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89Parameters of Cerebral Hemodynamics

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.

in our case series led, as hypothesized, to a distinct decrease in CBF and increased CCT but only to a nonsignificant trend toward a reduced CBV. As a simple bedside test, the method has the potential to help char-

acterize the hemodynamic state of patients in danger of raised intracerebral pressure, such as those with head trauma, intracranial hemorrhage, or global cerebral hypoxia.

Table A3.3 Cerebral blood volume (CBV) data. Depending on the method used, either relative (/100 g) or global values are given. Values in italics are calculated data, assuming an average brain weight of 1,400 g (Ho et al 1980).

Authors Method CBV/100 g Global CBV

Nylin et al 1961

P erythrocytes 6.9 mL 97 ± 6 mL

Grubb et al 1978 PET 4.3 ± 0.4 mL 60 mL

Phelps et al 1979 PET 4.2 ± 0.4 mL 59 mL

Sakai et al 1985 SPECT 4.8 ± 0.4 mL 67 mL

Reinstrup et al 2001 SPECT 4.3 ± 0.6 mL 60 mL

Steiger et al 1993 CT 5.8 ± 1.2 mL 82 mL

Muizelaar et al 1997 CT 6.1 ± 0.9 mL 85 mL

Rempp et al 1994 MRT 6.6 mL 92 mL

Vonken et al 1999 MRT 5.6 mL 78 mL

Elwell et al 1994 NIRS 2.9 ± 1 mL 41 mL

Doepp et al 2003 Ultrasound 5.5 mL 77 ± 13 mL

X. Liu et al 2014 Ultrasound 5.3 mL 74 ± 19 mL

Pathogenesis of Stroke

Arterial Ischemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90

Pathophysiology . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 90

Classiﬁ cation of Arterial Stroke . . . . . . . . . . . . . . . . . . . 91

Microembolic Signals . . . . . . . . . . . . . . . . . . . . . . . . . 100

Arterial Ischemia

Pathophysiology

The pathophysiologic correlate of cerebral ischemia is the inadequate delivery of glucose and oxygen to the brain. This is caused by a critical reduction of cerebral blood ﬂ ow (CBF), mostly due to occlusion of a brain-supplying vessel. On the basis of early animal studies (Astrup et al 1981, Heiss 1983) and positron emission tomography (PET) analyses in acute stroke patients (Baron 1999) a “three-compartment” model of stroke comprising different degrees of CBF reduction has been developed. The three compartments of the model are the ischemic core, the penumbra, and a surrounding region of oligemia (Fig. A4.1). Normal CBF is ~50–60 mL/100 g per minute (Kety 1950). CBF within the ischemic core is <20% of

Fig. A4.1 Schematic of the three compartments of cerebral ischemia: 1 = ischemic core (CBF <10 mL/100 g per minute); 2 = penumbra (CBF 10–20 mL/10 0 g per minute); 3 = oligemia (CBF 20–50 mL/100 g per minute).

Spontaneous Microemboli . . . . . . . . . . . . . . . . . . . . . . 100

Detection of Microemboli in Patent

Foramen Ovale . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 102

Venous Ischemia . . . . . . . . . . . . . . . . . . . . . . . . . . . . . . 103

normal values (<10 mL/100 g per minute) which leads

to irreversible tissue damage. The core is surrounded

by the penumbra—an inhomogeneous zone with a crit-

ical reduction down to 20–40% of normal CBF values

(10–20 mL/100 g per minute), which is below the func-

tional threshold but above the threshold for morphologic

integrity. Depending on the pace and magnitude of rep-

erfusion and the functionality of collaterals, the ﬂ ow in

the penumbra may either completely normalize without

induction of structural damage and with improvement of

clinical symptoms, or it may further decrease and lead to

an enlargement of the ischemic core. The penumbra itself

is surrounded by a region of oligemia with only mildly

reduced CBF values (20–50 mL/100 g per minute) which

is equally inﬂ uenced by the above factors. In addition, the

time factor is as important as the magnitude of hypoper-

fusion. Within 3 hours of stroke onset a penumbra can be

found in the majority of patients which may persist for

more than 16 hours (Baron 1999), but may also last for

more than 24 hours as we know from clinical experience.

For analysis of the ischemic penumbra in a clinical

setting, magnetic resonance imaging (MRI) using diﬀ u-

sion-weighted imaging (DWI) and perfusion-weighted

imaging (PWI) has almost completely replaced the PET

technique. The MR-deﬁ ned penumbra is determined by

the mismatch between the area of impaired diﬀ usion

(i.e., ischemic core) and the area of impaired perfusion

(DWI–PWI mismatch). However, there are some meth-

odological peculiarities of MRI that need to be consid-

ered. Not all areas with impaired diﬀ usion will result

in infarction. In fact, there is some regression of the

MRI-deﬁ ned infarct core in up to 20% of cases within

a 6-hour time window (Fiehler et al 2004). Further-

more, MRI and PET-deﬁ ned penumbra is not congruent

although an MRI-determined time-to-peak (TTP) de-

lay between 4 and 6 seconds seems to correspond well

with a PET-derived CBF <20 mL/100 g per minute (Heiss

et al 2004).

