J Neurol (2002) 249 : 85–93© Steinkopff Verlag 2002 ORIGINAL COMMUNICATION

Emre KumralNazire AfsarDursun KırbasKaan BalkırTolga Özdemirkıran

Spectrum of medial medullary infarction: clinical and magnetic resonance imaging findings

Introduction

Preliminary pathological studies have demonstratedthat infarction of the medial medulla oblongata rarelyoccurs [11, 12, 49]. Despite the description of severalmedullary syndromes, only the medial medullary in-farction (MMI) of Dejerine has been accepted as a com-plete, recognizable syndrome. The typical neurologicalsigns associated with unilateral medial medullary syn-

drome or syndrome of Dejerine include hemiparesissparing the face contralateral to the infarct, andhemisensory loss of the posterior column type con-tralateral to the infarct, and weakness of the tongue ip-silateral to the infarct [13]. Dejerine also described thecombination of MMI with lateral medullary infarction(LMI) (the hemimedullary syndrome later called asBabinski and Nageotte syndrome) [2].During the 1970 s,autopsy proven reports of the discrete unilateralsyndrome were published. Later, in the mid-1980 s the

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■ Abstract Among 4200 consecu-tive patients admitted to three hos-pitals with acute ischemic stroke,we found only 11 patients in whommagnetic resonance imaging

Received: 21 February 2001Received in revised form: 22 February 2001Accepted: 17 May 2001

Emre Kumral M. D. (�) · Kaan Balkır ·Tolga ÖzdemirkıranStroke Unit, Department of NeurologyEge UniversityFaculty of MedicineBornova, Izmir, 35100, TurkeyTel.: +90-5 32-2 16 52 13Fax: +90-2 32-4 63 97 26E-Mail: ekumral @ med.ege.edu.tr

Nazire AfsarDepartment of NeurologyMarmara UniversityIstanbul, Turkey

Dursun KırbasDepartment of NeurologyBakırköy State HospitalIstanbul, Turkey

(MRI) had proved that they hadmedial medullary infarction(MMI). In our centers, patientswith MMI were less than 1 % ofthose with vertebrobasilar stroke.The infarcts documented by MRIwere unilateral in 10 patients andbilateral in one. On clinico-topo-graphical analysis there were fourclinical patterns: (1) Classical De-jerine’s syndrome was the most fre-quent, consisting of contralateralhemiparesis, lemniscal sensory lossand ipsilateral lingual palsy in 7 ofthe eleven patients. (2) Pure hemi-paresis was present in 2 patients;(3) Sensorimotor stroke was pre-sent in 1 patient with contralateralhemiparesis, hypesthesia and milddecrease in pain sensation withoutlingual palsy; (4) Bilateral MMIsyndrome in 1 patient, accompa-nied by tetraparesis, bilateral lossof deep sensation, dysphagia, dys-phonia and anarthria. Presumedcauses of MMI were intrinsicbranch penetrator artery disease

with concomitant vertebral arterystenosis in 6 of the 11 patients, ver-tebral artery occlusion in 2,dolichoectatic vertebrobasilar ar-teries in 2, a source of cardiac em-bolism in 1. Prognosis at 3 monthswas favorable in 8 patients, but thepatient with bilateral MMI syn-drome had persisting motor deficitcausing limitation of daily activi-ties, and 2 died from systemiccauses. The classical triad of acuteMMI facilitates the diagnosis, al-though the recognition of this syn-drome in patients with incompletemanifestations can be difficult andoccurs more frequently than com-monly thought. Moreover, vertebralartery atherosclerosis and branchatheromatous disease of the pene-trating arteries are the main causesof medullary infarction.

■ Key words Stroke · Ischemia ·Medial medullary infarction ·Lingual palsy

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documentation of MMI by brain magnetic resonanceimaging (MRI), allowed us to recognise the neuro-oph-thalmological signs of MMI, and confirmed the occur-rence of bilateral MMI and combined MMI and LMI.Posterior infarcts of the medulla were both anatomicallyand clinically overshadowed by a consistantly associatedcerebellar infarct in the posterior inferior cerebellarartery (PICA) territory and considered together withanterolateral infarcts as a subgroup of lateral medullaryinfarcts [10, 11, 26, 45].

