Neurologic complications of aortic diseases and aortic surgery.

Handbook of Clinical Neurology, Vol. 119 (3rd series) Neurologic Aspects of Systemic Disease Part I Jose Biller and Jose M. Ferro, Editors © 2014 Elsevier B.V. All rights reserved

Chapter 16

Neurologic complications of aortic diseases and aortic surgery RICHARD HERSHBERGER* AND JAE S. CHO Division of Vascular Surgery and Endovascular Therapy, Loyola University Chicago, Stritch School of Medicine, Maywood, IL, USA

INTRODUCTION Aortic disease processes have a wide range of clinical manifestations. The inflammatory disease process of Takayasu’s arteritis differs dramatically from the visceral ischemia of aortic dissection. The catastrophic event of aortic rupture tends to overshadow life-altering events such as stroke and paraplegia. However, these neurologic manifestations of aortic diseases have dramatic effects that extend beyond the individual patient to include both social and financial ramifications. This chapter focuses on the major aortic disease processes and how they can initiate, both directly and indirectly, adverse neurologic events. Included in this chapter is a basic discussion of spinal cord blood supply. Subsequently, we proceed through the major disease processes which affect the aorta. This discussion not only includes the more common entities such as aneurysm formation and dissection, but also includes giant cell arteritis, Takayasu’s arteritis, aortic coarctation, and syphilitic aortitis. Medical and surgical treatment for these disease processes are also discussed where appropriate. The chapter concludes with a brief discussion of aortic surgery, how interventions on the aorta can cause neurologic complications, and techniques to avoid these feared adverse neurologic outcomes.

SPINAL CORD BLOOD SUPPLY The spinal cord receives its blood supply from three longitudinal arteries, one of which is anterior and two of which are posterior. The anterior spinal artery supplies the motor column of the spinal cord via perfusion of

the ventral horns and anterior and lateral columns. The posterior spinal arteries perfuse the dorsal horns and posterior columns. With this distribution, the anterior spinal artery provides perfusion to two-thirds of the spinal cord and the paired posterior spinal arteries perfuse the remaining third. The anterior spinal artery is formed from a confluence of descending branches of the intracranial segment of the vertebral arteries (Santillan et al., 2012a). However, flow provided by the vertebral arteries is sufficient to supply only the most cranial aspect of the spinal cord (Greathouse et al., 2001). In addition, the anterior spinal artery has a variable caliber throughout its course, being thinnest in the mid to upper thoracic region. The anterior spinal artery, therefore, requires supply from multiple sources throughout its course, and is better envisioned as a series of anastomotic vascular loops rather than a single straight artery (Hong et al., 2008). These loops have flow provided by radiculomedullary arteries at various levels of the spinal cord. The feeder arteries must be distinguished from the radicular arteries. The radicular arteries are present at every spinal level and provide flow to the dura and nerve roots (Santillan et al., 2012a). Both radicular and radiculomedullary arteries receive their flow from segmental arteries (intercostal and lumbar arteries) as well as the vertebral, subclavian, and iliac arteries. One study of thoracoabdominal patients showed that lumbar arteries and pelvic circulation are responsible for spinal cord perfusion in 25% of cases (Jacobs et al., 2006). The most prominent radiculomedullary artery, the artery of Adamkiewicz, is fed by the segmental arteries at the T8–L1 level (Christiansson et al., 2001) (Fig. 16.1).

*Correspondence to: Richard Hershberger, M.D., Assistant Professor, Surgery, Division of Vascular Surgery and Endovascular Therapy, Loyola University Chicago Stritch School of Medicine, 2160 S. First Ave., EMS Building 110 Rm. 3218, Maywood, IL 60153, USA. Tel: þ1-708-327-2686, E-mail: [email protected]

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R. HERSHBERGER AND J.S. CHO Posteriorly, the spinal cord receives blood from the paired posterior spinal arteries. The posterior spinal arteries travel along the right and left posterolateral surface of the spinal cord. The pair receives blood from posterior radiculomedullary arteries. At times, they may become discontinuous, with the contralateral posterior spinal artery crossing the midline to provide flow to the discontinuous side (Santillan et al., 2012b). Each posterior spinal artery forms a “ladder-like” longitudinal network, with each network originating either directly from the vertebral artery or indirectly from the posterior inferior cerebellar artery. A watershed area exists between the two trunks in the midline. At this level, only small, anastamotic vessels connect the two networks (Hong et al., 2008). When the artery of Adamkiewicz reaches the anterior spinal artery, it forms the classic “hairpin” loop as it gives off a more prominent descending branch (Fig. 16.2). Although the artery of Adamkiewicz is the most prominent radiculomedullary artery, it has a variable anatomic course. In a study of 90 cadavers, one artery was found in 74% of dissections with the remaining cadavers possessing two. The majority (72%) originate from left-sided segmental arteries. In those cadavers with two identified Adamkiewicz arteries, 57% of cadavers had a unilateral

Fig. 16.1. Anatomic illustration which demonstrates the segmental blood supply to the anterior spinal artery. Of note, the segmental artery providing direct flow to the artery of Adamkiewicz is occluded. 1, Spinal cord; 2, vertebral artery; 3, anterior spinal cord; 4, left subclavian artery; 5, aneurysmatic aorta; 6, Adamkiewicz artery; 7, intersegmental collateral; 8, segmental artery indirectly supplying the Adamkiewicz artery; 9, anastomotic loop to the posteriorspinal artery; 10, filum terminale artery; 11, common iliac artery; 12, external iliac artery; 13, internal iliac artery (hypogastric artery); 14, iliolumbar artery. (Reproduced from Backes et al., 2008.)

Fig. 16.2. Preoperative MR angiogram demonstrating an occlusion of the segmental artery providing flow to the artery of Adamkiewicz. The artery of Adamkiewicz demonstrates its classic hairpin turn. SA, segmental artery; AKA, artery of Adamkiewicz; ASA, anterior spinal artery; COL, intersgmental collateral. (Reproduced from Nijenhuis et al., 2007.)

