Version May 2024
INTRODUCTION — Spinal cord infarction is a rare but often devastating disorder caused by one of several etiologies. Patients typically present with acute paraparesis or quadriparesis, depending on the level of the spinal cord involved. The diagnosis is generally made clinically, with neuroimaging to confirm the clinical diagnosis and exclude other conditions.
This topic discusses the epidemiology, anatomy, and causes of spinal cord infarction. The clinical features, diagnosis, treatment, and chronic complications of spinal cord infarction are discussed separately.
●(See "Spinal cord infarction: Clinical presentation and diagnosis".)
●(See "Spinal cord infarction: Treatment and prognosis".)
●(See "Chronic complications of spinal cord injury and disease".)
Other causes of myelopathy are also discussed elsewhere. (See "Disorders affecting the spinal cord".)
EPIDEMIOLOGY — The incidence of spinal cord infarction has not been specifically reported. It has been estimated that spinal cord infarction accounts for approximately 1 percent of all strokes [1,2]. Extrapolating from estimates of total stroke incidence in the United States, which range from 540,000 to 780,000 per year, it is expected that 5000 to 8000 cases of spontaneous spinal cord infarction occur per year [3,4]. This may be an underestimate, as these figures likely do not include spinal cord infarction complicating major surgery, which is the most common cause of spinal cord infarction.
Spinal cord infarction typically occurs in adults; this is expected, as it is usually a direct or indirect complication of atherosclerotic vascular disease; in one series, the mean age was 64 years [5]. However, children, even neonates, can develop spinal cord infarction in specific circumstances [6]. (See 'Etiologies' below.)
SPINAL CORD ANATOMY — The spinal cord is contained within the spinal column and extends from the base of the skull to the conus medullaris adjacent to the first lumbar vertebral body. The spinal cord is divided into four longitudinal regions: cervical, thoracic, lumbar, and sacral (figure 1). Each region contains numbered segments corresponding to the vertebral body where its spinal nerves traverse the neuroforamina. At each level, the spinal cord consists of gray matter and surrounding white matter tracts as well as a pair of ventral and dorsal roots that form the paired spinal nerves (figure 2).
The anatomy of the spinal cord is discussed in greater detail separately. (See "Anatomy and localization of spinal cord disorders", section on 'Spinal cord anatomy'.)
VASCULAR ANATOMY — Three major vessels arising from the vertebral arteries in the neck supply the spinal cord (figure 3) [7]. There is one anterior spinal artery (ASA) and a pair of posterior spinal arteries (PSAs). The ASA supplies the anterior two-thirds of the spinal cord. The ASA and PSAs anastomose distally at the conus medullaris [8].
Anterior spinal artery — The ASA arises from the vertebral arteries at the level of the foramen magnum. It runs along the center of the anterior aspect of the spinal cord in the anterior median sulcus from the foramen magnum to the conus medullaris, making it the longest artery in the body [8]. Although it is typically continuous throughout its course, the diameter of the ASA varies considerably throughout its length [9]. It is smallest in the thoracic segment and largest in the lumbosacral region [10].
Along its course, the ASA is augmented by radicular arteries. These small arteries enter the spinal canal through the intervertebral foramen and supply blood to the emerging nerve roots. They originate from the vertebral arteries, intercostal arteries, or in rare instances, directly from the aorta. Typically, just 6 to 10 of the 31 pairs of radicular arteries (one pair at each spinal level) contribute to the ASA [11]. These arteries usually enter the spinal canal from the left neural foramen, but may be bilateral, particularly in the cervical spine. The thoracic spinal cord is particularly dependent on radicular contributions and may be the most vulnerable to infarction [10,11]. The most prominent thoracic radicular artery is the artery of Adamkiewicz, also known as the artery of the lumbar enlargement. The artery of Adamkiewicz contributes to the ASA between the T9 to T12 level in 75 percent of individuals, but may be found above and below this level [8].
From the ASA, sulcal arteries run into the center of the cord and then branch to the right or the left to supply the deep structures of the spinal cord. The ASA also contributes to a peripheral arterial plexus, which gives off radial branches to supply the periphery of the cord. The ASA supplies blood to the anterior horns of the gray matter, spinothalamic tracts, and corticospinal tracts.
