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(BQ) Part 2 book Warlow’s stroke has contents: Wha t caused this subarachnoid hemorrhage, a prac tical approach to the management of stroke and transient ischemic attack, specific treatment of acute ischemic stroke, specific treatment of aneurysmal subarachnoid hemorrhage,... and other contents.
437 What caused this subarachnoid hemorrhage? Matthew B Maas and Andrew M Naidech Department of Neurology, Northwestern University, Chicago, IL, USA CHAPTER MENU 9.1 9.2 9.3 9.4 9.5 9.6 Basic overview of subarachnoid hemorrhage, 437 Mechanisms of subarachnoid bleeding, 438 Neuroimaging patterns and findings, 443 Personal and genetic influences on subarachnoid hemorrhage, 447 Examination features in patients with subarachnoid hemorrhage, 449 Investigative course, 450 9.1 Basic overview of subarachnoid hemorrhage 9.1.1 Anatomic overview A basic grasp of the anatomy of the brain and its vascular supply is crucial to understanding the pathophysiology of bleeding in different intracranial compartments The brain surface and skull are separated by three layers of membranes, or meninges The pia is a thin membrane directly adherent to the brain surface, and the dura is adherent to the skull surface The arachnoid adheres to the inner surface of the dura Although the space between the pia and brain, the dura and skull, and the arachnoid and dura are only potential spaces with no separation under normal circumstances, the subarachnoid space that lies between the arachnoid and pia is filled with cerebrospinal fluid In addition, the major cerebral arteries and their large branches travel in the subarachnoid space, only entering the brain tissue in the form of small penetrating arterioles Thus, subarachnoid hemorrhage (SAH) occurs either from a source vessel traveling in the subarachnoid space, or when a hemorrhage that originates in brain tissue dissects through the thin pia membrane and into the suba rachnoid space Similarly, rupture of subarachnoid arteries may cause intraparenchymal extension with development of an intracerebral hemorrhage simultaneously with SAH, again because the pia provides little mechanical barrier support In the second section of this chapter, we will review the multiple specific conditions and mechanisms that lead to SAH Subarachnoid hemorrhage occurs either from a source vessel traveling in the subarachnoid space, or when a hemorrhage that originates in brain tissue dissects through the thin pia membrane and into the subarachnoid space Several additional anatomic peculiarities are worth noting First, the arteries in the subarachnoid space are large and exposed to the full systemic blood pressure, as vascular autoregulation occurs in the small, distal blood vessels of the brain As a consequence, rupture of these arteries can quickly extravasate a large volume of blood with devastating consequences Second, because the sub arachnoid space is an open, fluid‐filled space, in contrast to the epidural and subdural potential spaces, there may be less tamponade effect as there is no threshold of pressure required to dissect open a space to be filled with blood Third, whereas the anatomic structure of the epidural and subdural spaces inherently work to contain hemorrhages within those compartments and anatomi cally isolate them from other intracranial structures, the Warlow’s Stroke: Practical Management, Fourth Edition Edited by Graeme J. Hankey, Malcolm Macleod, Philip B. Gorelick, Christopher Chen, Fan Z Caprio and Heinrich Mattle © 2019 John Wiley & Sons Ltd Published 2019 by John Wiley & Sons Ltd 438 9 What caused this subarachnoid hemorrhage? subarachnoid space is a fairly large container of cerebro spinal fluid, continuous over the outer surface of the brain and spinal cord This fact may be exploited when seeking to confirm a diagnosis of SAH by lumbar p uncture, but can also be deleterious as the proinflammatory blood products spread to intracranial, ophthalmic, and spinal structures distant from the site of hemorrhage Finally, because multiple important structures traverse (cerebral arteries, cranial nerves) or project into (hypothalamus, arachnoid granulations) the subarachnoid space, the release of blood into the compartment and subsequent inflammation can provoke a wide