This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kim, J. S. Articles by Chung, C. S. Search for Related Content PubMed PubMed Citation Articles by Kim, J. S. Articles by Chung, C. S.

(Stroke. 1995;26:1548-1552.)
© 1995 American Heart Association, Inc.

Articles

Medial Medullary Syndrome

Report of 18 New Patients and a Review of the Literature

Presented in part at the 4th European Stroke Conference, Bordeaux, France, June 1-3, 1995.

Jong Sung Kim, MD; Hyeon Gak Kim, MD Chin Sang Chung, MD

From the Department of Neurology, University of Ulsan, Asan Medical Center, Seoul (J.S.K., H.G.K.), and Department of Neurology, Chungnam National University Hospital, Taejon (C.S.C.), South Korea.

Correspondence to Jong S. Kim, MD, Department of Neurology, Asan Medical Center, Song-pa PO Box 145, Seoul 138-600, South Korea.

	Abstract

Top Abstract Introduction Subjects and Methods Results Discussion References

 
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.

Key Words: cerebral infarction • magnetic resonance imaging • medulla oblongata

	Introduction

Top Abstract Introduction Subjects and Methods Results Discussion References

 
With the advent of MRI, infarctions occurring in the medulla can be more easily identified. Clinical^{1 2} and MRI^{3 4 5} characteristics of LMS, the most common type of medullary stroke, are well documented. MMS, a rarer type of stroke, has also been identified more frequently.^{6 7 8 9 10} To date, however, only approximately 30 cases have been reported,^{6 7 8 9 10 11 12 13 14 15 16 17 18 19 20 21 22 23 24 25 26 27 28} and the clinical and radiological characteristics of MMS have not been investigated extensively. Furthermore, in our experience MMS appears to be much more benign than previously thought. Therefore, in this report we describe our experience with 18 patients with MMS and review the previously reported cases.

	Subjects and Methods

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Eighteen patients who had clinical and MRI findings consistent with MMS were examined at two large tertiary hospitals (Asan Medical Center and Chungnam National University Hospital) between January 1991 and February 1995. The 15 men and 3 women ranged in age from 41 to 75 years (mean, 62 years). All except for 2 (patients 10 and 15) were examined within 5 days after the onset. Risk factors for stroke included hypertension in 13, diabetes mellitus in 11, cigarette smoking in 8, hyperlipidemia in 5, and a history of coronary heart disease in 4 patients. One had atrial fibrillation.

All patients underwent MRI, which was performed with a 1.5-T superconducting magnet (GE). An axial T₂-weighted (TR, 2500 milliseconds; TE, 80 milliseconds) scan was performed in the horizontal plane at 5- or 6-mm intervals. T₁-weighted (TR, 600 milliseconds; TE, 20 milliseconds) axial and sagittal images were also obtained. Using the T₂-weighted axial cuts, we evaluated the images rostrocaudally as follows: the upper medulla was characterized by dorsolateral bulging of the restiform body, the middle medulla by ventral-lateral bulging of the inferior olivary nucleus, and the lower medulla by its round shape.⁵

	Results

Top Abstract Introduction Subjects and Methods Results Discussion References

 
Clinical Features
Clinical features of the 18 patients are summarized in Fig 1. Three patients (patients 6, 8, and 15) had concurrent lateral medullary infarction on the side ipsilateral to the medial medullary stroke and had symptoms of a combination of MMS and LMS. One (patient 5) had a right lateral medullary infarction and a right basal pontine infarction 3 years and 8 months before the medial medullary infarction. Before the episode of MMS, this patient had mild residual sensory changes in the extremities.

View larger version (22K): [in this window] [in a new window]   Figure 1. Chart shows clinical and MRI findings of the patients. Pt indicates patient; Ipsi, ipsilateral; Par, paresthesia; PP, pinprick; VB, vibration; PO, position; Nyst, nystagmus; FP, facial paresis; DA, dysarthria; DP, dysphagia; and LP, lingual paresis.

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).

