Cervical myelopathy disease is generally characterized by a progressive worsening when caused by spondylar-disc-arthrosis. Acute cervical myelopathy etiopathological diagnosis is challenging2.
In our case report, clinic acutely onset in two episodes: the second one causing marked neurological worsening if compared to the first one. Clinical history would suggest a cardiovascular event followed by spinal cord infarction. Nevertheless, patient is young; she does not have cardiovascular risk factors (hypertension, atrial fibrillation, heart disease) nor hypercoagulability pathological conditions. No imaging examination was positive for thrombo-embolic lesions; CT aortic angioCT scan study was negative for dissecting lesions.
On the other hand, laboratory CSF tests by rachicentesis did not document any inflammatory or demyelinating diseases.
Myelopathy onset was diagnosed by cervical spine MRI, revealing an altered intramedullary signal area, following a hypothetic cardiovascular event. Cervical spine cord signal alteration was documented 12 hours later neurological symptoms onset, when the first embolic cleavage probably occurred. 24 hours later, as a consequence of a following probable embolic event, patient presented further acute neurological worsening: it produced a severe tethraparesis (ASIA C). Latency interval between the onset of the symptoms and the radiological evidence would suggest an ischemic problem.
Acute myelopathy by spine cord infarction would result spinal cord swelling inside a narrow cervical canal. Anterior triple discectomy decompression surgery would produce inside cervical canal pressure reduction, favoring medullary perfusion and secondary ischemic damage prevention.
FCE could contribute to explain the event4, 5, 6. As already proposed in other previous papers, spinal cord infarction is a rare disease and accounts for about 1% of all strokes3, 7. If no other obvious causes on imaging and laboratory tests are present, it can be a pathophysiological cause, albeit extremely rare. Its diagnosis is exclusive8, 9, 10, 11.
Peaks in the incidence of FCE are made up adolescence and middle age4, 12, 14. Hypothesized mechanism is migration of material from the nucleus pulposus into the vessels that supply the medulla2, 4, 5, 9, 10. Typical presentation includes neck or lumbar pain, followed by neurological deficits, up to supply territory of the occluded vessel. More frequently, ASA closure brings to bilateral motor deficits with possible asymmetry and sensory deficit from involvement of the spino-thalamic tract2, 3, 4, 8.
Unfortunately FCE diagnosis would be possible only with anatomopathological examination (and can be performed post-mortem)14, 16. CSF analysis is mandatory to exclude inflammatory, infectious and autoimmune pathological forms, as well as demyelinating diseases. As well as the already published cases, in our case the only data detected is a mild hyperprotidorrachia8, 15.
24 hours later onset of symptoms MRI study documented spine cord swelling and an alteration signal in T2 sequences, confirming SCI.
Proposed algorithm for the FCE diagnosis is: establish the diagnosis of myelopathy and the level involved; exclude traumatic and compressive etiologies; exclude inflammatory etiologies; establish the diagnosis of medullary infarction; establish the possible diagnosis of FCE (related to minor spinal trauma or episodes of increased intradiscal pressure and/or Valsalva maneuvers, presence of disc degeneration, especially Schmorl's hernietion or close to the level of myelopathy and absence of cardiovascular risk factors)4.
According to literature clinical practice, therapeutic strategies were: hypothermia; systemic hypertension; spinal fluid drainage; oxygen therapy; pharmacological neuroprotection; prevention of secondary ischemic damage2.
Secondary damage prevention is provided by perfusion pressure adjustment (by increasing mean arterial pressure and/or reducing CSF pressure with the external lumbar drainage); in our case, cervical canal via anterior decompression protected spine cord from secondary damage, before second ischemic insult could determine more serious effect than the first embolism.
The question remains whether it would be more appropriate to operate soon after the first clinical manifestation, earlier than the second episode occurred, despite spine cord ischemia was not revealed by MRI scan and self-resolution of the tetraparesis in the following 24 hours.