Posterior spinal artery — The PSAs originate from the vertebral arteries and travel the length of the cord in the posterior lateral sulci bilaterally. The PSAs vary greatly in diameter throughout their course and may even be discontinuous. The PSAs are supported by a greater number of radicular arteries than the ASA, commonly between 10 and 23 [11]. These radicular arteries typically originate from the left but are more frequently bilateral than those contributing to the ASA. The PSAs frequently anastomose with each other and are heavily connected to the peripheral and posterolateral plexuses [8,10]. The PSAs supply the dorsal columns and the posterior horns [10].
Venous system — Two major spinal veins, one anterior and one posterior, drain into a series of radicular veins, then into intravertebral and paravertebral plexuses, and finally into the azygous and pelvic venous systems [12]. Because spinal veins contain no valves, Valsalva and increased intra-abdominal pressure can lead to increased venous pressure and decreased spinal cord perfusion [10].
Factors that modulate blood flow — As in the brain, spinal blood flow is influenced by metabolic demand and responds to both hypoxia and hypercapnia with increased blood flow [12]. Metabolic demand and blood flow is highest in the gray matter, which is most abundant in the cervical and lumbar enlargements [13,14].
Blood flow to the spinal cord is also influenced by perfusion pressure, which is the difference between mean arterial and intraspinal canal pressure. Through autoregulation, spinal blood flow is maintained at a constant level over a range of mean arterial pressures. However, there are lower and upper limits of systemic blood pressure beyond which autoregulation fails [13,15]. As a result, systemic hypotension or increased intraspinal canal pressure may decrease perfusion and put the cord at risk. Because the spinal cord exists in a fixed space, intraspinal canal pressure is sensitive to changes in the contents of the spinal canal and may rise significantly in pathologic states.
ETIOLOGIES — A broad spectrum of diseases can cause spinal cord infarction (table 1) [10]. Diseases or procedures involving the thoracoabdominal aorta are common identifiable causes. Other spinal abnormalities such as vascular malformations or fibrocartilaginous embolism can also cause spinal cord infarction. Other embolic and thrombotic conditions that may lead to cerebral infarction can also cause spinal cord infarction. The mechanisms underlying these can be broadly categorized:
●Arterial occlusion resulting from arteriosclerosis, vasculitis, infection, embolic occlusion, thrombosis
●Systemic hypoperfusion
●Venous infarction
Aortic surgery — Surgery to repair thoracic and thoracoabdominal aortic aneurysms is the most common cause of spinal cord infarction [1,5,10,12,16-18]. Rates of spinal cord ischemia following thoracic aortic surgery have been reported to be as high as 29 percent, but are more usually reported as 10 to 11 percent [19]. Both open surgery and endovascular repair are associated with spinal cord ischemia. Risks may be lower with an endovascular approach, but data are conflicting and selection bias of patients may play a role in this finding [20-23].
Spinal cord ischemia after thoracic aortic surgery may be clinically apparent immediately after surgery, or after a period of normal neurologic functioning [24]. Delayed spinal cord ischemia has been reported as late as 27 days after surgical repair [25].
Many factors may play a role in this complication. These include systemic hypotension, before, during, or after the procedure; aortic cross-clamping causing decreased arterial perfusion and increased spinal canal pressure; and occlusion of important feeding arteries such as the artery of Adamkiewicz or other intercostal arteries either by ligation, resection, or embolization. Episodes of systemic hypotension in many cases appear to be temporally associated with delayed onset of ischemia [24,25].
Risk factors for spinal cord ischemia following aneurysm repair have been reported to include advanced age, aortic rupture, history of cerebrovascular disease, prior aortic surgery, more extensive aortic disease (eg, Crawford II/III repairs), postoperative bleeding, long cross-clamp duration, intraoperative hypotension, sacrifice of intercostal vessels, renal insufficiency, and atrial fibrillation [19,25-27].
Efforts to reduce the risk of spinal cord ischemia have included placement of lumbar drains, reimplantation of intercostal arteries, intraoperative neurophysiologic monitoring, epidural cooling, use of distal aortic perfusion, and arterial blood pressure augmentation [16,19,24,26-30]. While these interventions appear to improve outcomes, these have not been studied in a randomized or carefully controlled fashion.
Aortic dissection — Acute dissection of the descending aorta is often a catastrophic event and is associated with a high mortality (10 to 50 percent). Survivors of the acute event often contend with complications resulting from acute occlusion of branch vessels that include celiac, superior mesenteric, and renal arteries, as well as radicular arterial supply to the spinal cord. The incidence of spinal cord infarction with aortic dissection is reported to be 4 percent; spinal cord ischemia as the presenting symptom of aortic dissection is more unusual, but has been described in a number of cases [31-35].
