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A 63-year-old man with a history of hypertension, paroxysmal atrial fibrillation, and dyslipidemia had a sudden intense chest pain radiating to his left arm, and he lost control of his legs. He was not on anticoagulant therapy and had no history of back trauma. During transport, he was hypotensive (blood pressure 88/51), his right arm was pale, and he was not able to move his legs. ECG showed inferolateral ST-segment depressions. He was given 250 mg aspirin and morphine for pain. With intravenous fluid-replacement therapy, his blood pressure rose and the activity of his legs improved. Aortic dissection was suspected, and the patient was urgently admitted to the surgical emergency room within the university hospital. In the emergency room, his blood pressure was 108/62. Cardiac and pulmonary auscultation and abdominal palpation were normal, and peripheral pulses were symmetrical. Computed tomography of the aorta revealed a hematoma next to the ascending aorta, raising a suspicion of type A aortic dissection reaching from the ascending aorta to the beginning of the left renal artery. The aortic valve was intact.
一位63歲男性患者，既往有高血壓病、陣發(fā)性房顫、高脂血癥史，突然出現劇烈胸痛并放射至左側上肢，伴雙下肢無力。未曾接受抗凝治療，否認背部外傷史。往醫(yī)院轉送過程中，患者出現低血壓（血壓88/51mmHg），右側上肢蒼白，雙下肢不能平移。心電圖顯示下側壁ST段壓低，給予口服阿司匹林腸溶片250mg和嗎啡止痛。給予靜脈補液后，患者血壓逐漸上升，雙下肢運動障礙改善。懷疑主動脈夾層，患者被緊急送往大學醫(yī)院的外科急診室。在急診室，患者血壓108/62mmHg。心肺聽診及腹部觸診正常，外周動脈搏動對稱。主動脈CT顯示升主動脈旁有一血腫，高度懷疑從升主動脈到左側腎動脈起始段的A型主動脈夾層，主動脈瓣完整。
During an emergency operation, the ascending aorta and a part of the aortic arch were replaced with a prosthetic graft. The arrest time was 24 minutes, and closure of the aorta took 112 minutes. In the beginning, the patient needed vasoactive support because of hypotension but later on his hemodynamic was stable. However, the next day, the patient had to undergo a resternotomy because of postoperative bleeding. After the operation, he was hypertensive and was treated with antihypertensive medication.
急診手術中，升主動脈和部分主動脈弓用人工移植物代替。停搏時間為24分鐘，主動脈夾閉時間為112分鐘。因為血壓過低，患者一開始需要血管活性藥物維持血壓，但后來血流動力學平穩(wěn)。然而第2天，患者因為術后出血，不得不行開胸手術治療。術后血壓高，給予降壓藥物治療。
The patient was extubated on the second postoperative day and mobilization was started the next day, when it was noticed that the patient could not stand on his feet and coordination of his lower limbs was impaired. On the fourth postoperative day, a neurologist was consulted. The patient was somnolent but oriented, and denied any back or limb pain. His cranial nerves were intact, and his upper limbs had normal strength and sensation. He could hold his left leg up for 5 and his right leg for 3 s in a prone position. He could not press/push against resistance neither distally nor proximally, the right leg being somewhat weaker, and tonus of his lower limbs was weak-ened. The patient reported impaired sensation for pain and light touch on his feet. Reflexes were normal, and Babinski sign was negative. There was no impaired sensation in upper body. Diuresis was monitored by means of urinary catheter.