91Arterial Ischemia

Despite these shortcomings, the MRI mismatch con-

cept allows us to suﬃ ciently identify the brain tissue with critically low perfusion and therefore enables selection of patients with regard to intravenous thrombolysis within the 4.5–6-hour time window.

In contrast with myocardial ischemia, in which local atherosclerotic vessel wall disease is practically the only underlying pathomechanism, in ischemic stroke a variety of etiologies have to be considered. Cerebral ischemia can be classiﬁ ed according to several diﬀ erent criteria, e.g., by the temporal pattern, by the infarct pattern, by the a ﬀ ected vascular territory, by its etiology, and ﬁ nally by its pathogenesis. Usually all these criteria will be incorporated into the ﬁ nal diagnosis, although an exact classiﬁ - cation is not always possible. Also, stroke mimics such as migraine with aura, Todd paresis following focal seizures, peripheral vestibular syndromes, neuropathies, acute hypoglycemia, and cerebral venous thrombosis may be challenging, especially in the acute stage of the disease. The following section presents the diﬀ erent approaches to stroke classiﬁ cation.

Classiﬁ cation of Arterial Stroke

Temporal Pattern

The temporal pattern is an important aspect from both the clinician’s and the patient’s perspective. If clinical symptoms completely cease within 24 hours of stroke onset, the episode is deﬁ ned as a transient ischemic attack (TIA), whereas persisting symptoms are deﬁ ned as a com- pleted stroke. The concept of a reversible ischemic neurologic deﬁ cit (RIND)—symptoms that do not last longer than 7 days—has been abandoned as it falsely suggests transient ischemia without a morphologic correlate. The deﬁ nition of a TIA, which was developed at a time when the current imaging methods were not available, is also under critical review now, as it suggests that no structural damage has occurred. The term “acute cerebrovascular syndrome,” analogous to the “acute coronary syndrome,” was recently proposed by Japanese groups instead of the term TIA (Okada 2014). MRI sequences, including DWI, show that small structural lesions can be found in up to 60% of cases after a TIA (Brazzelli et al 2014). TIA-related DWI abnormalities are associated with prolonged duration of TIA (Inatomi et al 2004). Although they may regress completely in a short time (Carpentier et al 2012), their presence indicates a higher risk of subsequent stroke (Redgrave et al 2007). In addition, the arbitrary 24-hour cut-oﬀ seems problematic. About half of all TIAs are lim- ited to 30 minutes duration. If the symptoms last longer than an hour, the probability of a clinical deﬁ cit that will persist beyond the 24-hour cut-oﬀ reaches 86% (Levy

1988). Furthermore, the start of symptoms may represent not the onset of vessel occlusion but the onset of collateral failure, which also indicates the need to redeﬁ ne our con- cepts of cerebral ischemia by shifting from a clinical timebased to a morphology-based view of stroke.

Nevertheless, the term TIA is of great practical importance as it points out the risk of developing a subsequent completed stroke and therefore requires urgent etiological clariﬁ cation. In a meta-analysis of patients with

completed stroke, 23% reported a prior TIA. Of these, 43% had their last TIA within the week before and 17% on the day of the completed stroke. The TIAs and the subsequent strokes were mostly located within the same vascular territory (Rothwell and Warlow 2005). The risk of having a completed stroke after TIA is especially high in patients with an intracranial vessel occlusion or with a lesion on DWI MRI. Coutts et al (2005) found that the 90-day stroke risk in patients without intracranial vessel occlusion and without a DWI lesion was 4.3%, increasing to 10.8% in those with a positive DWI ﬁ nding alone and to 32.6% in those with an additional intracranial vessel occlusion. The overall 90-day stroke risk was 11.7%. In patients with a symptomatic ICA stenosis the 90-day stroke risk was

20.1% after a hemispheric TIA (Eliasziw et al 2004). Based on clinical data alone and considering age (A), blood pressure (B), clinical signs (C), duration of symptoms (D), and diabetes (D) an ABCD2 score was developed (Johnston et al 2007). The stroke risk after a TIA within 2 days was highest with 8.1% probability in patients aged 60 years or over with vascular risk factors, motor symptoms, and duration longer than 1 hour. Considering the heterogeneous data it becomes clear why the current concept of TIAs is under debate. A useful proposition might be to limit the diagnosis of TIA to neurologic deﬁ cits persisting less than 1 hour and in those in whom DWI MRI does not depict structural lesions (Albers et al 2002).