NEUROLOGIC COMPLICATIONS OF AORTIC DISEASES AND AORTIC SURGERY 225 origin while the remaining 43% had a bilateral origin media are different in the thoracic aorta when com(Koshino et al., 1999). pared to the abdominal aorta (Ruddy et al., 2008). Several studies have investigated the success of identiThroughout the aorta, the media provides both elasticity fying the artery of Adamkiewicz via computed tomograand strength through a balance of elastin, collagen, and phy or magnetic resonance angiography (CTA or MRA) smooth muscle cells that collectively form lamellar units. (Yamada et al., 2000; Hyodoh et al., 2007; Nijenhuis The thoracic aorta contains 55–60 lamellar units, a poret al., 2007). Although selective angiography of the artery tion of which is vascularized. However, the abdominal of Adamkiewicz is considered the gold standard, it has aorta contains 28–32 units, none of which are vascularbeen abandoned due to the risk of embolization ized (Wolinsky and Glagov, 1969). Furthermore, growth (Christiansson et al., 2001). A recent review of the literawithin the media is different. In the thoracic aorta, ture pooled identification of the artery of Adamkiewicz growth of the media is accomplished by synthesizing by MRA and CTA. They identified 11 papers from 2000 new lamellar units, whereas in the abdominal aorta, to 2008 describing successful visualization of the artery expansion occurs through widening of individual lamelof Adamkiewicz in 84% of patients (Melissano et al., lar units (Wolinsky, 1970). The increase in lamellar unit 2009). However, results are mixed in that one study which number may help explain the increased concentration of was published after the review detected the artery of elastin found in the thoracic aorta (Halloran et al., 1995). Adamkiewicz by CTA in only 18% of patients (Zhao As aneurysm formation is contingent upon elastin fraget al., 2009). Of note, one group was particularly successmentation, smooth muscle cell death and subsequent ful in locating the artery of Adamkiewicz by MRA, idenmedial degeneration, the abdominal aorta is at considertifying the artery in 97% of patients. They advocate the use ably higher risk of aneurysm formation due to a combiof MRA over CTA in that CTA cannot differentiate nation of fewer lamellar units, decreased elastin content, between the artery of Adamkiewicz and outlet veins, and poor vascularization (Ruddy et al., 2008). Further whereas MRA can differentiate between inlet artery differences pointing to a different etiology of aneurysm and outlet vein (Nijenhuis et al., 2007). formation in the abdominal aorta when compared to the thoracic aorta include differences in susceptibility to athNEUROLOGIC COMPLICATIONS erosclerotic plaque (Ruddy et al., 2008), differences in OF AORTIC DISEASES expression and source of matrix metalloproteinases (Freestone et al., 1995; Longo et al., 2002; Jones et al., Aortic aneurysm 2006; Sinha et al., 2006; Schmoker et al., 2007), and difAn artery is considered aneurysmal if it is 50% larger ferent levels of tissue inhibitors of metalloproteinases in than its expected diameter (Johnston et al., 1991). The the thoracic and abdominal aorta (Tamarina et al., 1997; ascending thoracic aorta is considered aneurysmal at Schmoker et al., 2007). 4.5 cm, whereas the abdominal aorta is considered aneuNeurologic symptoms caused by aortic aneurysms are a rysmal at 3 cm. The average age of individuals with thorare event, reported only as isolated cases in the literature. racic aortic aneurysms is 65 years of age, with a male to Symptomatology is related to compressive symptoms. female ratio of 1.7:1 (Bickerstaff et al., 1982). This is in Multiple neurologic findings have been described, to contrast to the abdominal counterpart of which mean include sciatica (Ashleigh and Marcuson, 1993), age is 75 years with a male to female ratio of 6:1 lumbosacral plexopathy (Lainez et al., 1989; Lacasa et al., (Pleumeekers et al., 1995). The majority of thoracic 1994), lumbosacral radiculopathy (Wilberger, 1983), and and abdominal aortic aneurysms are asymptomatic at cauda equina syndrome (Nogues et al., 1987; Jauslin presentation and found incidentally. The etiology of et al., 1991). William Osler, in 1905, was the first to recogthe majority of thoracic and abdominal aortic aneurysms nize that abdominal aortic aneurysms may present with is considered degenerative (Panneton and Hollier, 1995; neurologic symptoms, namely pain radiating down the Sinha et al., 2006). The aortic wall is composed of three leg (Osler, 1905). The more recent literature discusses layers, the intima, media, and adventitia. Aneurysm forhow nerve root compression by an aneurysm sac may promation in the thoracic as well as abdominal aorta is felt to duce sciatic pain, foot drop, or quadriceps paralysis be due to degradation and remodeling of the media (Eastcott, 1969). (Ruddy et al., 2008). However, the mechanism of action Thoracic aortic aneurysms have been described to of aneurysm formation in the two regions is felt to be cause cardiovocal syndrome. Cardiovocal, or Ortner’s different, with medial necrosis being the pathologic drivsyndrome is due to hoarseness caused by recurrent laryning force in the thoracic aorta and inflammation from geal nerve palsy. Several case reports of large saccular atherosclerosis being the driving force in the abdominal aneurysms causing cardiovocal syndrome from comaorta (Guo et al., 2006). This concept is reinforced with pression of the recurrent laryngeal nerve have been the discovery that the structural components of the described (Stoob et al., 2004; Gulel et al., 2007;