術后第2天拔除氣管插管，第3天患者下床活動時發(fā)現雙下肢站立不能，伴共濟失調。術后第4天請神經科醫(yī)生會診?；颊叱适人癄顟B(tài)，但定向力正常，否認背部或者四肢痛。顱神經檢查正常，雙上肢運動及感覺未見異常?；颊哐雠P位時，左下肢抬起能堅持5秒，右下肢3秒，肢體近端及遠端均不能抵抗阻力，右側下肢比左側肌力更差，肌張力低。雙下肢痛覺和輕觸覺減退，腱反射正常存在，巴賓斯基征陰性。上半身感覺正常。通過留置導尿管監(jiān)測到多尿。
Next, Magnetic Resonance Imaging of the Spinal Cord Was Performed. What Would You Expect to Find? 下一步行脊髓MRI檢查，你希望能發(fā)現什么呢？
Magnetic resonance imaging showed increased signal intensity of the anterior spinal cord between T11 and conus in T2-weighted images with edema and restricted diffusion in diffusion-weighted images. The finding suggested an ischemic lesion.
磁共振顯示胸11至脊髓圓錐段脊髓前部T2加權像高信號，伴有水腫，彌散加權像受限，結果提示脊髓缺血性病變。
On the 19th postoperative day, sensory deficits were no longer found. The patient was able to walk with assistance of a walker, but distal and motor weakness was still detected, the right side being weaker. Proprioceptive and temperature sense was normal. Vibration sense was impaired in both upper and lower limbs, probably unrelated to the acute situation. Bowel function was normal but the patient was still catheter-bound, partially because of the postoperative complication (bleeding in the groin area).
手術后19天，雙下肢感覺恢復正常。在他人攙扶下可行走，但雙下肢遠端肌力仍差，右下肢較明顯。本體感覺和溫度覺正常。四肢振動覺均受損，可能與此次發(fā)病無關。排便功能正常，但患者一直留置導尿，部分原因為術后并發(fā)癥（出血在腹股溝區(qū)）
A few days later, the patient was transferred to the intensive care unit because of septic shock, esophageal perforation, and gastrointestinal bleeding. Despite recurrent surgical interventions, antibiotics, maximal vasoactive medication, massive blood transfusions, and renal replacement therapy, the patient died on the 27th day after admission.
幾天后，患者因為感染性休克、食道穿孔、消化道出血被轉至重癥監(jiān)護病房。雖然給予多次手術治療、抗生素、最大量的血管活性藥物、大量輸血和腎臟替代治療，但患者在入院后第27天死亡。 Our patient had a motor paraparesis with mild sensory findings and possible paresis of the urinary bladder, suggesting of anterior spinal cord infarction but preserved dorsal column function. We concluded that aortic dissection had caused the infarction, the probable mechanism being occlusion of the anterior segmental medullary artery supplying lower thoracic and upper lumbar level. The fact that the patient had reported paraparesis preoperatively suggested that the causative factor was the dissection and not the operation. An alternative mechanism is hypoperfusion of the spinal cord because of the documented hypotension. The transient alleviation of symptoms after intravenous fluid therapy suggests that hypotension was at least a contributory factor.
患者有截癱伴輕度感覺障礙，可能有膀胱括約肌功能障礙，提示脊髓前部發(fā)生梗死，后索功能保留。我們推測是主動脈夾層導致了脊髓梗死，其發(fā)病機制是供應胸下段至腰上段水平的脊前動脈部分閉塞?；颊咝g前出現過雙下肢癱瘓，提示脊髓梗死的誘發(fā)因素為動脈夾層而非手術。由于患者有低血壓史，所以另外一種發(fā)生脊髓梗死的機制可能是低灌注。特別是給予靜脈輸液后癥狀有短暫性改善，提示低血壓至少是促發(fā)因素。
Infarction of the spinal cord is a rare cause of paraparesis. It is commonly caused by atheromas involving the aorta and is a potential complication of thoracoabdominal surgery. Other causes include collagen-vascular disease, syphilitic angiitis, embolic infarction, pregnancy, sickle cell disease, neurotoxic effects of iodinated contrast agents, compression of the spinal arteries by tumor, systemic arterial hypotension, and decompression sickness.1
脊髓梗死導致截癱極為罕見。脊髓梗死的常見病因為主動脈粥樣硬化，同時也是胸腹部手術的一種潛在并發(fā)癥，其他的病因包括：膠原血管病、梅毒性血管炎、血栓栓塞、妊娠、鐮狀細胞病、碘對比劑的神經毒性作用、腫瘤壓迫脊髓動脈、全身性低血壓和減壓病。
Arteries supplying the spinal cord are branches of the vertebral, thyrocervical, costocervical, intercostal, lumbar, and lateral sacral arteries. Two anterior thirds of the spinal cord are supplied by the anterior spinal artery and the posterior third by 2 posterior arteries, running along the entire length of the cord. They are joined by 6 to 9 large segmental medullary arteries originating from the same arteries except for lateral sacral arteries. In the cervical region, the blood supply is rich in collateral branches. In the thoracic region, the anterior spinal artery is joined by only a few branches from the thoracic aorta, making it more vulnerable to ischemia. Lower thoracic and lumbosacral areas are supplied by the largest medullary artery, the great anterior segmental medullary artery of Adamkiewicz, usually found at level L-1 or L-2 (occasionally as high as T-12 or as low as L-4). Conus and cauda equina are also supplied by the sacral branches ascending from the iliac arteries.
