Novy Jan, Carruzzo Alain, Maeder Philippe, Bogousslavsky Julien
Department of Neurology, Centre Hospitalier Universitaire Vaudois BH10, 1011 Lausanne, Switzerland.
Arch Neurol. 2006 Aug;63(8):1113-20. doi: 10.1001/archneur.63.8.1113.
The natural history and pathogenesis of ischemic spinal cord infarction remain largely unknown because most clinical studies have included mostly patients with ischemic lesions associated with aortic surgery or prolonged arterial hypotension.
To assess the pathogenetic mechanisms and outcomes of these cord infarctions based on clinical findings and spinal vascular anatomy.
Retrospective review.
We analyzed the clinical, laboratory, imaging, and outcome data for 27 patients with acute spinal cord infarction admitted between 1990 and 2003. There were 11 men and 16 women (age range, 19-80 years [mean age, 56 years]).
Ten patients had anterior spinal artery patterns, 4 each had anterior and posterior unilateral patterns, 3 had central patterns, and 2 each had posterior spinal artery patterns, transverse syndromes, and unclassifiable clinical pictures. Twenty patients had no identifiable etiology. Patients with a central or transverse infarct showed a high frequency of peripheral vascular disease, and all transverse infarcts occurred following prolonged arterial hypotension. The onset of all other infarcts was associated with mechanical triggering movements (P = .02), and these patients frequently had diseases of the spine (P = .003) at the level of the spinal lesion, with the clinical data suggesting root involvement at the level of the spinal cord lesion and pointing to mechanical injury of a radicular artery. The outcomes were favorable, with only 13 patients showing significant gait impairment on leaving the hospital.
There are 2 main types of spinal cord ischemia: (1) radicular artery territory infarct (bilateral anterior or posterior spinal artery infarcts and unilateral infarcts) and (2) extensive spinal cord hypoperfusion (central and transverse infarcts). Each type has characteristic clinical, imaging, pathogenetic, and prognostic features.
由于大多数临床研究主要纳入了与主动脉手术或长时间动脉低血压相关的缺血性病变患者,缺血性脊髓梗死的自然病史和发病机制仍 largely 未知。
基于临床发现和脊髓血管解剖结构评估这些脊髓梗死的发病机制和结局。
回顾性研究。
我们分析了 1990 年至 2003 年间收治的 27 例急性脊髓梗死患者的临床、实验室、影像学和结局数据。其中男性 11 例,女性 16 例(年龄范围 19 - 80 岁[平均年龄 56 岁])。
10 例患者为脊髓前动脉型,4 例为前侧和后侧单侧型,3 例为中央型,2 例为脊髓后动脉型、横贯性综合征和无法分类的临床表现。20 例患者病因不明。中央型或横贯性梗死患者外周血管疾病发生率高,所有横贯性梗死均发生在长时间动脉低血压之后。所有其他梗死的发作与机械触发动作有关(P = 0.02),这些患者在脊髓病变水平经常患有脊柱疾病(P = 0.003),临床数据提示脊髓病变水平有神经根受累,并指向根动脉的机械损伤。结局良好,仅 13 例患者出院时存在明显步态障碍。
脊髓缺血主要有 2 种类型:(1)根动脉供血区梗死(双侧脊髓前动脉或后动脉梗死及单侧梗死)和(2)广泛脊髓低灌注(中央型和横贯性梗死)。每种类型都有特征性的临床、影像学、发病机制和预后特征。