226 R. HERSHBERGER AND J.S. CHO Matteucci et al., 2012a). These symptoms can be resolved are divided into two classifications, type A and type B. with interventions, either open surgical or percutaneous. Type A dissections involve the ascending thoracic aorta, Although one patient refused intervention (Gulel et al., type B dissections involve the descending thoracic aorta 2007), one patient had resolution of his symptoms foland typically originate at the origin of the left subclavian lowing open repair (Matteucci et al., 2012b), and the final artery. Although the majority of patients present with patient had resolution of hoarseness with endovascular tearing chest pain (Hagan et al., 2000), 5–15% of patients repair (Stoob et al., 2004). Paraplegia has been described present without symptoms. Complicating the diagnosis, as a very uncommon initial presentation for abdominal 17–40% of patients can present with significant aortic aneurysm (AAA). Fewer than a dozen cases have neurologic symptoms (Gaul et al., 2008). This been described in the literature. One case involved a 75range likely results from a failure to document a year-old woman who presented with three episodes of thorough neurologic exam in emergent, critical acute neurologic deficit. Her symptoms included urinary situations, leading to an underestimation of the inciincontinence, asymmetric lower extremity weakness dence of neurologic complications of aortic dissection with sensory impairment. These symptoms progressed (Blanco et al., 1999). on the contralateral side such that the patient had bilatThe incidence of aortic dissection is dependent upon eral ankle clonus with plantar extension. She lost anal patient population risk factors, and ranges from 5 to 30 sphincter tone and developed a painful paresthesia from cases per million people. Men are most commonly the gluteal level down (Desai et al., 1989). affected, with a male:female ratio ranging from 2:1 to AAAs, particularly mycotic aneurysms, have been 5:1 (Khan and Nair, 2002), and a mean age of 63 described to erode vertebral bodies. Radiculopathy (Hagan et al., 2000). Hypertension is the most common may develop secondary to vertebral body erosion causative factor for aortic dissection, occurring in (Boonen et al., 1995). A conus-cauda equina syndrome 62–78% of patients. Marfan syndrome is the most comfrom a thoracoabdominal aortic aneurysm (TAAA) mon cause of dissections in patients younger than has been reported in a 65-year-old man presenting with 40 years of age (Khan and Nair, 2002). urinary retention, constipation, and subacute progresWith regards to neurologic complications of acute sive weakness of bilateral lower extremities (Nadkarni aortic dissection, ischemic stroke is the most common et al., 2009). The patient was found to have sensorimotor presenting neurologic symptom (Alvarez et al., 1989; loss affecting L1 to S1 bilaterally, with the most promiBlanco et al., 1999; Meszaros et al., 2000; Kazui et al., nent symptoms being in the L4–S1 distribution. The 2002; Gaul et al., 2007). Most frequently, ischemic stroke patient had erosion of the T12 and L1 vertebral bodies has been reported in type A dissections as the dissection and compression of the conus medullaris by a TAAA. extends into the carotid arteries. However, preoperative Ischemia of the conus medullaris from ruptured AAAs ischemic stroke in type B dissections has been described. has also been reported (Jones, 1976; Kamano et al., Rarer presentations resembling transient global amnesia 2005). AAA may also cause meralgia paresthetica from (Mondon et al., 2007) or with a Horner’s syndrome have compression of the lateral femoral cutaneous nerve by also been described (Condon and Rose, 1969). the aneurysm (Brett and Hodgetts, 1997). Both focal cerebral ischemic symptoms as well as In general, surgical repair of all thoracic aneurysms global ischemic symptoms have been described. In should be considered when they reach a size greater than addition, Mondon et al. describe a case of transient 6 cm. AAAs should be addressed if they are greater than global amnesia associated with a painless aortic dissec5 cm. Aneurysms in either location can be repaired with tion (Mondon et al., 2007). With regards to focal cerebral open or endovascular techniques, with more complex ischemia, it is felt to be secondary to advancement of the aneurysms having the potential to require hybrid repairs. dissection flap toward and within the aortic arch vessels. In the event of rupture, the patient needs immediate, Global ischemia is due to hemodynamic instability with urgent intervention. resultant global central nervous system (CNS) hypoperfusion (Blanco et al., 1999). Gaul et al. provide a thorough description of patients suffering from stroke Aortic dissection secondary to type A aortic dissections (Gaul et al., Among aortic pathologies, aortic dissection has the 2007). The cause of ischemic stroke was most commonly highest associated mortality, both in initial presentation due to the carotid circulation (81.2%) and predominately and following surgical management. Although the right-sided (69.2%). Finally, extension of the dissection pathologic process is similar in all cases, the developinto the supra-aortic vessels does not lead to cerebral ment of an intimal tear with subsequent separation of ischemia in all patients, as transient ischemic attack the intima and media from the adventitia, aortic dissec(TIA) or stroke was seen in only 22.7% of these patients tion has a wide range of presentations. Aortic dissections (Gaul et al., 2007).

NEUROLOGIC COMPLICATIONS OF AORTIC DISEASES AND AORTIC SURGERY With the advent of the use of recombinant tissue plasminogen activator (rt-PA) for acute stroke treatment, caution must be used in screening patients for contraindications to thrombolytic therapy. Cases of worsened outcomes due to administering rt-PA in patients with painless aortic dissections have been reported (Fessler and Alberts, 2000; Gaul et al., 2007). One patient died after developing cardiac tamponade and intrapleural hemorrhage following administration of rt-PA (Gaul et al., 2007). Current recommendations to avoid poor outcomes are to obtain an emergent chest X-ray prior to rt-PA administration as well as a careful pulse exam of all four extremities. This has been documented to avoid inappropriate rt-TP in patients with painless aortic dissection (Flemming and Brown, 1999). With extension of the dissection into the thoracic aorta, spinal cord ischemia can develop as the blood flow to the spinal cord via the intercostals is disrupted. Temporary or permanent paraplegia can develop as well as acute cauda equina syndrome (Patel et al., 2002), anterior spinal cord syndrome (van Zeggeren et al., 2011), Brown–Sequard syndrome, or a progressive myelopathy (Holloway et al., 1993). Paraplegia with acute dissection is a fairly rare event, occurring in 2–5% of patients (DeBakey et al., 1982). Although described in numerous case reports, an even rarer event is the patient presenting with painless paraplegia (Gerber et al., 1986; Zull and Cydulka, 1988; Inamasu et al., 2000; Joo and Cummings, 2000; Colak et al., 2012). Reversal of paraplegia with surgical intervention (Colak et al., 2012), as well as conservative management (Beggs et al., 2005; van Zeggeren et al., 2011), has been described. Finally, as the dissection continues into the iliac vessels, it can compromise blood flow to the lower extremities, leading to an ischemic neuropathy. Patient presentation with a pulse deficit is not uncommon. Bossone et al. reported that 29% of their patients presented with a pulse deficit. However, only 12% of presenting patients developed limb ischemia (Bossone et al., 2007). Rates of ischemic neuropathy have been reported between 6% and 11% (Alvarez et al., 1989; Blanco et al., 1999; Meszaros et al., 2000; Gaul et al., 2007). Lower extremity ischemic neuropathy is a result of the dissection extending beyond the aortic bifurcation and into the iliac and femoral arteries. Should the dissection flap become occlusive, loss of arterial flow to the lower extremity will result in pain, pallor, and paresthesia. If the ischemia is prolonged, loss in motor function will occur. Neurologic symptoms tend to develop distally first, traveling more proximally with prolonged ischemia. Aortic dissections can cause symptoms of peripheral nerve involvement through peripheral nerve compression or ischemic plexopathies. Two case reports of cardiovocal syndrome, also known as Ortner’s syndrome,