Infarct Pattern and Vascular Territory

Stroke requires cerebral imaging. In most places the ﬁ rst imaging modality is cranial CT (CCT) which is often followed by cerebral MRI. CCT is a well-established method of excluding intracranial bleeding (e.g., intracerebral hematoma, subarachnoid hemorrhage, subdural and epidural hematoma) which can be found in up to 15% of stroke patients. More recently, MRI with its blood-sensitive susceptibility weighted and T2* weighted, as well as ﬂ uid attenuated inversion recovery (FLAIR) sequences, have been shown to be able to detect intracranial hemorrhage with a sensitivity equal to that of CCT or even better. CCT, and better MRI, allow classiﬁ cation of ischemic infarcts according to their pattern and corresponding v a s c u l a r t e r r i t o r y . W e c o n s i d e r t e r r i t o r i a l i n f a r c t i o n s , lacunar infarctions, and border zone infarctions as i n d e p e n d e n t e n t i t i e s ; t h e l a t t e r m a y d e v e l o p w i t h i n o n e vascular territory or between several vascular territories.

Territorial Infarction

The brain comprises circumscribed regions that are supplied with blood via one main artery and its tributaries (Fig. A4.2). The classic concept that blocking a certain ar- tery leads to infarction of the complete territory of supply has been refuted. Due to the extensive pattern of extra- and intracranial collateral ﬂ ow a territorial infarct may there- fore either incompletely (partial territorial infarction) or completely (total territorial infarction) involve the area of a brain-supplying artery. The underlying pathogenesis in these cases is an intracranial arterial occlusion of the dedicated artery. In elderly patients these occlusions are mostly of embolic nature, for example deriving from a

92 4 Pathogenesis of Stroke

Anterior cerebral artery (ACA) Middle cerebral artery (MCA) Posterior cerebral artery (PCA) Anterior choroidal artery (AChA)

Fig. A4.2 Schematic of the arterial territories of the brain. Left: Axial plane. Right: Coronal plane. (Adapted from Duus et al

2005.).

cardiac source or from upstream macroangiopathic vessel wall alterations. However, an in-situ atherothrombosis on the basis of preexisting macroangiopathy may also be present (Lhermitte et al 1970). In younger patients rare conditions such as vasculitis, dissection, and vasoconstriction or nonatherothrombotic in-situ thrombosis with underlying genetic predisposition have to be considered.

The infarct size depends on several factors. In cases with an embolic event the location of the occlusion (proximal or distal), the duration of the occlusion, and the quality of the leptomeningeal collaterals (LMC) determine the dimension of the induced lesion; for further details about leptomeningeal collaterals, see Chapter 5, “Secondary Collaterals (Ophthalmic Artery and Leptomeningeal Collaterals)” under “Intracranial Collateral Pathways”/“Intracranial Collateral Pathways in ICA Occlusive Processes.” In the following, examples are given of the most commonly aﬀ ected intracranial artery, the middle cerebral artery (MCA). In case of a main-stem M1-MCA occlusion, which includes the lenticulostriate arteries (LSAs), total MCA territorial infarction will occur if timely r e c a n a l i z a t i o n d o e s n o t o c c u r a n d i f t h e L M C a r e i n s u f ﬁ cient (Fig. A4.3). If good LMC are present, the infarct size may—despite an identical location of the occlusion— be restricted to the striatocapsular area. In M1-MCA occlusion, this region is almost always aﬀ ected as the LSAs supply blood to end zone territories that are not reached by other vessels (Fig. A4.4). Occasionally, LSAs may in part or completely arise from a proximal M2-MCA branch, especially if the M1 segment is short, in which case an M1-MCA occlusion might not aﬀ ect the basal gan- glia. In between these two extremes diﬀ erent patterns of partial territorial infarctions with variable sizes, with or without subcortical involvement, can be observed in patients with a proximal MCA occlusion. Preserved “cortical islands” that derive their blood supply from LMC are a frequent ﬁ nding (Fig. A4.5). In case of an M1-MCA oc- clusion distal of the LSA origin, the basal ganglia will be preserved. In a “best case scenario” a circumscribed distal M1-MCA occlusion could be endured without infarction— but only in the case of excellent leptomeningeal blood supply and if embolus fragments have not migrated into

Fig. A4.3 Var iants o f MC A terri torial infa rcti on in p roxim al M 1 - M C A o c c l u s i o n . C r a n i a l C T , a x i a l p l a n e . ( A) Hyperdense media sign (arrow). (B) Complete MCA infarction.

Fig. A4.4 Var iants o f MC A terri torial infa rcti on in p roxim al M 1 - M C A o c c l u s i o n . C r a n i a l C T , a x i a l p l a n e . ( A) Hyperdense media sign (arrow). (B) Partial MCA infarction leading only to a large s t r i a t o c a p s u l a r i n f a r c t .