In this study, we present a consecutive series of pa-tients with MMI proven by MRI, and attempt to classifyclinical entities with regard to lesion topography andclinical findings.

Materials and methods

Stroke data files of three Neurology Department were searched forpatients with MMI during the period from1993 to 2000. There were 6patients with MMI from Izmir (among 2200 patients with ischemicstroke), 3 patients from Marmara University (among 1250 patients),and 2 from Bakırköy State Hospital, Istanbul (among 750 patients).Allpatients were hospitalized within the first day of stroke onset and ex-amined by at least one of the authors. Magnetic resonance imagingMRI (T1-, T2- and proton density weighted images by 5-mm thick sec-tions with and without gadolinium contrast) and magnetic resonanceangiography (MRA) were performed in all patients with 1.5 T MR sys-

tems, and readings were carried out by a neuroradiologist blinded tothe findings on neurological evaluation. T1-weighted (repetition time[RT] 450–600 ms; echo-time [ET], 12–20 ms), T2-weighted (RT,2000–5500 ms; ET, 80–120 ms), proton density-weighted (RT,2000–5500 ms; ET,10–40 m) MR examinations and MRA (three di-mensional time-of-flight technique) were performed in the first weekafter stroke.Systematic stroke assessment was performed with a stan-dard protocol including complete blood cell count and urinalysis,transcranial Doppler, duplex sonography of the carotid and vertebralarteries, 12-lead electrocardiography (ECG), and in selected casestransthoracic or transesophageal echocardiography (in 3 cases) anddigital substraction angiography (DSA) by Seldinger’s method (in 2cases). We recorded risk factors such as hypertension, diabetes, regu-lar smoking, hypercholesterolemia, venous hematocrit at admission,history of migraine and heart disease.

Vascular territories of the medulla were defined according to themap of brainstem territories from the anatomical studies of Duver-noy [15, 48]: (1) Anteromedial medullary arteries territory arise fromthe vertebral artery (VA) at the upper medulla and from the anteriorspinal artery (ASA) at the lower medulla; (2) Anterolateral medullaryarteries arise mostly from the ASA; (3) Lateral medullary arteries ter-ritory arise from the VA and posterior inferior cerebellar artery(PICA); (4) Posterior medullary arteries territory arise from the me-dial branches of the PICA. In figure 1, the vascular territories (A) andthe main vascular arteries (B) of the medulla were illustrated. Thetopography of the stroke was assessed from anatomical diagrams ofthe medulla at four levels used in the MRI findings (i.e, uppermedulla, middle medulla, lower medulla and cervicomedullary junc-tion).Presumed stroke causes and cardiovascular risk factors were as-sessed according to previously defined criteria [30].

Fig. 1 Axial schematic view of vascular territories (A) and the main vascular arte-ries (B) of the medulla (anatomy and vascularization after Duvernoy [15]).

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Tabl

e1

Clin

ical

char

acte

ristic

s of 1

1 pa

tient

s with

med

ial m

edul

lary

infa

rctio

n.

