(Stroke. 1997;28:809-815.)
© 1997 American Heart Association, Inc.
Articles |
Paramedian Pontine Infarction
Neurological/Topographical Correlation
From the Department of Neurology, Kanazawa Medical University, Daigaku, Ishikawa, Japan.
Correspondence to Satoshi Kataoka, MD, Department of Neurology, Kanazawa Medical University, Daigaku, Uchinada-machi, Kahoku-gun, Ishikawa 920-02, Japan.
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Abstract |
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Background and Purpose There have been few reports of pontine syndromes secondary to paramedian pontine infarctions. To clarify the clinicotopographical correlation and prognosis of paramedian pontine infarct syndromes, we analyzed the clinical signs and their association with MRI findings.
Methods We studied 49 patients with acute paramedian pontine infarcts and classified them into three subtypes on the basis of lesion location on MRI. Patient clinical status was assessed by Rankin Disability Scale (RDS) scores on admission and at 60 days after onset of stroke.
Results Twenty-seven patients had basal infarcts. Clinical findings included dysarthria (n=27), hemiparesis with upper extremity predominance (n=15), brachial monoparesis (n=4), and pathological laughing (n=3). Fifteen patients had basal-tegmental infarcts. Clinical findings presented with hemiparesis and horizontal gaze abnormalities, including abducens nerve palsy (n=1), internuclear ophthalmoplegia (INO) (n=5), horizontal gaze palsy (n=1), one-and-a-half syndrome (n=1), and superficial or proprioceptive sensory dysfunction (n=8). Seven patients had tegmental infarcts. Clinical findings included INO (n=1), horizontal gaze palsy (n=2), one-and-a-half syndrome (n=3), and sensory changes (n=2). On both admission and 60 days later, the RDS scores of the patients with upper pontine lesions were significantly better than those with lower pontine lesions (P<.01). The RDS scores of the patients with basal-tegmental infarct in the upper pons were significantly better than those with infarct in the lower pons (P<.02).
Conclusions Paramedian pontine infarcts, which are usually due to thrombosis of perforating arteries, presented with a faciobrachial dominant hemiparesis with dysarthria, somatosensory disturbance, and horizontal gaze abnormalities. The favorable outcome may be related to the level of the pontine lesion, which influences the effect on the corticospinal tract.
Key Words: basilar artery • cerebral infarction • lacunar infarction • pons • thrombosis
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Introduction |
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Foix and Hillemand1 elucidated the vascular supply of the pons and midbrain and described classic pontine syndromes including paramedian, circumferential, and tegmental syndromes. Thereafter, Lhermitte and Trelles2 recognized the following pontine syndromes resulting from basilar arteriosclerosis: pontine hemiplegia, paraplegia, and pontocerebellar pseudobulbar paralysis. The most common syndrome of paramedian basilar artery branch disease has been thought to be pure motor hemiplegia or hemiparesis with dysarthria and ataxia.3 In the 1970s, Fisher and Caplan4 5 described occlusion of BA branches in patients with paramedian pontine lesions, which manifested as motor signs and gaze abnormalities. Lacunar infarct syndromes, such as pure motor hemiparesis, dysarthria–clumsy hand syndrome, and ataxic hemiparesis, also can result from paramedian pontine lesions.6 7 8 9 10 Many case studies and classifications of pontine infarct syndrome have been presented in the literature8 9 10 11 12 ; however, paramedian pontine syndromes due to occlusive disease of the paramedian perforating artery have not been fully characterized. Therefore, we investigated clinical signs and symptoms in relation to the location of the pontine lesions as documented by MRI and compared the patients' RDS scores on admission with those at 60 days later.