Fig. A4.5 Variants of MC A terr itorial i nfarc tion in proxi mal M1-M CA occlusion. (A) Cerebral DW MRI, axial plane. Large MCA infarct with a vital parenchymal “island.” (B) Cerebral MRI, FLAIR image, axial plane. Large MCA infarct predominantly within the frontal and parietal opercula sparing most of the temporal parenchyma.

93Arterial Ischemia

Fig. A4.6 Varian ts of MC A terr itorial infa rction in dista l M1-M CA

occlusion. Cerebral DW MRI, axial plane. (A) Partial, predominantly subcortical MCA infarct with spots of cortical involvement. (B) Partial MCA infarct aﬀ ecting mainly the insula and sparing the basal ganglia.

the periphery. Most commonly, however, an inhomogeneous partial territorial infarct is seen, involving a variable amount of the corresponding cortex (Fig. A4.6). Apart from large and almost total striatocapsular infarction other subcortical infarct patterns may also occur in the centrum semiovale which may be diﬃ cult to distin- guish from lacunar stroke (Wessels et al 2005). If an MCA branch occlusion is present, the size (large or small) and extent (complete or incomplete) of infarction depends on the site of occlusion and the time-course of recanalization (Fig. A4.7). Because of their mostly clear localization, supratentorial infarctions are usually named according to the aﬀ ected vascular territory.

The distribution pattern of strokes in the anterior and posterior circulation roughly resembles the relation of both territories with regard to the total CBF. In a clinically orientated, community-based study of 675 patients, 68% of territorial infarctions were assumed to aﬀ ect the anteri- or and 32% the posterior circulation (Bamford et al 1991). An identical proportion (68%) of strokes in the anterior circulation was found in the hospital-based Lausanne stroke registry, which included 1,000 consecutive stroke patients who underwent CCT diagnostics. Distribution of infarcts within the anterior circulation was as follows: 96% within the MCA, 3% within the ACA, and 1% combined within the MCA and ACA territories. Embolic ACA infarctions are rare because of the ACA’s unfavorable angulation at the distributary from the terminal ICA. Emboli therefore tend to follow the ﬂ ow into the MCA. Large ACA vessels, e.g., also feeding the contralateral ACA or having a diameter similar to the ipsilateral MCA or larger, favor emboli into the ACA territor y (Shoamanesh et al 2014). Vertebrobasilar and PCA territory ischemia was seen in 26% of patients. Hemodynamic infarction and mixed patterns were seen in 3% of cases. Lacunar infarcts in this study were attributed to the corresponding vascular territory (Bogousslavsky et al 1988). Clinically, supratentorial territorial and lacunar or infratentorial ischemia can be diﬀ erentiated as the for- mer demonstrates cortical signs such as aphasia, apraxia, hemineglect, visuospatial impairment, and hemianopsia

Fig. A4.7 Va riants of ter ritor ial MCA inf arct ion in MC A bran ch o c c l u s i o n . C e r e b r a l D W M R I , a x i a l p l a n e . ( A) Large left anterior partial MCA infarction of an M2/3 segment leading to Broca’s aphasia. (B) Small left cortical MCA infarction within the left precentral gyrus (Rolandic artery, M4) leading to right brachiofacial hemiparesis.

Fig. A4.8 Microcirculation of the brain. (A) Schematic. (Adapted from Spatz 1939, Fig. 1, with kind permission of Springer Science and Business Media.) (B) Postmortem angiogram, axial plane: Note the distinct ramiﬁ cation of small perforating arteries in the basal ganglia. (Adapted from http://www.radnet.ucla.edu/sections/DINR/Part%2018/Part18B11.htm by courtesy of Professor G. Salamon, Radiology, UCLA, Los Angeles, USA).

in combination with motor or sensorimotor deﬁ cits. How- ever, large subcortical and thalamic infarcts can present similar signs but have a somewhat better prognosis.

Lacunar Infarction

Lacunar infarctions result from occlusion of small arterial branches or a single perforating artery itself. They have an average diameter between 100 μm and 400 μm, and arise directly from much larger arterial vessels in a perpendicular direction (Fig. A4.8). Causes of lacunar stroke may vary and are subject of ongoing debate (Del Bene et al 2013, Wardlaw 2005). Histopathologic analysis of smaller lacunar infarcts often reveals nonatherosclerotic subintimal vessel wall hyalinosis, lipohyalinosis, and ﬁ brinoid necrosis (Lammie et al 1997). Hypertension and diabetes