No/s

ex/a

geLe

sion

site,

Risk

Caus

eIn

itial

com

plai

nts

Dysa

rthr

iaDy

spho

nia

Faci

alFa

cial

Mot

orSe

nsor

yGa

gLi

ngua

lGa

itNy

stag

mus

Late

roRa

nkin

loca

lisat

ion

fact

ors

palsy

hype

sthe

sialo

ssre

flex

palsy

atax

iapu

lsion

Scal

elo

ss

1/M

/42

Righ

t, AM

Ht, s

mk

BAD

hem

ipar

esis

+–

++

M4

+–

+–

––

1

2/M

/43

Left,

AM

Smk,

hko

lBA

Dhe

mip

ares

is+

–+

–M

2+

++

+–

–3

dysa

rthr

ia

3/M

/68

Righ

t, AM

HtBA

Dhe

mip

ares

is+

–+

–M

3+

++

+ho

rizon

tal

–2

rota

tory

4//M

/56

Left,

AM

Ht, h

kol

LAD

num

bnes

s+

––

–M

4–

+–

––

–1

5/M

/66

Left,

AM

Ht,S

mk,

BAD

dysa

rthr

ia+

––

–M

4+

–+

––

3Dm

, MI,

hem

ipar

esis

Ca

6/M

/80

Left,

AM

Ht, h

kol

DEhe

mip

ares

is+

+–

–M

2+

–+

+–

+4

7/F/

70Ri

ght,

–BA

Ddi

zzin

ess

++

+–

M4

++

++

horiz

onta

l–

1AM

+AL

8//F

/26

Left,

PFO

CEhe

mip

ares

is+

–+

+M

3+

–+

+–

+1

AM +

AL

dizz

ines

s, at

axia

9/M

/52

Righ

t,Ht

, MVP

LAD

hem

ipar

esis

––

––

M0

+–

–+

horiz

onta

l+

4He

mim

edul

ladi

plop

ia, v

ertig

o

10/M

/63

Righ

t, AM

Ht, D

mBA

Dhe

mip

ares

is+

–+

–M

3+

–+

+–

+1

11/M

/57

Bila

tera

l, AM

Ht,sm

k,DE

dysa

rthr

ia+

++

+Bi

late

ral,

Bila

tera

l+

++

Upbe

at,

+5

hkol

atax

iar,M

3; l,

M4

horiz

onta

lro

tato

ry

AM: a

nter

omed

ial;

AL: a

nter

olat

eral

; L: l

ater

al te

rrito

ry; M

VP: m

itral

e va

lve

prol

apsu

s; PF

O: p

aten

t for

amen

ova

le; C

a: ca

rcin

oma

(bla

dder

); Dm

: dia

bete

s mel

litus

; Ht:

hype

rten

sion;

hko

l: hy

perc

hole

ster

olem

ia; s

mk:

smok

-in

g; B

AD: i

ntra

cran

ial b

ranc

h at

hero

mat

ous d

iseas

e; D

E: v

erte

bro-

basil

ar a

rter

y do

licho

ecte

sia; M

: the

seve

rity

of p

ares

is, 5

(nor

mal

) to

0 (c

ompl

ete

pare

sis)

88

Results

There were 11 patients with acute MMI, 9 men and 2women, with the mean age of 57±15 years (range26–80). None of the patients had an acute infarct in theother arterial territories of the vertebrobasilar system.In 10 patients the infarction was unilateral, and only 1patient had bilateral MMI. The clinical features are pre-sented in Table 1.

■ Risk factors

The main vascular risk factors were hypertension in 8cases, hypercholesterolemia 4 cases, cigarette smokingin 4 cases, diabetes mellitus in 2 cases, myocardial in-farction in 1 case, bladder carcinoma in 1 case of the pa-tients. Patients 3 and 5 had a history of vertebrobasilartransient ischemic attacks consisting of diplopia, hemi-hypesthesia and bilateral visual disturbance. Themedullary ischemic stroke had a non-progressive onsetof symptoms (stabilized < 1 hour) in 9 patients, while itwas progressive (over 3 hours) in 2 (patient 6 and 7).

Lesion localization and arterial pathologies wereshown in figure 2. Presumed cause of infarction wasatheromatous disease of an intracranial branch withconcomitant VA stenosis in 6 patients,VA occlusion in 2,dolichoectesia of the vertebral and basilar arteries in 2,and a source of cardiac embolism in 1.

■ Clinical findings

Motor weakness (72 %), dizziness and vertigo (27 %)were the most frequent initial complaints. Patients 6, 7and 11 had two to five episodes of drop attacks beforeadmission to hospital. Patient 11 with bilateral MMI hadsomnolence in the acute phase of stroke. Facial weak-ness occurred in 7 patients with unilateral infarct, beingalways contralateral to the lesion. In these patients,4 hadinfarcts in the upper medulla and 3 in the middlemedulla.Weakness of the tongue was found ipsilateral in9 patients, and was accompanied by a homolateral palsyof the accessory nerve in patient 9. Motor deficits werepresent in all patients and progressed over more thanone hour in two of them. All patients had brachiocruralparesis, and in the acute stage muscle tone was flaccid inpatients 2, 3, 8, 9, 10, 11 and mildly decreased in patients1, 4, 6, 7. The degree of paresis was moderate to severe inseven patients (M0–M3) (13),and mild (M4) in the otherfour. Muscle reflexes were increased in all but only in pa-tients 6,9,10,11 was Babinski’s sign present. Sensory dis-turbances on the same side as the hemiparesis were pre-sent in all but patients 9 and 11 had bilateral deepsensory deficits. Touch, pain, and vibration sensorymodalities was diminished in 10 patients and postural