MRI and Vascular Studies
MRI results are depicted (copied from original films) in Fig 1. The lesions were located in the upper medulla in 10, in the middle medulla in 2 (patients 1 and 9), and in the lower medulla in 3 (patients 13, 15, and 17). Two (patients 2 and 5) had lesions extending from the lower to the upper medulla, and 1 (patient 18) had the lesion in the upper and middle medulla.

In 16 patients the lesion involved the paramedian-ventral region. However, 1 (patient 2) had bilateral lesions that caused unilateral clinical symptoms. The lesions of patients 3, 16, and 18 extended dorsally. Two (patients 12 and 17) had paramedian lesions sparing the ventral part of the medulla. Four had additional lesions in the posterior-lateral medulla. The lesion of patient 16 extended to the lower pons, and patient 2 had additional lesions in the bilateral middle cerebellar peduncle. MRI flow void signal was investigated with the use of both T₁- and T₂-weighted images, as described previously.^{29 30} Absent vertebral flow void signal was noted in the side ipsilateral to the lesion in 6 patients (patients 2, 3, 4, 8, 10, and 16) and in the side contralateral to the lesion in 1 (patient 18). Patient 6 had a hypoplastic vertebral artery in the side ipsilateral to the lesion. Three underwent angiography and 6 MR angiography, the results of which showed normal findings in 3 and vertebral artery occlusion or narrowing in 6 (in the side ipsilateral to the lesion in 5 and contralateral to the lesion in 1). Although 1 had atrial fibrillation, MR angiography results showed a severe narrowing of the vertebral artery favoring atherothrombosis as a likely pathogenetic mechanism. Including this patient, none had a cardiac valvular disease or echocardiographic evidence of thrombosis.

Literature Review
The 26 cases from previous literature are summarized in the Table. The patients included 14 men and 12 women, aged 28 to 84 years (mean, 57 years). Twenty-one patients were diagnosed by pathological examination, 4 by MRI, and 1 by both. Thirteen patients had unilateral lesions, and 13 had bilateral infarcts. Clinical manifestations included quadriparesis in 11, hemiparesis in 15, hemihypesthesia in 9, and quadrihypesthesia in 7 patients. Lingual paresis was described in 12 patients. Respiratory difficulty was noted in 6 patients with bilateral lesions and in 1 with a unilateral lesion.⁴ The cause of the infarction was usually atherothrombosis of the vertebral^{10 12 13 17 18 22} or the anterior spinal artery.^{12 13 14 18} Rarely, embolic occlusion of anterior spinal artery by talc²³ or fibrocartilaginous material²⁵ was documented, and syphilitic arteritis^{11 16} or compression of the anterior spinal artery by meningioma¹³ was the cause of MMS in 2 and 1 cases, respectively. The prognosis was good in 6 patients and poor in the remaining patients. More recently, Bernasconi et al¹⁰ briefly described 6 additional patients with MMS diagnosed by MRI. Among them, 4 with an infarct above the pyramidal decussation had contralateral sensorimotor (3 cases) or pure motor stroke (1 case), 3 of whom had ipsilateral lingual paresis. Two patients with an infarct below the decussation presented with sensorimotor stroke in the side ipsilateral to the lesions.

View this table: [in this window] [in a new window]   Table 1. Summary of Previously Reported Cases With MMS

	Discussion

Top Abstract Introduction Subjects and Methods Results Discussion References

 
MMS, first described in the early part of this century,^{31 32} remains a rare occurrence, and our 18 patients are by far the largest collection of this stroke syndrome. In our series the patients with MMS most commonly presented with benign hemisensorimotor stroke. Seventeen of the patients had hemiparesis, contralateral to the site of infarction in 15. Hemisensory symptoms occurred in 15 patients.