variety of secondary injuries such as cerebral vasospasm, cranial neuropathies, hydrocephalus, and diabetes insipidus Injury from SAH is a combination of harm caused by local effects at the site of bleeding, concurrent intraparenchymal injury, disrup tions of cerebrospinal fluid dynamics with hydrocephalus and elevated intracranial pressures, and harm to other structures in the subarachnoid space 9.1.2 Epidemiology of subarachnoid hemorrhage According to recently compiled data, approximately 800 000 people experience a new or recurrent stroke each year in the United States, of which 3% are SAHs [1] Similar to ischemic stroke and intracerebral hemorrhage, the incidence of SAH is higher in black, Hispanic, and Native American populations A large prospective cohort study of stroke in Mexican Americans, for example, found that the age‐adjusted risk ratio for SAH was 1.57 compared with non‐Hispanic white populations, and double for black populations [2, 3] The incidence appears to be greater yet among Native American and Pacific Islander populations, although among all race groups the proportion of SAH to all stroke types is typi cally near 3% [4–6] Not only are the rates of SAH greater in non‐white racial groups, but mortality rates are uni formly higher as well [7] Studies have not found a clear difference in care access or delivery, suggesting the increased mortality represents intrinsic disease‐related factors, such as known differences in aneurysm burden and location by race [8] Other risk factors for aneurys mal SAH include cigarette smoking, nicotine, caffeine and cocaine use, hypertension, low body mass index, and lower educational achievement [9] Approximately 3% of the 800 000 strokes each year in the United States are subarachnoid hemorrhages, with a higher incidence in black, Hispanic, and Native American populations One‐fifth of patients present stuporous with severe deficits, and around 15% have no identifiable cerebrovascular lesions on angiography Describing the severity spectrum of SAH cases with precision is difficult Over 40 grading schemes have been proposed for the disease [10] Commonly used schemes, such as the Hunt and Hess Scale, have only fair to moder ate interrater reliability and many studies indicate little statistical difference in outcome between grades [10] A reasonable approximation is that about 22% of patients with SAH due to ruptured aneurysms present stuporous and with severe deficits, or worse [11] Approximately 15% of patients presenting with subarachnoid bleeding have no identifiable cerebrovascular lesions on angiogra phy [12, 13] These patients are generally milder in sever ity and experience better outcomes [13, 14] An important caveat that must be kept in mind whenever interpreting literature on SAH is that most publications focus exclusively on hemorrhages caused either by rup tured intracranial aneurysm or idiopathic SAHs where no underlying primary lesion or mechanism is identified This is primarily driven by the fact that a large preponderance of cases are caused by ruptured intracranial aneurysms, and because the course, m anagement, and prognosis of sec ondary SAHs (e.g bleeding from superficial melanoma metastases, subarachnoid extension of a primary intracer ebral hemorrhage) are primarily driven by the underlying primary disease process For example, given that the inci dence of intracerebral hemorrhage is more than three times greater than primary (aneurysmal or idiopathic) SAH, and that 40% of patients with intracerebral hemorrhage develop secondary SAH, we would expect that there would be more SAH cases yearly due to secondary causes than from an aneurysmal or idiopathic source [1, 15] Again, because the significance and management of secondary SAH is poorly understood for most nonaneurysmal processes, the inci dence is not clearly reported for most nonaneurysmal con ditions and is difficult to estimate Subarachnoid hemorrhage secondary to conditions such as subarachnoid extension of intracerebral hemorrhage, hemorrhagic metastases, and other processes are common 9.2 Mechanisms of subarachnoid bleeding In this section, we will consider in greater detail the various pathologic mechanisms that have been associ ated with subarachnoid bleeding, expanding upon the basic anatomic ideas already