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(Stroke. 1995;26:950-955.)
© 1995 American Heart Association, Inc.

Articles

Syndromes of Pontine Base Infarction

A Clinical-Radiological Correlation Study

Jong S. Kim, MD; Jay H. Lee, MD; Joo H. Im, MD Myoung C. Lee, MD

From the Department of Neurology, University of Ulsan, Asan Medical Center, Seoul, 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
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 *Abstract
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 down arrowSubjects and Methods
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Background and Purpose Although there have been sporadic reports of lacunar syndromes due to pontine base infarction, studies of clinical-radiological correlation in sufficient numbers of patients have not yet been reported.

Methods We studied the clinical features of 37 patients with acute infarcts that mainly involved the base of the pons and correlated the clinical syndromes with the radiological findings.

Results The clinical presentations included pure motor hemiparesis (PMH) in 17, sensorimotor stroke in 3, ataxic hemiparesis (AH) in 4, and dysarthria–clumsy hand (DA-CH) syndrome in 6 patients. Variants of AH included 1 patient with dysarthria-hemiataxia and 2 with quadrataxic hemiparesis, and in 4 patients dysarthria–facial paresis syndrome was considered a variant of DA-CH syndrome. Hypertension was the single most common and important risk factor, and the pathogenetic mechanisms of ischemia were likely to be small arterial (lacunar) occlusion or basilar atheromatous branch occlusion in most of the patients. Our clinical-radiological correlation study suggested that large lesions involving the paramedian caudal or middle pons correlate with severe hemiparesis (PMH), whereas lesions of similar size located in the paramedian rostral pons tended to produce DA-CH syndrome. Lesions producing AH were located variously but tended to spare the pyramidal tracts. The prognosis of these patients is fair or good, although residual hemiparesis remained in patients with initially severe hemiparesis.

Conclusions Our data suggest that the various lacunar syndromes that follow pontine base infarcts reflect the balance of the involvement of the corticospinal, corticopontocerebellar, and corticobulbar tracts. Analysis of radiological findings aids in determining the clinical-anatomic correlation in patients with pontine base infarction.


Key Words: cerebral infarction • diagnostic imaging • lacunar infarction • pons


*    Introduction
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 up arrowAbstract
 *Introduction
down arrowSubjects and Methods
 down arrowResults
 down arrowDiscussion
 down arrowReferences
 
There have been sporadic reports of pontine base infarction producing clinical syndromes of pure motor hemiparesis (PMH),1 2 3 4 5 6 sensorimotor stroke (SMS),6 ataxic hemiparesis (AH),6 7 8 9 10 11 12 13 14 15 16 and dysarthria–clumsy hand (DA-CH) syndrome.15 17 18 19 However, reports of sufficient numbers of patients are rare, and a clinical-radiological correlation study has not yet been performed. Therefore, in this report we describe 37 patients with pontine base infarction, correlating their clinical findings with imaging results.


*    Subjects and Methods
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 up arrowAbstract
 up arrowIntroduction
 *Subjects and Methods
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We studied 37 patients with unilateral pontine base infarcts who were examined at Asan Medical Center between September 1990 and December 1994. All were evaluated with CT scan (n=30), MRI (n=32), or both (n=25). We excluded patients who had (1) infarcts the extent of which were not clearly delineated on CT scan or MRI; (2) large lesions involving bilateral areas of the pons; (3) simultaneous lesions in the medulla or midbrain; (4) lesions mainly involving the tegmentum (usually presenting with predominant or pure sensory symptoms and/or ocular motor dysfunction); or (5) residual neurological deficits from previous strokes or who presented with pseudobulbar palsy.

The clinical syndromes were classified as PMH, SMS, AH, DA-CH, and their variants according to previous descriptions.1 7 17 20 In the first two groups, motor weakness of the proximal part of the limbs was graded in five categories (0, no contraction; 1, flicker or trace of contraction; 2, active movement possible only with gravity eliminated; 3, active movement against gravity but not resistance; 4, active movement against resistance and gravity; and 5, normal power).21 When the grade was different between the arm and leg, that of the arm was used in this study. Dysarthria and facial paresis were graded as follows: -, none; +, mild; and ++, moderate to marked (Fig 1Down). AH and DA-CH were defined as follows: AH, patients with obvious cerebellar ataxia and hemiparesis mild (grade IV) enough to perform reliable cerebellar function tests; DA-CH, clumsy limbs (muscle strength greater than grade IV) with relatively severe dysarthria.