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Subjects and Methods |
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We studied 49 consecutive patients with isolated paramedian pontine infarcts, defined as a stroke syndrome involving the paramedian pontine region in the territory of the paramedian branch arteries of the BA as seen on MRI. History and neurological examination were performed by members of the neurology staff for all patients. All patients were assessed by at least two of the three main investigators (S.K., A.H., and G.H.) on admission and at 3 to 7 days after the onset. All examiners agreed on the acute neurological findings within the first 7 days, which were analyzed as the final neurological deficit. Because some information on neurological symptoms and findings was retrospectively assembled from the medical records of the Department of Neurology, specific details regarding the mode of onset, quality of symptoms, and chronic neurological findings were not uniformly assessed.
The pontine perforating branches of the BA have been subdivided into
three groups based on a previously described
classification.13 14 15 16 The first group consists of the
median and paramedian perforating arteries (anteromedial group), which
comprise the short and long anteromedial arteries. The former mainly
supply the medial basis pontis, including the corticospinal tract, and
do not extend to the medial lemniscus dorsally. The latter arteries,
which are the most medially located, supply the medial pontine
tegmentum, including the floor of the fourth ventricle, abducens
nucleus, MLF, and PPRF. The second group consists of short
circumferential arteries (anterolateral group), which supply the
lateral basis pontis and tegmentum. The third group comprises the long
circumferential arteries (lateral group), which supply the most lateral
part of the pontine base and tegmentum. These main vascular territories
are illustrated in Fig 1
. This classification was used
for the topographical localization of the paramedian pontine infarcts
in this series. These infarcts were divided into three types based on
the topography: (1) paramedian basal infarcts that involved the short
anteromedial arteries, (2) paramedian basal-tegmental infarcts that
involved the short and long anteromedial arteries, and (3) paramedian
tegmental infarcts that involved the long anteromedial arteries.
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The MRI examinations were performed on either a 0.5-T or 1.5-T superconducting magnet with a quadrature head coil within the first 7 to 14 days after the onset of stroke, when the surrounding edema and mass effect had resolved and the fogging effect was not present. Each examination included spin-echo sagittal T1-weighted images (repetition time [TR], 600 ms; echo time [TE], 15 ms) and axial T2-weighted (TR, 2500 ms; TE, 90 ms) images. The images were 5 mm thick with a 2.5-mm gap. The image acquisition matrix was 256x192. Gadolinium-DTPA–enhanced spin-echo T1-weighted images were also obtained. MR angiography was performed using three-dimensional time-of-flight imaging. A coronal two-dimensional phase-contrast scout image was obtained to locate the vertebrobasilar arteries. Conventional angiography including retrograde brachial or vertebral angiography using the Seldinger method was performed to detect occlusive lesions in the vertebrobasilar arteries. Our criterion for stenosis was a reduction of the caliber of the artery by at least 30% on a lateral or anteroposterior view of the conventional angiogram17 or 50% narrowing on an anteroposterior or lateral view from an MR angiogram.18 19 The topographical localization of the paramedian pontine infarcts was determined for each patient using transverse anatomic templates of the pons at three different levels, ie, upper, mid, and lower levels of the pons.20 Patients with extensive brain-stem infarcts involving the midbrain or medulla, such as pontomesencephalic infarcts, and recent or previous cerebellar or supratentorial infarcts were excluded.
We analyzed multiple variables, risk factors, and associated disorders, including a history of cigarette smoking, hypertension, diabetes mellitus, hyperlipidemia, hyperuricemia, IHD, valvular heart disease, and peripheral vascular disease. These baseline risk factors and associated disorders were diagnosed according to previously defined criteria.21 We compared the incidence of these variables for two types of infarct: an infarct extending to the surface of the pontine base and the infarct not extending to the surface of the pontine base.
Functional outcome was assessed on admission and at 60 days after the stroke with the use of the RDS, which has five grades (1, no significant disability; 2, slight disability; 3, moderate disability; 4, moderately severe disability; and 5, severe disability).22 We also compared the RDS score of patients with paramedian basal, basal-tegmental, and tegmental infarcts at the three pontine levels.
To assess the difference in the clinical variables among the
infarct types, the 
2 test was used. Student's
t test was used to detect the significance in the RSD score
among the infarct groups. Statistical significance was defined as a
value of P<.05.