Tingling or numb sensation was a common sensory symptom in our patients and the cases previously reported,* which probably is attributed to an involvement of the medial lemniscus.³³ The area of sensory symptoms occasionally included the periotic region or even half of the face (patients 9, 16, 17, and 18). In these patients a part of the ascending trigeminal tracts may have been involved (Fig 2). Among sensory modalities, vibration sense was most commonly affected, being abnormal in 14 patients. Selective impairment of vibration sense was recorded in 3 of our patients and in a few previous cases.^{7 22} Although position sense was also commonly impaired in our series, it occasionally remained intact despite pathological evidence of the medial lemniscal involvement,^{16 18 19 20 24 26} suggesting that partial involvement of the medial lemniscus may not cause significant loss of position sense. The mildly impaired pinprick sense noted in 7 of our patients without LMS was also observed in cases described previously.^{12 14 15 27} MRI findings of patients 1, 13, 16, and 18 suggest that the lesions may have partially involved the spinothalamic pathway, which is located in the superficial-lateral part of the medulla (Fig 2). Alternatively, pain sensation not carried through the spinothalamic pathways³⁴ might have been affected.

View larger version (30K): [in this window] [in a new window]   Figure 2. Schematic drawing of the upper medulla and its important structures.

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 (Fig 2). The small lesions usually limited to the paramedian-ventral area may explain the paucity of tongue weakness in our patients. The absence of respiratory symptoms in our patients may also be explained in a similar manner since significant respiratory disturbances were usually associated with bilateral, extensive medullary lesions.^{8 9 12 16 23} The upbeat nystagmus shown in 2 of our patients was described previously,^{11 12 14 16 23 25} and the presence of gaze paresis or sixth nerve palsy observed in patient 16 and previously reported cases^{8 35} suggests that the lesions extended to the lower pons. These ocular signs, if present, can be of help in localizing the lesion.

Patient 12 was of interest in that she had bilateral gait ataxia without sensorimotor symptoms. The lesion was located in the paramedian pontomedullary junction, sparing the most ventral region. We were unable to find a similar case in the literature. However, bilateral gait ataxia was reported in patients with paramedian midpontine^{36 37} or midbrain³⁸ infarcts that spared the ventral surface. Presumably, involvement of the fastigial-pontine efferent or afferent fibers, which tend to project bilaterally,³⁹ may be responsible for this clinical symptom.

The results of angiography, MR angiography, and signal void analysis of MRI are in accordance with previous reports with documented vertebral artery thrombosis^{10 12 13 17 18 22} and illustrate that the most common cause of MMS is a thrombosis of the vertebral artery. However, since the lower two thirds of the medulla is supplied by the anterior spinal arteries, atherosclerosis in these vessels may also be related to MMS.^{12 13 14 18} In patients with unilateral MMS with good prognosis, however, the major arteries often remained patent.^{19 20 24} Occlusion of small paramedian vessels appears to be responsible for the infarction in these patients.^{15 22}

Considering the close relationship between MMS and vertebral artery disease, it is not surprising to see some of our patients experiencing both MMS and LMS, either concurrently (patients 6, 8, 15) or as separate events (patient 5). Combined MMS and LMS was first described by Déjérine³² and has been reported as usually occurring in separate episodes.^{12 40} Hauw et al⁴¹ identified 4 patients with combined MMS and LMS among 49 pathologically examined cases of medullary infarction. In rare occurrences, the whole hemimedulla can be involved, producing so-called Babinski-Nageotte syndrome.^{42 43}

Although our patients did not show any mental or emotional disturbances, previous reports have described patients presenting with pathological crying,^{12 13} laughing,^{12 13 26} or psychotic behaviors,^{15 26} symptoms often observed in patients with pontine^{37 44 45 46 47} or capsular⁴⁸ strokes. However, these reported patients had a previous history of depression,¹⁵ evidence of an involvement of the pontine basilar branches,¹² or additional lesions in the pontine base.^{13 26} Therefore, it remains to be investigated whether these symptoms can be caused by a pure medullary lesion.

In summary, our data suggest that MMS is most commonly manifested as hemisensorimotor stroke characterized by tingling sensation and impaired deep sensation, with the face usually but not always spared. Ipsilateral lingual paresis was rare, and identification of nystagmus or other ocular motor dysfunction may be of help in localizing the lesion. The lesion detected by MRI was generally small, unilateral, and usually involved the paramedian-ventral region of the upper medulla. 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.^{49 50 51 52}

	Selected Abbreviations and Acronyms

 

LMS = lateral medullary syndrome MMS = medial medullary syndrome TE = echo time TR = repetition time

	Footnotes

 
¹ References 7, 11-13, 15, 16, 22, 23, 26, 27.