脊髓動脈供應主要來自椎動脈、甲頸干動脈、肋頸干動脈、肋間動脈、腰動脈和骶外側動脈的分支。脊髓前2/3血液供應主要來自脊髓前動脈，后1/3的血液供應由二條貫穿脊髓全長的后動脈供應，除了骶外側動脈，起自上述這些動脈的6到9支大的節(jié)段性髓動脈也參與供血。頸段脊髓側支血供非常豐富，在胸段，脊髓前動脈僅接收胸主動脈發(fā)出的幾根分支的血供，從而使其容易發(fā)現缺血，下胸段和腰骶段脊髓由最大的髓動脈供血，較大的前根動脈Adamkiewicz動脈（AKA）,常位于腰1或者腰2水平（偶爾高至胸12或者低至腰4）。脊髓圓錐和馬尾有來自髂動脈的骶分支供應。
Aortic dissection begins with an intimal tear whereby blood enters the vessel wall and splays apart the laminar planes of the media to form a false lumen. The dissecting hematoma spreads along the laminar planes and may lead to occlusion of its branches. It may also rupture through the adventitia and cause massive hemorrhage, leading to hypotensive shock. The most common place for spontaneous dissections is the proximal ascending aorta that is susceptible to the greatest sheer stress. Aortic dissections are classified into 2 types. Type A involves the ascending aorta, whereas type B arises after the origin of the great vessels of the aortic arch. The most important risk factor for aortic dissection is hypertension.2
主動脈夾層起源于血管內膜撕裂，血液流入血管壁中，使動脈中層被剝離分開從而形成假腔。夾層中的血腫可能沿著層狀平面擴散，導致分支動脈閉塞。也可以是動脈血管外膜破裂，導致大出血，出現低血壓性休克。自發(fā)性動脈夾層最常見的位置是升主動脈的近端，因為此處血管易受到較大的血流剪應力。主動脈夾層分2型，A型為升主動脈受累，B型為主動脈弓大血管受累。主動脈夾層最主要的危險因素為高血壓。
The typical manifestation of aortic dissection is acute intense chest pain that may radiate to back and propagate downward. If it affects the ascending aorta, it may cause cardiac complications such as myocardial infarction, aortic valve insufficiency, or cardiac tamponade. By occluding the arteries originating from the aorta or under general hypotension, dissection can cause hypoperfusion and ischemia of brain, kidneys, limbs, bowel, or spinal cord.