sensation was mildly decreased in five, accompanied bymarked truncal lateropulsion, which was always to thecontralateral side (patients 6, 8, 9, 10, 11), but patients7and 11 had bilateral deep sensory loss. Three patientshad contralateral facial hypesthesia. Additional clinicalpictures included dysarthria in 10 patients, gait ataxia in8, dysphagia in 3, nystagmus in 4 (beating contralateralto lesion in 2, rotatory in 1, upbeating and rotatory in 1).Four patients had gag reflex loss without respiratory dis-turbances.

The topography of the infarcts on MRI in each pa-tient are illustrated in figure 2. The infarct was located inthe upper medulla (n=1), middle medulla (n=3), or overmost levels of the medulla (n=7). In patients 9 and 11, le-sion extended to the upper cervical cord (figure 3), andin patients 7,8 and 9 it involved anterolateral medulla.Patient 5 had an old infarction in the left cerebellar cor-tical region.Patients 3,5,6,8 and 11 had leukoaraiosis onMRI.

■ Prognosis

At review after 3 months nine patients had survived anddid not need any assistance in daily living,except patient11 with bilateral MMI. Patients 1, 4, 7 and 10 had a goodmotor recovery with a mild impairment of fine fingermovements, and three patients (nos. 2, 3, 9 and 10) had apersisting motor deficit with mildly limitation. Patient 5died from bladder carcinoma and systemic metastases,and patient 6 died because of aspiration pneumonia onemonth after stroke onset.

Discussion

In our centers, the frequency of patients with MMI waslow, being fewer than 1 % of posterior circulation in-farcts. In the literature, we found 52 MMI patients withdefinite clinico-topographic documentation, during theperiod 1894–1997 [4, 5, 9, 11, 12, 16, 18, 21, 24, 27, 33, 36,37, 46, 49]. In our series, all patients had pure MMI ex-cept patient 5 who had an old cerebellar infarct, but inother series some patients had involvement of lowerpons, cerebellum, upper cervical cord, basal ganglia, andposterior cerebral artery territory [4, 11, 22, 27, 36, 50].

The analysis of clinical pictures of MMI patients de-tected by MRI in previous and the present series showedfour specific clinico-topographic patterns [4, 18, 22, 27,29, 36, 46, 51, 53]. Table 2. Depending upon the differentextension of medullary ischemia, the clinical pictures ofMMI is heterogeneous owing to a variable involvement ofthe arteries, and the anastomotic net between them. Inour series, the classic clinical triad of the Dejerine syn-drome was the most common clinical picture,accompanied by contralateral hemiparesis, ipsilateral

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Fig. 2 Lesion topography and vascular pathologies in 11 patients with medial medullary infarction.

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hypoglossal palsy and lemniscal sensory decrease.Hemi-paresis is the constant finding of MMI syndrome [4,9,27,32, 43, 44, 46]. It is usually the first symptom of MMI, andthe motor deficit is commonly in the upper extremity,and in the distal portion of the affected limbs [4].In somepatients, crural hemiparesis with involvement of theproximal portion of the limbs was observed, implying amore ventral topography of the lesion. Proximal paresisof the limbs may suggest a dorsolateral lesion disruptingcorticoreticular pathways rather than corticospinalpathways [47]. Moreover, spasticity occurred in allpatients within a few weeks, often, with flexion of theupper limb and extension of the lower limb.A mild facialpalsy, usually contralateral to a lesion in the uppermedulla, was found in two thirds of our patients. Themechanism of contralateral facial weakness may be re-lated to recurrent supranuclear facial fibers exiting fromthe pyramid tract at the level of medulla and taking a ros-tral course to the contralateral pontine tegmentum [20].

