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99Arterial Ischemia

Valdueza et al., Neurosonology and Neuroimaging of Stroke: A Comprehensive Reference, Second Edition (ISBN 978-3-13-141872-2), copyright © 2017 Thieme Medical Publishers All rights reserved. Usage subject to terms and conditions of license.

Fig. A4.25 Schematics illustrating the area variations of the PCA territory. Horizontal lines indicating maximal PCA perfusion area, additional vertical lines indicating minimal PCA perfusion area. (A) Axial sections from the cella media plane (left) to the basal ganglia plane (right). (B) Medial surface view (top) and lateral s u r f a c e v i e w ( bottom). (Reproduced with permission from van der Zwan et al 1992.)

cell disease, see Case 43), mitochondriopathies, migraine (for further reading, see Case 22), and cerebral venous thrombosis (CVT) (for further reading, see Case 29).

TOAST Classiﬁ cation

Ideally, a stroke classiﬁ cation system should consist of all the aspects discussed above. However, such a classiﬁ ca- tion would be too long and time consuming for everyday clinical application, and therefore it could only be sensibly used in research studies. A practical classiﬁ ca- tion which was also the ﬁ rst proposed system based on stroke mechanism is the TOAST classiﬁ cation. This clas- siﬁ cation includes the radiologic infarct pattern as well as etiological aspects. Nevertheless, it remains compact and manageable, and has a good interobserver agreement (Adams et al 1993). The classiﬁ cation criteria distinguish ﬁ ve groups:

1. Macroangiopathy (large-vessel disease): The presence of a stenosis >50% or occlusion of an intra- or extracranially located brain-supplying artery corresponding to the clinical symptoms and with a territorial cortical infarc-

2. Microangiopathy (small-vessel disease): The presence of a typical lacunar syndrome with normal CT/ MRI or an infarct of <1.5 cm of diameter on CT/MRI without stenosis of an ipsilateral brain-supplying a r t e r y > 5 0 % .

3. Cardioembolism: The presence of a source of cardiac embolism (in general from atrial ﬁ brillation, valvu- lar heart disease, acute myocardial infarction, patent foramen ovale and atrial septum aneurysm, and cardiac masses) with brain infarction in more than one territory or a territorial cortical infarct or subcortical infarct >1.5 cm.

Fig. A4.26 Schematic of ischemic stroke causes. (Adapted from Schünke et al 2006; drawing: Markus Voll.) Note that an intracranial stenosis may cause three types of stroke alone or in combination: artery-to-artery embolism leading to a territorial infarction, hemodynamic ischemia leading to a BZI, and perforator stroke, caused by in-situ (= autochthonic = local atherothrombotic) blockade of a perforating artery at its origin.

Macroangiopathy

(large-vessel disease)

Unknown etiology

22.7%

Concurrent etiologies

Other etiologies

Microangiopathy

(small-vessel disease)

Fig. A4.27 Etiologic subgroups of ischemic stroke according to the Stroke Data Bank of the German Stroke Foundation (Grau et al

2001).

6.9%

3.5%

20.5%

20.9%

25.6%

Cardioembolism

4. Other determined etiologies: E.g., the presence of dissection, vasculitis, coagulopathies, and hematologic disorders.

5. Undetermined etiologies: If the etiology cannot be determined, or a complete examination has not been done, or two or more potential causes of stroke have been found.

Some authors add a subgroup “concurrent etiology” to point 5, which includes those patients in whom at least two potential causes of stroke are present. Applying these criteria, the Stroke Data Bank of the German Stroke Foundation—a multicenter hospital-based stroke registry including 5,017 patients with ischemic stroke—reported the following distribution of stroke pathogenesis:

100 4 Pathogenesis of Stroke

Cardiac embolism (25.6%) was most common, followed by macroangiopathy (20.9%) and microangiopathic causes (20.5%). Other etiologies were rare. Cervical artery dissection, vasculitis, coagulation disorders, hematologic diseases, or nonspeciﬁ ed etiologies were found in

3.5% of cases. No etiology was found in 22.7% of cases, despite complete and extensive investigations in most instances. Concurrent etiologies were observed in 6.9% of cases. In the macroangiopathy group, territorial infarction was present in 89% and BZI in 11% (Grau et al 2001) (Fig. A4.27). In young stroke populations a diﬀ erent pat- tern is observed (Yesilot Barlas et al 2013). For further reading see also Case 6.

Besides its use for clinical studies the TOAST classiﬁ cation also has several limitations which have to be discussed. Its main weakness is that it underrates the macroangiopathic cause in two ways: First, it excludes artery-to-artery embolism from the carotid artery in all cases of distinct atherosclerotic macroangiopathy but stenosis <50%, although such a mechanism is highly likely if no competing causes are present. Second, in-situ atherothrombotic lesions of large basal arteries leading to extended subcortical basal ganglia, capsular, thalamic, or pontine infarction is not included as a stenosis of the parent artery seldom reaches >50%. According to the TOAST criteria these infarctions are then classiﬁ ed as small- vessel disease if the lesions are less than 15 mm, but they ﬁ t better into the category of large-vessel disease. This is of special interest in the Asian population where, in contrast to whites, intracranial arteriosclerosis rather than extracranial arteriosclerosis is the main cause of stroke (Gorelick et al 2008, Kim and Kim 2014, Wong 2006). A further critical point is that two relevant categories, cardioembolism and macroangiopathy, share the same pathogenesis with embolism leading to territorial infarcts. In cardioembolism this mechanism refers to all strokes, as the name implies. In macroangiopathy artery-to-artery embolism is the main mechanism. However, hemodynamic strokes with BZI or impaired embolic clearance may also occur in extra- and intracranial macroangiopathy, and a third possibility, intracranial macroangiopathy (plaque or thrombus formation) causing perforator artery occlusion, has to be taken into account.