presented 9.2.1 Arterial malformations and injuries As described earlier, SAH due to rupture of vascular structures within the subarachnoid space is among the 9.2 Mechanisms of subarachnoid bleeding most common and lethal forms of primary hemorrhages in that intracranial compartment Here we describe these vascular anomalies in greater detail Saccular (berry) aneurysm Hemorrhage from saccular aneurysm rupture is the best‐studied cause of SAH Saccular (or “berry”) aneu rysms are focal outpouchings of a thinned and weakened artery wall Although saccular aneurysms may form in any location of the arterial vascular system, in practice they are overwhelmingly observed at or near vessel bifurcations on first‐ or second‐order arterial branches of the vessels emanating from the circle of Willis Histopathology of intracranial saccular aneurysms show defects in the media of the vessel wall, in particular, degeneration of the muscularis and elastica [16, 17] Important parts of saccular aneurysms are the neck and the dome The neck is the channel joining the aneurysm sac to the parent vessel lumen As discussed in Chapter 15, certain ultrastructural characteristics of the aneurysm, such as the ratio of the neck diameter to sac diameter, can influence endovascular options for aneu rysm obliteration The dome is the distal portion of the aneurysm sac opposite to the neck The dome of the aneurysm is the site at highest risk for rupture When aneurysms grow larger than 4 mm portions of the dome can become extremely thin and become foci for rupture and hemorrhage [16] Another important factor in patients with intracranial saccular aneurysm is that the presence of multiple aneurysms in the same patient is common The International Study of Unruptured Intracranial Aneurysms reported that 55.2% of all patients in the observational cohort had more than one unruptured aneurysm [18] Saccular aneurysms near the circle of Willis are the most common cause of primary subarachnoid hemorrhage About half of all patients with intracranial aneurysm have more than one aneurysm Most intracranial aneurysms never rupture Aside from typical locations at proximal bifurcation points of the main cerebral arteries, saccular aneurysms also develop in association with arteriovenous malfor mations (“flow aneurysms”) and from septic emboli in distal branches of cerebral arteries The histological structure of these less common secondary aneurysms is essentially identical to that of idiopathic saccular aneurysms [19] Aneurysms are believed for form in association with arteriovenous malformations due to the combined effect of congenitally abnormal and weak blood vessel walls in the high flow lesion, as well as the chronic effects of turbulent flow Although ruptured aneurysms account for the majority of severe cases of primary SAH, most cerebral aneurysms never rupture The prevalence of unruptured intracranial aneurysms is estimated to be 3.2% in the general popula tion, and substantially higher in groups with known risk factors for aneurysm such as polycystic kidney disease, positive family history, and brain tumor [20] A recent meta‐analysis of 19 studies including 6556 unruptured aneurysms in 4705 patients found a 1.3% rupture risk in subjects followed >10 years, with increased age, female sex, size >5 mm, posterior circulation location, symptomatic status, and particular ethnicity (Japanese or Finnish) being factors associated with increased risk of rupture [21] Patients who have been treated for a ruptured cerebral aneurysm in the past are at substantially increased risk of recurrent SAH from either the index or a different aneurysm One large study found that the risk of bleeding is 22 times higher than expected in an age‐ and sex‐matched population over the 10 years after first hemorrhage, with smoking, age, and the presence of multiple aneurysms at the time of initial SAH being identified as risk factors [22] Dissecting aneurysms When dissection along the wall of an artery progresses to the point of disrupting the internal elastic membrane and muscularis, aneurysmal swelling of the vessel may occur The true frequency of dissecting aneurysms is unknown as many not come to attention and, unlike saccular aneurysms, these vascular lesions may heal and resume normal radiographic