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Results |
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Between January 1984 and June 1995, 644 patients with acute brain infarcts were admitted to our neurological service at Kanazawa Medical University Hospital. Of these, we studied 49 patients (7.6%) with paramedian pontine infarcts (31 men and 18 women; mean age, 67.2 years) who represented 28.3% of 173 patients with vertebrobasilar territory infarcts. Twenty-seven patients had a paramedian basal infarct, 15 patients had a basal-tegmental infarct, and 7 patients had a tegmental infarct. The neurological findings on admission are summarized in Table 1
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Paramedian Basal Infarcts
An infarct localized to the paramedian pontine base was seen in 27
patients (55.1%). Among these, a unilateral basal infarct was found in
25 patients and bilateral infarcts in 2 patients. Dysarthria was noted
in all 27 patients and supranuclear facial palsy in 21 (77.8%). Four
patients (14.8%) had a brachial monoparesis. Nineteen patients
(70.4%) had a hemiparesis (Fig 2A). Eleven of these patients had pure
motor hemiparesis. Fifteen patients (55.6%) had dysarthria and
hemiparesis with brachial predominance. Dysarthria–clumsy hand
syndrome was diagnosed in 4 patients (Fig 2B) and ataxic hemiparesis in
1 patient. Other neurological signs included decreased perception of
light touch and pain in 3 patients, with contralateral facial
distribution in 2 and facial/brachial distribution in 1. A pseudobulbar
affect with pathological laughing was seen in 3 patients.
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Paramedian Basal-Tegmental Infarcts
This infarct was usually wedge-shaped and extended from the basal
surface of the pons to the floor of the fourth ventricle dorsally. It
was seen in 15 patients (30.6%). All 15 patients had a contralateral
hemiparesis. Fourteen patients (93.3%) had dysarthria, and 13 (86.7%)
had a supranuclear facial palsy as well. Eight patients had sensory
disturbances. Two had abnormal proprioception, and 6 had
disturbed light touch and pain sensation. Other neurological signs
included INO in 5 patients, one-and-a-half syndrome in 1, horizontal
gaze palsy in 1 (Fig 3), nuclear abducens
nerve palsy (lateral gaze palsy) with supranuclear facial palsy in 1,
and skew deviation in 3. A pseudobulbar affect with pathological crying
was seen in 1 patient.
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Paramedian Tegmental Infarcts
This infarct, localized to the medial tegmentum, was seen in 7
patients. Five patients had dysarthria, and 4 patients had supranuclear
facial palsy. Decreased perception of pinprick and light touch on the
contralateral face area and decreased vibration sense in the toes were
seen in 2 patients. Other neurological signs included INO in 1 patient,
one-and-a-half syndrome in 3, horizontal gaze palsy in 2, and abducens
nerve palsy in 1 (Fig 4). Skew deviation,
primary-position downbeating nystagmus, and ocular bobbing were seen in
1 patient each.
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Vertebrobasilar Angiography
Conventional vertebrobasilar angiography was performed in 30
patients and MR angiography in 5 patients. Unilateral occlusion of the
VA at the V4 segment was seen in 1 patient, unilateral VA
stenosis of the V4 segment in 12, and an irregular VA in 6
patients. Three patients (8.5%) had stenosis in a middle or
distal segment of the BA. Eight patients (22.8%) had irregularity of
the BA. No abnormality was detected in 13 patients. MR angiography
showed a mild VA stenosis in 2 patients, but no
stenotic or occlusive BA disease.
Distribution of Infarcts
An infarct extending to the surface of the pontine base was seen
in 24 patients. In contrast, an infarct not extending beyond the
pontine base was seen in 25 patients (Table 2).
Unilateral infarcts were seen in 45 patients (91.8%), of which 22 had
a lesion on the right side and 23 had a lesion on the left side.
