Article under review: Novy J, Carruzzo A, Maeder P, Bogousslavsky J. Spinal cord ischemia: clinical and imaging patterns, pathogenesis, and outcomes in 27 patients. Arch Neurol 2006;63:1113-20.
Background: The spinal cord is supplied rostrally from braches of the vertebral arteries, with more caudal contributions from radicular arteries that enter the spinal canal with the nerve roots. These radicular arteries are somewhat variable, but commonly have major vascular contributions around C3, C7, T7, between T9-T12 (artery of Adamkiewicz), and sometimes at the conus (artery of Desproges-Gotteron originating from the internal iliac artery). As a result there are several major rostral-caudal arterial territories of the spinal cord: cervicothoracic (C1-T3), midthoracic (T3-T7), and thoracolumbar (T8 to the conus medullaris).
The intrinsic vasculature of the spinal cord is from a single anterior spinal artery and 2 posterior spinal arteries and their associated peripheral (circumferential) vascular plexus. The posterior spinal arteries run along the posterolateral sulcus of the spinal cord and give off penetrating branches. The anterior spinal artery gives off central arteries that run horizontally in the central sulcus, supplying most of the central gray matter and the adjacent white matter including the corticospinal tracts.
Spinal cord infarction has been recognized since 1658, when it was first described by Wepfer (Silver 2003). Recognition of spinal cord infarction increased markedly after World War II when it was identified as a complication of aortic surgery (Silver 2003).
Purpose: To characterize the pathogenesis and outcomes of spinal cord infarction.
Design: Retrospective review.
Methods: Patients with acute spinal cord infarction were identified among 72 patients admitted for investigation of acute myelopathy.
Patients underwent extensive investigation:
* depending on the level of the lesion
Results and discussion: 27 patients (11 men and 16 women) had acute ischemic myelopathies with a mean age of 56 years (range 19 to 80 years).
|Syndrome||Motor||Lemniscal sensory||Spinothalamic sensory|
|Anterior spinal artery||bilateral*||bilateral|
|Posterior spinal artery||bilateral*||bilateral|
* quadriparesis or paraparesis depending on the cord level affected
# hemiparesis or monoparesis depending on the cord level affected
Investigations: Other than spinal MRI, investigations were normal or nonspecific. Blood studies were unrevealing except for previously known diabetes and hypercholesterolemia. Cerebrospinal fluid studies showed an elevated protein concentration in almost half (n=12, 44%). One patient had a known aortic valve replacement. Imaging disclosed no further potential sources of cardioemboli and no instances of vertebral artery dissection.
MRI showed an ischemic lesion in a well-defined arterial spinal cord territory in two thirds of the patients (n=18, 67%). Sagittal and axial T2-weighted images were most useful. An abnormal MRI was more frequent in those with severe weakness (but the breakdown of cases was not given). Although evidence of vertebral body infarction on MRI has been reported to be a useful confirmatory sign of spinal cord infarction (Yuh et al 1992; Faig et al 1998; Amoiridis et al 2004), this is apparently insensitive as only 1 patient had a concomitant vertebral body infarction. None had evident arteriovenous malformation or fistula.
The breakdown of cases by spinal segments affected was not given, but lesions apparently clustered in the following general segments: C1-C7, T3-T7, T8-L1, corresponding approximately to the territories identified as most susceptible in previous studies (eg, Cheshire et al 1996; Masson et al 2004).
It should be noted that the distribution of vascular syndromes and the distribution of etiologies in this study differ from those in several other studies because of the inclusion/exclusion criteria. For example, by excluding cases associated with surgery (eg, aortic surgery) or trauma, there are fewer cases associated with hypotension and a larger proportion with causes that were not clearly identified. Nevertheless, Masson and colleagues also reported that a definite cause of spinal cord infarction was identified in less than half of patients (Masson et al 2004).
The authors also provided a further analysis of potential etiologic factors. This analysis must be considered exploratory for a number of reasons: (1) data were obtained retrospectively and are susceptible to various forms of bias (recall, ascertainment, etc.); (2) sample sizes within each group were quite small; (3) comparisons were not specified a priori and all comparisons made were not elaborated; (4) given the nature of the reported statistically significant differences by Fisher's exact test it is likely that multiple comparisons were made, with no statistical adjustment made for multiple comparisons.
Mechanical stress and damage to radicular arteries was considered a likely factor in a number of patients. Degenerative spinal disease was present in 11 patients at the level of the cord infarct, and ischemic symptoms developed immediately after a presumed triggering movement in 13 patients (48%) that could have stressed that level. Anterior spinal artery, posterior spinal artery, and unilateral infarcts—but not central or transverse infarcts—were felt to be associated with mechanical triggering movements and with acute and chronic spinal disease.
Degenerative spinal disease may directly compress or damage vessels with triggering movements (especially radicular arteries), impair venous drainage, and induce foraminal and subarachnoid fibrosis—all of which reduce collateral blood flow and increase susceptibility to ischemia. Acute damage to radicular arteries with mechanical stress may result in acute spinal cord infarction.
Hypotension can produce severe transverse lesions which reduce to central lesions at the superior and inferior poles of the lesions (Zülch and Kurth-Schumacher 1970). Such lesions often involve the thoracolumbar region, presumably due to a high density of motoneurons and frequent atherosclerotic disease of the aorta and iliac arteries (Duggal and Lach 2002).
Outcomes: The outcomes reported in the present study are difficult to judge as (1) outcome categories were not clearly defined, and (2) the tabular data and the textual data do not clearly correspond (25 patients tabulated in the table with some overlapping outcome categories).
Nevertheless, the outcomes were felt to be generally favorable and only about half of the patients (n=13, 48%) had significant gait impairment on leaving the hospital and only about 40% (10 of 25 in Table 4) required assistance with walking. Treatment varied and could not be related to outcome in this small retrospective study. Post-hospital outcomes were not available in this study.
Masson and colleagues reported that about two thirds of the 28 patients in their study were unable to walk at onset and one third required assistance (Masson et al 2004). The initial severity of neurologic deficits is the best (though imperfect) predictor of neurologic outcome (Masson et al 2004). Salvador de la Barrera and colleagues reported that about a fifth (22%) of the 38 patients in their study died during the initial hospitalization, and of the survivors more than half were unable to walk at discharge (57%), a quarter were ambulatory with assistance (25%), and only 18% were fully ambulatory (Salvador de la Barrera et al 2001). The outcome at 2 months is worse with either proprioceptive impairment, walking impairment, or bladder dysfunction at onset (Masson et al 2004). Patients frequently have residual pain, especially those with anterior spinal artery territory infarcts involving the spinothalamic tracts (Pelser and van Gijn 1993; Masson et al 2004).
To date no therapy for acute spinal cord infarction has been demonstrated to be beneficial.