A ﬁ rst adaptation of the TOAST system was published in 2005 and called Stop-Stroke-Study TOAST (SSS-TOAST). There, embolic infarctions with stenosis of the corresponding vessel less than 50% were classiﬁ ed as large- vessel disease. The size of lacunar infarcts was changed from <15 mm to <20 mm and even more, if no other stroke category seemed likely. Applying this approach resulted in a marked reduction of numbers in the group of undetermined stroke etiology (Ay et al 2005). In 2009 the ASCO system was presented (Amarenco et al 2009). In this acronym A stands for “atherosclerosis,” S for “small-vessel disease,” C for “cardiac source,” and O for “other causes.” Each of the four categories was additionally graded according to the level of diagnostic certainty: 1, deﬁ nite; 2, potential; 3, unlikely; and 0, absent. A 9 is given if no grading is possible. A patient with atrial ﬁ brillation, small lacunar stroke, and diabetes would be classiﬁ ed as A3-S1-C1-O3. The deﬁ nition of the stroke categories was adapted from the TOAST system. However, the required

grade of ipsilateral intra- or extracranial stenosis for A1 was deﬁ ned to be at least 70% and for A2 to be 50–70%. A couple of years later, the same group extended the score by including a category D for dissection (ASCOD system). Simultaneously, the required grade of stenosis for A1 was changed to 50–99% and for A2 to 30–50% (Amarenco et al

2013)—but the problem of stroke caused by macroangiopathy in cases of stenosis <50% still remains.

Asian proposals to classify stroke mainly focus on intracranial atherosclerosis. Deﬁ ning intracranial stenoses <50% as causative if the stenosis matches the infarction pattern led to a higher proportion of large-vessel disease compared with small-vessel occlusions (J.T. Kim et al

2006). A further modiﬁ cation included the deﬁ nition of a small-vessel stroke if a single subcortical stroke in the territory of a perforator was visible and no macroangiopathy on angiography was detectable (Han et al 2007). Recently a Chinese group suggested considering largeartery disease if any degree of parental artery stenosis or even a plaque was present in high-resolution MRI (Gao et al 2011).

None of the latter proposals has so far become generally accepted and TOAST remains the most used stroke classiﬁ cation system. However, considering the global burden of stroke, the high prevalence of intracranial large-vessel diseases in the Asian population, the above-discussed diverse causes of stroke to be determined, and the advances in noninvasive imaging methods such as high-resolution MRI and ultrasound techniques, new classiﬁ cation systems with worldwide acceptability will inevitably emerge.

Microembolic Signals

Ultrasound permits the detection of spontaneous as well as artiﬁ cially induced microembolic signals (MES) which appear within the Doppler spectrum in the form of high-intensity transient signals (HITS). Spontaneous MES might be derived from embolic sources within the heart or from mostly atherosclerotic vessel wall changes of the brain-supplying arteries. Artiﬁ cial MES, induced by intravenous injection of an echo contrast agent, are used for the detection of right-to-left cardiac or pulmonary shunts (RLS).

Spontaneous Microemboli

Following the introduction of transcranial Doppler (TCD) as a routine clinical diagnostic method more than 30 years ago, the phenomenon of MES assessed by TCD was quickly discovered. The occurrence of MES during carotid endarterectomy in 1990 was the ﬁ rst systematic description (Spencer et al 1990). To date Doppler sonography is still the only diagnostic method that can detect clinically silent emboli originating from the heart or (supra-)aortal vessels. This is easily achieved by continuous Doppler spectrum monitoring of the intracranial arteries but may also be accomplished by monitoring the neck arteries, e.g., the extracranial ICA, if the embolic source is presumed to be located more proximally. For practical reasons (consistent

Fig. A4.28 Spontaneous microembolic signal. TCD, transtemporal

approach. Top and bottom: Doppler spectrum analysis at the carotid-T junction, MCA signal above the zero line, ACA signal below the zero line. Unilateral microembolic signals within the Doppler spectrum. Note that microembolic signals are present in the MCA spectrum only, which is an important criterion for diﬀ erentiation from, e.g., motion artifacts.

and symmetric vessel anatomy) and because of its clinical relevance the main-stem MCA is the most frequently studied vessel. However, MES can be assessed in any of the detectable intracranial arteries including the posterior circulation and the basilar artery (Hwang et al 2012). Recently, transorbital Doppler of the distal ICA was proposed as an alternative approach in patients with an insuﬃ cient acoustic temporal bone window (Saedon et al 2014).

The greatest methodological challenge, which has led

to continuous improvements of the technique, is diﬀ er- entiating between MES and mechanical or electronic artifacts which are most frequently caused by movements of the patient. In 1995 diagnostic criteria were published for the ﬁ rst time:

1. MES have a characteristic clicking or chirping noise that is easy to distinguish acoustically.

2. The signal intensity is ≥3 dB above the background noise level of the Doppler spectrum, usually lasting less than 300 ms.