appearance A very high proportion of dissecting aneurysms reported in the lit erature are described in conjunction with SAH, although due to discovery bias, the true risk of hemorrhage is unknown [23] There is evidence to indicate that repeti tive intramural hemorrhages from inadequately healed dissections may eventually progress to chronic fusiform aneurysm formation [24] Fusiform aneurysms Fusiform aneurysms are malformations characterized by irregular, circumferential dilation of an artery These ectatic, tortuous vessels (also known as dolichoectasia) are most often observed in the vertebrobasilar system These nonsaccular aneurysms account for about 3–13% of intracranial aneurysms Although SAH can occur, many remain asymptomatic or present with symptoms caused by ischemia or from compression of local structures [24–26] Blister aneurysms Although most focal aneurysms are saccular aneurysms arising at vessel bifurcations, a small number of intracranial 439 440 9 What caused this subarachnoid hemorrhage? aneurysms occur at nonbranching sites of the terminal internal carotid artery, or less commonly, the basilar and other intracranial arteries These focal lesions demonstrate an unusual morphology of thin, fragile walls with poorly defined necks, and are referred to as blood blister‐like aneurysms, or simply blister aneurysms [27] These unu sual entities account for between 0.5% and 6.6% of all intracranial aneurysms [28–30] Blister aneurysms are assumed to develop secondary to small, focal dissections Infectious arteriopathies Infection is a rare but serious cause of cerebral artery injury Although ischemic stroke from embolic occlusion or inflammation‐mediated luminal stenosis is a more common manifestation, rupture of weakened blood ves sel walls is a well‐described phenomenon, especially in infectious endocarditis In the context of either systemic bacteremia or endocarditis lesions causing release of septic emboli, bacteria‐laden material travels through the bloodstream to distal sites within the cerebral circulation Pathologic studies of bacterial mycotic aneu rysms report visualization of embolic fragments in the peripheral portions of diseased artery walls It is pre sumed that septic material enters the vasa vasorum of these distal vessels and then degrades the vessel wall due to inflammation and microabscess formation [31] In contrast to typical saccular aneurysm near the circle of Willis, infectious (mycotic) aneurysms typically arise in the distal vasculature and cause superficial cortical hemorrhages In contrast to bacterial mycotic aneurysms, fungal v asculitis occurs by direct luminal or adventitial surface invasion, usually sparing the vasa vasorum [32] Injury to the artery walls can be irregular, and focal saccular pro trusions may not be seen, although vessel wall rupture leading to SAH occurs Similarly, viral vasculopathies caused by pathogens such as varicella zoster cause irregular but widespread blood vessel injury The predominant risk in severe cases is ischemic stroke, although SAH can occur Angiographic studies reveal a mixture of large and small arteries affected with segmental constrictions and poststenotic dilatation [33] 9.2.2 Arteriovenous malformations and fistulas Abnormal connections between arteries and veins lack ing a normal capillary bed can occur in two patterns: arteriovenous malformations existing in the brain paren chyma, and dural arterial venous fistulas, in which the abnormal arterial–venous connectivity involves dural veins or venous sinuses Arteriovenous malformations A recent, large population‐screening study reported an annual arteriovenous malformation detection rate of 1.34 cases per 100 000 person‐years, with 0.51/100 000 presenting with hemorrhage The estimated prevalence of hemorrhage among detected cases was 0.68 per 100 000 [34] Depending on the location of the malfor mation, hemorrhages can present in the parenchyma, subarachnoid space, or both Aside from hemorrhages, other presenting symptoms may include seizure, head ache, or focal neurologic deficits Many arteriovenous malformations are noted to have associated aneurysms, which may become a source of hemorrhage as points of particular blood vessel wall weakness [35] Most cases of arteriovenous malformation are presumed to be congen