The second most common clinical picture was sen-sorimotor stroke without lingual palsy.According to thepresent and previous reports [4, 21, 27, 32], lingual palsymay be absent for several reasons.The medial medullarylesion may not extend laterally to interrupt the hy-poglossal nerve fibers or dorsally to involve the hy-poglossal nucleus. The hypoglossal nucleus is a cell col-umn 18 mm long in the medulla and a lesion in a smallportion of it may not cause any detectable deficit. In ad-dition, hypoglossal nerve fibers sometimes appear to bepreserved in an area of infarction [11, 46]. In one study,only 6 out of 13 patients had hypoglossal nerve palsy,but

in other series only two of 18 patients presented with lin-gual palsy [27]. In the series of Kim et al. the most com-mon picture was sensorimotor stroke with involvementof different sensory modalities [27]. The classic patternof sensory loss is contralateral lemniscal sensory loss ofthe entire hemibody with or without facial involvement.Dissociated loss of lemniscal modalities with absence ofvibration and intact postural sense or vice versa can oc-cur even in the presence of involvement of the mediallemniscus [18, 34, 46, 52]. Pain sensation was also de-creased in most of our patients, oftenly in associationwith preserved temperature sensation and hyperesthe-sia as seen in the previous series [4, 28, 51]. This can beexplained by involvement of the fibers at the level of themedial lemniscus,as well as fibers in the adjacent medialmedullary reticular formation carrying nociceptive in-formation [8]. In a previous series, two patients with ho-molateral lemniscal sensory loss secondary to a lesionextending to the medullo-cervical junction causing dis-ruption of crossing sensory fibers or below their decus-sation were reported [4]. We observed only two patientshaving bilateral lemniscal sensory loss, one with a lesionextending to cervico-medullary junction, and the otherwith bilateral MMI.

The third clinical picture is pure motor hemiparesiswithout lingual palsy, and was present in only one pa-tient, implying involvement of the pyramid tract with-out extension of the lesion to hypoglossal nucleus or hy-poglossal fibres. Pure motor hemiparesis with lingualpalsy has been reported in most of the large series [4, 22,27, 50].

Fig. 3 T2-weighted MRI A axial, and B coronal sections) of patient 9 with medial medullary infarction.

A B

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Bilateral MMI is usually associated with tetraparesis,bilateral disturbance of deep sensation, dysphagia, dys-phonia, lingual paralysis, and anarthria as seen in ourpatient 11 [23, 27, 29, 36, 41, 50]. In the review of Ho andMeyer, bilateral medullary involvement occurred in 7 of15 cases of MMI [22]. In bilateral MMI, atypical MMIsyndromes such as bilateral pure motor hemiparesis,quadriparesis without tongue paralysis, unilateral com-plete plus contralateral sensorimotor stroke without lin-gual palsy, may develop according to infarct size and lo-cation [18]. Respiratory disturbances may be seen in thebilateral extensive medullary lesions with bilateral MMIor combined MMI and lateral medullary infarctionwhich are related to either impairment of voluntary res-piratory control secondary to the corticospinal lesion ordisturbance of autonomic respiratory control [6, 12, 29,34, 38, 40, 50]. Disturbances of consciousness with som-nolence, hallucinations and delirium, suggesting therole of the medial medulla in the modulation of vigi-lance by the medial medullary reticular formation haverarely been reported in bilateral MMI [12, 24, 27, 40].

In our series, dysphagia with pharyngeal weaknesswas seen infrequently as has been previously reported.In a previous report,10 of 23 patients with medullary in-farction manifested aspiration on swallowing, and mosthad a lesion at the middle level of the medulla [28].A le-sion running the length of the middle and lower medullalevels always resulted in aspiration.Dysfunction of swal-lowing suggests an extension of the lesion to the lateralmedulla with involvement of the nucleus ambiguus. Inthe nucleus ambiguus, vagal motoneurons innervatingthe larynx are located more caudally than those control-ling the pharynx [42].We observed dysarthria almost inall cases, which could be explained either by facio-palato-glossal dysfunction or by the disruption of cere-bellopetal pathways.

Ocular motor disturbances are uncommon in MMI,and have been reported mainly as upbeat and rotatorynystagmus, the amplitude of which may increase duringthe up or lateral gaze [4,25,33,34]. In MMI,upbeat couldbe attributed to involvement of the ipsilateral mediallongitudinal fasciculus or the region of the perihy-poglossal nuclei, both of which lie dorsal to the mediallemniscus [3, 39]. Horizontal rotatory nystagmus is of-ten associated with involvement of vestibular nuclei andtheir connections to the cerebellum in the lateralmedulla [26, 54]. Transient gaze paresis and a long-last-ing sixth nerve palsy in a patient with pontomedullaryjunction infarction, and ocular bobbing have been re-ported only once in MMI [24, 50].