94 4 Pathogenesis of Stroke

Fig. A4.9 Morphologic variants of supratentorial microangiopathy. (A) Cerebral DW MRI, axial plane. Right-sided lacunar thalamic infarct assumed to correspond to small-vessel disease. (B) Cerebral MR T2-weighted image, axial plane. Pronounced periventricular conﬂ uent white matter changes (leukoaraiosis), predominantly in the parietooccipital area, and small lacunar lesions of the basal ganglia.

mellitus are predisposing factors for this type of vessel affection but may clinically be overlooked. Larger perforating arteries may show a proximal intraluminal atheroma, also called arteriolosclerosis, or an atherosclerotic plaque located at the origin of the vessel. Also a small embolus may enter and occlude an LSA as has been demonstrated in a monkey model (Macdonald et al 1995). However, a single small subcortical infarction is most unlikely to be caused by a proximal embolic source, as the embolus would need to pass the unfavorable branching-oﬀ of the perforating artery from the parent artery. Even in the presence of a suggestive cardioembolic cause, such as atrial ﬁ brillation other etiologies should be taken into account whenever cortical areas are spared by the ischemia. The most frequently aﬀ ected perforating arteries are the LSA arising from the MCA stem, the thalamoperforating and thalamogeniculate arteries arising from the proximal PCA and posterior communicating artery, and the paramedian branches of the BA. Corresponding infarcts are usually found within the basal ganglia, the internal and external capsule, the centrum semiovale, the t h a l a m u s , a n d t h e b r a i n s t e m , m a i n l y p o n t i n e ( Fig. A4.9 and Fig. A4.10). Lacunar infarcts are by deﬁ nition small, not exceeding 15 mm, most of them being smaller than 10 mm. The true dimension of a subcortical infarct can only be determined if at least two MR planes are used. Infarctions with a small round or oval shape in all imaging planes are true microinfarctions due to nonatherosclerotic vessel diseases (Fig. A4.10 and Fig. A4.11). In contrast, an infarct appearing small and oval-shaped in one plane but tubular, club-, or fan-like-shaped in at least one of the other two planes and exceeding the above-deﬁ ned 15 mm can be considered as in-situ (local) thrombotic or atherothrombotic (in atherosclerosis), i.e., aﬀ ecting the complete vascular area of a single perforating artery (see “Infarctions of Uncertain Classiﬁ cation” below).

Most lacunar strokes present as characteristic syn-

dromes as they aﬀ ect the above-mentioned circum- scribed brain regions. These are generally pure motor

Fig. A4.10 Variants of lacunar paramedian pontine stroke assumed to correspond to small-vessel disease. Top: Cerebral DW MRI, axial plane. Bottom: T2-weighted images, sagittal plane. (A) Medium-sized left-sided paramedian pontine infarct. (B) Small left-sided pontine infarct (arrow).

Fig. A4.11 (A) Cerebral DW MRI, axial plane. Right-sided lacunar thalamic infarct assumed to correspond to small-vessel disease. (B,C) Cerebral MR T2-weighted image, coronal plane (B) and s a g i t t a l p l a n e ( C), both showing the infarct small and oval-shaped, suggestive of a microangiopathic lesion (arrow).

strokes, found in up to 50% of cases; pure sensory strokes; sensorimotor strokes; dysarthria–clumsy hand syndrome; and ataxic hemiparesis. However, these clinical syndromes are not pathognomonic of lacunar stroke. A study in 73 patients with clinically lacunar syndromes revealed a diﬀ erent pathomechanism in 23% of cases, half of them attributable to a cardiac embolic source, and half of them due to a relevant proximal arterial stenosis (Wessels et al 2005). It may be helpful to note that subcortical strokes usually lead to complete motor, sensory, or sensorimotor signs aﬀ ecting limbs and face, whereas cortical infarctions usually spare one limb or the face. In pure motor stroke a proportional hemiparesis equally a ﬀ ecting arm and leg indicates a subcortical lesion while cortical MCA or ACA infarctions usually present a more arm- or leg-dominating hemiparesis.

95Arterial Ischemia

Fig. A4.12 Var iants of anteri or ext ernal BZI . (A) Cranial CT, axial plane. Hypodense BZI located between the left MCA and ACA territory. (B) Cerebral DW MRI, axial plane. Left anterior BZI, larger and located more laterally.