ital with no predisposing family history, although an association with Wyburn–Mason and Osler–Weber– Rendu disease has been reported [36] Depending on the location of the arteriovenous malformations, hemorrhages can occur in the brain parenchyma, subarachnoid space, or both Dural arteriovenous fistulas Dural arteriovenous fistulas occur throughout the brain and spinal cord surface, and consist of multiple connec tions between branches of dural arteries and veins or venous sinuses Although many arteriovenous malforma tions in brain parenchyma are thought to be congenital, venous sinus thrombosis is believed to predispose to dural fistulas [37] It is believed that leptomeningeal and cortical venous reflux elevates the risk of hemorrhage, and this is observed in approximately half of all lesions that are discovered Of those in the higher risk group, the annual hemorrhage risk is approximately 8.1% [37] 9.2.3 Subarachnoid extension of spontaneous and tumor‐associated intraparenchymal hemorrhages The meninges serve to compartmentalize SAH within the subarachnoid space and intracerebral hemorrhages within the brain parenchyma, although large or superficial hemorrhages may breach the meningeal membranes Approximately 40% of patients with primary intracerebral hemorrhage are found to have extension of bleeding into the subarachnoid space, more frequently in patients with lobar hemorrhages and with larger hematoma volumes Development of secondary SAH independently contributes to worse functional outcomes in such cases [15] Similarly, rare instances of SAH in the context of pituitary apoplexy have been reported [38] Symptoms can range from sud den death (very rare), nonlocalizing symptoms such as headache, nausea, vomiting, and signs related to anatomic 9.2 Mechanisms of subarachnoid bleeding location, and compression on nearby structures, such as decreased visual acuity, bitemporal hemianopsia, ocular palsies, and endocrine abnormalities [38, 39] Subclinical pituitary hemorrhage probably occurs nearly twice as frequently as clinically apparent pituitary apoplexy [40] Subarachnoid hemorrhage as a secondary phenomenon in spontaneous intracerebral hemorrhage is more common than primary subarachnoid hemorrhage, but etiology and management are defined by the underlying parenchymal brain hemorrhage Vascular integrity is poor in rapidly growing tumors, frequently resulting in hemorrhage Certain cancer types show a predilection to metastasize to the brain surface, where tumor‐associated hemorrhage can cause suba rachnoid bleeding There are numerous reports of meta static melanoma causing SAH, but most commonly as xanthochromic cerebrospinal fluid or small collections of localized blood, rather than thick, diffuse SAH Similar patterns of low‐ volume subarachnoid bleeding have been reported with many other tumor types, most n otably lung cancer, glioblastoma multiforme, lower grade gliomas, medulloblastoma, subependymoma, choroid plexus papilloma, acoustic neuroma, and sarcoma [41– 43] Finally, similar to the pathophysiology of mycotic aneurysms, metastasis of cardiac myxoma to the intrac ranial vasculature with secondary aneurysmal vessel wall injury and SAH has been reported [44] 9.2.4 Trauma SAH occurs in approximately 40% of patients with moderate to severe traumatic head injuries Autopsy studies indicate that the source of bleeding in most cases is injured cortical arteries or diffusion of blood from superficial brain contu sions [45] The presence of traumatic subarachnoid blood is strongly linked with poor outcomes, potentially mediated by the disproportionately high rate of subdural hemorrhage and parenchymal brain damage seen in association with subarachnoid blood in those cases [46] The extent of trau matic SAH also identifies patients most at risk for worsening of traumatic brain contusions [47] Arteriography studies in patients with moderate to severe head injuries have shown that 19% demonstrate some degree of arterial narrowing, although clinically symptomatic vasospasm is less common than with aneurysmal SAH [48] 9.2.5 Reversible cerebral vasoconstriction syndrome Reversible cerebral vasoconstriction syndrome is an uncommon acute vasculopathy of unclear etiology Predominantly affecting middle‐aged women, the onset of this syndrome is