Medial medullary infarction from fibrocartilaginous embolism to the anterior spinal artery.

Abstract

SUMMARY A previously healthy young woman presented with sudden onset of quadriplegia, anesthesia below the C3 dermatome, respiratory paralysis, vertical nystagmus, ocular bobbing and cortical blindness. After partial resolution of the latter deficits, she remained quadriplegic, with a C3 level of anesthesia, and in respiratory paralysis until death from complications of a fulminant pulmonary infection. Autopsy disclosed bilateral infarctions of the medial aspect of the medulla and the upper cervical cord, in the distribution of the anterior spinal artery. Multiple sites of arterial occlusion by fibrocartilaginous material were found in branches of the anterior spinal artery, in correspondence with the sites of infarction. A review of the literature disclosed only 2 examples of medial medullary syndrome from embolism to the anterior spinal artery.Stroke, Vol 14, No. 3, 1983 INFARCTION IN THE MEDULLA OBLONGATA is usually unilateral and limited to its dorso-lateral aspect. Medial medullary infarction occurs rarely, and it results from occlusion of the vertebral or anterior spinal artery (ASA).1 -2 Bilateral symmetric involvement of this area by vascular lesions has been described on three instances before, [3][4][5] in one of them as a result of embolic occlusion of ASA branches. 4 This report describes the case of a young patient with bilateral embolic medial medullary infarctions. The topography of the medullary lesions and the associated vascular pathology were studied by serial sections, which disclosed multiple occlusions of the ASA branches by fibrocartilaginous emboli.Case Report A 23 y/o female bank clerk complained of sudden occipital headache while at work, and vomited once. Taken immediately to the hospital, on her way she developed bilateral arm weakness, rapidly followed by weakness of the legs. By the time of her arrival in the emergency room a few minutes after onset, she had become unresponsive, had shallow respirations at a rate of 3 per minute and then suffered a respiratory arrest. Because of marked trismus, intravenous diazepam (Valium) was required to perform oral endotracheal intubation. After 10 minutes of mecnanical ventilation she was able to open her eyes spontaneously. Physical examination showed regular pulse at 72 per minute, temperature 37 degrees C. She was able to open and close the eyes spontaneously and on verbal command, and the extraocular movements were conjugate and full in all directions. Testing of visual func-

Bilateral distal upper limb amyotrophy and watershed infarcts from vertebral dissection.

“…Anterior spinal artery embolism produces a clinical picture and autopsy findings of infarction of the entire anterior spinal artery territory. 8 Embolism would be unlikely to result in bilateral symmetrical, pencil-shaped infarcts restricted to the anterior horns. That nonvascular, compressive conditions such as spondylotic myelopathy and ossification of the posterior longitudinal ligament may result in similarly located spinal cord MR hyperintensities ("snakeeyes") 9 or probable ischemic lesions at autopsy 10 supports a hypoperfusion etiology in the present case.…”

Lateral and Medial Medullary Infarction

“…[1][2][3] For this reason, only a limited number of cases could be examined. Since the advent of MRI, the clinical diagnosis of MI has been made possible, and several clinical studies of MI are available.…”

Bilateral medial medullary infarction with oculomotor disorders.

“…6 Gaze palsy is usually caused by a lesion in the pons or midbrain, and vertical oculomotor abnormality is a classic feature of midbrain lesions, related to the rostral interstitial nucleus of the MLF. 7 Three clinicopathologic reports on medial medullary infarction, however, described the presence of oculomotor disturbance 3 " 5 : bobbing eye, 3 upward and lateral gaze palsy, 5 and poor maintenance of depression of gaze. 4 All of the pathologically verified lesions were limited to the bilateral medial medulla, extending to the pontomedullary junction in one case 5 ; the mechanism, however, was not detailed.…”