Fibrocartilaginous Embolism in Anterior Spinal Artery Syndrome

Spinal cord infarction in childhood is extremely rare. Characteristics of an anterior spinal artery syndrome are subacute pain with transition to paraplegia and a dissociated paresthesia with concomitant vesicorectal dysfunction.

In 2013, we treated two patients with peracute nontraumatic paraplegia after the initial pain in the upper thoracic/cervical spine.

Patient 1, a 14-year-old boy, experienced a stinging pain in the thoracic spine after minimal strain and rapidly developed a weakness. At admission, he showed an incomplete paraplegia concentrating on the right lower extremity and vivid muscle reflexes. Furthermore, he displayed a reduced sensibility and a voiding dysfunction. The magnetic resonance images (MRI) showed long distance signal alterations in the cervical myelon (C2/3 and C5-7), which were considered as edema. Extensive diagnostics including vascular, thrombophilic, cerebrospinal fluid, and autoimmune parameters did not yield any etiologic risk factors. After rehabilitation, the boy achieved major improvement of function.

Patient 2, a 15-year-old boy, suffered from weakness of the legs while walking around. He reported a major pain in the neck the day before without any trauma. He developed an incomplete tetraparesis with paresthesia and voiding dysfunction within a few hours. The MRI showed lesions with partially barrier dysfunction in the cervical myelon (C3-C6), which were considered as spinal ischemia. In the axial sequences, T2w hyperintensities in the anterior myelon were visible, known as “snake bite.” After rehabilitation, the patient regained almost complete resolution of all functions.

In both the patients, vascular disease (ischemia, bleeding, and vessel malformation), inflammatory disease (acute myelitis transversa, multiple sclerosis, and neuroborreliosis), and spinal tumors were excluded. On the basis of nontraumatic pain in the recent past and otherwise unknown etiology, we suggest a fibrocartilaginous embolus as the pathogenetic cause of a spinal ischemia. Hereby, particles of an acute vertical disk herniation of the nucleus pulposus material are mobilized under strain and are embolized through microlesions into the anterior spinal artery.