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have been described (Khan et al., 1999; Lee et al., 2006b). Unique to both cases was that the only presenting symptom of the patient was hoarseness. In the one patient undergoing repair, the hoarseness of the patient’s voice resolved (Khan et al., 1999). Finally, there is a case report of a patient presenting with unilateral weakness and numbness. The etiology of the patient’s symptoms was felt to be from an ischemic lumbosacral plexopathy (Lefebvre et al., 1995). Surgical repair of type A dissections is an emergent operation. Repair is performed with an open technique and involves replacement of the aortic arch. Type B dissections only require intervention if signs of renal, mesenteric, or extremity malperfusion develop. A wide range of techniques, both open and endovascular, can be used to improve perfusion. If patients with type B dissections are medically managed, they will require serial imaging of their aorta as they are at risk for aneurysmal degeneration. Surgical repair of type A aortic dissections can result in a variety of neurologic complications which include hypoxic encephalopathy, ischemic stroke, ischemic neuropathy, and spinal cord ischemia. Cerebral ischemia, both focal and global, is the most common neurologic complication. The former is considered to be caused by advancement of the false channel into the cerebral vessels, whereas the latter is secondary to perioperative, global central nervous system hypoperfusion (Blanco et al., 1999). Neurologic complications following repair of thoracic aortic aneurysms secondary to type B dissections are primarily paraparesis and paraplegia. With the use of adjunctive measures such as cerebral spinal fluid drainage and distal aortic perfusion, the rate of paraplegia and paraparesis following repair of thoracic aortic aneurysmal degeneration secondary to aortic dissection is not statistically different form the rate of neurologic complications seen following repair of nondissecting TAAA (Safi et al., 2002).

Giant cell arteritis Also known as temporal arteritis, giant cell arteritis (GCA) is the most common idiopathic vasculitis of large and medium vessels. It is an autoimmune disease that primarily involves the arteries originating from the aortic arch. Most typically the branches of the external carotid artery, including the posterior ciliary arteries that supply the optic nerve, are involved, but inflammation of the aorta and its primary or secondary branches may occur. In fact, it has recently been recognized that large artery involvement, especially the aorta, is a common but under-recognized event. Involvement of the aorta and large vessels usually occurs years after the onset of

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the disease (Nuenninghoff et al., 2003a; Nesher et al., 2004a; Butler et al., 2010). GCA affects individuals older than 50 years, with increasing incidence with age; its incidence is highest in those aged between 70 and 80 years. People of Scandinavian descent are more commonly afflicted with it, while it is rare in black people and Asians. Women are more commonly affected than men at a ratio of 2:1. In Olmsted County, Minnesota, the incidence of GCA has remained stable over the past 20 years, with an average annual incidence of 18.8 cases per 100 000 persons aged 50 years and older. The median time from diagnosis to the detection of aortic complications ranges from 3 to 8 years verses 1.1 years for subclavian, axillary, and/or brachial stenosis (Klein et al., 1975; Nuenninghoff et al., 2003b; Gonzalez-Gay et al., 2004; Bongartz and Matteson, 2006). Signs and symptoms of aortic involvement include aneurysm formation, dissection, and death; symptoms for large vessel involvement include upper and lower extremity claudication and, when cervical arteries are afflicted, cerebrovascular symptoms. Large artery (axillary, femoral, internal carotid and vertebral) (Fig. 16.3) complications have been reported to occur in up to 27% of patients with GCA. The incidence rate for aortic aneurysm or dissection was reported at 15–18% in population-based studies (Nuenninghoff et al., 2003a; Butler et al., 2010). Finally, great vessel (supra-aortic trunk: innominate, common carotid, and subclavian arteries). involvement has been reported to occur in 10–15% of patients. Involvement of the great vessels may result in ischemic neurologic or peripheral vascular symptoms (Evans et al., 1995; Salvarani et al., 2002; Bongartz and Matteson, 2006).

Fig. 16.3. Right upper extremity angiogram of a patient with axillary artery stenosis from giant cell arteritis. Brach, brachial artery; Sten Ax, stenotic axillary artery; Ax, axillary artery; SC, subclavian artery; Vert, vertebral artery. (Reproduced from Casserly and Messenger, 2009.)

The thoracic aorta has a much higher propensity to develop complications than the abdominal aorta in patients with GCA. GCA patients are 17 times more likely to develop thoracic aortic aneurysm compared to the general population, while for abdominal aortic aneurysm the figure is 2.4 (Evans et al., 1995). The most common neurologic symptom in patients with GCA is new-onset headache in the setting of systemic inflammation. Headache may be accompanied by scalp and temporal tenderness and thickening or nodularity of the temporal arteries. Ocular symptoms such as decreased vision and diplopia occur less commonly. Permanent blindness is the best known and most feared complication of GCA. In one study of 161 patients with biopsy-proven GCA, 26% of patients had some visual manifestations; 15% of these ultimately developed permanent visual loss, of whom only 7.5% experienced antecedent amaurosis fugax. Anterior ischemic optic neuropathy accounted for permanent blindness in 91.7% of cases and central retinal artery occlusion in 8.3%; cortical blindness from occipital lobe infarction was the cause in only one patient (Loddenkemper et al., 2007). Similarly, in another study, visual symptoms were documented in 30.1% of patients with partial or total visual deficits developing in 19.1%. Again, the majority (92.3%) of cases of blindness were due to Anterior ischemic optic neuropathy and only 7.7% of cases were due to central retinal artery occlusion (Salvarani et al., 2005). Visual damage in GCA is due to ischemic injury to the optic nerve. Once it occurs, it is not reversible. This is precipitated by intimal hyperplasia and thrombosis of the ciliary artery. Predictors of visual loss are older age, optic disc swelling, hypertension, jaw claudication and cerebrovascular symptoms (TIA and stroke) (Nesher et al., 2004a). It is of interest that the presence of systemic symptoms (weight loss, weakness and fever) was protective against the development of cerebral ischemic symptoms (Nesher et al., 2004a; Borg et al., 2008). Stroke and transient ischemic attack from stenosis or occlusion of the carotid or vertebral arteries occurs less frequently, in about 3–4% of patients (Nesher et al., 2004a; Borg et al., 2008). Amaurosis fugax responds to steroids (Joyce, 1986). Jaw claudication, although present in only one third of patients, is a characteristic symptom of GCA. Constitutional symptoms such as fatigue, weight loss, or fever may also feature. About one third of patients with GCA experience symptoms of polymyalgia rheumatica, including pain and stiffness in the neck and proximal extremities. Patients with large vessel arteritis may present with claudication symptoms or asymmetric blood pressures. However, early detection may be difficult as typical symptoms of headache, visual loss, and jaw claudication, which are characteristic of mediumsize vessel disease, may not manifest.