heralded by thunderclap headache in 85% of cases, raising immediate suspicion for aneurysmal SAH Angiographic imaging reveals segmental cerebral artery vasoconstriction A large case series of 139 patients with reversible cerebral vasoconstriction syndrome reported that imaging of the brain parenchyma is initially normal in about half of patients, although 81% ultimately develop brain lesions including infarcts, lobar hemor rhages, and brain edema Convexity SAH occurs in 34% of these cases, although no underlying vascular malfor mation source is identifiable There is thought to be an association with prior migraine and vasoconstrictive drug exposure No clearly beneficial targeted therapy has been identified, and evidence suggests that corticoster oid therapy may be associated with worse outcomes [49, 50] SAH due to reversible cerebral vasoconstriction syn drome is more common in patients who are younger, have a higher number of affected arteries, bilateral arte rial narrowing, lower Fisher and Hunt–Hess grade, and female sex [51] 9.2.6 Posterior reversible encephalopathy syndrome Posterior reversible encephalopathy syndrome describes a group of pathologic processes that manifest in response to relative cerebrovascular hypertension leading to increased capillary filtration pressure, and endothelial dysfunction causing failure of the blood–brain barrier A common element in the disease process is the failure of brain vascular autoregulation to maintain arteriolar perfusion pressures within a physiologically normal range, either due to impaired arteriolar autoregulation reflexes or overwhelming systemic hypertension Several individually recog nized disorders fall within this umbrella descriptor, including malignant hypertension, hypertensive enceph alopathy, preeclampsia–eclampsia, and autonomic dysreflexia The primary abnormality seen on neuroimaging is extensive, relatively symmetric areas of vasogenic edema, with patchy enhancement identifying the areas with the most extensive blood–brain barrier compromise Patchy areas of sulcal SAH are seen in approximately 15% of cases [52] This condition can be distinguished from other causes of SAH by the relatively small volumes of cortical subarachnoid blood, the spatial proximity of subarachnoid blood to areas of extensive vasogenic brain edema, lack of malformations or other abnormalities on angiographic imaging, and identification of a pre cipitating process such as pregnancy, severe systemic hypertension, or recent exposure to immunomodulating or chemotherapeutic drugs which are known to induce endothelial dysfunction 441 442 9 What caused this subarachnoid hemorrhage? Reversible cerebral vasoconstriction syndrome and posterior reversible encephalopathy syndrome are uncommon conditions where small‐volume cortical subarachnoid hemorrhage is one of many associated abnormalities The pattern of symptoms and blood deposition is distinct from that of aneurysmal and idiopathic hemorrhages 9.2.7 Bleeding from cervical spinal canal sources The subarachnoid space is contiguous between the cranium and spinal canal Rarely, vascular lesions in the spinal subarachnoid space can rupture and cause SAH, with extension of blood into the inferior brain cisterns SAH has been described due to spinal arteriovenous malformations, dural arteriovenous fistulas, and spinal artery fusiform aneurysms One recent review of the literature identified 36 cases in patients ranging in age from to 72 years old The majority of lesions were at the craniocervical junction or within the cervical spinal canal The severity of spinal SAHs is lower than what is seen in intracranial hemorrhages, with 72% of patients having no disabling deficits at discharge or follow‐up [53, 54] It is not possible to accurately estimate the rela tive incidence of these lesions, other than to note that even large cohorts of patients with SAH contain only one or two such cases 9.2.8 Idiopathic subarachnoid hemorrhages In the preceding portion of this section, we have reviewed an extensive array of common and rare disorders known to result in subarachnoid bleeding Excluding cases due to other obvious primary processes, such as sponta neous intracerebral hemorrhage or cerebral metastases, approximately 85% of patients presenting with intracra nial SAH are