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  		Figure 1. Chart shows characteristics of patients with pure motor hemiparesis or sensorimotor stroke. D indicates dysarthria; F, facial paresis; U, upper extremity; L, lower extremity; SM, cigarette smoking; CA, cardiac disease; HT, hypertension; DM, diabetes mellitus; HL, hyperlipidemia; PMH, pure motor hemiparesis; SMS, sensorimotor stroke; C, CT scan; M, middle pons; R, rostral pons; Lg, large; Sm, small; C, caudal pons; and Me, medium.

MRI was performed with the use of a 1.5 T-superconducting magnet (GE). An axial T2-weighted (repetition time [TR], 2500 milliseconds; echo time [TE], 80 milliseconds) scan was performed in a horizontal plane at 5- or 6-mm intervals. T1-weighted (TR, 600 milliseconds; TE, 20 milliseconds) axial and sagittal images were also obtained. Evaluation of the lesions generally depended on T2-weighted axial cuts. The images were evaluated rostrocaudally22 as follows: the rostral pons was characterized by its relatively round shape with small, round-shaped aqueduct; the middle pons was characterized by its square-shaped fourth ventricle, large middle cerebellar peduncles, and silhouettes of trigeminal nerves; and the caudal pons was characterized by its shape similar to the middle pons but with images of the facial/acoustic nerves and grooves instead of trigeminal nerves. In 5 patients in whom only CT scan was performed, the morphology of the pons was used for the evaluation. Three patients (patients 1, 5, and 19) underwent angiogram, and 3 (patients 15, 17, and 20) underwent MR angiography. In 32 patients evaluated with MRI, vertebrobasilar artery flow void signals were examined with the use of T2- and T1-weighted images. The radiological evaluation was performed by one of the authors who was blind to the patients' clinical histories. The size of the lesion was defined as large when the value of the longest diameter of the lesion (or dominant lesion when the lesions were seen in more than one cut) multiplied by its longest intersecting line was greater than 2 cm2, as small when it was less than 1 cm2, and as medium when it was between these two.


*    Results
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 *Results
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Thirty-seven patients (19 men and 18 women; age, 36 to 85 years [mean, 61 years]) were studied; the details of each patient are summarized in Figs 1 through 3UpDownDown. Risk factors for stroke included hypertension in 31, diabetes mellitus in 10, cigarette smoking in 9, and history of coronary heart disease in 3 patients. One (patient 19) did not have any risk factors. The presence of hypertension was based on the history and serial check-up of blood pressure during hospitalization. None had arrhythmia at the time of event, and the echocardiogram in 29 patients did not reveal the presence of valvular diseases or possible emboligenic abnormalities. Radiological examination showed that the rostral, middle, and caudal pons were involved in 9, 10, and 6 patients, respectively. Eleven patients had lesions in both the rostral and middle pons, and 1 had a lesion in the middle and caudal pons. The radiological findings are depicted (drawn from the original films) in Figs 1 through 3UpDownDown. Among 6 patients in whom angiogram or MR angiography was performed, none had occlusion or severe stenosis of basilar artery. However, 2 (patients 17 and 20) had diffuse stenosis or occlusion of the internal carotid arteries. None had abnormal basilar artery flow void signal.



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  		Figure 2. Chart shows characteristics of patients with ataxic hemiparesis and its variants. HT indicates hypertension; HL, hyperlipidemia; DM, diabetes mellitus; Hemi, hemiparesis; M, middle pons; Lg, large; R, rostral pons; Sm, small; Me, medium; and C, caudal pons.



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  		Figure 3. Chart shows characteristics of patients with dysarthria–clumsy hand syndrome and its variants. HT indicates hypertension; SM, cigarette smoking; DM, diabetes mellitus; CA, cardiac disease; R, rostral pons; Lg, large; M, middle pons; Me, medium; and Sm, small.

