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A computed tomography scan of his cervical spine showed multilevel degenerative changes that were most severe at C3-4 but no fracture. Magnetic resonance imaging of his cervical spine demonstrated significant spondylotic spinal canal stenosis at the level of C3-4, increased intramed- ullary T2-weighted signal, and spinal cord atro- phy at that level. The paraspinal soft tissues were within normal limits (Figure 1). The radiological picture was indicative of chronic spondylotic cer- vical myelopathy.


Because the clinical status of our patient was not worrisome, he was assigned to an intermedi- ate hospital bed, and neurological and vital signs were monitored every 2 hours. On 2-hour vital sign controls, his systolic and diastolic blood pressures were above 120mmHg and above 70mmHg, respectively, throughout his stay and his heart rate was within the normal range of 70 to 85 beats per minute. Oxygen saturation was above 90% on 2 liters by nasal cannula. Through- out his hospital stay, our patient complained of intermittent subjective symptoms, such as par- esthesias, whole-body pain, and fear of death, but the results of regular 2-hour exams did not show any worsening of the motor exam results. Approximately 8 hours after admission, a urinary catheter was introduced for increasing difficulty with urination. Two hours after placement of the urinary catheter, he was still stable. On the next 2-hour check (4 hours after the catheter place- ment), he was found in bed unresponsive. Im- mediate resuscitation was initiated but was not successful.


The autopsy revealed macroscopic signs of spinal cord necrosis extending along the entire cervical spinal cord to the mid-thoracic region (Figure 2). The microscopic examination showed diffusely scattered large eosinophilic degenerat- ing neurons in a background of disintegrating glial tissue consistent with ischemic necrosis.


Discussion Delayed


spontaneous post-traumatic cervical


spinal cord infarction in adults is a devastating condition that, to the best of our knowledge, has not been described yet. Cases of spinal cord isch- emia after minor trauma are well documented in children7,8


. Nance and Golomb2 reviewed a series


of children with spinal cord infarction without vertebral fracture and concluded that hypoten- sion and fibrocartilaginous embolism were the principal etiological factors of spinal cord infarc- tion after minor trauma or extensive physical exercise. Ischemia of the spinal cord is believed to be the underlying mechanism of spinal cord injury without radiographic abnormality9,10


.


The exact mechanism of delayed spinal cord infarction in our case remains unknown, but we


Figure 1 . Magnetic resonance imaging (MRI) of the cervical spine shows cervical spinal ca- nal stenosis at the C3-4 segment. (A) T1-weighted MRI image without contrast. (B) T2-weight- ed MRI image. The T2-weighed sagittal image shows intramedullary hyperintensity and no signs of spinal cord swelling. The images are compatible with chronic spondylotic cervical myelopathy.


speculate that premorbid degenerative spinal canal stenosis played an important role in this respect. The mid-cervical region with chronic cervical myelopathy at the C3-4 level seems to have represented a hemodynamically fragile territory. Experimental evidence in cats shows that vascular autoregulation is deranged even after mild spinal cord trauma leading to transi- tory hyperemia11


. Experimental studies on rats


demonstrated that mild spinal cord injury was followed by a transitory decrease in SCBF12


and


this decrease was paralleled by a transitory drop in mean arterial blood pressure (MABP)13


. Given the results of these experimental stud-


ies, it is conceivable that the delayed spinal cord infarction in our patient was the end result of several pathophysiological processes. First, our patient withstood a mild head injury after being struck by a dragline weight. This blow to his head provoked hyperflexion of the cervical spine, which caused spinal cord compromise in the nar- row cervical spinal canal, hence the mild sensory symptoms in the upper and lower extremities at admission. Second, this mild cervical spinal cord affliction (even if the clinical symptoms were minimal) had the further pathophysiological con- sequence of post-traumatic hyperemia because of perturbed vascular autoregulation. We hypoth- esise that the combination of locally decreased SCBF and transitory diminution of MABP dur- ing the night ultimately triggered infarction of the cervical spinal cord.


Vascular territory involvement is another im- portant topic in the pathophysiology of spinal cord infarction. Pathological studies of infarcted human spinal cords indicate that infarctions oc- cur most frequently in the most metabolically active lumbosacral and cervical segments14


. This


finding is contrary to the historical concept of ischemic vulnerability of the “watershed zone” centered at the mid-thoracic levels but is plau- sible in the context of the angiosome concept of blood supply to the spinal cord. Based on the an- giosome concept, the arterial supply to the spinal cord follows a segmental, rather than longitudi- nal, distribution15


. So, during arterial hypoten-


sion, the most vulnerable spinal cord segments are those that are the most active metabolically. The fact that our patient had an infarction to the cervical intumescence is in good agreement with the above findings. With respect to pial versus sulcal artery involvement, Ishizawa et al.16


, in a


histopathological study of hemodynamic spinal cord infarction, showed that the infarction in- volved the gray matter supplied by the central artery while the periphery of the spinal cord sup- plied by the pial arteries remained intact. In our patient, the pathological finding was altered by the pre-existing cervical spondylotic myelopathy, and delineation between pial versus sulcal vascu- lar territories was not possible.


Conclusions In this case report, we describe a catastrophic Autumn 2012 | SpinalSurgeryNews | 27


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