3. MES occur unidirectionally within the spectrum and have an irregular temporal pattern without any relation to the cardiac cycle (Consensus Committee 1995, Ringelstein et al 1998) (see Fig. A4.28 and Video

A4.1).

Physically, MES are caused by an impedance diﬀ er-

ence between blood and embolus, caused by an increased reﬂ ection of ultrasound waves at the embolus surface. MES can be caused by thrombocyte aggregations, small atheroma particles, fat particles, or small gaseous microbubbles. The signal intensity of a MES increases with its size but also depends on its composition: Gaseous emboli cause higher impedance diﬀ erences than solid par- ticles and solid atheromatous particles result in stronger signals than thrombocyte aggregations. As both factors inﬂ uence signal intensity simultaneously, no conclusion can be drawn about size and composition from the ultrasound signal (Markus and Brown 1993).

101Microembolic Signals

The number of spontaneous MES that can be detected over time varies considerably. In MCA stenosis up to 102 per 30 minutes have been reported (Gao et al

2004). Generally, however, MES counts are far lower. In patients with carotid, aortic, or cardiac embolic sources MES counts vary between 0 and 13 per hour. If analyzed over 4 hours, even more intraindividual variations, e.g., between 0.25 and 8 per hour, can be found (Droste et al

1996). This makes standardized evaluations problematic: they are time consuming and expensive, as ideally long-time online observations over several hours would be required. Furthermore, several approaches including the use of a neuronal network, multichannel techniques, and automated embolus detection have been developed. However, their diagnostic reliability does not yet compare with the analytic abilities of an experienced sonographer (Cullinane et al 2000, Kemény et al 1999, Ringelstein et al 1998). For practical reasons, the current consensus is a compromise and includes detection of microembolic signals over a period of 1 hour.

Clinical Applications

In general, MES originate from the heart or the brain-supplying arteries. MES of cardiac source typically occur bilaterally, i.e., in any insonated vessel. MES caused by supra-aortic vessel diseases usually occur downstream ipsilateral to the side of the embolic source, e.g., an ICA stenosis. However, in the anatomic ACA variant, in which both ACA territories are supplied by one A1-ACA-segment, emboli from an ICA stenosis may also enter the contralateral A2-ACA segment.

MES in Cardiac Sources of Embolism

MES can almost always be identiﬁ ed during cardiac sur- gery, especially during aortic clamping as well as during the initial phase of reperfusion (Barbut et al 1994). A potential relationship between the number of MES and the occurrence of postoperative cerebral ischemia or of neuropsychological deﬁ cits has been postulated (Barbut et al 1997, Clark et al 1999, Sylivris et al 1998). MES can frequently be found in patients with artiﬁ cial heart valves which cause cavitation-induced microbubbles (gaseous MES). The extent of these strongly depends on the type of the implanted valve (Sliwka and Georgiadis 1998). The question whether MES may in addition be caused by emboli from valvular thrombi (solid MES) is still being debated, as an unequivocal diﬀ erentiation between gaseous and solid MES is not possible (Dittrich and Ringelstein

2008). MES have also been observed in other cardiologic conditions such as symptomatic and asymptomatic atrial ﬁ brillation, congestive heart failure, myocardial in- farction, cardiomyopathy, endocarditis, patent foramen ovale, aortic or mitral stenosis, or patients with intracardiac thrombi. The prevalence of MES might be similar between these diﬀ erent cardiac diseases and therefore is not helpful for diﬀ erentiating between them (Sliwka et al 1995). Interestingly, there is so far no evidence that MES are a true predictor of the occurrence of stroke in the above conditions (Cullinane et al 1998, Dittrich and Ringelstein 2008, Georgiadis et al 1997). For instance, in patients with cardioembolic stroke, only 38% of patients

102 4 Pathogenesis of Stroke

demonstrate MES immediately after the event, signiﬁ - cantly decreasing over time (Sliwka et al 1997b).

MES in Arterial Sources of Embolism

A large number of studies have been conducted in carotid surgery. Here, a raised MES incidence correlates with the occurrence of postoperative cerebral ischemia (Ackerstaﬀ et al 1995). In particular the number of postoperative MES seems to correlate with the risk of recurring ischemia and local postoperative thrombosis (Ackerstaﬀ et al 2000, Levi et al 1997). Depending on the applied technique, percutaneous angioplasty might lead to the occurrence of MES. However, a correlation with ischemic events or clinically silent new DWI lesions on MRI has not been found (Jordan et al 1999, Rosenkranz et al 2006).

Numerous studies have analyzed the impact of MES on the stroke risk in carotid stenosis. A meta-analysis of 19 studies conﬁ rmed a signiﬁ cantly higher prevalence of MES in patients with high-grade carotid stenosis and in symptomatic (43%) compared with asymptomatic (10%) carotid stenosis (Ritter et al 2008). In another meta- analysis of eight studies the same authors found a signiﬁ cantly increased risk of TIA and stroke in patients with MES compared with MES-negative cases with symptomatic as well as asymptomatic carotid stenosis. Furthermore, MES in patients with TIA indicate a higher ischemic stroke risk (Liu et al 2013). These ﬁ ndings were conﬁ rmed in a large pro- spective observational trial, the Asymptomatic Carotid Emboli Study (ACES), which analyzed 467 patients with asymptomatic carotid stenosis of at least 70% according to NASCET criteria. The absolute annual risk of ipsilateral stroke or TIA was 7.13% versus 3.04% and remained s i g n i ﬁ cant after controlling for anti platelet therapy, degree of stenosis, and other vascular risk factors (Markus et al