Bilateral infarcts were seen in 4 patients (8.2%). On sagittal images,
an upper pontine lesion was seen in 18 patients (36.7%), a mid-pontine
lesion in 21 (42.9%), and a lower pontine lesion in 10 (20.4%) (Table 3). In the upper to mid pons, a paramedian basal infarct
was found in 24 patients and a basal-tegmental infarct in 11. In the
mid to lower pons, a paramedian basal infarct was found in 16 patients
and basal-tegmental infarct in 10. Contrast-enhanced images were
obtained in 7 patients. Lesion enhancement was seen in 5 patients
within 2 weeks after stroke onset. Two patients did not have
enhancement effect within 3 weeks after stroke onset.
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Risk Factors and Associated Disorders
Hypertension was present in 34 patients (69.4%). Nineteen
patients (38.8%) had diabetes mellitus. Fourteen patients (28.6%) had
hyperlipidemia. Thirty patients (61.2%) were current
smokers. Seventeen patients had heart disease. Nine patients (18.4%)
had IHD (old myocardial infarction in 4, angina pectoris in 5), and 8
patients (16.3%) had valvular heart disease (mitral
stenosis in 1, mitral regurgitation in 6, and
aortic regurgitation in 1). In age-matched logistic
regression analysis, the incidence of smoking in patients with
pontine infarcts extending to the basal surface was significantly
higher than in patients with infarcts not extending to the basal
surface (Table 2
). In this series, 12 patients (24.5%) had a potential
cardiac source of embolism: valvular heart disease in 8 and IHD
in 4.
Disability After Stroke
Functional evaluation on admission using the RDS classified 5
patients as grade 5, 9 as grade 4, 17 as grade 3, and 18 as grade 2.
Sixty days after stroke onset, 5 patients showed grade 4 disability, 10
grade 3, 14 grade 2, and 20 grade 1. Twenty patients (42.8%; 14
patients with paramedian basal infarcts, 2 with basal-tegmental
infarcts, and 4 with tegmental infarcts) improved to grade 1 by 60 days
after admission. In regard to the severity of the deficit on admission
and the three pontine levels, the mean±SD RDS score in patients with
lesions involving the upper pons was 2.8±0.9; mid pons, 3.0±1.0; and
lower pons, 3.9±1.1. Statistical analysis revealed that the
RDS score in patients with upper pontine lesions was significantly
better than in those with lower pontine lesions on admission
(P<.01) and 60 days after stroke onset (P<.01).
Also, in the paramedian basal-tegmental infarct group, the RDS score in
patients with upper pontine lesions was significantly better than in
those with lower pontine lesions on admission (P<.02) and
60 days after stroke onset (P<.02). There was no
significant difference between the RDS score in patients with upper
pontine lesions and mid-pontine lesions (Table 3).
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Discussion |
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We have shown that paramedian pontine infarcts are common (28.3%) infarcts of the vertebrobasilar system. The main motor abnormality in this syndrome was dysarthria with either contralateral hemiparesis, which predominated in the upper extremity, or brachial monoparesis. Facial and upper-extremity dominant hemiparesis are known to be the usual manifestations in cases of small cortical infarctions of the anterior rolandic or opercular area and corona radiata.23 24 25 However, the combination of dysarthria with either brachial monoparesis or hemiparesis (worse in the upper extremity) can also be seen in patients with a ventral pontine lesion, as well as a supratentorial infarct, such as an infarct in the medial third of the posterior internal capsule.26 27 28 The motor deficit in paramedian basal infarcts follows the topography of the arrangement of the corticospinal tract, in which the fibers of the upper extremity are located more ventromedially than the fibers of the lower extremity. Because of the somatotopic organization of the corticospinal tract in the basis pontis, the fibers of the lower extremity were not affected by a paramedian ischemic event. Pontine pseudobulbar palsy is similar to that of cerebral pseudobulbar syndrome. At the pontine level, the corticobulbar fibers that terminate directly in or indirectly around the motor nuclei of the trigeminal and facial nerves are the most medially located.29 30 31 32 Previous studies have also shown that lesions of the paramedian pontine base result in pure dysarthria.10 33 Because the supranuclear fibers of the facial nerve, which are thought to be in the region of the pontine base, extend to the tegmentum, a paramedian basal infarct can be present with dysarthria and supranuclear facial palsy. Pathological laughing and crying (one of the components of pseudobulbar palsy or affect) are usually seen in patients with bilateral or unilateral cerebral hemispheric lesions. The responsible lesion in the corticobulbar tract is thought to be in either the genu of the internal capsule or in the brain stem.10 33 34 35 Although unilateral or bilateral lesions involving the paramedian pons may contribute to pathological crying and laughing, the precise mechanism remains unknown.