The outcome of unilateral MMI confined to the upperthird of medulla is favorable, although earlier reports ofMMI based on autopsy were biased towards a poor out-come. In our series, one patient with bilateral MMI wasmildly dependent, but previous series suggest that bilat-eral MMI and hemimedullary infarction have worse out-

come than limited unilateral infarction in associationwith patent VA and ASA [4, 9, 22, 27]. Two of our patientswith unilateral MMI died from systemic causes ratherthan MMI. Most of our patients had satisfactory recov-ery of motor strength despite severe pyramidal tract in-volvement at stroke onset. This may be related to theemerging ipsilateral corticospinal pathways or other de-scending motor pathways that are organized bilaterally[17, 20].

Our data showed that the most common etiology wasatherothrombosis of VA and ASA as observed in otherprevious series [4, 20, 23, 27, 44]. The present findingswere similar to those of previous pathologic and angio-graphic studies reporting an incidence of VA occlusionor narrowing in 67 % to 70 % of patients [16,51].The rar-ity of MMI despite the high frequency of VA disease maybe due to paired vertebral arteries and the wide anasto-motic net connecting perforating arteries supplying themedial medulla. Two thirds of our patients had VA wallirregularity and stenosis with vascular risk factors, andtherefore they have been accepted as having intracranialbranch atheromatous disease of the penetratingbranches which has been proposed as one of the majorcauses of posterior circulation infarctions [7]. In patient11, simultaneous bilateral infarction of the medulla maybe related to the involvement of an unpaired ASA as ananatomical variation. Contralateral VA atheroscleroticdisease – as seen in our patient 2 – may cause unilateralMMI, since rostral median branches of the VA penetrateand cross the midline between the pyramids, and cansupply the contralateral anteromedial arterial territory[1, 19]. Only one young patient (no. 8) in the present se-ries had an embolusl from heart disease, and angiogra-phy showed an occluded VA probably due to cardioem-bolism. We found dolichoectesia of the vertebrobasilararteries in two patients, in whom the probable cause ofstroke was either compression of the ventral surface ofbrainstem or thrombosis of penetrating branches of themedulla [36]. Among the rare causes of MMI, dissectionof VA [4, 7, 51, 55], syphilis [34, 53], embolic occlusion ofthe ASA by talc or fibrocartilaginous material [24], arte-rial compression by fusiform aneurysm [31, 55], drugabuse [37] have been reported.

In conclusion, according the present and previous se-ries, the main clinical pictures of MMI are classical De-jerine syndrome accompanied by brachiocrural hemi-paresis, decrease of deep sensation with lingual palsy;sensorimotor stroke without lingual palsy; pure motorhemiparesis without lingual plasy; bilateral MMI in-cluding tetraparesis, bilateral loss of deep sensation,dysphagia/dysphonia, anarthria, and respiratory diffi-culties. The clinical outcome was generally poor in bi-lateral MMI in contrast to unilateral medial medullarylesion. Vertebral artery atherosclerotic disease and in-trinsic branch penetrator disease seem to be moreprevalent in MMI patients.

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1. Akar ZC, Dujovny M, Gomez-Tortosa E(1995) Microvascular anatomy of theanterior surface of the medulla oblon-gata and olive. J Neurosurg 82:97–105

2. Babinski J, Nageotte J (1902) Hemia-synergie, lateropulsion et myosis bul-baires avec hemianesthesie et hémi-plegie croisées. Rev Neurol(Paris)10:358–365

3. Baloh RW, Yee RD (1989) Spontaneousvertical nystagmus. Rev Neurol(Paris)145:527–532

4. Bassetti C, Bogousslavsky J, Mattle H,Bernasconi A (1997) Medial medullarystroke. Report of seven patients andreview of the literature. Neurology48:882–890

5. Bogousslavsky J, Fox AJ, Barnett HJM,Hachinski VC, Vinitski S, Carey LS(1986) Clinico-topographic correlationof small vertebrobasilar infarcts usingmagnetic resonance imaging. Stroke17:929–938

6. Bogousslavsky J, Khourana R, DeruazJP, Hornung JP, Regli F, Janzer R, PerretC (1990) Respiratory failure and uni-lateral caudal brainstem infarction.Ann Neurol 28:668–673