Border Zone Infarction

Border zone infarction (BZI) is considered to be caused by a low-ﬂ ow state in large brain-supplying arteries due to high-grade stenosis or occlusion of an upstream artery or profound hypotension. An incomplete cerebral arterial circle (circle of Willis) is probably another important risk factor for BZI (for further details, see Case 30). Brain lesions may be located in the anterior and in the posterior circulation at the boundary of the territorial blood supply from the major intracranial vessels. They are best discussed in the anterior circulation, but even here there is considerable concern about the nature and signiﬁ cance of these lesions (Caplan and Hennerici 1998, Momjian-Mayor and Baron 2005). Within the supratentorial parenchyma, two categories can be distinguished: external and internal BZIs, the ﬁ rst also referred to as cortical BZIs. External BZIs are located between two or all three cortical territories of the MCA, ACA, and PCA. The lesions aﬀ ect mainly the cortical area in a wedge-shaped manner, but they may extend into the subcortical areas and may vary considerably in size. An anterior external BZI between the MCA and ACA is mainly observed in ICA pathology (Fig. A4.12). A posterior external BZI, located between the MCA and PCA territory, may be present in ICA pathology in combination with fetal-type PCA or in additional steno-occlusive disease of the vertebrobasilar circulation (Fig. A4.13). However, there is no extensive data correlating the distribution of cortical BZI with the vascular status. The internal border zone involves a subcortical area within the corona radiata between the superﬁ cial and deep perforators of the MCA or between the superﬁ cial perforators of the MCA and ACA (Fig. A4.14). An internal BZI may have a distinct rosary-like pattern of small inline white matter lesions or a more prominent cigar-shaped conﬂ uent pattern (Fig. A4.15). Both patterns may occur separately or in combination (Fig. A4.16). The reported proportion of hemodynamic strokes varies. From clinical and autopsy studies it is assumed that ~10% of all brain infarctions are of hemo-

Fig. A4.13 Variants of poste rior e xtern al BZI . (A) Cerebral MR FLAIR image, axial plane. Subcortical left hyperintense BZI between the MCA and PCA territory. (B) Cerebral MR T2-weighted image, axial plane. Similar infarct location. Note that the wedge-shaped infarct extends to the cortical area.

A B

Fig. A4.14 Variants of internal BZI. ( A) Cerebral MRI, FLAIR image, coronal plane: Corona radiata lesion between the superﬁ cial and deep MCA perforators (lower lesion, blue arrow) and between the superﬁ cial perforators of the MCA and ACA (upper lesion, red arrow). (B) Postmortem angiogram, axial plane (adapted from http://www.radnet.ucla.edu/sections/DINR/Part%2018/ Part18B11.htm by courtesy of Professor G. Salamon, Radiology, UCLA, Los Angeles, USA): Image showing corresponding areas with clearly reduced number of small arterial vessels as the normal anatomic situation (blue and red circles).

dynamic origin (Bladin and Chambers 1994, Jörgensen and Torvik 1969). In the Lausanne stroke registry only 3% of patients were considered to suﬀ er from BZI (Bo- gousslavsky et al 1988). In symptomatic high-grade ICA stenoses or ICA occlusions of atherosclerotic origin ipsilateral hemodynamic lesions have been observed in ~50% of cases (Szabo et al 2001).

Cortical BZIs may present as distinct clinical syndromes. Lesions of the speech-dominant anterior cortical border zone result in transcortical motor aphasia. Speech production is aﬀ ected, as in Broca’s aphasia, but patients retain their ability to repeat words and sentences. Other patients with BZI present with mood

96 4 Pathogenesis of Stroke

Fig. A4.15 Varia nts of inte rnal BZI. Ce rebra l MR FLA IR ima ge, axial plane. (A) Rosary-like internal BZI pattern in the left hemisphere at the cella media level of the lateral ventricles indicating hemodynamic ischemia in the MCA territory. (B) Conﬂ uent cigar-shaped internal BZI pattern in the corona radiata of the left hemisphere indicating hemodynamic ischemia between the MCA and ACA territory.

Fig. A4.17 Variants of small centrum semiovale infarction. Cerebral MR diﬀ usion-weighted image, axial plane. (A) Left centrum semi- ovale lesion of ~1 cm near the lateral ventricle. (B) Similar lesion, located more medially.

Fig. A4.16 Variants of com bined i ntern al and exte rnal BZI. Ce rebral MR FLAIR image, axial plane. (A) Large right anterior external and small posterior external BZI in combination with a conﬂ uent internal BZI. (B) Large right posterior external BZI and small inline white matter lesions representing an internal BZI.

Fig. A4.18 Variants of i n-situ (at hero)th rombotic l arge pa ramedian pontine infarction. (A) Cerebral MR FLAIR image, axial plane. Large signal increase within the right paramedian pons. (B) Cerebral MR T2-weighted image. Lesion in similar location.

d i s t u r b a n c e s . A b i l a t e r a l a n t e r i o r c o r t i c a l B Z I c a n p r o voke the “man-in-the-barrel” syndrome, characterized by paresis of both arms with intact facial and leg strength. Unilateral posterior cortical BZI of the speech-dominant side may lead to transcortical sensory aphasia. Again, patients can repeat words, phrases, or sentences but, like patients with Wernicke’s aphasia, their comprehension is impaired. Other cortical signs such as apraxia or neglect may also be present but do not help in diﬀ erentiation from territorial infarctions. Bilat- eral posterior cortical BZI may produce variable types of visual agnosia, the most remarkable of which is Balint’s syndrome. This is a combination of gaze apraxia, leading to diﬃ culties in eye ﬁ xation, optic ataxia, the inability to move the hand to a speciﬁ c object by visual control, and simultanagnosia, which restrict the patient’s ability to perceive more than one object at a time.