主動脈夾層典型的臨床表現為急性劇烈胸痛，放射至背部并向下擴散。如果累及升主動脈，可能會引起心臟并發(fā)癥，如心肌梗死、主動脈瓣關閉不全或心包填塞。通過堵塞主動脈分支動脈或引起全身性低血壓，主動脈夾層可導致腦、腎臟、四肢、腸道或者脊髓血流灌注不足和缺血。
Neurological symptoms of aortic dissection include persistent or transient ischemic stroke, hypoxic encephalopathy, spinal cord ischemia, and ischemic neuropathy.3 Neurological involvement is reported in 17% to 40%.4 Proposed risk factors for neurological complications in type A aortic dissections include advanced age and classic type of dissection.5 At the onset, patients with neurological symptoms are more often pain free than those without (33% versus 5.6%).6 Neurological symptoms often manifest early after dissection and may rapidly resolve. It is speculated that this might be explained by transient arterial occlusion during the propagation of dissection.4 In some studies, neurological complications predicted poor outcome whereas others could not find a correlation.5,6
主動脈夾層的神經系統(tǒng)癥狀包括持續(xù)性或短暫性缺血性卒中、缺氧性腦病、脊髓缺血和缺血性神經病。神經系統(tǒng)受累約占17%—40%。A型主動脈夾層引起神經系統(tǒng)并發(fā)癥的高危因素包括：高齡和夾層的典型分型。發(fā)病時，有神經系統(tǒng)癥狀的患者無痛的比例高于無神經系統(tǒng)癥狀的（33% 對 5.6%）。主動脈夾層后神經系統(tǒng)癥狀通常出現早，且很快緩解，推測這可能是由于主動脈夾層撕裂過程出現短暫性血管閉塞有關，有些研究認為出現神經系統(tǒng)并發(fā)癥提示愈后不良，而其他研究未發(fā)現有相關性。
Spinal cord ischemia is reported in 1% to 9% of type A aortic dissections.4 However, it is more common in distal dissections, ranging ≤10%.7 Spinal cord ischemia in patients with aortic dissection can be caused by occlusion of the intercostal and lumbar arteries, the Adamkiewicz artery, or the thoracic radicular arteries or by hypotension. The most frequent location of infarction is the watershed zone in the middle thoracic spinal cord.1,7
1%—9%A型主動脈夾層出現脊髓缺血，然而，動脈遠端夾層中更常見，小于或者等于10%。主動脈夾層患者脊髓缺血的原因可能是肋間動脈、腰動脈、腰膨大動脈或者胸神經根動脈的閉塞，或者低血壓。胸中段脊髓的分水嶺區(qū)為梗死好發(fā)部位。
The classic clinical presentation of spinal infarction is the anterior spinal artery syndrome: sudden (primarily plegic) paraplegia, local and radicular pain, sphincter symptoms, loss of pain, and temperature sensation but preserved proprioception and vibration because of sparing of the dorsal columns.1 Importantly, partial syndromes are also seen because of vascular border zones created by anastomosis from penetrating branches of the spinal arteries. If ischemia affects only the motor horns of the spinal cord, pure motor clinical manifestations can be seen.1 It can also manifest as a transverse spinal cord infarction, Brown–Séguard syndrome, progressive myelopathy or transient spinal cord ischemia.4
脊髓梗死的典型臨床表現為脊髓前動脈綜合征:突然截癱（主要是癱瘓）、局灶性神經根性疼痛、括約肌功能障礙、痛溫覺缺失，但本體感覺和振動覺保留，因為脊髓后索未累及。重要的是，由于脊髓動脈穿通支的吻合形成血管的分水嶺區(qū)，可表現為脊前動脈部分綜合征。如缺血僅影響到運動前角，臨床表現就會出現純運動障礙。也可以表現為橫斷性脊髓梗死、脊髓半切綜合征、進行性脊髓病或一過性脊髓缺血。
Surgical treatment is always indicated in type A aortic dissections, whereas uncomplicated type B dissections can be treated conservatively. Medical treatment aims at managing blood pressure to prevent propagation of dissection without compromising adequate perfusion to vital organs. Two approaches are used in surgical treatment: open surgery, and, more recently, endovascular stent graft repair (TEVAR), which is mainly used in type B dissections. In open surgery, the dissected segment of the aorta is replaced with a prosthetic vascular interposition graft during cross-clamping of the aorta, usually during temporary circulatory arrest in type A. In TEVAR, an endovascular stent graft is placed in the true lumen through the femoral artery while avoiding cross-clamping of the aorta. Both techniques require temporary or permanent interruption of arterial collaterals supplying the spinal cord.