Typically, spinal cord infarction in this setting involves the mid and lower thoracic cord levels. Severe "tearing" pain and abnormal distal pulses suggest this diagnosis [32,36]. However, 5 to 15 percent of acute aortic dissections are painless, requiring a high degree of suspicion for this diagnosis [33,34,37]. Chronic hypertension, underlying atherosclerotic vascular disease, and Marfan syndrome are among the risk factors for aortic dissection [38]. (See "Clinical features and diagnosis of acute aortic dissection".)
Aortic thrombosis from venoarterial extracorporeal oxygenation — Peripheral venoarterial extracorporeal membrane oxygenation (V-A ECMO) is a form of advanced life support that is used for patients with circulatory or cardiac failure. In V-A ECMO, blood is drained from a central vein, oxygenated extracorporeally, and reinfused into an artery. It typically requires arterial and venous cannulation of the large vessels, cardiopulmonary bypass, and anticoagulation.
Several complications of V-A ECMO may occur, including spinal cord infarction [39]. Retrograde blood flow in the aorta and subsequent stasis in the aortic root or left ventricle may contribute to thromboembolism. While the exact etiology remains unclear, occlusion of critical spinal radicular arteries from the iliac arteries and turbulent aortic blood flow may also contribute to the risk of spinal cord infarction [39]. (See "Extracorporeal life support in adults: Management of venoarterial extracorporeal membrane oxygenation (V-A ECMO)", section on 'Cardiac or aortic thrombosis'.)
Other aortic pathologies — Spinal cord infarction can complicate traumatic aortic rupture [12]. Other pathologies involving the descending aorta, such as aneurysm formation and thrombosis, have also been presumed to be causative in some patients with acute spinal cord infarction [12,17,40-42]. Coarctation of the aorta and its corrective surgery is a less common cause of spinal cord infarction [43]. Spinal cord infarction can also complicate aortography [44].
Nonaortic surgeries — A number of other surgical procedures are associated with spinal cord ischemia. Of these, spine surgery is the most common; however, bowel resection, hepatectomy, caesarean section, hip and prostate surgery, and many other open procedures have also been associated with spinal cord infarction [5,10,12,17,45-47]. Spinal cord infarction has also been reported after endovascular procedures including percutaneous coronary intervention, neurointerventional procedures, and others [48-52].
Surgical injury to a radicular feeding artery probably plays a role in many of these cases. Others have wondered about the role of epidural anesthesia possibly causing direct injury to an artery or inducing vasospasm in some cases [40,46]. In some patients, intra- or perioperative hypotension appeared to be contributory. Others have noted that many patients with perioperative spinal cord infarction have underlying aortic disease and/or prior aortic surgery, perhaps increasing their susceptibility to this complication.
Fibrocartilaginous embolism — Fibrocartilaginous embolism (FCE) is a rare phenomenon that can cause spinal cord infarction. FCE originates from herniated intervertebral discs. A temporal relationship to minor head or neck injury or heavy lifting is a clue to this etiology, but is not always present. A broad age range of patients (7 to 78 years) can be affected by this phenomenon [53-57]. Most cases involve the cervical cord; some involve the lower medulla or upper thoracic cord. Neck pain typically precedes neurologic symptoms by 15 minutes to 48 hours [55,57-60]. Magnetic resonance imaging (MRI) may show a collapsed intervertebral disc at the appropriate level. Because the upper cervical cord is involved, case fatality rates appear to be relatively high.
The pathogenesis of this phenomenon is uncertain. It is hypothesized that axial loading forces on the spinal column produce a high intradisc pressure causing the injection of semifluid disc material into the disc vasculature and/or to the bone marrow and venous sinuses of the vertebral bodies [57]. This material may then spread retrograde to involve blood vessels supplying the spinal cord. Autopsy has shown fibrocartilaginous material occluding local arteries and/or veins in some cases; however, autopsy is rarely performed, and it has also been postulated that spinal hyperextension can cause vascular compression and spinal infarction without FCE [57,61-63].
Systemic hypotension — The spinal cord is vulnerable to ischemic injury during episodes of systemic hypotension (eg, cardiopulmonary arrest, systemic bleeding, etc). One autopsy series found evidence of ischemic myelopathy in 46 percent of adults who died after a cardiac arrest or severe hypotensive episode [64]. The predominant level of involvement was the lumbosacral cord. This phenomenon is also described in neonates, particularly premature neonates, after episodes of hypotension in the perinatal period [65]. Among survivors, ischemic myelopathy can be obscured by hypoxic-ischemic encephalopathy; however, in a number of cases, spinal cord infarction is the principal complication [12,40,66].