Infarctions of Uncertain Classiﬁ cation

Occasionally stroke patterns occur that make exact classiﬁ cation diﬃ cult, e.g., subcortical ischemic le- sions in the centrum semiovale, pons, thalamus, and basal ganglia are often classiﬁ ed as lacunar lesions of suspected microangiopathic origin. Small centrum semi ovale infarcts (SCOI) are sometimes caused by an occlusion of a superﬁ cial penetrating artery originating from the MCA (Fig. A4.17). A comparison of 38 patients with this infarct pattern and 60 patients with lacunar infarctions in the basal ganglia, all deﬁ ned as lesions <15 mm, showed signiﬁ cantly higher rates of sudden clinical onset (63% versus 26%), potential cardiac embolic sources (34% versus 12%), and occlusive MCA and/ or ICA occlusive process (53% versus 19%) in the SCOI group. Contrary, a clinical lacunar syndrome was more frequent in the lacunar stroke group (81% versus 50%)

97Arterial Ischemia

Brainstem

Sagittal plane Axial plane

Fig. A4.19 Schematic of pontine infarction patterns, sagittal and axial plane. (A) Infarction in occlusion of a distal perforating artery or in one of its branches caused by a small-vessel microangiopathic disease results in a small round or ovoid lesion. (B) A proximal penetrating artery occlusion by a microatheroma (B1) or by an atherothrombotic vessel lesion of the parent artery (B2) leads to a small infarction a c c o r d i n g t o t h e p e r f u s i o n a r e a o f t h e a ﬀ ected perforating artery.

(Yonemura et al 2002). In clinical practice this implies that SCOIs require an extensive search for a treatable embolic source.

Paramedian pontine infarctions may also have diﬀ er-

ent etiologies and may be divided into microangiopathic (small-vessel) or macroangiopathic (large-vessel) disease. In macroangiopathy an atherosclerotic plaque of the BA blocks the origin of a perforator (luminal plaque / parent vessel disease) or a plaque continues into the perforating artery (junctional plaque). Also, a small atheroma may block the proximal segment of a perforating artery ( F i s h e r a n d C a p l a n 1 9 7 1 ) . I n t h e s e c i r c u m s t a n c e s t h e i s chemic lesion is usually a large, longish, tubular paramedian pontine infarction, extending to the basal surface of the pons (Fig. A4.18). A microangiopathic pontine lesion, however, originating from nonatherosclerotic disease of a distal perforator segment or one of its branches, is located more centrally within the tegmentum pontis and has a rounded or ovoid shape (Fig. A4.10 and Fig. A4.19). A total vessel occlusion of the parent artery, i.e., the BA, with blockade of all its perforating branches, will lead to a complete infarction of the ventral pons area and clinically results in a partial or complete locked-in syndrome (Fig. A4.20). The same diﬃ culties in separating small- from large-vessel diseases may occur in thalamic and striatocapsular infarctions. Considering striatocapsular infarctions, atherosclerosis with or without MCA stenosis has been shown to be a major clinical determinant in the Asian population (Bang et al 2002, Yoon et al 2013) (Fig. A4.21). A total blockade of the LSA results in large subcortical infarction mainly of the basal ganglia and internal capsule and a clinical manifestation of severe media syndrome (Fig. A4.22). According to the TOAST criteria (see below), a club-like striatocapsular infarction of 15 mm length has to be deﬁ ned as macroangiopathic, i.e., as large-vessel disease if the parent artery (e.g., the M1-MCA) has a stenosis greater than 50%. The same infarct pattern with a ﬂ at, nonstenosing plaque is, however,

Fig. A4.20 (A) Cranial CT, axial plane. Hyperdense BA sign at the midpontine level (arrow) indicating complete BA occlusion at its midpart. (B) Cerebral MR FLAIR-weighted image, axial plane showing an almost complete cross-sectional infarction of the pons caused by a bilateral blockade of the short and circumferential perforators of the BA at the level of the occlusion.

Fig. A4.21 (A) Schematic of MCA, LSA, and the basal ganglia, c o r o n a l v i e w . N o t e t h e s m a l l o r a n g e - c o l o r e d p l a q u e s , o n e o f them blocking a LSA artery. (B,C) Cerebral MR T2-weighted image, coronal plane (B) and sagittal plane (C), showing an elongated (>20 mm) but tall striatocapsular infarct (arrowheads) which a p p e a r s c l u b - l i k e i n t h e s a g i t t a l v i e w f a v o r i n g a m a c r o a n g i o p a t h i c lesion of the parent M1-MCA.

classiﬁ ed as small-vessel disease, which makes the con- cept of lacunar stroke problematic.

