Tuesday, August 7, 2012

Medial Medullary Syndrome Practical Aspects

Medial Medullary Syndrome: Report of 18 New Patients and a Review of the Literature. Jong Sung Kim, Hyeon Gak Kim, Chin Sang Chung. Stroke. 1995;26:1548-1552
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Abstract
Background and Purpose With advanced imaging techniques, infarctions occurring in the medulla are now more easily identified. To date, however, only approximately 30 cases of medial medullary infarction syndrome (MMS) have been reported, and the clinical and radiological characteristics of MMS remain to be studied.
Methods We studied 18 patients (15 men, 3 women; mean age, 62 years) who had compatible clinical and MRI findings of MMS and reviewed the previously reported cases.
Results Seventeen patients had a unilateral lesion usually involving the upper medulla, and 1 had bilateral lesions. Fifteen patients had unilateral sensorimotor stroke, while 2 presented with pure motor stroke. The face was usually but not always spared. The degree of hemiparesis varied, and a tingling sensation with decreased vibration and position sense was the most common sensory manifestation. Two patients had lingual paresis, and none suffered respiratory difficulties. One patient presented with bilateral gait ataxia without sensorimotor dysfunction. Angiography or MR angiography performed in 9 patients showed vertebral artery disease in 6. Three patients had concurrent lateral medullary infarction, and 1 had a previous history of lateral medullary syndrome. The prognosis was generally good, although residual hemiparesis remained in patients with initially severe hemiparesis. Review of 26 previously reported cases showed that they frequently had bilateral lesions, often presenting with quadriplegia, lingual paresis, respiratory symptoms, and a grave prognosis.
Conclusions Our data illustrate that MMS is most often manifested as benign hemisensorimotor stroke frequently associated with tingling sensation and impaired deep sensation. This benign form of MMS should be much more common than MMS with poor prognosis and may have been frequently misdiagnosed as capsular or pontine stroke before the era of MRI. 
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A few clinical details
Hemiparesis was the most common clinical manifestation of MMS; 15 had contralateral hemiparesis, and 2 (patients 15 and 13) had ipsilateral hemiparesis and crural monoparesis, respectively. One (patient 12) did not have motor weakness but had transient bilateral gait ataxia. In 2 (patients 5 and 14), motor weakness was the only clinical manifestation (pure motor stroke), although patient 5 had slight residual sensory symptoms due to previous LMS. At the peak of the weakness, the degree of the hemiparesis (motor power of the proximal limbs) was severe (0 to 2 on a scale of 5) in 3, moderate (3 on a scale of 5) in 5, and mild (4 or clumsiness on a scale of 5) in 9. Generally, the distal part of the limb (hand and foot) was more severely affected compared with the proximal part. In patients with significant motor deficit, the progression of weakness usually evolved for several hours or days. During this progression, muscle tone was generally flaccid but became spastic during the recovery phase.
Hemisensory symptoms were the second most common clinical manifestation, occurring in 15 patients (including 3 with LMS). Initially, 12 patients felt tingling or a numb sensation. The face was usually spared, but the area of paresthesia occasionally ascended to the periotic area (patients 3 and 11) or even to the midface (patients 9, 16, 17, and 18). Vibration sense was impaired in 14 patients, and decreased position sense was noted in 10. However, only 1 (patient 16) had severely decreased position sense, and none described the vibration sense as reduced more than 50% of the intact side. Seven patients without LMS stated that the pinprick sense was also mildly impaired.
Headache (3 cases) and nausea/vomiting (3 cases) were uncommon, and dizziness/ vertigo was noted in 9 patients. One (patient 18) had transient ipsilateral lingual paresis, and patient 3 showed clumsy tongue movements bilaterally. Including these 2 patients, 4 without LMS had dysarthria, while 2 (patients 2 and 18) had dysphagia. Mild facial paresis was noted in 4 patients. None had respiratory disturbances. One had horizontal nystagmus, 1 had upbeat nystagmus, and 1 had both. Patient 16 had transient gaze paresis and long-lasting sixth nerve palsy.
The patients were followed up for 14 days to 41 months (mean, 11 months). None died during the follow-up period. All were able to walk unassisted, although mild residual paresis remained in patients with initially moderate to severe motor weakness. Uncomfortable paresthesia over the palm or foot became the most distressing symptom in some patients (patients 9, 11, 16, and 17). 
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Lingual paresis
Unexpectedly, lingual paresis, described in 12 of 26 cases reported in the literature, was observed in only 2 of our patients, with the lesions extending dorsally. Lingual paresis is caused by lesions extending into the lateral part of the medulla, affecting the fibers of the hypoglossal nerves or fascicles, or lesions extending deep into the hypoglossal nucleus.
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Differences from previous reports
The paucity of lingual paresis and respiratory symptoms along with the patients’ benign outcome was strikingly different from previously described subjects in whom prognosis was generally poor. These differences may be explained in several ways. First and most importantly, the diagnosis of MMS was made by MRI in our patients, whereas that of most of the previously reported cases was based on autopsy. Second, since hypertension seems to be more prevalent and large-vessel atherosclerosis less common in oriental than Western countries, relatively small vessels might have been more often affected in our Korean patients than in previously reported cases. Finally, it may also be possible that the recent progress on risk factor management has led us to encounter more benign cerebrovascular diseases today than before.

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