2010). The assumption that MES are an independent risk factor of stroke is supported by further studies. In patients with asymptomatic carotid stenosis a hypoechoic plaque morphology indicates a higher stroke risk which increased signiﬁ cantly further in MES-positive patients (Topakian et al 2011). Neovascularization and inﬂ ammation within the plaques, known as further factors of vulnerability, were also associated with MES occurrence (Moustafa et al 2010, Zhou et al 2013). However, contradictory results have been reported regarding the prevalence of MES in ulcerating plaques (Stork et al 2002, Valton et al 1995). Furthermore, MES seem not to be associated with intraplaque hemorrhage or ruptured ﬁ brous cap, which have been identiﬁ ed as signs of plaque vulnerability in symptomatic carotid stenosis (Truijman et al 2014).

Carotid endarterectomy of ICA stenoses is known to reduce MES (Siebler et al 1994a, van Zuilen et al 1995). Contradictory results have been published regarding the eﬃ ciency of medical secondary MES prevention in symp- tomatic carotid artery stenosis. A ﬁ rst study found that intravenous heparin reduces the number of detectable MES (Siebler et al 1994b) which was not conﬁ rmed by a second study (Georgiadis et al 1994). More consistent data are available regarding platelet aggregation inhibitors. They do reduce the number of MES, and patients who have a medication-induced reduction of MES revealed a notably lower risk of re-ischemia (Goertler et al

2002). Dual antiplatelet therapy with clopidogrel and aspirin more eﬀ ectively lowered MES than aspirin alone in patients with recently symptomatic ICA or MCA stenosis, as has been shown in the CARESS and CLAIR studies (Markus et al 2005, Wong et al 2010). A signiﬁ cant decline of MES and cardiovascular events was reported due to a combined nonmedical and medical therapy of several vascular risk factors (Spence et al 2010). Of note, depending on the underlying stroke etiology, the number of detectable MES changes over time. In many cases they decrease with increasing elapsed time to the ischemic event (Grosset et al 1994, Lund et al 2000).

Acute cervical artery dissection is another cause of MES, especially in patients who present with stroke (Ritter et al 2008). It also indicates a higher risk of stroke in patients with dissection in whom cerebral ischemia is not the initial disease manifestation (Molina et al 2000). Approximately one-third of patients with suspected aortic embolism show MES with a higher prevalence in patients with large plaques compared with patients with smaller plaques (Ritter et al 2008). However, no data exist to indicate whether MES in these patients predict a higher stroke risk.

Unlike extracranial arterial stenoses, asymptomatic intracranial stenoses usually do not cause MES (Segura et al 2001, Sliwka et al 1997a). MES however are present in symptomatic intracranial stenosis with the highest prevalence in the acute stage (Ritter et al 2008). In a large study including 114 patients with acute symptomatic MCA stenosis a high MES count was the only predictor of recurrent stroke (Gao et al 2004). In intracranial MCA stenosis and proximal extracranial ICA stenosis, analyses of pre- and poststenotic MCA segments facilitate the allocation of the embolic source in patients with competing stenoses (Nabavi et al 1996).

In patients with moyamoya disease MES independently predict ischemic cerebral events (J. Chen et al 2014).

In conclusion, MES analysis remains a promising ﬁ eld of research, giving insight into important aspects of stroke pathophysiology. MES monitoring can be considered as an important additional diagnostic tool in patients with symptomatic and asymptomatic carotid artery stenosis to assess the risk of recurrent stroke, but has not yet found its accreditation in diagnostic pathways. The clinical impact in other arterial or cardiac sources of cerebral ischemia remains unclear. Foreseeable potential future indications for MES detection could be the analysis of treatment eﬀ ectiveness, e.g., of diﬀ erent antiplatelet agents in secondary stroke prevention after TIA and stroke and the detection of critical plaques without relevant stenosis. As a monitoring tool in interventions of cardiac surgery and surgery or in interventions of the brain-supplying arteries, TCD is already well accepted worldwide.

Detection of Microemboli in Patent Foramen Ovale

A patent foramen ovale (PFO) is a remnant of the fetal circulation present in 20–30% of the population. It can be directly diagnosed by transthoracic echocardiography (TTE) or by combined contrast-enhanced and color

103Venous Ischemia

Fig. A4.29 PFO detection. (A,B) Bilateral TCD monitoring of the right and left MCA Doppler spectrum. Image during Valsalva maneuver. (A) Grade 3 PFO (>20 HITS, no curtain phenomenon) according to the consensus criteria. (B) Grade 4 PFO (curtain phenomenon).

D o p p l e r m o d e s o f t r a n s e s o p h a g e a l e c h o c a r d i o g r a p h y (TEE), the current gold standard. A recent Medline review of all prospective studies assessing the accuracy of TEE to detect a PFO in comparison to autopsy, cardiac surgery, and/or catheterization found data on 164 patients. The resulting TEE sensitivity was 89.2% and the speciﬁ city

91.4% (Mojadidi et al 2014a). Indirect PFO diagnosis can be achieved by TCD analysis. In comparison to TEE, TCD is more comfortable for the patient, a suﬃ cient Valsalva maneuver (VM) is easier to perform, and moreover the method can detect the rare cases of pulmonary RLS. H o w e v e r , T C D c a n n o t l o c a l i z e t h e s h u n t a n d s h o u l d t h e r e fore be used primarily as complementary test to TEE. In TEE-negative patients, TCD PFO testing might be useful in those with cryptogenic stroke. In a recent meta-analysis of 27 studies with 1968 patients comparing TCD with TEE as the reference, TCD attained 97% sensitivity and 93% speciﬁ city (Mojadidi et al 2014b).

