Acute traumatic central cord syndrome: magnetic resonance imaging and clinical observations

Abstract

Object. Acute traumatic central cord syndrome has been classically thought to be caused by a hemorrhage that primarily affects the central part of the spinal cord and that destroys the axons of the inner part of the corticospinal tract devoted to the motor control of the hands. Some authors, however, have proposed that its pathogenesis is based on the destruction of the motor neurons supplying the muscles of the hand. To test the validity of these two theories, the authors retrospectively studied the magnetic resonance (MR) images obtained in 18 cases of acute traumatic central cord syndrome (ATCCS) to assess the presence of intramedullary blood and to define the distribution of the abnormal signal intensities in the cervical spinal cord. Methods. The authors used the American Spinal Injury Association (ASIA) motor scale to assess upper- and lower-limb deficits and to evaluate its metameric distribution. The abnormal intramedullary signal was then compared with the distribution of the motor deficit. All MR imaging sessions performed in the acute stage revealed a hyperintense signal on T2-weighted sequences without any signal change suggesting the presence of intramedullary blood. The localization of this signal was distributed predominantly from the C3–4 to the C5–6 disc levels. The mean ASIA motor score was 74.3 of 100, with an unequal representation between the upper and lower limbs (32 of 50 compared with 42.3 of 50, respectively). The metameric distribution of the deficit was also unequal, with a major deficit in hand function (C8—T1) compared with the more proximal cord segments (5.2 of 10 compared with 7.8 of 10, respectively). This demonstrates the absence of any correlation between the hyperintense signal and the motor deficit distribution. Conclusions. Acute traumatic central cord syndrome cannot be explained by the injury to the gray matter at the level of motor neurons supplying the hand muscles. In agreement with recently published data, the results of this series confirm the absence of intramedullary hemorrhage and corroborate the hypothesis that ATCCS may be explained by the impairment of the corticospinal tract, which can be affected globally.