found to have a saccular aneurysm as the culprit, and 70%) stenosis of the innominate artery has multiple repercussions in blood flow in different arterial segments of the extracranial brain circulation Carotid duplex of extracranial arteries matched with arrows with a time‐of‐flight MRA of extracranial vessels (stenosis represented with an X within a circle, (c)) Left internal carotid artery (ICA) showing compensatory increased velocities (d), left vertebral artery (VA) showing normal waveform (g), right common carotid artery (CCA) showing velocities within normal ranges but lower than contralateral CCA with systolic flow deceleration (f ), right VA showing inversed diastolic flow (subclavian steal, (e)) and left ICA showing blunted flow with decreased velocities and severe systolic flow deceleration (b) (a) (b) (c) (d) (e) (f) (g) (h) (i) Plate 5B.3 Right vertebral artery presenting with normal waveform and antegrade flow toward the head (in red) (a) Left vertebral artery (in blue) showing reversed flow toward the arm (b) Left vertebral artery and left vertebral vein presenting with the same color on carotid duplex (d) Venous Doppler signal (e) CT angiography showing the occlusion of the origin of the left subclavian artery (c, f ) Transcranial color‐coded duplex showing the vertebrobasilar junction (reversed Y appearance; (g)); note that right VA and BA are shown in blue, indicating normal blood flow direction to the head On the contrary, left VA flow is reversed (in red) Note the antegrade low‐resistance waveform of right intracranial VA (h) and alternating flow (reversed during systole and antegrade during diastole) of the left VA (i) (a) (c) (b) (d) Plate 5B.5 Right middle cerebral artery (MCA) stenosis on transcranial color‐coded duplex showing aliasing (a) Loss of signal (arrow) indicates high‐grade stenosis (b) Focal increase in velocities corresponding to a focal stenosis >70% (c) Post‐stenotic decrease in velocities with very low pulsatility (pulsatility index 0.28, (d)) (a) (b) (c) (d) (e) (f) (g) (h) (i) (j) (k) Plate 5B.11 A 68‐year‐old male patient, smoker, who had been irradiated in the neck years before for pharynx cancer, presented with transient aphasia Carotid duplex revealed left internal cerebral artery (ICA) stenosis (a) Transcranial Doppler (TCD) showed left posterior cerebral artery compensatory increase in velocities due to collateralization via PCoA (b) The patient was referred for stenting of the symptomatic left ICA (c) A week later he developed another episode of aphasia and diffusion‐weighted imaging revealed new ischemic lesions in left MCA territory (e, f ) CDU disclosed focal increase in velocities within the stent in left common carotid artery (d) Digital subtraction angiography of the left CCA confirmed intraluminal filling defects in the proximal third of the stent with focal stenosis due to recoil of the stent and thrombus formation (left external carotid artery had been occluded; (g)) TCD identified microembolic signals (MES, arrow) in the left MCA at a rate around 8 MES per minute (h, i) LMWH (lower molecular weight heparin) at therapeutic dose resulted in MES disappearance The patient has remained hospitalized for aspiration pneumonia and developed new aphasic symptoms and right hemiparesis two weeks later TCD once again revealed MES (arrow) in the left MCA (h) Repeat CDU confirmed focal acceleration in CCA velocities within the stent corresponding to a >70% stenosis (j) The patient was referred for repeat stenting of left ICA/CCA After the second stenting the patient was shifted to double antiplatelet therapy with no MES on TCD nor focal acceleration on CDU (k) (a) Plate 5C.4 Computed tomography angiography of the lower abdomen and pelvis The left ventricular thrombus had embolized and caused complete occlusion of the infrarenal abdominal aorta and bilateral common iliac arteries (red arrow) ((a) is a 3D runoff spin.) Plate 5C.7 Three‐dimensional TEE evaluation of left atrial myxoma (red arrow) (c) (d) Plate 5C.11 TEE study focusing on the mitral valve in a 44‐year‐old man who presented with fever, chills, and right upper extremity paresthesia who deteriorated rapidly and developed an acute right MCA infarct and massive cerebral edema There is severe mitral regurgitation through that