The TCD technique uses intravenously administered air-containing echo contrast agents that are not capable of passing through the pulmonary circulation. In case of a cardiac or pulmonary RLS, these air bubbles pass into the arterial body circulation and can be detected by TCD in the form of HITS (Fig. A4.29). TCCS is also able to detect HITS (Video

4.1). Reports on three types of contrast are avail-

able: mechanically agitated saline containing pure air bubbles alone, agitated gelatin-based solutions (Haemaccel), or D-galactose-based micro air bubbles (Echovist, Bayer HealthCare). The production of Echovist was stopped in 2011 and it is no longer commercially available.

An international consensus meeting (Jauss and Z a n e t t e 2 0 0 0 ) r e c o m m e n d e d a s t r i c t l y s t a n d a r d i z e d protocol for TCD examination. The patient should be studied in a supine position with no relevant head elevation. Preferably both M1-MCA Doppler spectra should be recorded. Examination should be done at rest and during a VM. The VM has to be practiced before the injection of the contrast agent. As a measure of an adequate VM, ﬂ ow velocities during the maneuver fall and will then show an overshoot several seconds after its end. In antecubital

injection (preferably with a large 18-gauge needle), the VM can be started as soon as the injection of intravenous contrast (e.g., a mixture of 9 mL of isotonic saline or gelatine-based solution and 1 mL of air) is ﬁ nished; the injection should not last longer than 5 seconds. In more distal venous injection sites (e.g., near the wrist) the VM should be initiated 5 seconds later. The duration of the VM itself should be at least 10 seconds.

If used in combination with a VM, all TCD studies have been shown to reach a sensitivity of 90% and speciﬁ city be- tween 92% and 100% compared with TEE (Jauss et al 1994, Klötzsch et al1994, Mas 1996). Adding 1 mL of the patient’s own blood to the above mixture results in an improved detection of RLS and signiﬁ cantly increased number of HITS (Gentile et al 2014). Also, the use of a femoral vein injection may be helpful: it has been reported to increase TCD test sensitivity and may be considered in selected cases (Gevorgyan et al 2014, Hamann et al 1998).

The magnitude of the RLS can be semiquantitatively assessed by counting the number of HITS in both MCAs. Following the consensus conference of 2000 on TCD PFO diagnostics, four diﬀ erent grades, separately documented at rest and during VM for each MCA, can be distinguished (Jauss and Zanette 2000):

• Grade 1—normal: No HITS.

• Grade 2—small RLS: 1–10 HITS.

• Grade 3—moderate RLS: >10 HITS and no “curtain.”

• Grade 4—large RLS: “Curtain” pattern with uncounta-

ble HITS.

Some authors subdivide the large RLS category further into a “shower” pattern (>25 HITS) and a “curtain” pattern with uncountable HITS (Serena et al 2008).

The prevalence of RLS is signiﬁ cantly higher in crypto- genic strokes than in strokes of known etiology (atherothrombotic, lacunar, cardioembolic) or in healthy subjects. Particularly large RLS with shower or curtain HITS patterns seem to be strongly associated with cryptogenic stroke and a higher risk of stroke (Serena et al 1998). Small studies suggested that the amount of RLS might correlate with risk of recurrent stroke in patients with PFO-related stroke (An zol a e t a l 20 03) . H owev er, the se ﬁ ndings were not con- ﬁ rmed in a larger prospective study describing a similar stroke risk in patients without or with small or massive RLS (Serena et al 2008). In patients with acute RLS- related ischemic events HITS might rather be associated with a small ischemic lesion than with territorial infarcts (J.W. Kim et al 2013). The clinical impact of PFO detection in cryptogenic stroke, however, is probably low. Three recently published randomized trials, CLOSURE-1, RESPECT, and the PC-Trial, found no signiﬁ cant diﬀ erences between PFO closure, anticoagulation, and antiplatelet therapy regarding the recurrent stroke risk (see also Case 22).

Venous Ischemia

Venous stroke diﬀ ers considerably from arterial is- chemia. It occurs less frequently and often has a subacute temporal pattern. It is often accompanied by headaches, has a high incidence of epileptic seizures and intracranial hemorrhage, responds to heparin treatment, and

104 4 Pathogenesis of Stroke

Ascending veins to the SSS Descending veins to the TS/SiS Deep venous drainage to the StS Descending veins to the SpPS/CS

Fig. A4.30 Schematic of the venous territories of the brain. (Adapted from Schünke et al 2006; drawing: Markus Voll.) CS = cavernous sinus; SiS = sigmoid sinus; SpPS = sphenoparietal sinus; SSS = superior sagittal sinus; StS = straight sinus; TS = transverse sinus.

shows a better potential with regard to regression of clinical symptoms. CVT accounts for <1% of all strokes. It may present suddenly, mimicking arterial stroke, and in rare instances may even result in subarachnoid hemorrhage (Oppenheim et al 2005). The vast majority of patients, however, develop symptoms over days and weeks. Intracranial hemorrhage in arterial ischemic stroke occurs as a reperfusion phenomenon. In CVT, the venous congestion leads to raised venous and capillary pressures, which cannot be compensated for and subsequently results in hemorrhage (Villringer et al 1994). Another diﬀ erence between arterial and venous stroke is the size of the ischemic penumbra which, as shown in animal experiments, seems to be larger in CVT (Frerichs et al 1994). In patients with CVT, the area with a prolonged mean transit time (MTT) in perfusion-weighted MRI can be considered as the morphologic correlate of the penumbra (Doege et al 2001). The large proportion of brain tissue in CVT that is only functionally impaired explains the frequently observed excellent clinical recovery even in cases with delayed diagnosis and when venous congestion infarcts or hemorrhage are present.

