The spinal cord is part of the central nervous system that extends from medulla oblongata to lumbar region (level of vertebral body L1-L2).
It is made by H-shaped grey matter that forms the most inner part of the spinal cord and white matter around it. Grey matter forms anterior and posterior horns and split white matter into funiculus (anterior, medial and posterior) (Fig. 1)
The spinal cord is irrigated by three arteries: two posterior spinal arteries (PSAs) and one anterior spinal artery (ASA) (Fig. 2 and Fig. 3). Spinal arteries receive blood supply from spinal branches that arise from various parent vessels depending on the segment of spinal cord.
There are 3 main segments of spinal cord arterial irrigation (Fig. 4):
- C1-D3 segment with blood supply form vertebral arteries and cervical ascending arteries.
- D3-D7 with supply from intercostal arteries.
- and below the D8 with supply from the Adamkiewicz artery.
ASA irrigates the anterior two-thirds of the spinal cord and PSAs supply the one-third of the spinal cord.
Anterior and posterior circulation is connected by pial anastomoses called vasocorona that supply the outermost part of the medulla.
Vertebral bodies share blood supply with the spinal cord and often infarct together (Fig. 5).
There are two main incidence peaks of spinal cord infarct: first one during childhood and second in adult patients (>65 years old).
In childhood, the most frequent causes are cardiac malformations and trauma.
In adults the main causes are arteriosclerosis and aortic pathology (aneurysms, aortic dissection and aortic surgery), followed by embolisms, arterial hypotension and A-V malformations although in more than 40% of cases have no proven origin.
- The rapid development of neurological symptoms (loss of bladder and sphincter control as well as motor and sensitivity deficits).
- Back pain (can be present even several days before the neurological clinic).
- Severity and type of clinic depend on vascular territory and affected levels.
- Especially dangerous is the involvement of segments C3-C5 and D4-D9. First one forms phrenic nerve (motor innervation of the diaphragm) and second splanchnic nerve (vasomotor tone) that can cause respiratory failure and hypotension.
Spinal cord widening and oedema (it’s important to differentiate oedema with space-occupying lesion).
Hyperintense intramedullary signal changes can be seen in T2/STIR that appear during the first 2 days after clinical appearance and affect one of the vascular territories.
In the hyperacute phase, MRI exploration can be normal (lack of alterations in MRI in case of clinical suspicion supports the diagnosis of spinal cord infarct).
Mild contrast enhancement can be seen during the acute phase because of the blood-brain barrier destruction.
DWI sequence is the most sensitive and detects alterations even in the hyperacute phase. Unfortunately, they are more difficult to interpret given low spatial resolution and artefacts by fluid movements.
Anterior spinal artery syndrome (Fig. 6 and Fig. 7):
The most common syndrome with an affectation of the vascular territory of the anterior spinal artery.
The typical clinic is:
- Loss of bilateral motor function.
- Loss of sensitivity of pain and heat.
- Conservation of proprioception and vibration.
May have an incomplete presentation.
Anterior horn syndrome:
Incomplete anterior syndrome with a motor deficit but without a sensory deficit.
Only affects anterior horns that have greater metabolic activity and are more vulnerable to ischemia.
Owl eyes sign (Fig. 8) - hyperintense T2 lesions of anterior horns (Fig. 9).
Posterior spinal artery syndrome (Fig. 11 and Fig. 12):
Affectation of the territory of one of posterior spinal arteries.
Uncommon and mainly unilateral syndrome.
- loss of sensitivity at the level of injury.
- loss of proprioception and vibration below the injury.
- when motor symptoms exist they are minimal and transitory.
Sulcal artery syndrome (Fig. 13):
Sulcal arteries are paired branches of the anterior spinal artery that supply the spinal cord.
Clinical presentation is similar to occlusion of anterior spinal artery but unilateral (decrease in ipsilateral strength with decrease sensitivity to pain and heat without loss of sensation of vibration and proprioception).
Central and transverse spinal infarction:
Infarcts caused by hypoperfusion and microemboli that affect poorly perfused locations (watershed areas).
Clinic depends on the size of the lesion:
- Small centrally localised lesions (Fig. 14) cause loss of heat and pain sensitivity at the level of injury. Sensitivity below the injury is not affected. There is no loss of motor function or sphincter control.
- An extensive area that affects all parts of the spinal cord (Fig. 15) and causes loss of motor function and all modalities of sensitivity below the lesion.
Peripheral spinal cord supplied by vasocorona is not affected.
Differential diagnosis should be made with:
- Spinal cord compression due to trauma or neoplasia - lack of morphological abnormalities of the spinal canal, infarction rarely enhances.
- Demyelinating diseases such as SM or transverse myelitis- the appearance of a very sudden neurological clinic, lack of alterations in the hyper-acute phase, restriction of DWI.
- Spontaneous epidural hematoma - collection in epidural space.