perforation (c) A 3D rendering of the mitral valve shows the large vegetation sitting on the mitral valve with a perforation of the posterior leaflet (red arrow) (d) (b) Plate 5C.16 TEE study (biplane view at 110 degrees) (b) shows blood flow from left to right (b) Plate 5C.18 TEE of the aortic arch (0 and 90 degrees) in a 39‐year‐old woman with acute left MCA stroke There is no evidence of obstruction to flow on color flow Doppler (b) On repeat imaging, this thrombus had completely resolved after the initiation of anticoagulation Target Flow-mediated vasodilation Adhesion molecules Macrophages MMPs Cathepsin Process Endothelial dysfunction Endothelial activation Inflammation Proteolysis Apoptosis Lipid core Fibrous cap αvβ3 integrin Fibrin Platelets αllbβ3 integrin Tissue factor Angiogenesis Thrombosis Thrombus Fibrous cap Monocyte recruitment ↓ NO production Lipid-rich necrotic core Internal elastic lamina Angiogenesis I Approximate American Heart Association lesion stage αvβ3 integrin MMP II III IV Apoptotic cell Collagen fibril Endothelial cell Platelet Smooth muscle cell VCAM1, ICAM, selectins V Fibrin VI Foam cell LDL Plate 6.3 Growth, progression, and complications of atheromatous plaques Source: Choudhury RP, et al Molecular, cellular and functional imaging of atherothrombosis Nat Rev Drug Discov 2004;3:913–925 Reproduced with permission of Springer Nature (c) Plate 6.11 Paradoxical embolism A postmortem specimen showing: (c) A reproduction of paradoxical embolism Source: Courtesy of Dr John Webb Cortical borderzone between ACA and MCA Internal borderzone Cortical borderzone between MCA and PCA Plate 6.21 Borderzone areas Boundary zones between the territories of the middle (yellow, MCA), anterior (red, ACA), and posterior (green, PCA) cerebral arteries Deeper structures are supplied by the lenticulo‐striate (orange) and anterior choroideal arteries (blue) The internal borderzone is the boundary area between lenticulo-striate perforators and the deep penetrating branches of the MCA or at the borderzone of deep white matter branches of the MCA and the ACA Source: http://www.radiologyassistant.nl/en/p484b8328cb6b2/ brain-ischemia-vascular-territories.html Reproduced with permission MTT CBF CBV (b) Plate 6.25 (b) Computed tomography perfusion study showing prolonged mean transient time (MTT), decreased cerebral blood flow (CBF), and preserved cerebral blood volume (CBV) in the left MCA territory consistent with territorial hypoperfusion Plate 6.33 Transcranial Doppler signals from the middle cerebral artery Arrow shows the high intensity microembolic signal (MES) of an embolus Note that the embolic signal does not extend beyond the Doppler trace and is of higher intensity (brightness) than the rest of the Doppler signal Pyriform sinuses Esophagus Back Airway entrance Valleculae Epiglottis Base of tongue Front (a) Yogurt spilling over the aryepiglottic fold into the laryngeal vestibule Residue of yogurt in the pyriform sinus Vocal cords Residue of yogurt in the valleculae Front (b) Pharyngeal residue after the swallow with risk of aspiration Plate 11.16 Photographs taken during a fiberoptic endoscopic evaluation of swallowing showing the main anatomic structures (a) (b) (c) Plate 15.7 Intraoperative views under the surgical microscope depicting a ruptured right posterior communicating artery (PCOMM) aneurysm with a titanium clip across the aneurysm neck (arrow) and an unruptured right anterior choroidal artery aneurysm (curved arrow) (a) (b) Clipping of the anterior choroidal artery aneurysm Perforators from the PCOMM and anterior choroidal artery are visualized (arrow) with gentle manipulation of the artery (c) ... 20 05;36(11) :23 94 23 99 451 4 52 9 What caused this subarachnoid hemorrhage? 23 Yamaura A, Watanabe Y, Saeki N Dissecting 38 Wakai S, Fukushima T, Teramoto A, Sano K Pituitary 24 39 25 26 27 28 29 30 31 32 33... unruptured intracranial aneurysms Brain 20 00; 123 (2) :20 5 22 1 Vega C, Kwoon JV, Lavine SD Intracranial aneurysms: current evidence and clinical practice Am Fam Physician 20 02; 66(4):601–608 Ruigrok YM, Buskens... 75 25 Number at risk 3373 1 821 Survival time (years) 125 7 794 10 4 82 269 Figure 10.5 Cumulative survival up to 10 years after stroke in the South London Stroke Register Source: Wolfe et al 20 11