Received February 2, 1995; revision received May 22, 1995; accepted May 22, 1995.

	References

Top Abstract Introduction Subjects and Methods Results Discussion References

 
1. Sacco RL, Freddo L, Bello JA, Odel JG, Onesti ST, Mohr JP. Wallenberg's lateral medullary syndrome: clinical-magnetic resonance imaging correlations. Arch Neurol. 1993;50:609-614. [Abstract/Free Full Text]

2. Norrving B, Cronqvist S. Lateral medullary infarction: prognosis in an unselected series. Neurology. 1991;41:244-248. [Abstract/Free Full Text]

3. Ross MA, Biller J, Adams HP, Dunn V. Magnetic resonance imaging in Wallenberg's lateral medullary syndrome. Stroke. 1986;17:542-545. [Abstract/Free Full Text]

4. Bogousslavsky J, Fox AJ, Barnett HJM, Hachinski VC, Vinitski S, Carey LS. Clinico-topographic correlation of small vertebrobasilar infarct using magnetic resonance imaging. Stroke. 1986;17:929-938. [Abstract/Free Full Text]

5. Kim JS, Lee JH, Suh DC, Lee MC. Spectrum of lateral medullary syndrome: correlation between clinical findings and magnetic resonance imaging in 33 subjects. Stroke. 1994;25:1405-1410. [Abstract]

6. Fox AJ, Bogousslavsky J, Carey LS, Barnett HJM, Vinitski S, Karlik SJ, Vinuela F, Pelz DM, Hachinski V. Magnetic resonance imaging of small medullary infarction. AJNR Am J Neuroradiol. 1986;7:229-233. [Abstract]

7. Sawada H, Seriu N, Udaka F, Kameyama M. Magnetic resonance imaging of medial medullary infarction. Stroke. 1990;21:963-966. [Abstract/Free Full Text]

8. Toyoda K, Hasegawa Y, Yonehara T, Oita J, Yamaguchi T. Bilateral medial medullary infarction with oculomotor disorders. Stroke. 1992;23:1657-1659. [Abstract/Free Full Text]

9. Kleinert G, Fazdkas F, Kleinert R, Schmidt R, Payer F, Offenbacher H, Lechner H. Bilateral medial medullary infarction: magnetic resonance imaging and correlative histopathologic findings. Eur Neurol. 1993;33:74-76. [Medline] [Order article via Infotrieve]

10. Bernasconi A, Bassetti C, Bogousslavsky J. Medial medullary stroke: clinical-MRI study of 6 patients. Cerebrovasc Dis. 1994;4:253. Abstract.

11. Tyler KL, Sandberg E, Baum KF. Medial medullary syndrome and meningovascular syphilis: a case report in an HIV-infected man and a review of the literature. Neurology. 1994;44:2231-2235. [Free Full Text]

12. Davison C. Syndrome of the anterior spinal artery of the medulla oblongata. Arch Neurol Psychiatry. 1937;37:91-107. [Abstract/Free Full Text]

13. Davison C. Syndrome of the anterior spinal artery of the medulla oblongata. J Neuropathol Exp Neurol. 1944;3:73-80.

14. O'Brien FB, Bender MB. Localizing value of vertical nystagmus. Arch Neurol Psychiatry. 1945;54:378-380. [Abstract/Free Full Text]

15. Brown WJ, Fang HCH. Spastic hemiplegia in man associated with unilateral infarct of the corticospinal tract at the pontomedullary juncture. Trans Am Neurol Assoc. 1956;81:22-26.

