The incidence of spinal vascular disease is much lower than that of cerebrovascular disease because the spinal cord is supplied with blood through several routes, with vascular redundancy. Specifically, the spinal cord is usually supplied with blood by 6 to 8 main root medullary arteries from the craniovertebral junction to the conus medullaris. This collateral circulation makes the spinal cord significantly more tolerant of ischaemia than brain tissue. However, the disadvantage of this redundant blood supply is the watershed region between the two arterial blood-supply areas. This watershed area has reduced blood supply and is thus more vulnerable to ischaemic damage. The blood flow in the cervical and lumbar segments of the spinal cord is significantly higher than that in the thoracic segment, especially the upper thoracic segment [2]. This paper reports a rare case of long-segment spinal cord infarction. The lesions involved the C6–T7 segment of the spinal cord, mainly covering the thoracic segment. The lesions were extensive and unusual.

The causes of spinal cord infarction include not only common factors, such as atherosclerosis, vasculitis, hypertension, dyslipidaemia, diabetes, hyperfibrinogen, and long-term heavy smoking, but also the following factors [3,4,5,6]: fibrocartilage embolism, congenital heart disease surgery or spinal cord decompression, aortic dissection aneurysm or aortic thrombosis, hypotension, percutaneous vertebroplasty, multiple rib fractures, spinal cord arteriovenous malformations, epidural abscess, epidural haematoma, intervertebral disc prolapse, adhesive arachnoiditis and bacterial meningitis.

In addition to the spinal cord MRI that suggested long-segment spinal cord infarction, the brain MRI also suggested multiple acute lacunar infarctions in this patient. Therefore, after further discussion, we determined that the most likely stroke mechanism was embolic infarction; such emboli originate from the atherosclerotic aortic arch. The following findings support this inference. First, the chest CTA showed that the aortic arch exhibited noncalcified plaque with stenosis and multiple ulcers; an external force could have knocked loose the noncalcified plaque when the patient set down the heavy object. Second, we did not find evidence of atrial fibrillation on the ambulatory ECG or obvious abnormality on the colour Doppler echocardiography, thus ruling out cardiogenic embolism. Third, the vascular anatomy could explain why the spinal cord infarction and cerebral infarction occurred simultaneously. The spinal cord infarction could have been caused by vertebral artery embolism, and the multiple cerebral infarctions could have been caused by internal carotid artery embolism. The multiple infarct lesions could also be explained by embolic infarction. However, this case suggests that there is merit to further exploration of the aetiology.

Spinal cord infarction is an ischaemic spinal vascular disease with a stroke-like onset; it often reaches a peak within a few minutes or hours. Given his clinical manifestations, this patient was considered to have anterior spinal artery syndrome, specifically, anterior 2/3 syndrome [4, 7], which is more common in the thoracic segment. Generally, the first symptom of this condition is severe nerve root pain located at the corresponding level of the lower boundary of the affected segment. Most cases involve dissociative sensory disorders with the loss of sensation involving pain and temperature and the retention of deep sensation. More obvious manifestations are dysfunctions of urination and defecation. After 3 months of follow-up, the neurological deficit in this patient was significantly improved. Therefore, we recommend that the initial treatment of such patients include medication and active rehabilitation treatment.

The incidence rate of spinal cord infarction is relatively low, and the aetiology and clinical manifestations of this disease are quite distinct. Clinically, spinal cord infarction is effectively differentiated from Guillain–Barre syndrome, acute myelitis, spinal cord demyelinating disease, spinal cord injury and other spinal cord diseases [8]. MRI examination is very important for the diagnosis of this disease and the assessment of the patient’s condition. Currently, there is no universal scheme for treating spinal cord infarction, and most therapies are based on the treatment scheme for cerebral infarction. With deepening clinical understanding of spinal cord infarction, the clinical treatment of this disease will improve.

In conclusion, long-segment spinal cord infarction is quite rare and can be complicated with cerebral infarction. The specific aetiology merits further exploration.

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