Vascular malformation — The most common presentation of a spinal vascular malformation is that of a progressive, step-wise myelopathy. However, some patients may have a more abrupt or stroke-like presentation [12,67]. (See "Disorders affecting the spinal cord", section on 'Vascular malformations'.)
Other causes — Among case series, between 44 to 74 percent of patients with spinal cord infarction do not have an identified etiology [1,5,6,17,40,41,68-72]. In many of these cases, atherosclerotic risk factors are prevalent, and atherothrombotic disease is presumed to be responsible for at least some of these cases. However, this pathology has not been specifically described. Moreover, a small percentage of patients in many series includes patients with no identifiable etiology and no vascular risk factors [40,41].
Other causes of spinal cord infarction are numerous (table 1) [10]. A few of the more common of these rare conditions include:
●Vasculitis resulting from bacterial or syphilitic infection, systemic lupus erythematosus, polyarteritis nodosa, and giant cell arteritis, which can be a cause of spinal cord infarction [1,12,68,69,73,74].
●Vertebral artery atheroma and dissection, which has been associated with rostral cervical cord infarction [17,41,75,76].
●Both inherited and acquired hypercoagulable conditions such as prothrombin gene mutations, as well as sickle cell disease, which appear to underlie some cases of spinal cord infarction [12,77-83].
●Cervical spondylosis, which has been postulated to be a cause of spinal cord infarction, perhaps by causing dissection or compression of a radicular artery [12,40,84].
●Umbilical artery catheters used in newborns, which can rarely cause occlusion of the artery of Adamkiewicz, resulting in spinal cord infarction [85,86].
●Cocaine-related arteriopathy, which has been thought to cause spinal cord infarction in a few patients [17].
●Emboli from a variety of cardiogenic sources (artificial valves, vegetations), which have also been implicated as the cause of spinal cord infarction in a number of cases [17,40,68,87-89].
Embolic spinal cord infarction has also been reported as a complication of therapeutic bronchial artery embolization to treat hemoptysis [90,91]. (See "Evaluation and management of life-threatening hemoptysis", section on 'Efficacy and adverse effects'.)
●Decompression sickness myelopathy, which may have a vascular pathogenesis. (See "Disorders affecting the spinal cord", section on 'Decompression sickness myelopathy'.)
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Stroke in adults".)
SUMMARY
●Epidemiology – Spinal cord infarction is a rare condition accounting for approximately 1 percent of strokes. Spinal cord infarction typically occurs in adults. However, children, even neonates, can develop spinal cord infarction. (See 'Epidemiology' above.)
●Anatomy – The spinal cord is divided into four longitudinal regions: cervical, thoracic, lumbar, and sacral (figure 1). Each region contains numbered segments corresponding to the vertebral body where its spinal nerves traverse the neuroforamina. At each level, the spinal cord consists of gray matter and surrounding white matter tracts as well as a pair of ventral and dorsal roots that form the paired spinal nerves (figure 2). (See 'Spinal cord anatomy' above.)
Three major vessels arising from the vertebral arteries in the neck supply the spinal cord (figure 3). There is one anterior spinal artery (ASA) and a pair of posterior spinal arteries (PSAs). The ASA supplies the anterior two-thirds of the spinal cord. Along its course, the ASA and PSAs are augmented by radicular arteries. The thoracic spinal cord is particularly dependent on radicular contributions and may be the most vulnerable to infarction. (See 'Vascular anatomy' above.)
●Common etiologies – The most common cause of spinal cord infarction is surgical repair of the thoracoabdominal aorta. (See 'Aortic surgery' above.)
Spinal cord ischemia can also result from other pathologies involving the aorta, including aortic dissection. (See 'Aortic dissection' above and 'Other aortic pathologies' above.)
●Less common causes – Spinal cord infarction can also complicate other nonaortic surgeries, as well as episodes of profound systemic hypotension such as those occurring during cardiopulmonary arrest. (See 'Nonaortic surgeries' above and 'Systemic hypotension' above.)
Other causes of spinal cord infarction are diverse (table 1). A large proportion of spontaneous spinal cord infarction does not have an identified etiology; many of these are presumably secondary to atherothrombotic disease. (See 'Other causes' above.)
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