A型主動脈夾層通常選擇手術治療，而不復雜的B型主動脈夾層可以保守治療。內科治療的目的是控制血壓，防止動脈夾層撕裂延長，導致重要臟器功能障礙。外科手術治療有2種方法，一種是開胸手術，另一種是最近主要應用于B型主動脈夾層的血管內介入支架修復(TEVAR)。在A型開胸手術中，暫時性循環(huán)停止，在主動脈橫向鉗閉時主動脈撕裂部分血管用人工血管移植物代替。在血管內支架修復術中，血管內支架移植物穿過股動脈被植入真腔，而不需要橫向夾閉主動脈。這兩種技術均需要暫時或永久性阻斷供應脊髓的側支血管。
The reported frequency of spinal cord ischemia after thoracoabdominal surgery varies widely between 2.6% and 28% in open surgery and between 4% and 7% in endovascular procedures.8,9 Risk factors for postoperative spinal cord ischemia in thoracoabdominal surgery include aneurysm extent, open surgical repair, previous distal aortic operations, cross-clamp duration, the sacrifice of T9–L1 intercostal vessels, emergency operation, severe peripheral vascular disease, perioperative hypotension, and anemia.9,10 Different strategies for spinal cord protection and early detection of ischemia have been used. These include minimizing the surgical time, using hypothermia and pharmacological neuroprotection, protecting spinal cord perfusion by maintaining adequate mean arterial pressure, CSF drainage and by reimplantation of intercostal and lumbar segmental arteries, and using intraoperative monitoring of somatosensory and motor evoked potentials.10
據報道在胸腹部手術后出現脊髓缺血的概率范圍很大，在2.6%—28%之間，而血管內介入手術出現的概率在4%-7%。胸腹部手術術后導致脊髓缺血的危險因素包括：動脈瘤的大小、打開手術修復、既往遠端主動脈手術史、阻斷時間、受累的T9–L1肋間血管、急診手術、嚴重的周圍血管疾病、圍手術期低血壓、貧血。各種不同的脊髓保護和早期發(fā)現缺血的方法已經被使用，其中包括縮短手術時間，采用低溫和神經保護藥物、維持足夠的平均動脈壓以保證脊髓灌注、腦脊液引流和肋間和腰椎節(jié)段動脈再植術、術中監(jiān)測體感和運動誘發(fā)電位。
TAKE-HOME POINTS
總 結