16. Meyer JS, Herndon RM. Bilateral infarction of the pyramidal tracts in man. Neurology. 1962;12:637-642.

17. Fisher CM, Curry HB. Pure motor hemiplegia of vascular origin. Arch Neurol. 1965;13:30-44.

18. Trelles JO, Trelles L, Urquiaga C. Le ramollissement médian du bulbe: a propos de deux cas anatomo-cliniques. Rev Neurol (Paris). 1973;129:91-104. [Medline] [Order article via Infotrieve]

19. Chokroverty S, Rubino FA, Haller C. Pure motor hemiplegia due to pyramidal infarction. Arch Neurol. 1975;32:647-648. [Abstract/Free Full Text]

20. Leestma JE, Noronha A. Pure motor hemiplegia, medullary pyramidal lesion, and olivary hypertrophy. J Neurol Neurosurg Psychiatry. 1976;39:877-884. [Abstract/Free Full Text]

21. Nardelli E, Lannucci A, Rizzuto N. Bilateral infarction of pyramidal tracts. Acta Neurol. 1978;33:130-136. [Medline] [Order article via Infotrieve]

22. Ropper AH, Fisher CM, Kleinman GM. Pyramidal infarction in the medulla: a case report of pure motor hemiplegia sparing the face. Neurology. 1979;29:91-95. [Abstract/Free Full Text]

23. Mizutani T, Lewis RA, Gonatas NK. Medial medullary syndrome in a drug abuser. Arch Neurol. 1980;37:425-428. [Abstract/Free Full Text]

24. Ho KL, Meyer KR. The medial medullary syndrome. Arch Neurol. 1981;38:385-387. [Abstract/Free Full Text]

25. Kase CS, Varakis JN, Stafford JR, Mohr JP. Medical medullary infarction from fibrocartilaginous embolism to the anterior spinal artery. Stroke. 1983;14:413-418. [Abstract/Free Full Text]

26. Paulson GW, Yates AJ, Paltan-Ortiz JD. Does infarction of the medullary pyramid lead to spasticity? Arch Neurol. 1986;43:93-95. [Abstract/Free Full Text]

27. Jagiella WM, Sung JH. Bilateral infarction of the medullary pyramids in humans. Neurology. 1989;39:21-24. [Abstract/Free Full Text]

28. Milandre L, Habib M, Hassoun J, Khalil R. Bilateral infarction of the medullary pyramids. Neurology. 1990;40:556.

29. Biller J, Yuh WTC, Mitchell GW, Nruno A, Adams HP Jr. Early diagnosis of basilar artery oclusion using magnetic resonance imaging. Stroke. 1988;19:297-306. [Abstract/Free Full Text]

30. Knepper L, Biller J, Adams HP, Yuh W, Ryals T, Godersky J. MR imaging of basilar artery occlusion. J Comput Assist Tomogr. 1990;14:32-35. [Medline] [Order article via Infotrieve]

31. Spiller WG. The symptom-complex of a lesion of the uppermost portion of the anterior spinal and adjoining portion of the vertebral arteries. J Nerv Ment Dis. 1908;35:775-778.

32. Déjérine J. Semiologie des affections du système nerveux. Paris, France: Masson et Cie; 1914.

33. Tasker RR. Somatotopographic representation in the human thalamus, midbrain, and spinal cord: the anatomical basis for the surgical relief of pain. In: Morley TP, ed. Current Controversies in Neurosurgery. Philadelphia, Pa: WB Saunders Co; 1976:485-495.

34. Haerer AF. DeJong's the Neurological Examination. 5th ed. New York, NY: JB Lippincott Co; 1992:47-66.

35. Satake M, Kira J-I, Yamada T, Kobayashi T. Raymond syndrome (alternating abducent hemiplegia) caused by a small haematoma at the medial pontomedullary junction. J Neurol Neurosurg Psychiatry. 1995;58:261. Letter.