Similar to the arterial vascular territories, the venous circulation also comprises areas that correspond to the drainage of particular veins or sinuses (Fig. A4.30). The dorsal frontoparietal regions of the cerebral convexity are drained by ascending superﬁ cial veins, usually 12 on each side, which drain into the superior sagittal sinus. Each vein drains a wedge-shaped area of the frontoparietal cortex. One of these is the slightly dominating superior anastomotic vein (vein of Trolard) located over the postcentral region. Within the descending veins, the inferior anastomotic vein (vein of Labbé) dominates the posterior aspects, draining the blood from the lateral, basal, and posterior temporal lobe and itself draining into the distal end of the transverse sinus, just at the junction to the sigmoid sinus. The anterior regions, especially the areas around the sylvian ﬁ ssure, are drained

Fig. A4.31 Top: Schematic drawing of venous infarct patterns. (Adapted from Schünke et al 2006; drawing: Markus Voll.) Bottom: Corresponding radiologic examples. (A,B) Cortical/ subcortical frontal lobe infarction in ascending vein thrombosis. (C,D) Cortical/subcortical temporal lobe infarction in vein of Labbé thrombosis. (E,F) Bilateral thalamic infarction and basal ganglia i n f a r c t i o n i n d e e p c e r e b r a l v e i n t h r o m b o s i s .

by sylvian veins which then run toward the sphenoparietal sinus and the cavernous sinus. The deep venous system, comprising the paired basal veins of Rosenthal and internal cerebral veins as well as the straight sinus drains the temporomesial regions, large aspects of the basal ganglia and the thalamus. Depending on the affected vessels, a venous thrombosis may lead to a corresponding venous territorial infarction as well as to concomitant clinical symptoms (Fig. A4.31).

Four main clinical patterns can be distinguished relating to the location of thrombosis and involvement of the parenchyma. In thrombosis of the superior sagittal sinus without involvement of the adjacent cortical veins, patients may present with isolated intracranial hypertension, also referred as pseudotumor cerebri. The only clinical manifestations may then be headaches and bilateral papilledema but no focal neurologic signs. Sometimes an additional horizontal diplopia may occur, caused by cranial nerve VI palsy. In the second and most common variant an extension of thrombosis to the ascending frontoparietal cortical veins will lead to circumscribed wedge-shaped infarctions which may resemble circumscribed arterial cortical infarction. Focal motor or sensory deﬁ cits may be present and are often associ- ated with focal seizures with secondary generalization. The risk of seizures is particularly high if the Rolandic vein within the central sulcus or the vein of Trolard in the postcentral sulcus is aﬀ ected. Depending of the site of a cortical vein thrombosis a variety of cortical signs and neuropsychological syndromes may occur. Because of the predominant distal aﬄ iction, the leg tends to be more aﬀ ected, and bilateral signs may be observed. In transverse sinus occlusion, local signs such as otalgia and cervical tenderness may be present. Venous infarction within the temporal lobe may lead to aphasia or other neuropsychological deﬁ cits including confusion if the vein of Labbé is aﬀ ected. Venous temporal lobe in- farction may resemble partial territorial MCA infarction

105Venous Ischemia

or herpes encephalitis. Thrombosis of the deep venous system is the third typical pattern which mainly leads to unilateral or bilateral infarctions of the basal ganglia and/or the thalamus. Bilateral thalamic infarctions may also be caused by arterial stroke if both thalamoperforating arteries are aﬀ ected, but the resulting infarct area is usually smaller in size and spares the dorsal thalamic region. Clinically, not only alterations of mood and

consciousness but also extrapyramidal signs have been observed. The last pattern to be mentioned is (mostly infectious) cavernous sinus thrombosis which is now rarely observed. Local signs including orbital pain, chemosis, exophthalmus and cranial nerve III–VI palsies are typical signs. For neuroimaging and neurosonology in CVT, see also Chapter 5, “Cerebral Venous Thrombosis” under “Venous Pathology,” and Case 29.