7. Caplan LR, Tettenborn B (1991) Verte-brobasilar occlusive disease: review ofselected aspects. Part 1. Spontaneousdissection of extracranial and in-tracranial posterior circulation arte-ries. Cerebrovasc Dis 2:256–265

8. Casey KL (1969) Somatic stimuli,spinal patways, and size of cutaneousfibres influencing unit activity in themedial medullary reticular formation.Exp Neurol 25:35–36

9. Chokroverty S, Rubino FA, Haller C(1975) Pure motor hemiplegia due topyramidal infarction. Arch Neurol32:647–648

10. Currier RD, Giles CL, de Jong RN(1961) Some aspects on Wallenberg’slateral medullary syndrome. Neurol-ogy 11:778–791

11. Currier RD (1969) Syndromes ofmedulla oblongata. In Vinken PJ,Bruyn GW (eds) Handbook of clinicalneurology, vol 2. North-Holland, Ams-terdam pp 217–237

12. Davison C (1944) Syndrome of the an-terior spinal artery of the medulla ob-longata. J Neuropathol Exp Neurol3:73–80

13. Dejerine J (1926) Sémiologie des affec-tions du système nerveux. Paris: Mas-son et Cie.

14. De Jong RN (1950) The neurologic ex-amination. New York: Hoeber.

15. Duvernoy HM (1995) The humanbrainstem and cerebellum: surface,structure, vascularization and three di-mensional sectional anatomy withMRI. New York: Springer-Verlag

16. Escourolle R, Hauw JJ, Agopian PD,Trelles L (1976) Les infarctus bulbaires:étude de lésions vasculaires dans 26observations. J Neurol Sci 28:103–113

17. Fries W, Danek A, Scheidtmann K,Hamburger C (1993) Motor recoveryfollowing capsular stroke: role of de-scending pathways from multiple mo-tor areas. Brain 116:369–383

18. Gan R, Noronha A (1995) Themedullary vascular syndromes revis-ited. J Neurol 242:195–202

19. Gillilan LA (1964) The correlation ofthe blood supply to the human brain-stem with clinical brainstem lesions. JNeuropathol Exp Neurol 23:78–108

20. Haines DE (1987) Neuroanatomy. AnAtlas of structures, sections and sys-tems. Baltimore: Urban andSchwarzenberg

21. Hauw J, Agopian P, Trelles L, EscourelleR (1976) Les infarctus bulbaires. J Neu-rol Sci 28:83–102

22. Ho KL, Meyer KR (1981) The medialmedullary syndrome. Arch Neurol38:385–387

23. Jagiella WM, Sung JH (1989) Bilateralinfarction of the medullary pyramidsin humans. Neurology 39:21–24

24. Kase CS, Varakis JN, Stafford JR, MohrJP (1983) Medial medullary infarctionfrom fibrocartilaginous embolism tothe anterior spinal artery. Stroke14:413–418

25. Kato I, Nakamura T, Watanabe J (1985)Primary position upbeat nystagmus:localizing value. Arch Neurol42:819–821

26. Kim JS, Lee JH, Sulh DC, Lee MC(1994) Spectrum of lateral medullarysyndrome: correlation between clinicalfindings and magnetic resonanceimaging in 33 subjects. Stroke25:1405–1410

27. Kim JS, Kim HG, Chung CS (1995) Me-dial medullary syndome. Report of 18patients and review of the literature.Stroke 26:1548–1552

28. Kim H, Chung C-S, Lee K-H, RobbinsJR (2000) Aspiration subsequent to apure medullary infarction. Lesion sites,clinical variables, and outcome. ArchNeurol 57:478–483

29. Kleinert G, Fazekas F, Kleinert R(1993) Bilateral medial medullary in-farction: Magnetic resonance imagingand correlative histopathologic find-ings. Eur Neurol 33:74–76

30. Kumral E, Ozkaya B, Sagduyu A, SirinH, Vardarlı E, Pehlivan M (1998) TheEge Stroke Registry: A hospital-basedstudy in the Aegean Region, Izmir,Turkey. Cerebrovasc Dis 8:278–288