The horizontal gaze abnormalities in these pontine infarcts included
abducens nerve palsy, INO, horizontal gaze palsy, and one-and-a-half
syndrome. A lesion involving the abducens nerve fasciculus passing
through the medial tegmentum to the basis pontis at the mid-pontine
level can cause an isolated unilateral lateral rectus
palsy.36 37 38 Thus, supranuclear facial palsy with a sixth
nerve palsy may be indicative of a paramedian pontine infarct. A
horizontal gaze palsy can be produced by a focal lesion involving the
ipsilateral PPRF. The PPRF and the sixth nucleus are anatomically
commingled, and thus an infarct generally produces a horizontal gaze
palsy rather than an isolated abducens palsy.39 40 41 Lesions
that affect the PPRF and the ipsilateral MLF produce one-and-a-half
syndrome.42 43 Paramedian tegmental infarcts that
present with one-and-a-half syndrome usually result from a single,
unilateral, small lesion of the dorsomedial in the lower pons. In
contrast, a paramedian basal-tegmental infarct involving the short and
long arteries caused hemiparesis with horizontal gaze abnormalities
(Fig 3). Terminal or segmental occlusion of the anteromedial long
arteries can present with horizontal gaze palsy (Fig 4) or
one-and-a-half syndrome. The pontine tegmentum is supplied by the
lateral group of the arteries, the superior cerebellar artery and
anterior inferior cerebellar artery, which create a
capillary network on the lateral aspect of the
tegmentum.1 2 14 15 16 Because of the extensive collateral
circulation, paramedian basal-tegmental infarcts usually do not involve
the entire territory of the anteromedial arteries. On contrast-enhanced
images, we detected a small discrete ischemic lesion in the
area of the sixth nerve nucleus and ipsilateral MLF, which caused
horizontal gaze palsy with INO (Fig 4). Gadolinium-DTPA is useful for
distinguishing recent pontine infarcts from other old lesions within
the first 2 to 3 weeks after stroke.44
Contralateral vibratory perception and proprioception were decreased in 3 patients. The long paramedian arteries supply the medial part of the medial lemniscus, and thus sensory deficits may be due to partial involvement of the medial lemniscus. These 3 patients also had mild disturbances in pinprick and light touch in a contralateral facial or faciobrachial distribution, which has been reported previously.45 46 47 The fibers of the ventral trigeminothalamic tract, which convey pain and thermal and tactile sensations of the face, originate from the spinal trigeminal nucleus. The lateral spinothalamic tract conveys pain and light touch in the upper extremities. Because the fibers of the ventral trigeminothalamic tract usually cross at various locations in the lower brain stem and ascend in association with the contralateral medial lemniscus,32 a decreased perception of pinprick on the contralateral face area and upper extremity may be due to involvement of the crossing fibers in the paramedian pons.
Previous studies have shown that the presumed mechanism of isolated small pontine infarcts is due to lipohyalinosis of pontine perforating arteries.8 9 10 11 12 25 28 In the current study, BA stenosis was seen in 3 patients (8.5%). Larger infarcts that extended to the basal surface were the result of ostial occlusion of the basilar perforating arteries without BA stenosis. In contrast, intrinsic small lacunar infarcts are probably due to occlusion of these perforators by lipohyalinosis.6 9 12 Cardioembolism is a potential cause of the bilateral pontine infarcts extending to the pontine base. Twelve patients had a potential source of cardiac embolism in this series, but no cardioembolic infarcts were diagnosed according to clinical criteria.48 49 50 Thus, on the basis of the distribution of infarcts and risk factors, there are probably two mechanisms of paramedian pontine infarction: (1) atherothrombotic occlusion at the origin of the perforating arteries and (2) segmental or terminal lipohyalinosis.