36. Nabatame H, Fukuyama H, Akiguchi I, Kameyama M, Nishimura K, Torizuka K. Pontine ataxic hemiparesis studied by a high resolution magnetic resonance imaging system. Ann Neurol. 1987;21:204-207. [Medline] [Order article via Infotrieve]

37. Kim JS, Lee JH, Im JH, Lee MC. Syndromes of pontine base infarction: a clinical-radiological correlation study. Stroke. 1995;26:950-955. [Abstract/Free Full Text]

38. Bogousslavsky J, Maeder P, Regli F, Meuli R. Pure midbrain infarction: clinical syndromes, MRI, and etiologic patterns. Neurology. 1994;44:2032-2040. [Abstract/Free Full Text]

39. Carpenter MB, Sutin J. Human Neuroanatomy. 8th ed. Baltimore, Md: Williams & Wilkins Co; 1983:454-492.

40. Harris TH, Hauser A. Occlusion of the right posterior inferior cerebellar artery and right vertebral artery. Arch Neurol Psychiatry. 1931;26:396-400. [Abstract/Free Full Text]

41. Hauw JJ, Der Agopian P, Trelles L, Escourolle R. Les infarctus bulbaires: etude systématique de la topographie lésionnelle dans 49 cas. J Neurol Sci. 1976;28:83-102. [Medline] [Order article via Infotrieve]

42. Mossuto-Agatiello L, Kniahynicki C. The hemimedullary syndrome: case report and review of the literature. J Neurol. 1990;237:208-212. [Medline] [Order article via Infotrieve]

43. Nakane H, Okada Y, Sadoshima S, Fujishima M. Babinski-Nageotte syndrome on magnetic resonance imaging. Stroke. 1991;22:272-275. [Abstract/Free Full Text]

44. Helgason CM, Wilbur AC. Basilar branch pontine infarction with prominent sensory signs. Stroke. 1991;22:1129-1136. [Abstract/Free Full Text]

45. Andersen G, Ingeman-Nielsen M, Vestergaard K, Riis JO. Pathoanatomic correlation between poststroke pathological crying and damage to brain areas involved in serotonergic neurotransmission. Stroke. 1994;25:1050-1052. [Abstract]

46. Drake ME Jr, Pakalnis A, Phillips B. Secondary mania after ventral pontine infarction. J Neuropsychiatry Clin Neurosci. 1990;2:322-325. [Abstract/Free Full Text]

47. Kim JS, Lee JH, Lee MC, Lee SD. Transient abnormal behavior after pontine infarction. Stroke. 1994;25:2295-2296. Letter. [Medline] [Order article via Infotrieve]

48. Ceccaldi M, Poncet M, Milandre L, Rouyer C. Temporary forced laughter after unilateral strokes. Eur Neurol. 1994;34:36-39.

49. Ahmed OI, Orchard TJ, Sharma R, Mitchell H, Talbot E. Declining mortality from stroke in Allegheny County, Pennsylvania: trends in case fatality and severity of disease, 1971-1980. Stroke. 1988;19:181-184. [Abstract/Free Full Text]

50. Howard G, Toole JF, Becker C, Lefkowitz DS, Truscott L, Rose L, Evans GW. Changes in survival following stroke in five North Carolina counties observed during two different periods. Stroke. 1989;20:345-350. [Abstract/Free Full Text]

51. McGovern PG, Burke GL, Sprafka JM, Xue S, Folsom AR, Blackburn H. Trends in mortality, morbidity and risk factor levels for stroke from 1960 to 1990: the Minnesota Heart Survey. JAMA. 1992;268:753-759. [Abstract/Free Full Text]

52. McGovern PG, Pankow JS, Burke GL, Shahar E, Sprafka JM, Folsom AR, Blackburn H. Trends in survival of hospitalized stroke patients between 1970 and 1985: the Minnesota Heart Survey. Stroke. 1993;24:1640-1648.[Abstract/Free Full Text]

This article has been cited by other articles:

				J. S. Kim, K. -D. Choi, S. -Y. Oh, S. -H. Park, M. -K. Han, B. -W. Yoon, and J. -K. Roh Medial medullary infarction: Abnormal ocular motor findings Neurology, October 25, 2005; 65(8): 1294 - 1298. [Abstract] [Full Text] [PDF]

				M. Kwon, J. H. Lee, and J. S. Kim Dysphagia in unilateral medullary infarction: Lateral vs medial lesions Neurology, September 13, 2005; 65(5): 714 - 718. [Abstract] [Full Text] [PDF]