 譯文全文 一位63歲男性患者，既往有高血壓病、陣發(fā)性房顫、高脂血癥史，突然出現劇烈胸痛并放射至左側上肢，伴雙下肢無力。未曾接受抗凝治療，否認背部外傷史。往醫(yī)院轉送過程中，患者出現低血壓（血壓88/51mmHg），右側上肢蒼白，雙下肢不能平移。心電圖顯示下側壁ST段壓低，給予口服阿司匹林腸溶片250mg和嗎啡止痛。給予靜脈補液后，患者血壓逐漸上升，雙下肢運動障礙改善。懷疑主動脈夾層，患者被緊急送往大學醫(yī)院的外科急診室。在急診室，患者血壓108/62mmHg。心肺聽診及腹部觸診正常，外周動脈搏動對稱。主動脈CT顯示升主動脈旁有一血腫，高度懷疑從升主動脈到左側腎動脈起始段的A型主動脈夾層，主動脈瓣完整。
急診手術中，升主動脈和部分主動脈弓用人工移植物代替。停搏時間為24分鐘，主動脈夾閉時間為112分鐘。因為血壓過低，患者一開始需要血管活性藥物維持血壓，但后來血流動力學平穩(wěn)。然而第2天，患者因為術后出血，不得不行開胸手術治療。術后血壓高，給予降壓藥物治療。
術后第2天拔除氣管插管，第3天患者下床活動時發(fā)現雙下肢站立不能，伴共濟失調。術后第4天請神經科醫(yī)生會診?；颊叱适人癄顟B(tài)，但定向力正常，否認背部或者四肢痛。顱神經檢查正常，雙上肢運動及感覺未見異常?；颊哐雠P位時，左下肢抬起能堅持5秒，右下肢3秒，肢體近端及遠端均不能抵抗阻力，右側下肢比左側肌力更差，肌張力低。雙下肢痛覺和輕觸覺減退，腱反射正常存在，巴賓斯基征陰性。上半身感覺正常。通過留置導尿管監(jiān)測到多尿。
下一步行脊髓MRI檢查，你希望能發(fā)現什么呢？ 磁共振顯示胸11至脊髓圓錐段脊髓前部T2加權像高信號，伴有水腫，彌散加權像受限，結果提示脊髓缺血性病變。
手術后19天，雙下肢感覺恢復正常。在他人攙扶下可行走，但雙下肢遠端肌力仍差，右下肢較明顯。本體感覺和溫度覺正常。四肢振動覺均受損，可能與此次發(fā)病無關。排便功能正常，但患者一直留置導尿，部分原因為術后并發(fā)癥（出血在腹股溝區(qū)）
幾天后，患者因為感染性休克、食道穿孔、消化道出血被轉至重癥監(jiān)護病房。雖然給予多次手術治療、抗生素、最大量的血管活性藥物、大量輸血和腎臟替代治療，但患者在入院后第27天死亡。 患者有截癱伴輕度感覺障礙，可能有膀胱括約肌功能障礙，提示脊髓前部發(fā)生梗死，后索功能保留。我們推測是主動脈夾層導致了脊髓梗死，其發(fā)病機制是供應胸下段至腰上段水平的脊前動脈部分閉塞?；颊咝g前出現過雙下肢癱瘓，提示脊髓梗死的誘發(fā)因素為動脈夾層而非手術。由于患者有低血壓史，所以另外一種發(fā)生脊髓梗死的機制可能是低灌注。特別是給予靜脈輸液后癥狀有短暫性改善，提示低血壓至少是促發(fā)因素。
脊髓梗死導致截癱極為罕見。脊髓梗死的常見病因為主動脈粥樣硬化，同時也是胸腹部手術的一種潛在并發(fā)癥，其他的病因包括：膠原血管病、梅毒性血管炎、血栓栓塞、妊娠、鐮狀細胞病、碘對比劑的神經毒性作用、腫瘤壓迫脊髓動脈、全身性低血壓和減壓病。
脊髓動脈供應主要來自椎動脈、甲頸干動脈、肋頸干動脈、肋間動脈、腰動脈和骶外側動脈的分支。脊髓前2/3血液供應主要來自脊髓前動脈，后1/3的血液供應由二條貫穿脊髓全長的后動脈供應，除了骶外側動脈，起自上述這些動脈的6到9支大的節(jié)段性髓動脈也參與供血。頸段脊髓側支血供非常豐富，在胸段，脊髓前動脈僅接收胸主動脈發(fā)出的幾根分支的血供，從而使其容易發(fā)現缺血，下胸段和腰骶段脊髓由最大的髓動脈供血，較大的前根動脈Adamkiewicz動脈（AKA）,常位于腰1或者腰2水平（偶爾高至胸12或者低至腰4）。脊髓圓錐和馬尾有來自髂動脈的骶分支供應。