Regarding the prognosis of paramedian pontine strokes, 20 patients (42.8%) improved to RDS grade 1 within 60 days. Thus, the favorable outcome of isolated pontine infarcts is consistent with results of previous prospective studies.9 10 12 In addition, the outcome of paramedian infarcts involving the upper pons tended to be better than that of lesions of the lower pons. The corticospinal tract in the upper pontine level is located more laterally than in the lower pons. Furthermore, the fibers of the corticospinal tract tend to converge toward the ventromedial surface of the lower pontine base to form the compact bundle.15 32 Therefore, paramedian pontine infarcts in the upper pons do not injure the entire corticobulbar and corticospinal tracts. Because the lesions in our series occurred more frequently in the upper to mid pons (79.6%), the favorable outcome may be related to the distribution and level of the lesions. It is important to evaluate the extent and distribution of a lesion to predict the functional outcome from a paramedian pontine infarct.
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Selected Abbreviations and Acronyms |
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Acknowledgments |
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The authors wish to thank Dr Frank M. Yatsu, Department of Neurology at the University of Texas Medical School at Houston, for his critical comments on the manuscript.
Received March 21, 1996; revision received January 24, 1997; accepted January 24, 1997.
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References |
|---|
|
TopAbstractIntroductionSubjects and MethodsResultsDiscussionReferences |
|---|
1. Foix C, Hillemand P. Contribution à l'étude des ramollissements protubérantiels. Rev Med (Paris). 1926;453:287-305.
2. Lhermitte J, Trelles JO. L'artériosclerose du tronc basilaire et ses conséquences anatomo-cliniques. Jb Psychiat Neurol. 1934;51:91-107.
3. Silverstein A. Pontine infarction. In: Vinken PJ, Bruyn GW, eds. Handbook of Clinical Neurology. Amsterdam, Netherlands: North-Holland; 1972:13-36.
4.
Fisher CM, Caplan LR. Basilar artery branch
occlusion: a cause of pontine infarction. Neurology. 1971;21:900-905.
5.
Fisher CM. Bilateral occlusion of basilar
artery branches. J Neurol Neurosurg Psychiatry. 1977;40:1182-1189.
6.
Caplan LR. Intracranial branch
atheromatous disease: a neglected, understudied, and
underused concept. Neurology. 1989;39:1246-1250.
7.
Fisher CM. Lacunar strokes and infarcts: a
review. Neurology. 1982;32:871-876.
8. Glass JD, Levey AI, Rothstein JD. The dysarthria-clumsy hand syndrome: a distinct clinical entity related to pontine infarction. Ann Neurol. 1990;27:487-494. [Medline] [Order article via Infotrieve]
9. Toyoda K, Saku Y, Ibayashi S, Sadoshima S, Ogasawara T, Fujishima M. Pontine infarction extending to the basal surface. Stroke. 1994;25:2171-2178. [Abstract]
10.
Kim JS, Lee JH, Im JH, Lee MC. Syndromes of
pontine base infarction: a clinical-radiological correlation
study. Stroke. 1995;26:950-955.
11. Bassetti C, Bogousslavsky J, Barth A, Regli F. Paramedian pontine infarct: clinical-topographical correlation. Neurology. 1993;43(suppl 2):A159. Abstract.
12.
Bassetti C, Bogousslavsky J, Barth A, Regli F.
Isolated infarcts of the pons. Neurology. 1996;46:165-175.