106

Vascular Pathology

Arterial Pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 106

Vessel Wall Pathology . . . . . . . . . . . . . . . . . . . . . . . . . . 106

Tortuosity . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 107

Intima-media Thickness . . . . . . . . . . . . . . . . . . . . . . 108

Atherosclerotic Plaques . . . . . . . . . . . . . . . . . . . . . . 108

Arterial Stiﬀ ness . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113

Dissection . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 113

Fibromuscular Dysplasia (FMD) . . . . . . . . . . . . . . . . 114

Vasculitis/Arteritis . . . . . . . . . . . . . . . . . . . . . . . . . . . 115

Carotidynia and Carotid Artery Vasospasm . . . . . . 115

Stenoses and Occlusions . . . . . . . . . . . . . . . . . . . . . . . . 118

Ultrasound Criteria of Stenoses . . . . . . . . . . . . . . . . 118

Ultrasound Criteria of Occlusions . . . . . . . . . . . . . . 125

Extracranial Pathology . . . . . . . . . . . . . . . . . . . . . . . . . . 125

Extracranial Anterior Circulation . . . . . . . . . . . . . . . 125

Extracranial Posterior Circulation . . . . . . . . . . . . . . . 133

Intracranial Pathology . . . . . . . . . . . . . . . . . . . . . . . . . . 138

Stenoses . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 138

Occlusions . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 144

Intracranial Posterior Circulation . . . . . . . . . . . . . . . 153

Collateral Pathways . . . . . . . . . . . . . . . . . . . . . . . . . . . . 161

Intracranial Collateral Pathways . . . . . . . . . . . . . . . . 162

Intracranial Collateral Pathways in ICA

Occlusive Processes . . . . . . . . . . . . . . . . . . . . . . . . . 167

Intracranial Collateral Pathways in VA

Occlusive Processes . . . . . . . . . . . . . . . . . . . . . . . . . 172

Extracranial Collateral Pathways in VA

Occlusive Processes . . . . . . . . . . . . . . . . . . . . . . . . . 173

Clinical Relevance of Collateral Pathways . . . . . . . . 173

Venous Pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . 175

Cerebral Venous Thrombosis . . . . . . . . . . . . . . . . . . . . 175

Superior Sagittal Sinus Occlusion . . . . . . . . . . . . . . 175

Deep Cerebral Venous System Occlusion . . . . . . . . 176

Lateral Sinus (Transverse and Sigmoid Sinus)

Occlusion . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 176

Flow Abnormalities in Cerebral

Venous Thrombosis . . . . . . . . . . . . . . . . . . . . . . . . . . 176

Ultrasonography of the Internal Jugular

Vein in Intensive Care Patients . . . . . . . . . . . . . . . . . . . 178

Central Venous Cannulation . . . . . . . . . . . . . . . . . . 178

Indirect Assessment of Central Venous

Pressure (CVP) . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 178

Intracranial Stroke-related B-mode

Pathology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 178

Ventricles . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 178

Hydrocephalus . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 179

Papilledema and Optic Nerve Sheath Diameter . . . . . 179

Midline and Midline Shift . . . . . . . . . . . . . . . . . . . . . . . . 180

Intracranial Hemorrhage . . . . . . . . . . . . . . . . . . . . . . . . 180

Parenchymal Hemorrhage . . . . . . . . . . . . . . . . . . . . 180

Subdural and Epidural Hematoma . . . . . . . . . . . . . . . . 182

Arterial Pathology

Vessel Wall Pathology

On review of the arteries supplying the brain, diﬀ erent types of vascular and vessel wall alteration as well as different preferential sites may be observed in the large arteries. These changes can be physiologic in nature or may represent true pathologic ﬁ ndings.

In atherosclerosis, nonlaminar ﬂ ow in the carotid bulb as well as in the area of bifurcations favors the formation of atheromas and stenoses, which explains their preferential sites. Other pathologies are strictly extracranially located, aﬀ ecting the proximal segments as in Takayasu’s arteritis or the distal segments as in the dissections, the latter in part explained by the vessel segments prone to motion stress and in part by the vessel wall composition which may play a role in ﬁ bromuscular dysplasia. In contrast,

AB C

Fig. A5.2 DSA, selective CCA ﬁ lling, lateral view, of three patients with distinct coiling (arrows) of the extracranial ICA: (A) in the distal segment (not accessible to ultrasound); (B) in the middle (sometimes accessible to ultrasound); (C) proximal ICA (readily accessible to ultrasound).

107Arterial Pathology

Fig. A5.1 Distribution pattern of macroangiopathic lesions in

the brain-supplying arteries. Pink = atherosclerosis (unilateral or bilateral), green = ﬁ bromuscular dysplasia (bilateral), dark blue = Takayasu’s arteritis (bilateral), light blue = dissection (mostly unilateral), gray = carotidynia (unilateral), yellow = moyamoya (mostly bilateral carotid-T, rare in the proximal PCA), Dotted lines indicate the junction of the extracranial and intracranial vessel segments.

moyamoya strictly involves intracranial vessels, again presenting a typical pattern at the carotid-T, but also in the proximal posterior cerebral artery (PCA) (Fig. A5.1).

Tortuosity

Vessel tortuosity is a frequent ﬁ nding in extracrani- al brain-supplying arteries (Fig. A5.2) and can often be visualized by duplex ultrasound in proximal locations (Fig. A5.3). The general reported incidence varies between 10% and >40%, depending on the population studied (Ballotta et al 2005, Huber 1982, La Barbera et al 2006, Perdue et al 1975, Togay-Işikay et al 2005, Weibel and Fields 1965). Age and continuous strain due to long-term arterial hypertension as well as vessel wall alterations within the tunica media of the aﬀ ected arteries have been suggested as potential underlying precipitants (Del Corso et al 1998, La Barbera et al 2006). Vessel tortuosity can be diﬀ erentiated into three main groups (Fig. A5.4):

Fig. A5.3 Extracranial duplex, longitudinal view. Left: B-mode insonation revealing an S-shaped ICA elongation. Right: Color-mode image of the same vessel segment.

