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There have been several reports on MRI of the classic medullary vascular syndromes such as dorsolateral infarction and medial infarction.1-4 The syndrome with both dorsolateral and medial infarctions is known as hemimedullary (Babinski-Nageotte) syndrome.5 However, because of the separate arterial topography supplying the medulla, the simultaneous occurrence of ischaemic lesions of its medial and lateral parts would be extremely rare.6 7 We report MRI of a patient with an ipsilateral lateral medullary infarction (Wallenberg’s syndrome) followed by a medial medullary infarction with a 6 month interval. The initial stroke event on the central facial weakness of this patient was previously reported.8
A 40 year old man noted weakness of the right limbs and dysarthria. Since the age of 38, the patient had been on an antihypertensive drug regimen. He was conscious, and his blood pressure was 134/80 mm Hg. Neurologically, there were noted right supranuclear facial weakness, paralysis of the left hypoglossal nerve, paralytic dysarthria, and right hemiparesis with prominent weakness of the arm. Deep tendon reflexes were exaggerated in the right limbs and Babinski’s sign was positive on the right side. Light touch and vibratory sensations were slightly decreased in the right leg, but temperature and pain sensations were well preserved. There was no diabetes mellitus or hyperlipidaemia. No abnormalities were noted on ECG, transthoracic echocardiogram, and Holter monitoring. Brain MRI at 10 days after the onset showed a high signal intensity area (T2 weighted image) in the left ventromedial part of the upper medulla, which was diagnosed as an infarct (figure A). Cerebral angiography performed at 12 days after onset showed mild atherosclerotic changes of the vertebrobasilar artery. The right facial weakness and left tongue paralysis were gradually improved and the patient was discharged with persisting mild right hemiparesis after one month.
Six months later, however, he suddenly experienced a floating sensation and gait difficulty. At that time he was alert and had a blood pressure of 160/106 mm Hg. Neurological examination showed left Horner’s syndrome, skew deviation with slight downward position of the left eyeball, clockwise rotatory nystagmus, impairment of temperature and pain sensations of the left face, paralysis of the left soft palate, hoarseness, slight dysphagia, cerebellar ataxia of the left limbs, decreased temperature and pain sensations of the neck and all parts of the right side, and hypohidrosis of the left half of the body. Slight right hemiparesis was present. Brain MRI performed on the next day showed a high signal intensity area (T2 weighted image) in the left dorsolateral portion of the upper to middle medulla. A repeat MRI study at one month after this second attack clearly showed an infarct in a left dorsolateral portion of the medulla with a reduction of oedema, and showed a reduction of an infarct in the left ventromedial part from the first stroke (figure B).
The patient presented here developed a left dorsolateral medullary infarction 6 months after the onset of an infarction involving the left ventromedial part of the upper medulla. Both were clearly seen on MRI. The dorsolateral part and medial part of the medulla are supplied by separate branches from the posterior inferior cerebellar artery and the anterior spinal artery, both of which are indirectly supplied by the vertebral artery. Hence the occlusion of the vertebral artery could produce simultaneous hemimedullary syndrome.2 6 However, serial infarctions of the separate topographic areas of the medulla resulting in a hemimedullary syndrome have been suggested,3-5 serial events documented by MRI—such as in the present patient—have not been reported. The present case provided unequivocal evidence that the hemimedullary syndrome can occur as serial events of the medial and lateral medullary infarctions.
With the advent of MRI, it has recently become possible to see microvascular lesions in the brain stem that would in the past have been detected only by postmortem examination. In patients where such multiple ischaemic lesions occur at separate sites and times so as to form a certain distinct syndrome, serial observations with MRI will certainly prove the pathogenic background of this syndrome and be of great clinical interest.