主動脈夾層起源于血管內膜撕裂，血液流入血管壁中，使動脈中層被剝離分開從而形成假腔。夾層中的血腫可能沿著層狀平面擴散，導致分支動脈閉塞。也可以是動脈血管外膜破裂，導致大出血，出現低血壓性休克。自發(fā)性動脈夾層最常見的位置是升主動脈的近端，因為此處血管易受到較大的血流剪應力。主動脈夾層分2型，A型為升主動脈受累，B型為主動脈弓大血管受累。主動脈夾層最主要的危險因素為高血壓。
主動脈夾層典型的臨床表現為急性劇烈胸痛，放射至背部并向下擴散。如果累及升主動脈，可能會引起心臟并發(fā)癥，如心肌梗死、主動脈瓣關閉不全或心包填塞。通過堵塞主動脈分支動脈或引起全身性低血壓，主動脈夾層可導致腦、腎臟、四肢、腸道或者脊髓血流灌注不足和缺血。 主動脈夾層的神經系統(tǒng)癥狀包括持續(xù)性或短暫性缺血性卒中、缺氧性腦病、脊髓缺血和缺血性神經病。神經系統(tǒng)受累約占17%—40%。A型主動脈夾層引起神經系統(tǒng)并發(fā)癥的高危因素包括：高齡和夾層的典型分型。發(fā)病時，有神經系統(tǒng)癥狀的患者無痛的比例高于無神經系統(tǒng)癥狀的（33% 對 5.6%）。主動脈夾層后神經系統(tǒng)癥狀通常出現早，且很快緩解，推測這可能是由于主動脈夾層撕裂過程出現短暫性血管閉塞有關，有些研究認為出現神經系統(tǒng)并發(fā)癥提示愈后不良，而其他研究未發(fā)現有相關性。
1%—9%A型主動脈夾層出現脊髓缺血，然而，動脈遠端夾層中更常見，小于或者等于10%。主動脈夾層患者脊髓缺血的原因可能是肋間動脈、腰動脈、腰膨大動脈或者胸神經根動脈的閉塞，或者低血壓。胸中段脊髓的分水嶺區(qū)為梗死好發(fā)部位。
脊髓梗死的典型臨床表現為脊髓前動脈綜合征:突然截癱（主要是癱瘓）、局灶性神經根性疼痛、括約肌功能障礙、痛溫覺缺失，但本體感覺和振動覺保留，因為脊髓后索未累及。重要的是，由于脊髓動脈穿通支的吻合形成血管的分水嶺區(qū)，可表現為脊前動脈部分綜合征。如缺血僅影響到運動前角，臨床表現就會出現純運動障礙。也可以表現為橫斷性脊髓梗死、脊髓半切綜合征、進行性脊髓病或一過性脊髓缺血。
A型主動脈夾層通常選擇手術治療，而不復雜的B型主動脈夾層可以保守治療。內科治療的目的是控制血壓，防止動脈夾層撕裂延長，導致重要臟器功能障礙。外科手術治療有2種方法，一種是開胸手術，另一種是最近主要應用于B型主動脈夾層的血管內介入支架修復(TEVAR)。在A型開胸手術中，暫時性循環(huán)停止，在主動脈橫向鉗閉時主動脈撕裂部分血管用人工血管移植物代替。在血管內支架修復術中，血管內支架移植物穿過股動脈被植入真腔，而不需要橫向夾閉主動脈。這兩種技術均需要暫時或永久性阻斷供應脊髓的側支血管。 據報道在胸腹部手術后出現脊髓缺血的概率范圍很大，在2.6%—28%之間，而血管內介入手術出現的概率在4%-7%。胸腹部手術術后導致脊髓缺血的危險因素包括：動脈瘤的大小、打開手術修復、既往遠端主動脈手術史、阻斷時間、受累的T9–L1肋間血管、急診手術、嚴重的周圍血管疾病、圍手術期低血壓、貧血。各種不同的脊髓保護和早期發(fā)現缺血的方法已經被使用，其中包括縮短手術時間，采用低溫和神經保護藥物、維持足夠的平均動脈壓以保證脊髓灌注、腦脊液引流和肋間和腰椎節(jié)段動脈再植術、術中監(jiān)測體感和運動誘發(fā)電位。
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