• C- or S-shaped elongation with angles >90°.

• Coiling of the artery up to 360°.

• Kinking, considered as a variant of coiling with an angle <90°, likely to result in a lumen reduction and subsequent vessel narrowing.

Within the internal carotid artery (ICA), a straight vessel course is seen in 65–70% of individuals, a curved course in 23%, and coiling (including kinking) in 9–16%. Following Weibel an d Field s ( 1965 ) an in itial tor tuous C- or S-shaped elongation over ~4 cm in length occurs twice as often bilaterally as unilaterally, usually aﬀ ecting individuals old- er than 50 years. Coiling is usually found 4–8 cm distal of the bifurcation without side-to-side preferences and equal frequency bilaterally and unilaterally without any reported age dependency. Routine ICA ultrasound insonation should therefore be performed over the whole visible vessel length and as far distally as possible. Kinking predominantly involves the ICA, 2–4 cm distal of the bifurcation and is

108 5 Vascular Pathology

Fig. A5.4 Left: Schematic of the three types of vessel tortuosity: (A) C- or S-shaped elongation with angles >90°, (B) coiling of the vessel up to 360°, (C) kinking with angles <90°. Right: Corresponding color-mode images.

more common in elderly people. Unilateral kinking is twice as frequent as bilateral. There are no extensive analyses on the prevalence of kinking and the related grade of stenosis. The clinical importance of these vessel changes is under debate. Some authors regard elongations as an anatomic variant without any clinical implications (Togay-Işikay et al

2005), whereas others consider them to be responsible for symptomatic cerebrovascular disease (Ballotta et al 2005). Particularly problematic in this context is that elongations and atherosclerotic vessel changes frequently coexist, so a conﬁ dent diﬀ erentiation of causal proportion is diﬃ cult. Whenever elongations are found in symptomatic patients, careful consideration should be given to whether the symptoms match the aﬀ ected vessel and if other potential causes are not being overlooked. Kinking and coiling seem to be related to carotid artery dissection (Saba et al 2014) whereas vessel elongations or tortuosity are not (Dittrich et al 2011).

Intima-media Thickness

Within the process of developing atherosclerosis the ﬁ rst observable sign of vascular alteration may be an increasing intima-media thickness (IMT). However, increased IMT may not only reﬂ ect atherosclerosis but may also occur in other conditions that lead to smooth muscle cell hyperplasia or ﬁ brocellular hypertrophy (Touboul et al

2012). IMT can only be analyzed with duplex ultrasound. High insonation frequencies increase the spatial resolution and are therefore recommended. According to the Mannheim consensus criteria, IMT is deﬁ ned as follows: IMT is a double-line pattern visualized by B-mode sonography on both walls of the carotid arteries in a longitudinal image. It is made up of two parallel lines, which consist of the leading edges of two anatomic boundaries: the interface between the lumen and the intima and the interface between the media and adventitia (Fig. A5.5). IMT measurements should be performed in regions without atherosclerotic plaque, preferably in the CCA, but may also be

0.5 mm

QIMT 459 µm SD 13 µm

Fig. A5.5 Extracranial duplex, B-mode insonation, longitudinal view. Top left and ri ght : Single-point manual measurement of a normal (0.5 mm) and a pathologically raised IMT (1.4 mm) of the CCA. Bottom left and right: Multipoint automated IMT measurements of the CCA over a 2-cm distance given as mean ± standard deviation (normal 0.459 ± 0.013 mm, pathologic 1.326 ± 0.095 mm).

1.4 mm

QIMT 1326 µm SD 95 µm

performed in the carotid bulb as well as the ICA. If possible, measurements should be made on the far wall as near-wall evaluations are less reliable. Either manual measurements or an automated system can be used for IMT determination (Fig. A5.5). The latter allows repeated measurements with- in a predeﬁ ned vessel segment (preferably ≥10 mm) in a short time, the former requires rigorous quality control to keep the intra- and interobserver variability low (Touboul et al 2012). No consensus exists regarding the question of whether the maximum IMT or a mean IMT should be used and if the right and the left side should be averaged, as IMT values seem to be higher on the left side (Rodríguez Hernández et al 2003). Population-based values of IMT vary depending on age, gender, and ethnicity (Tabl e A5 .1) (Howard et al 1993). There is no clear accepted deﬁ nition of a raised IMT but a size >1 mm is generally considered abnormal. Raised IMT values have been associated with several classic vascular risk factors such as hypertension, smoking, cholesterol, homocysteine levels, C-reactive protein, and the presence of a metabolic syndrome or coronary artery disease (Crouse 2006). Prospective analyses have demonstrated that raised IMT values are associated with an increased number of myocardial infarctions and stroke in the elderly population, indicating a predictive value for future vascular events (Lorenz et al 2007, O’Leary et al 1999, Polak et al 2011, Silvestrini et al 2013).

Atherosclerotic Plaques

Loss of laminar ﬂ ow at a bifurcation or vessel widening like the carotid bulb leads to increased vessel wall shear stress and subsequently causes initiation and promotion of vessel wall arteriosclerosis and plaque formation in conjunction with vascular risk factors and age. It seems that the left carotid bulb is more vulnerable than the right for the development of atherosclerosis. In a large stroke-free population studied using MRI, bilateral plaques were seen in 85% but unilateral plaques were twice as prevalent on

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