NEUROLOGIC COMPLICATIONS OF AORTIC DISEASES AND AORTIC SURGERY Aortitis involves the proximal aorta most commonly, requiring aortic root replacement. The inflammatory process may also involve the entire aorta and cause aneurysmal dilitation. Stenosis or occlusion of the aorta occurs infrequently. Presenting symptoms may be those of aortic dissection, such as chest pain, shortness of breath, and pulselessness with hypotension, due to aortic rupture or aortic valve insufficiency. Predictors of aortic complications include the presence of aortic valve insufficiency at the time of diagnosis of GCA, coronary artery disease, hyperlipidemia and high ESR with polymyalgia (Bongartz and Matteson, 2006). Patients may present with acute aortic emergency as the initial presentation of GCA without any antecedent rheumatological symptoms. Thus, GCA should be suspected as a cause for aortic disease in patients without any risk factors. Early detection of large vessel GCA is difficult due to the lack of symptoms and biochemical markers. An elevated erythrocyte sedimentation rate (ESR) is a hallmark of this disease, although it may be normal in between 5% and 24% of cases, even in patients with biopsy-proven GCA (Weyand et al., 2000; Salvarani and Hunder, 2001). Biopsy should be considered in all patients suspected of having GCA, even in those treated with steroids; it may be positive in 35% of cases (Achkar et al., 1994). In patients with large vessel arteritis or aortitis, temporal artery biopsy is reported to be negative in about 50% of cases. A low ESR in these same patients may complicate obtaining an accurate diagnosis (Bongartz and Matteson, 2006). While GCA in small- and middle-sized vessels is usually localized, aortic involvement is more commonly continuous and diffuse. Characteristic angiographic findings include bilateral and symmetric progressive multiple focal taperings, poststenotic dilatation, and generous collateralization. Upper extremity lesions predominate, although lower extremity involvement has been observed. Most commonly affected arteries are the subclavian, axillary, brachial, profunda femoris, and superficial femoral; those in the forearm and calf are involved occasionally. The visceral, coronary, cerebral, and vertebral systems are rarely afflicted (Butler et al., 2010). Physical examination reveals bruits over the carotid, axillary, and brachial, as well as subclavian arteries. Asymmetric blood pressure and diminished or absent pulses indicate hypoperfusion of the extremities, which can lead, although rarely, to tissue necrosis. Systemic therapy for GCA is high-dose steroids with the dose tapered as per clinical responses. However, metachronous aortic aneurysm development has been observed in 38% of patients with GCA following ascending aortic aneurysm repair despite continued steroid therapy (Zehr et al., 2005). The duration of therapy

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remains to be elucidated. When refractory to steroid therapy, antirheumatic agents such as azathioprine or methotrexate should be added to the regimen. Aspirin appears to confer benefits in reducing cranial symptoms and the steroid dose requirement (Weyand et al., 2000; Nesher et al., 2004b; Lee et al., 2006a; Narvaez et al., 2008). The need for surgery is occasional and indications include aortic valve incompetence, aortic dissection, aneurysmal disease, and lifestyle limiting claudication despite adequate steroid therapy. Risk for graft thrombosis is higher if performed during the active phase.

Takayasu’s arteritis Bearing the name of Japanese ophthalmologist Mikito Takayasu, who described arteriovenous anastomoses of the ocular papilla in a wreath-like distribution in a 21-year-old woman with sudden vision loss in 1908, Takayasu’s arteritis (TA) is a systemic necrotizing vasculitis causing inflammation of the aorta, its major branches, and the pulmonary arteries (Fig. 16.4). It is predominantly a disease of young women in the in the second or third decade of life; women are affected three to eight times more frequently than men, depending on the region being studied. A population-based study in Olmstead County, Minnesota, found an incidence of 2.6 per million (Hall et al., 1985). Although not everyone presents in this order, systemic manifestation of TA classically begins with fever, fatigue, malaise, anorexia, and diffuse body aches (arthralgia and myalgia). It characteristically involves the aorta and its primary branch vessels, characterized by the presence of bruits and tenderness. Over the course

Fig. 16.4. Computed tomography angiogram reconstruction of a patient with Takayasu’s arteritis. Note the occluded proximal left subclavian and left common carotid artery in addition to the severely stenosed left-sided great vessels. (Figure courtesy of Jin Hyun Joh, M.D.)

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of time this leads to a postinflammatory stenosis or occlusion of the affected vessels, hence TA being referred to as pulseless disease. TA affects the pulmonary arteries less frequently. Involvement of great vessels (innominate, common carotid, and subclavian arteries) occurs in 31–54% of cases by angiographic examination (Kim et al., 2012). Mid-aortic syndrome (atypical aortic coarctation), presenting with renovascular hypertension and lower extremity claudication, is a common form of TA; in Japan, it accounted for 15.9% of surgically treated TA (Taketani et al., 2005). The most recent classification for TA was proposed at the Tokyo International Conference on Takayasu Arteritis. It divides TA into six patterns of disease (Table 16.1). Ectasia or aneurysmal degeneration occurs most commonly in the ascending aorta but may also develop in the distal thoracic and abdominal aorta. Aortic intramural hematoma and dissection with rupture have also been reported. The clinical presentation of patients with TA varies by geographic region. It occurs far more commonly in India and Asian countries than in the US or Europe. Nonetheless, cerebrovascular signs and symptoms are common because of the relatively high frequency of aortic arch and primary branch vessel involvement. Approximately 32% of patients present with carotodynia. Many patients report syncope/presyncope, lightheadedness, dizziness and headache at some point during the course of the disease. Stroke or transient ischemic attack has been observed in 5–20% of patients, while visual disturbances occur in up to 30% and are related to vertebral and common carotid artery stenosis or occlusion (Kerr et al., 1994). In one study, stroke accounted for 9.5% of deaths in TA patients (Mwipatayi et al., 2005). TA patients with great vessel involvement present with symptoms associated with cerebral hypoperfusion (rather than embolic). The presentation of these patients may be complicated by severe hypertension, which occurs frequently as a result of renal artery stenosis, baroreceptor dysfunction, Table 16.1 Angiographic classification of Takayasu’s arteritis* Type