				M Nakajima, M Inoue, and Y Sakai Contralateral pharyngeal paralysis caused by medial medullary infarction J. Neurol. Neurosurg. Psychiatry, September 1, 2005; 76(9): 1292 - 1293. [Abstract] [Full Text] [PDF]

				P. Zickler, R. J. Seitz, H.-P. Hartung, and H. Hefter Bilateral medullary pyramid infarction Neurology, May 24, 2005; 64(10): 1801 - 1801. [Full Text] [PDF]

				W. Kameda, T. Kawanami, K. Kurita, M. Daimon, T. Kayama, T. Hosoya, T. Kato, and for the Study Group of the Association of Cerebrov Lateral and Medial Medullary Infarction: A Comparative Analysis of 214 Patients Stroke, March 1, 2004; 35(3): 694 - 699. [Abstract] [Full Text] [PDF]

				H.-C. Fung, S.-T. Chen, L.-M. Tang, and L.-S. Ro Triparesis: MRI documentation of bipyramidal medullary infarction Neurology, April 9, 2002; 58(7): 1130 - 1130. [Full Text] [PDF]

				P. P. Urban, S. Wicht, G. Vucorevic, S. Fitzek, J. Marx, F. Thomke, A. Mika-Gruttner, C. Fitzek, P. Stoeter, and H. C. Hopf The course of corticofacial projections in the human brainstem Brain, September 1, 2001; 124(9): 1866 - 1876. [Abstract] [Full Text] [PDF]

				S.-H. Lee, D.-E. Kim, E.-C. Song, and J.-K. Roh Sensory Dermatomal Representation in the Medial Lemniscus Arch Neurol, April 1, 2001; 58(4): 649 - 651. [Abstract] [Full Text] [PDF]

				H. Kim, C.-S. Chung, K.-H. Lee, and J. Robbins Aspiration Subsequent to a Pure Medullary Infarction: Lesion Sites, Clinical Variables, and Outcome Arch Neurol, April 1, 2000; 57(4): 478 - 483. [Abstract] [Full Text] [PDF]

				J. S. Kim and S. Choi-Kwon Sensory Sequelae of Medullary Infarction : Differences Between Lateral and Medial Medullary Syndrome Stroke, December 1, 1999; 30(12): 2697 - 2703. [Abstract] [Full Text] [PDF]

				S TERAO, M IZUMI, S TAKATSU, J TAKAGI, T MITSUMA, A TAKEDA, M HIRAYAMA, and G SOBUE Serial magnetic resonance imaging shows separate medial and lateral medullary infarctions resulting in the hemimedullary syndrome J. Neurol. Neurosurg. Psychiatry, July 1, 1998; 65(1): 134a - 135. [Full Text]

				J. S. Kim, J. H. Lee, and C. G. Choi Patterns of Lateral Medullary Infarction : Vascular Lesion–Magnetic Resonance Imaging Correlation of 34 Cases Stroke, March 1, 1998; 29(3): 645 - 652. [Abstract] [Full Text] [PDF]

				S Terao, S Takatsu, M Izumi, J Takagi, T Mitsuma, A Takahashi, A Takeda, and G Sobue Central facial weakness due to medial medullary infarction: the course of facial corticobulbar fibres J. Neurol. Neurosurg. Psychiatry, September 1, 1997; 63(3): 391 - 393. [Abstract] [Full Text] [PDF]

				J. S. Kim and Y. H. Bae Pure or Predominant Sensory Stroke Due to Brain Stem Lesion Stroke, September 1, 1997; 28(9): 1761 - 1764. [Abstract] [Full Text]

				J. R. Keane Twelfth-Nerve Palsy: Analysis of 100 Cases Arch Neurol, June 1, 1996; 53(6): 561 - 566. [Abstract] [PDF]

				J. S. Kim and S. Choi-Kwon Discriminative Sensory Dysfunction After Unilateral Stroke Stroke, April 1, 1996; 27(4): 677 - 682. [Abstract] [Full Text]

This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Kim, J. S. Articles by Chung, C. S. Search for Related Content PubMed PubMed Citation Articles by Kim, J. S. Articles by Chung, C. S.