13. Gillilan LA. The correlation of the blood supply to the human brain stem with clinical brain stem lesions. J Neuropathol Exp Neurol. 1964;23:78-108. [Medline] [Order article via Infotrieve]
14. Duvernoy HM. Human Brainstem Vessels. Berlin, Germany: Springer-Verlag; 1978:11-15.
15. Duvernoy HM. The Human Brainstem and Cerebellum: Surface, Structure, Vascularization, and Three-Dimensional Sectional Anatomy With MRI. Vienna, Austria: Springer-Verlag; 1995.
16.
Tatu L, Moulin T, Bogousslavsky J, Duvernoy H.
Arterial territories of human brain: brainstem and
cerebellum. Neurology. 1996;47:1125-1135.
17. North America Symptomatic Carotid Endarterectomy Trial Collaborators. Beneficial effect of carotid endarterectomy in symptomatic patients with high-grade carotid stenosis. N Engl J Med. 1991;325:445-453. [Abstract]
18.
Korogi Y, Takahashi M, Mabuchi N, Miki H, Shiga H,
Watabe T, O'Uchi T, Nakagawa T, Horikawa Y, Fijiwara S, Furuse
M. Intracranial vascular stenosis and occlusion:
diagnostic accuracy of three-dimensional, Fourier
transform, time-of-flight MR angiography. Radiology. 1994;193:187-193.
19.
Wentz KU, Röther J, Schwartz A, Mattle HP,
Suchalla R, Edelman RR. Intracranial vertebrobasilar system: MR
angiography. Radiology. 1994;190:105-110.
20. Solsberg MD, Fournier D, Potts DG. MR imaging of the excised human brainstem: a correlative neuroanatomic study. AJNR Am J Neuroradiol. 1990;11:1003-1013. [Abstract]
21. Kataoka S, Saigan T, Michishita H, Hori A, Hirose G. Altered serum lipoproteins and apolipoproteins in carotid atherosclerosis. Cerebrovasc Dis. 1996;6:21-27.
22. Rankin J. Cerebral vascular accidents in patients over the age of 60, II: prognosis. Scott Med J. 1965;57:200-215.
23. Ashizawa T, Rolak LA, Hines M. Spastic pure motor monoparesis. Ann Neurol. 1986;20:638-641. [Medline] [Order article via Infotrieve]
24. Boiten J, Lodder J. Isolated monoparesis is usually caused by superficial infarction. Cerebrovasc Dis. 1991;1:337-340.
25.
Melo TP, Bogousslavsky J, van Melle G, Regli F.
Pure motor stroke: a reappraisal. Neurology. 1992;42:789-798.
26. Chamorro A, Sacco RL, Mohr JP, Foulkes MA, Kase CS, Tatemichi TK, Wolf PA, Price TR, Hier DB. Clinical-computed tomographic correlations of lacunar infarction in the Stroke Data Bank. Stroke. 1991;221:175-181.
27. Iwasaki Y, Kinoshita M, Ikeda K, Takamiya K, Shiojima T. A case of pure motor monoparesis due to pontine infarction. Int J Neurosci.. 1990;55:157-159. [Medline] [Order article via Infotrieve]
28.
Nighoghossian N, Ryvlin P, Trouillas P, Laharotte JC,
Froment JC. Pontine versus capsular pure motor
hemiparesis. Neurology. 1993;43:2197-2201.
29. Kuypers HGJM. Corticobulbar connections to the pons and lower brain-stem in man: an anatomical study. Brain. 1958;812:364-388.
30.
Hopf HC, Tettenborn B, Krämer G. Pontine
supranuclear facial palsy. Stroke. 1990;21:1754-1757.
31. Crosby EC, Humphery T, Lauer EW. Correlative Anatomy of the Nervous System. New York, NY: Macmillan Publishing Co; 1962:490-491.
32. Brodal A. Neurological Anatomy in Relation to Clinical Medicine. Oxford, UK: Oxford University Press; 1981:186-187.
33. Kim JS. Pure dysarthria, isolated facial paresis, or dysarthria-facial paresis syndrome. Stroke. 1994;25:1994-1998. [Abstract]
34. Poeck K. Pathological laughter and crying. In: Fredericks JAM, ed. Handbook of Clinical Neurology. Amsterdam, Netherlands: Elsevier Science Publishing Co; 1985:219-225.
