^{31 , 32}

Related posts:

25 Brainstem and Thalamic Intraparenchymal Hemorrhage 29 Endovascular Management of Brainstem and Thalamic Arteriovenous Malformations 30 Surgery for Thalamic and Brainstem Cavernous Malformations 27 Endovascular Management of Aneurysms of the Posterior Circulation 28 Surgical Management of Thalamic and Brainstem Arteriovenous Malformations 31 Revascularization of the Brainstem

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