Vessel involvement

Type I Type IIa Type IIb

Branches from the aortic arch Ascending aorta, aortic arch and its branches Ascending aorta, aortic arch and its branches, thoracic descending aorta Thoracic descending aorta, abdominal aorta and/or renal arteries Abdominal aorta and/or renal arteris Combined features of types IIb and IV

Type III Type IV Type V

*If coronary or pulmonary involvement occurs, the classification is designated as C(þ) or P(þ) (Fields et al., 2006).

or altered vascular compliance. Visual disturbances can occur as a result of central retinal hypoperfusion due to retinal involvement, a manifestation of the disease initially described by Takayasu. Finally, a case of Takayasu’s arteritis complicated by spinal cord compression due to thoracolumbar inflammatory epiduritis has been reported (Kim et al., 2009). Pathologically, TA manifests with granulomatous inflammation of the adventitia and media, with infiltration of lymphocytes, plasma cells, histiocytes, and multinucleated giant cells. Grossly, the lesions involved with TA are diffuse, long and thickened arterial wall. Diagnosis of TA rests on clinical suspicion and is confirmed by aortography in any young patient, particularly women, with absent or diminished pulses associated with bruits or ischemic ulcers, or a combination thereof. Characteristic aortographic findings include occlusion or stenosis of affected vessels, aneurysm formation, and increased collateral circulation. Systemic corticosteroids are the first-line agents, starting at 1 mg/kg/day for 1–3 months and tapering off as the patient improves clinically. Unlike giant cell arteritis, TA responds well to steroid therapy; remission rates have been between 40% to 60% of cases (Kerr et al., 1994). Cytotoxic agents, such as cyclophosphamide, methotrexate, and azathioprine, may be used in conjunction with steroids. Mycophenolate mofetil has also been used in patients who failed conventional therapy (Shelhamer et al., 1985; Mevorach et al., 1992; Shetty et al., 1998; Daina et al., 1999; Ozen et al., 2007). Surgical intervention, either percutaneous or open, may be indicated in the setting of end organ ischemia (i.e., renovascular hypertension) or aneurysmal degeneration. Intervention should be avoided, if possible, during the active phase of the disease. Patency rates have been reported to be inferior when bypass grafting was performed during active versus quiescent stage (Fields et al., 2006; Saadoun et al., 2012). Bypass grafting has been a mainstay in the treatment of complications associated with TA. Common carotid bypass is typically performed for stroke prevention. The common carotid lesions afflicted with TA are typically long and eventually thrombose, unlike atherosclerotic carotid lesions. As such, they are not amenable to endarterectomy and are best treated by bypass grafting. Endarterectomy in TA patients is difficult because of transmural inflammatory changes that render development of a dissection plane difficult. In a series from Cleveland Clinic, two-thirds of endarterectomy with patch angioplasty procedures failed (MaksimowiczMcKinnon et al., 2007). When constructing carotid bypass, inflow should originate from the aortic arch where the extent of disease is less compared with its branches (Giordano, 2002).

NEUROLOGIC COMPLICATIONS OF AORTIC DISEASES AND AORTIC SURGERY The new endovascular approach may provide a viable alternative to patients with TA. It has been thought that endovascular treatment for TA is more likely to be complicated with recurrent stenosis given the fibrotic changes of the arterial wall. Maksimowicz-Mckinnon has shown the restenosis rate following endovascualr intervention to be twice that of open surgical reconstruction (Maksimowicz-McKinnon et al., 2007). However, these results are disputed by a recent multicenter experience of a relatively large series of 166 revascularization procedures in 79 patients. Patients were treated with either open surgical or endovascular modalities and had a 6.5 year follow-up. The outcome of the study demonstrated that the underlying biological inflammation at the time of therapy, not the therapeutic modality, was the most important determinant of late complications (Saadoun et al., 2012).

Aortic coarctation Morgagni is credited with the discovery of aortic coarctation at an autopsy in 1760. Aortic coarctation can be seen at any aortic level. Typically it occurs at the level of the ligamentum arteriosum and is classified based on its relation to the ligament as preductal, postductal or ductal (Fig. 16.5). The most common manifestation is immediately distal to the ligamentum arteriosum. Pathologically, it is thought to develop from the same process that obliterates the ductus arteriosus. It is hypothesized that oxygen-sensitive smooth muscle tissue from the ductus becomes incorporated within the aortic wall. When these cells become exposed to high oxygen tension, they constrict leading to aortic narrowing. Coarctation affects 19 in 1000 live births worldwide (Hoffman and Kaplan, 2002). Of note, it is also the most common missed congenital heart disease (Punukollu RCC

LCC

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et al., 2011). If the affected survive infancy, the mean age of death without intervention is only 34 years of age. The majority of deaths are attributed to cardiac failure. Other causes of death are aortic rupture, bacterial endarteritis, and intracranial hemorrhage (Campbell, 1970). Although the patient can be asymptomatic, common complaints include intracranial hemorrhage, headache, nose bleeds, dizziness, claudication, or abdominal angina. Some 10% of patients with aortic coarctation also have intracranial aneurysms, an almost fivefold increase in frequency when compared to the general population (Connolly et al., 2003). Physical examination findings concerning for coarctation include a discordance in upper and lower extremity blood pressures, weak femoral pulses, or evidence of arterial collateralization to include palpable arteries over the scapulae or chest wall (Bedard et al., 2008). Coarctation can cause a variety of neurologic deficits due to its alteration of aortic blood flow. Two mechanisms exist by which coarctation can cause neurologic compression, steal and arterial collateralization. With regards to steal, the upper thoracic spinal cord segment is a watershed zone of spinal perfusion. Theoretically, blood flow could be shunted from the medullary arteries, away from the anterior spinal artery, in an attempt to provide blood flow to the descending thoracic aorta. These are extremely rare cases and the literature is limited to case reports. Kendal and Andrew reported on an 11-year-old boy who had spastic paresis as well as intermittent claudication. Walking a distance significant enough to elicit the claudication symptoms also caused a worsening in his spasticity and weakness. Contrast myelogram of the patient showed no spinal cord compression. Following correction of the patient’s coarctation, all symptoms resolved (Kendall and Andrew, 1972). More recently, a similar case was

LSA

COARC.

RSA LIG.