It is essential to examine MR images in at least two planes to conﬁ dently assess the extension of these sub- cortical lesions and to distinguish both entities. Clinically there are also diﬀ erences as larger subcortical infarctions often present a stuttering or undulating course of symptoms and more frequently have a worse outcome than small subcortical infarcts (Zhang et al, 2014).

Finally, classiﬁ cation may also be diﬃ cult when at- tempting to distinguish between territorial and border zone infarcts. A clear separation between an external BZI and a territorial infarct just at the territorial border is often diﬃ cult and one has to bear in mind that the variability

98 4 Pathogenesis of Stroke

Fig. A4.22 (A) Cerebral MR FLAIR-weighted image, coronal plane showing an elongated (>20 mm) striatocapsular infarction, more extended compared with Fig. A4.21. (B) Sagittal cerebral MR T2-weighted image reveals an infarct extension caused by compromising more than one LSA. (C) Cranial CT, axial plane. Hyperdense media sign indicating long-segment M1-MCA occlusion as the cause of stroke. (D) Cerebral MR DWI image, axial plane shows a complete striatocapsular infarction.

of the physiologic borders between arterial territories is larger than generally assumed (van der Zwan et al 1992) ( Fig. A4.23, Fig. A4.24, Fig. A4.25). Circle of Willis variants have shown to be the main reason for this phenomenon (van Laar et al 2006a). In chronic ICA disease the border zones may also be shifted, subsequently resulting in a smaller MCA territory. In such a case, a posterior external BZI may appear as a posterior MCA territorial infarct. I n t e r n a l B Z I m a y c a u s e d i ﬃ culties in delineation from lacunar stroke or SCOI when only small lesions are present. A strictly unilateral appearance is, however, uncommon in microangiopathy and points toward a hemodynamic origin.

Etiology and Pathogenesis

A variety of causes may lead to the development of stroke (Fig. A4.26). Vascular disease is the overall main cause of ischemic stroke. We distinguish between involvement of the aortic arch and other large extra- and intracranial brain-supplying arteries (macroangiopathy or large-vessel disease) and the involvement of the small arteries with a size <400 μm (microangiopathy or small-vessel disease). In macroangiopathy, atherosclerosis is the most common ﬁ nding. However, vessel dissection, vasculitis, vasospasm (e.g., following subarachnoid hemorrhage), radiation injury, and etiologically unclear vasculopathies such as ﬁ bromuscular dysplasia and moyamoya can be found aﬀ ecting large vessels in diﬀ erent preferential locations. In microangiopathy, lipohyalinosis is the main cause of disease. Cerebral amyloid angiopathy is an additional, more recently recognized vessel pathology, which may aﬀ ect small and medium-sized arteries (but also veins) in a more cortical location. One of its radiologic manifestations is cortical microbleeds (Kim and Lee 2013). The diﬀ erent preferential site separates this entity from the more subcortical locations of lipohyalinosis, the latter usually associated with arterial

Fig. A4.23 Schematics illustrating the area variations of the MCA territory. Horizontal lines indicating maximal MCA perfusion area, additional vertical lines indicating minimal MCA perfusion area. (A) Axial sections from the cella media plane (left) to the basal ganglia plane (right). (B) Lateral surface view. (Reproduced with permission from van der Zwan et al 1992.)

Fig. A4.24 Schematics illustrating the area variations of the ACA territory. Horizontal lines indicating maximal ACA perfusion area, additional vertical lines indicating minimal ACA perfusion area. (A) Axial sections from the cella media plane (left) to the basal g a n g l i a p l a n e ( right). (B) Medial surface view (top) and cranial surface view (bottom). (Reproduced with permission from van der Zwan et al 1992.)

h y p e r t e n s i o n a n d / o r d i a b e t e s . F i n a l l y , C A D A S I L ( c e r e b r a l autosomal dominant arteriopathy with subcortical infarcts and leukoencephalopathy) has to be mentioned as a rare but important small-vessel disease. All microangiopathic diseases can lead to lacunar lesions, diﬀ use white matter involvement (leukoaraiosis), or both (see Fig. A4.9). Cardioembolic infarcts are the third important group. There is a particularly high risk of embolism in atrial ﬁ brillation, valvular heart disease, and acute myo- cardial infarction and intracardiac thrombi. Paradoxical embolism in cases with a right–left cardiac shunt is still controversial. Less frequently observed causes of ischemic stroke include several hematologic diseases (for sickle

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