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Infarction in the territory supplied by the cervical anterior spinal artery occurs infrequently, especially in young people. The anterior spinal artery supplies the ventral two thirds of the spinal cord and provides its major blood supply. In the cervical cord, the anterior spinal artery is supplied by anterior radicular arteries arising from the cervical branches of the vertebral arteries and the ascending cervical arteries.1 There have been few reports of MRI in the first hours after the start of an anterior spinal artery syndrome. We describe a case of an acute anterior spinal cord syndrome appearing after two suppressed sneezes that was studied with MRI only four hours after the onset of symptoms.
A 37 year old previously healthy woman suddenly experienced severe anterior thoracic pain after two consecutive suppressed sneezes. Five minutes later, the pain irradiated to the arms and was followed by paresthesiae and weakness in both upper limbs. One hour later the weakness and paresthesiae had extended to the legs. On admission neurological examination showed tetraparesis, with a predominantly distal motor deficit in the arms (0/5 power distal and 3/5 proximal). There was an overall reduction in power to 3/5 in the legs. The deep tendon reflexes were diminished in the arms and absent in the legs. Plantar responses were indifferent. There was a loss of sensation for pain and temperature below the T2 dermatome. Light touch and vibratory and position sensitivity were preserved. The patient also developed a neurogenic bladder.
With these the clinical features, an infarction in the territory of the anterior spinal artery was suspected and an emergency MRI of the cervical spine was performed four hours after the onset of symptoms. This initial MRI, using fast spin echo sequences, failed to show any spinal cord signal abnormality (figure, A); immediately afterwards, a conventional sagittal dual echo long TR spin echo sequence showed a linear high signal intensity lesion affecting the anterior part of the cervical spinal cord between C3 and C7 (figure, B and C). No cord swelling was identified. All the findings were consistent with the clinical diagnosis of infarction of the anterior spinal artery.
Chest radiography, ECG, and routine laboratory examinations were normal. Chest CT performed to rule out aortic dissection was also normal. The patient was treated initially with intravenous methylprednisolone (1 g daily for three days).
Over the next 12 hours she developed flaccid paralysis of the lower and distal upper limbs, with continued diminished muscle power of the deltoid and biceps muscles. Deep tendon reflexes were abolished except for the biceps reflexes. The sensorial level was unchanged. An ECG failed to disclose thrombi. Somatosensory evoked potentials in the arms and legs showed no conduction blocks. Blood coagulation tests were normal. Antinuclear and antiphospholipid antibodies analysis were negative. Serological tests for HIV, Epstein-Barr virus, lues, Borrelia burdogferi, varicella zoster virus, and herpes simplex virus were negative. Four days later a follow up cervical spine MRI, including angiographic sequences of the vertebrobasilar system, was performed. Vertebral artery dissection could be ruled out, but the spinal cord showed pronounced swelling and on the long TR conventional spin echo sequences a diffuse high intensity signal covering almost the entire diameter of the cervical spine was identified that spared only its posterolateral borders (figure, D). The inferior extension of the signal abnormality reached the T1 level. Spinal angiography was not performed, as it was not considered to be clinically justified. A third MRI performed two months later showed an extensive area of atrophic myelomalacia of the cervical cord between C3 and T1.
The patient made a slow clinical recovery, and four months later appreciable tetraparesis persisted.
Infarction of the cervical spine cord is rare, especially in young people. We think that the patient presented with infarction of the anterior spinal cord because of the sudden onset and rapid development of typical clinical features after two violent sneezes, with no posterior column involvement (dissociated sensory impairment), absence of cord compression, and exclusion of other known neurological diseases, all of which point to anterior spinal artery syndrome as a result of infarction in the territory supplied by this artery.
Different causes of anterior spinal cord infarction have been described in young people—namely, arteriovenous fistula, spinal surgery, cardiac surgery, arteriography, fibrocatilagenous embolism, polyarteritis nodosa, and carotid or vertebral artery dissection. However, the final cause is not identified in half of the cases.2 3 Spinal cord or brainstem infarctions have been reported in association with chiropractic manipulation1 and hyperextension of the neck. Dissection of the vertebral artery was found in all these cases. In our patient this second diagnosis was ruled out with the combination of conventional MRI and MR angiography. Gutowski et al 4 reported another case of cervical posterior spinal artery infarction after sneezing. In our patient, the spinal cord infarction could have been caused by abnormal neck movements in association with the suppressed sneezes. The relation of extreme flexions of the neck (violent sneeze) with the abrupt onset of symptoms suggests vascular compression or obstruction of the vertebrobasilar system without arterial dissection.
Most cases of spinal cord infarction are associated with arteriovenous fistulas5 that are not always identified on MRI, and it has been suggested that spinal angiograms should be performed, at least in young patients, when no obvious cause is known. However, a more recent report shows a higher sensitivity of MRI in detecting this kind of malformation. In the presented case vertebral angiography was not considered clinically justified. The clinical contribution of angiography in those cases of anterior spinal infarction with an obvious traumatic event and in which a high quality cervical spine MRI has ruled out spinal vascular malformations and vascular dissection, may be limited and should not be considered mandatory.
MRI is a sensitive modality in the evaluation of the spinal cord for infarction. It rules out extradural compression, vascular malformations, and space occupying lesions. The differential diagnosis includes infectious or parainfectious myelitis, multiple sclerosis, and vasculitis. In inflamatory or demyelinating lesions, it is well known that T2 weighted images show lesions some time before the clinical onset, whereas with ischaemic lesions a normal or almost normal MRI is usually seen in the first few hours. The sudden onset of clinical symptoms after a rapid movement of the neck is very suggestive of infarction, but not of myelitis. In the acute phase after infarction the diameter of the spinal cord remains normal and diagnosis is based on signal abnormalities on the long TR sequences, which reflect the presence of cytotoxic oedema. However in the subacute phase, with the appearance of extensive vasogenic oedema, the high signal abnormalities are more evident and associated with cord swelling. In our case the anterior location and the temporal MRI changes, together with the sudden onset and rapid development of typical clinical symptoms, should help in differentiating spine infarction from other spinal cord lesions such as multiple sclerosis and neoplastic conditions.
We have not found any reported case of spinal cord infarction in which MRI was performed in the first four hours after the clinical event. In this acute phase only a subtle anterior linear hyperintensity was identified on the T2 weighted images. This abnormal intensity was not clearly seen on the fast spin echo sequence; however, we were able to identify it with a conventional spin echo sequence. Despite the fact that fast spin echo sequences have been accepted for routine use in the examination of spinal cord lesions, replacing conventional spin echo sequences, the second are more sensitive and should be used in selected cases, when obvious clinical lesions have not not been clearly shown on the fast spin echo sequences. Fast spin echo imaging of the spine is in most ways similar to conventional spin echo imaging. However, there may be difficulties in detecting very small intramedullary lesions.6
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