35. Ceccaldi M, Poncet M, Milandre L, Rouyer C. Temporary forced laughter after unilateral strokes. Eur Neurol. 1994;34:36-39.
36. Donaldson D, Rosenberg NL. Infarction of abducens nerve fascicle as cause of isolated sixth nerve palsy related to hypertension. Neurology. 1988;38:1654.
37.
Fukutake T, Hirayama K. Isolated abducens nerve
palsy from pontine infarction in a diabetic patient.
Neurology. 1992;42:2226.
38.
Kim JS, Kang JK, Lee SA, Lee MC. Isolated or
predominant ocular motor nerve palsy as a manifestation of brain stem
stroke. Stroke. 1993;24:581-586.
39.
Bronstein AM, Morris J, Du Boulay G, Rudge GP.
Abnormalities of horizontal gaze: clinical, oculographic and magnetic
resonance imaging findings, I: abducens palsy. J
Neurol Neurosurg Psychiatry. 1990;53:194-199.
40.
Bronstein AM, Rudge P, Gresty MA, Du Boulay G, Morris
J. Abnormalities of horizontal gaze: clinical, oculographic and
magnetic resonance imaging findings, II: gaze palsy and internuclear
ophthalmoplegia. J Neurol Neurosurg Psychiatry. 1990;53:200-207.
41. Hirose G, Furui K, Yoshioka A, Sakai K. Unilateral conjugate gaze palsy due to a lesion of the abducens nucleus: clinical and neuroradiological correlations. J Clin Neuro-ophthal. 1993;13:54-58. [Medline] [Order article via Infotrieve]
42.
Pierrot-Deseilligny CH, Chain F, Serdaru M, Gray F,
Lhermitte F. The `one-and-a-half' syndrome:
electro-oculographic analyses of five cases with deductions
about the physiological mechanisms of lateral
gaze. Brain. 1981;104:665-699.
43.
Wall M, Wray SH. The one-and-a-half syndrome—a
unilateral disorder of the pontine tegmentum: a study of 20 cases and
review of the literature. Neurology. 1983;33:971-980.
44.
Miyashita K, Naritomi H, Sawada T, Nakamura M, Kuriyama
Y, Ogawa M, Imakita S. Identification of recent lacunar lesions
in cases of multiple small infarctions by magnetic resonance
imaging. Stroke. 1988;19:834-839.
45.
Helgason CM, Wilbur AC. Basilar branch pontine
infarction with prominent sensory signs. Stroke. 1991;22:1129-1136.
46.
Hommel M, Besson G, Pollak P, Borgel F, Le Bas JF,
Perret J. Pure sensory stroke due to a pontine lacune.
Stroke. 1989;20:406-408.
47. Shintani S, Tsuruoka S, Shiigai T. Pure sensory stroke caused by a pontine infarct: clinical, radiological, and physiological features in four patients. Stroke. 1994;25:1512-1515. [Abstract]
48.
Ramirez-Lassepas M, Cipolle RJ, Bjork RJ, Kowitz J,
Snyder BD, Weber JC, Stein SD. Can embolic stroke be diagnosed
on the basis of neurologic clinical criteria? Arch
Neurol. 1987;44:87-89.
49.
Kittner SJ, Sharkness CM, Price TR, Plotnick GD,
Dambrosia JM, Wolf PA, Mohr JP, Hier DB, Kase CS, Tuhrim S.
Infarcts with a cardiac source of embolism in the NINCDS Stroke Data
Bank: historical features. Neurology. 1990;40:281-284.
50.
Bogousslavsky J, Cachin C, Regli F, Despland PA, van
Melle G, Kappenberger L. Cardiac sources of embolism and
cerebral infarction—clinical consequences and vascular concomitants:
the Lausanne Stroke Registry. Neurology. 1991;41:855-859.
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