31. Kurita H (2000) Dejerine syndromecaused by an aneurysmal compression.Arch Neurol 57:1639–1640

32. Leetsma JE, Noronha A (1976) Puremotor hemiplegia, medullary pyramidlesion, and olivary hypertrophy. J Neu-rol Neurosurg Psychiatry 39:877–884

33. Marinesco G, Draganesco S (1923)Hémisyndrome bulbaire révélant d’unramolissement de l’étage moyen dubulbe, suite de thrombus de l’artérevertébrale droite. Ann Méd 13:1–19

34. Meyer JS, Herndon RM (1962) Bilateralinfarction of the pyramidal tracts inman. Neurology 12:637–642

35. Milandre L, Habib M, Hassoun J, KhalilR (1990) Bilateral infarction of themedullary pyramids. Neurology 40:556

36. Milandre L, Arnaud O, Khalil R (1992)Infarction of the medullary pyramididentified on MRI. Cerebrovasc Dis2:183–184

37. Mizutani T, Lewis RA, Gonatas NK(1980) Medial medullary syndrome ina drug abuser. Arch Neurol 37:425–428

38. Mossuto-Agatiello L, Kniahynicki C(1990) The hemimedullary syndrome:case report and review of the litera-ture. Neurology 237:208–212

39. Munro NAR, Gaymard B, Rivaud S(1993) Upbeat nystagmus in a patientwith a small medullary infarct. NeurolNeurosurg Psychiatry 56:1126–1128

40. Nakane H, Okada Y, Sadoshima S, Fu-jishima M (1991) Babinski-Nageottesyndrome on magnetic resonanceimaging. Stroke 22:272–275

41. Nardelli E, Lannucci A, Rizzuto N(1978) Bilateral infarction of pyrami-dal tracts. Acta Neurol (Napoli)33:130–136

42. Orem J (1994) Respiratory neuronsand sleep. In: Kryger MH, Roth T, De-ment WC (eds) Principles and practiceof sleep medicine. 2nd Ed. W. B. Saun-ders

43. Paulson GW, Yates AJ, Paltan-Ortiz JD(1986) Does infarction of themedullary pyramid lead to spasticity?Arch Neurol 49:93–95

44. Ropper AH, Fisher CM, KleinmannGM (1979) Pyramidal infarction in themedulla: a case report of pure motorhemiplegia sparing the face. Neurology29:91–95

45. Sacco RL, Freddo L, Bello JA, Odel JG,Onesti ST, Mohr JP (1993) Wallenberg’slateral medullary syndrome: clinical-magnetic resonance imaging correla-tions. Arch Neurol 50:609–614

46. Sawada H, Seriu N, Udaka F,Kameyama M (1990) Magnetic reso-nance imaging of medial medullary in-farction. Stroke 21:963–966

47. Schneider R, Gautier JC (1994) Legweakness due to stroke. Site of lesions,weakness patterns and causes. Brain117:347–354

References

93

48. Tatu L, Moulin T, Bogousslavsky J, Du-vernoy H (1996) Arterial territories ofhuman brain: brainstem and cerebel-lum. Neurology 47:1125–1135

49. Tohgi H, Nakura H, Yamanouchi H(1980) Vascular disorders in themedulla oblongata. Jpn J Stroke2:84–86

50. Toyoda K, Hasegawa Y, Yonehara T(1992) Bilateral medial medullary in-farction with oculomotor disorders.Stroke 23:1657–1659

51. Toyoda K, Imamura T, Saku Y, Oita J,Ibayashi S, Minematsu K, Yamaguchi T,Fujishima M (1996) Medial medullaryinfarction: Analyses of eleven patients.Neurology 47:1141–1147

52. Trelles JO, Trelles L, Urquiaga C (1973)Le ramolissement median du bulbe. Apropos de deux cas anatomo-cliniques.Rev Neurol (Paris)129:91–104

53. Tyler KL, Sandberg E, Baum KF (1994)Medial medullary syndrome andmeningovascular syphilis: a case re-port in an HIV-infected man and a re-view of the literature. Neurology44:2231–2235

54. Vuilleumier P, Bogousslavsky J, Regli F(1995) Infarction of the lower brain-stem. Clinical, aetiological and MRI-topographical correlations. Brain118:1013–1025

55. Watanabe M, Murayama T, Mano K(1996) Medial medullary infarctionfollowing neck manipulation. RinshoShinkeigaku 36:43–46