LSA

COARC. Ao

PT

A

B

Fig. 16.5. Preductal (A) and postductal (B) aortic coarctation. Ao, Aorta; PT, pulmonary trunk; RSA, right subclavian artery; RCC, right common carotid artery; LCC, left common carotid artery; LSA, left subclavian artery; LIG, ligamentum arteriosum; COARC, coarctation. (Reproduced from Kilian, 2006.)

232 R. HERSHBERGER AND J.S. CHO reported in which a 30-year-old man presented with 4/5 be considered in children weighing more than 35 kg. In strength and hypotonia in all four extremities. Workup adult patients, whether the lesion is native or recurrent, revealed a dilated, tortuous anterior spinal artery with stent placement is the treatment of choice. The one excepno focal compression on the spinal cord. The patient gradtion to this final subset of patients is patients of advanced ually recovered and his coarctation was to be repaired age, or patients with a concomitant vasculitis (Golden and (Gill et al., 2011). Hellenbrand, 2007). More commonly, collateralization of blood flow between the thoracic aorta and the anterior spinal artery Syphilis aortitis can lead to aneurysmal dilatation of spinal or radicular arteries. Subsequently, these aneurysms can lead to a Before the discovery of penicillin, tertiary syphilis, myelopathy from spinal cord or nerve root compression. caused by the spirochete Treponema pallidum, was estiAlternatively, these dilated arteries can lead to sympmated to affect 15% of adults in the US in the nineteenth toms if they rupture. century and was the most common cause of thoracic aorCase reports of both occurrences are found in the littic aneurysm, resulting in 5–10% of cardiovascular erature. With regards to compression, a 71-year-old deaths (Roberts et al., 2009; Paulo et al., 2012). With the introduction of antibiotics, the incidence of late manwoman presented as Brown–Sequard due to an aneuifestations of syphilis has declined almost to a rare rysm of the radicular artery causing spinal cord compression at the C4 level. The patient’s symptoms included entity. However, the incidence rates of both congenital numbness in the right lower extremity that progressed and acquired syphilis have been increasing since 1985, to the right upper extremity. Neurologic examination primarily in patients afflicted with human immunodefirevealed a mild weakness of the right lower extremity ciency virus (HIV) (Hook and Marra, 1992). and a dissociated sensory disturbance below the level After a variable interval of latency, tertiary syphilis of C5 (Tsutsumi et al., 1998). A similar case was reported manifestations develop as gummatous (benign) cardiovascular or neurosyphilis in about one third of untreated in a 49-year-old man whose symptoms improved followpatients. The spirochete causes obliterative endarteritis ing repair of his coarctation (Herron et al., 1958). Several cases exist in the literature in which rupture of of the vasa vasorum resulting in necrosis of the elastic enlarged spinal arteries has led to hematomyelia and subfibers and connective tissue in the aortic media. The scarsequent neurologic deficits. A 59-year-old man with ring and thickening of the adventitia and thinning of the coarctation presented with paraplegia due to spinal hemmedia markedly reduces, if not completely obliterates, orrhage caused by rupture of a dilated spinal artery elastic fibrils and smooth muscle cells. This results in a (Iwata et al., 1997). Similarly, a 36-year-old man preweakened arterial wall that leads to aneurysmal degeneration of the aorta (Roberts et al., 2009; Paulo et al., sented with sudden onset of weakness of all four limbs, 2012). As such, the cardiovascular manifestations of late loss of sensation below the neck, and urinary and fecal incontinence. Workup was significant for hematomyelia syphilis are at least life-threatening, if not fatal. Syphiextending into the subarachnoid space, a coarctation of litic aortitis is a tertiary development, generally occurthe aorta, and aneurysmal dilatation of the anterior spiring 10–30 years after the initial infection. nal artery at the level of C6. The patient’s aneurysm had Neurosyphilis, however, is not limited to the tertiary to be repaired surgically (Sharma and Kumar, 2010). stage (Hook and Marra, 1992). Patients with central nerAnother presentation of aortic coarctation may vous system involvement are often asymptomatic. Those who present with symptoms may present with overlapping involve a compressive spinal cord extradural hematoma. symptoms that span all the stages of the disease. In one case an 11-year-old presented with neck stiffness without any headache or neurologic deficit. He was Meningeal syphilis, which is characterized by headache, found to have a hematoma in addition to a coarctation. stiff neck, nausea, and vomiting, usually occurs within His neurologic symptoms resolved with bed rest, the first year after infection. While it may invade cranial antihypertensive therapy and corticosteroids, and his nerves (visual and hearing disturbances and facial weakcoarctation was repaired 6 months later (Dauphin ness), it rarely afflicts the spinal cord. The next stage is et al., 2001). meningovascular type, which occurs 4–7 years after infection, presenting with ischemia or stroke. Ocular syphilis Surgical repair is indicated in symptomatic patients or (uveitis) is another early presenting symptom in the inadthose in which a > 30 mmHg gradient is present across the coarctation. Options include open surgical repair or equately treated patient. General paresis or tabes dorsalis, endovascular placement of stents. As a general rule, surmeaning “decay of the back,” follows 10–20 years later. gery is the treatment of choice for all native coarctation in Tabes dorsalis, the most common presentation of tertiary children less than a year of age. Balloon angioplasty can syphilis, is a progressive degenerative process involving be considered for recurrent stenosis. Stent placement can demyelination and inflammatory changes of the spinal

NEUROLOGIC COMPLICATIONS OF AORTIC DISEASES AND AORTIC SURGERY cord. It is manifested by a triad of neurologic symptoms: unsteady gait, lightening-type pains, urinary incontinence, and sexual dysfunction. In advanced cases, anterior horn cells may also be involved. Charcot joint, hyporeflexia, Romberg sign, and Argyll Robertson pupil (pupils that accommodate but do not react) are also relatively common findings in late-stage disease (Hook and Marra, 1992; Pandey, 2011).

