Acute central cord syndrome: injury mechanisms and stress features.

STUDY DESIGN

Numerical techniques were used to study the mechanisms of acute central cord syndrome.

OBJECTIVE

To analyze the features of stress distribution in the cervical cord under different injury conditions using finite element model of the cervical cord and to improve the understanding of the possible pathogenesis of acute central cord syndrome.

SUMMARY OF BACKGROUND DATA

Acute central cord spinal injury was initially attributed to hemorrhagic damage to the central portion of the spinal cord, but recent histopathologic studies showed that it was predominantly a white matter injury. The precise anatomic location of neuronal injury and the etiology of the clinical manifestation were poorly understood.

METHODS

Cervical cord injury was simulated using a finite element model of the cervical enlargement described previously, with the model loaded under 3 traumatic postures: neutral, flexion, and extension. Five traumatic conditions were simulated and analyzed: hyperextension with the pinch force directed to the anterior (A) or posterior (B); flexion injuries (C), vertical compression with the pinch force directed to the anterior (D) or posterior (E). After simulation, several representative cross-sections of each traumatic pattern were selected. In each cross-section, the average von Mises stress of 9 regions, such as anterior funiculus, lateral part of the lateral funiculus, medial part of the lateral funiculus, lateral part of the posterior funiculus, medial part of the posterior funiculus, anterior horn, the bottom of anterior horn, the cervix cornu posterioris, the caput cornu posterioris, and the apex cornu posterioris was recorded.

RESULTS

High localized stress occurred at the portion under compression injury and the level above it. High localized stress tended to occur at the lateral part of the anterior horn motor neurons innervating the hand muscles in traumatic conditions A and D. Under conditions A, D, and E, the average localized stress at the anterior and posterior horn of the gray matter was higher than that at the white matter in all selected cross-sections, and the stress was higher at the anterior funiculus, the medial part of the lateral funiculus, and the lateral part of the posterior funiculus in the white matter. Under conditions B and C, the differences of the localized stress between the gray and the white matter were not as significant as under conditions A, D, and E, and the stress was lower at the medial part of the lateral funiculus than that at the lateral part of the posterior funiculus. Under all traumatic conditions, the average stress at the lateral part was higher than that at the medial part of the posterior funiculus.

CONCLUSION

Three common traumatic patterns: hyperextension, flexion, and vertical compression, could be the possibly underlying injury mechanisms of the central cervical cord syndrome according to the results of the current finite element analysis. The stress features under different injury conditions were not in complete accord. High stress mainly occurred at the posterior horn, the anterior horn, and the adjacent white matter. The centermost lesion was not common in mild central cord injuries. The upper extremity weakness should be ascribed to the damage at the corticospinal tract and the motor neurons in the anterior horn. Hyperpathia probably resulted from injuries to the posterior horn, the anterior funiculus, and the fasciculus cuneatus. Just as there are varieties of the localized stress features in central cord injuries, variations in clinical presentations were common.