NEUROLOGIC COMPLICATIONS WITH AORTIC SURGERY Ischemia or embolism to the brain or spinal cord may result in stroke and/or spinal cord ischemia (SCI) following aortic surgery. SCI, paraplegia, or paraparesis, is one of the most feared complications of aortic surgery. It primarily results from ischemic injury to the spinal cord from either direct exclusion of the segmental spinal blood flow or from perioperative hypoperfusion of the spinal column. It is a devastating complication that changes the quality of life of both the afflicted and family members. Furthermore, it also adversely affects the operative mortality rates as well as late outcomes. Risk factors for developing SCI include: total aortic cross-clamp time, extent of aorta repaired, aortic rupture, patient age, proximal aortic aneurysm, and baseline renal dysfunction (Svensson et al., 1993; Cambria et al., 2002). The primary contributing factors to perioperative SCI revolve around permanent exclusion of critical segmental blood supply to the spinal cord following graft replacement. Alternatively, paraplegia and paraparesis can occur due to malperfusion of the spinal cord during

233

surgery. The development and degree of malperfusion is dependent upon the length of time the aorta is crossclamped, the extent of repair, and the presence of a collateral circulation. Therefore, the maintenance of spinal cord perfusion pressure (SCPP) is paramount when treating thoracoabdominal/thoracic aortic pathology in order to minimize risk of SCI. Incidence of neurologic complications and its mechanisms differ depending on the nature of disease and extent of aortic repair performed. TAAA is well known for its risk for spinal cord ischemia. In a landmark article by Crawford and colleagues, the incidence rates of SCI following repair of TAAA were reported to range from 4% for type IV TAAAs to 31% for type II TAAAs (Fig. 16.6) (Svensson et al., 1993). Since then, a number of advances in techniques and adjunctive measures have been taken to reduce the incidence of SCI. These include hypothermia, CSF drainage with lumbar drains, maintaining distal arterial perfusion pressure, monitoring of evoked potentials with reimplantation of the intercostal arteries when changes occur, and minimizing aortic cross-clamp time. With selective use of the aforementioned methods, centers of excellence have been able to diminish their paraplegia rates (Fig. 16.7). The experience at Baylor is one such example. After performing 2286 thoracoabdominal aneurysm repairs, they report an astoundingly low paraplegia rate of 3.8% (Coselli et al., 2007). Other centers mimic this experience, where paraplegia rates have been reported to be 5–10% (Estrera et al., 2001; Jacobs et al., 2006; Greenberg et al., 2010; Conrad et al., 2011). Similarly, the incidence rates of SCI with open repair of the descending thoracic aortic

Fig. 16.6. Crawford classification of thoracoabdominal aneurysms. (Reproduced from Conrad et al., 2007.)

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Fig. 16.7. Plot of observed/expected ratios for paraplegia based on 82 clinical series showing a significant (p < 0.001) decrease in paraplegia rates over the last 23 years. (Reproduced from Acher and Wynn, 2009.)

aneurysm (DTAA) range from 2.5% to 3% in centers of excellence (Coselli et al., 2004; Estrera et al., 2005). Although primarily described as a complication of intervention on the thoracic and thoracoabdominal aorta, paraplegia can also occur following infrarenal aortic procedures. The incidence of SCI following infrarenal abdominal aortic aneurysm repair is about 0.25% (Gloviczki et al., 1991). Delayed paraplegia may develop. It is usually associated with transient hypotension in the postoperative period, although extremes as long as 10 months postprocedure have been reported (Cho et al., 2008). Early recognition is critical as prompt restoration of hemodynamic stability with mean arterial pressure (MAP) above 90 mmHg and institution of CSF drainage are crucial for neurologic recovery. Hyperperfusion syndrome is another mechanism of stroke in patients undergoing bypass grafting of great vessels for occlusive diseases of great vessels, whether due to atherosclerosis or vasculitis. Increased blood flow to the brain following revascularization of severely stenotic carotid arteries result in brain edema, seizure, and potentially, intracranial hemorrhage and stroke. Intracerebral hemorrhage due to cerebral hyperperfusion syndrome has been observed in 4.8% (Fields et al., 2006) and 13.3% of patients (Kim et al., 2009). In order to prevent this complication, the need for tight control of blood pressure cannot be overemphasized. Staged, rather than simultaneous, carotid reconstruction in the setting of severe bilateralcarotid occlusive disease will also help reduce the risk of hyperperfusion syndrome.

Stroke following aortic intervention can be the result of either embolic or ischemic process. Ischemic strokes result from brain hypoperfusion from either clamping of the great vessels or perioperative hypotension. Concomitant cerebrovascular disease as well as heavily diseased aorta places patients at risk for perioperative stroke. As such, evaluation of extracranial carotid arteries by duplex scanning and of the aorta by CTA would be important to minimize the risk. Stroke risk has been shown to be directly related to aortic cross-clamp positioning. As the clamp is placed more distally, the stroke risk decreases. With clamp placement adjacent to the left subclavian artery (LSCA), stroke risk is 2.0%. This decreases to 1.5% when clamped near the midthoracic level and 0.4% when clamped near the diaphragm (Schmittling et al., 2000). When the atherosclerotic disease burden is prohibitive for aortic cross-clamping, hypothermic circulatory arrest (HCA) may be used selectively, albeit at an increased morbidity and mortality rate (Coselli et al., 2008; Safi et al., 1998). Although some espouse routine use of HCA (Fehrenbacher et al., 2007; Kulik et al., 2010), it has not been shown to particularly reduce the stroke risk compared with conventional methods (Safi et al., 1998). Embolic strokes can occur secondary to manipulation of atheroma-burdened aorta and consequent embolism. This may occur at the time of manipulation of the aorta either during open surgery or during endovascular intervention. Deployment of the proximal end of the endograft in zone 2 (proximal to the left subclavian artery) has been shown to have a strong association with perioperative stroke; this is most likely secondary to manipulation of the arch with catheters, wires, balloons, and stent-grafts at the origin of great vessels in patients with high disease burden of atheromatous debris (Criado et al., 2005; Cho et al., 2006; Thompson et al., 2007). Thus, the importance of preoperative identification and avoidance of aortic arch with atheroma, minimal manipulation in the arch, meticulous cleansing of guidewires and catheters, and use of balloon molding only inside the grafts cannot be overemphasized (Cho and Makaroun, 2010).

CONCLUSION A subset of patients with adverse neurologic events can attribute their symptoms to aortic disease processes. Diseases of the aorta can both directly and indirectly lead to a variety of neurologic presentations. Although rare at times, they must be kept in mind by the clinician, as neurologic manifestations of aortic disease can be the subtle sign of a more complex, life-threatening process. Surgical techniques continue to evolve in an attempt to improve neurologic outcome both prior to and after intervention.

NEUROLOGIC COMPLICATIONS OF AORTIC DISEASES AND AORTIC SURGERY

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