Pure Motor or Sensorimotor Stroke (Fig 1Up)
Seventeen patients had PMH, and 3 had hemiplegia plus mild sensory (pinprick and vibration) dysfunction. Patient 2 had transient, burning paresthesia on the right face. At the time of maximum severity, motor weakness was severe (grade 0 to II) in 12, moderate (grade III) in 5, and mild (grade IV) in 3. The weakness was equal between arm and leg in 11 and was more severe in the arm in 9 patients. Motor weakness was usually more severe in the distal than the proximal part of the limbs. The mode of onset was usually smoothly or stutteringly progressive for several hours or days, and heparinization, used in all patients with progressive hemiparesis, did not halt the progression. In some patients with a sluggishly progressive onset, initial symptoms resembled those of DA-CH or AH. Despite frequently severe hemiparesis, dysarthria and facial paresis were often mild or even absent in some patients (Fig 1Up). Dysarthria was moderate to marked in 8, and only 1 (patient 18) had marked dysphagia that required a nasogastric tube for feeding. Four patients (patients 13, 15, 17, and 18) showed distinct lingual paresis, and patients 12 and 1 had contralateral palatal-lingual and palatal-lingual- laryngeal hemiparesis, respectively.

The lesions were evaluated by MRI in 15 and by CT in 5 patients. They were situated in the caudal pons in 5, middle pons in 6, rostral pons in 1, and middle and rostral pons in 8 patients. The 12 patients with severe limb weakness had large lesions in 10, a medium-sized lesion in 1, and a small lesion in 1. All 3 patients with mild hemiparesis had small lesions.

Ataxic Hemiparesis and Its Variants (Fig 2Up)
Four patients had AH, 2 of whom also had transient sensory symptoms. Two (patients 25 and 26) showed AH and additional limb ataxia on the side ipsilateral to the lesions, which was worse in the leg. They had marked gait difficulty due to bilateral lower limb ataxia and hemiparesis and were designated as having quadrataxic hemiparesis. One (patient 27) showed dysarthria and hemiataxia but without hemiparesis or hemihypesthesia and was designated as having dysarthria-hemiataxia.

The lesions were evaluated with the use of MRI in all patients. The location was variable: caudal pons in 1, middle pons in 2, rostral pons in 1, caudal and middle pons in 1, and middle and rostral pons in 2 patients. Two had large infarcts: 1 in the middle pons and 1 in the rostral pons. Four had medium-sized and 1 had small lesions. In 4 (patients 22, 23, 25, and 27), the lesions were located relatively laterally.

Dysarthria–Clumsy Hand Syndrome and Its Variants (Fig 3Up)
Six patients had DA-CH syndrome, 1 of whom had transient hemisensory symptoms. Three patients had dysarthria and facial paresis without limb involvement, and 1 presented with isolated dysarthria. All the lesions were evaluated with the use of MRI. Seven patients had lesions in the paramedian rostral pons, which were large in 5 and small in 2. One had a medium-sized lesion involving the middle and rostral pons, and 1 had a medium sized mid-pontine lesion.

Other Clinical Features and Follow-up Findings
Patients 8 and 11 with PMH had sixth nerve palsy. Patients 24 and 32 presented with transient uncontrollable laughter, and patient 26 had excessive crying followed by inappropriate smiling. Patient 17 became depressed and had a suicidal idea, while patient 28 showed transient psychotic behavior. The patients were followed up for 1 to 47 (mean, 9) months. All survived the acute stage of stroke and improved gradually except patients 6 and 18, who remained bedridden. Patient 25 had a recurrent infarct in the corona radiata in 2 months. All others were able to walk, although patient 8 required assistance. The patients with initially severe limb weakness had persistent hemiparesis of variable degree. Seven patients manifested ataxia in the hemiparetic limb as their motor strength improved.


*    Discussion
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 up arrowIntroduction
 up arrowSubjects and Methods
 up arrowResults
 *Discussion
down arrowReferences
 
Risk Factors and Presumed Mechanism of Ischemia
In our patients hypertension was the single most important risk factor, and no patients had cardiac arrhythmia or valvular heart diseases. Unfortunately, angiogram and MR angiography were performed in only 6 patients, and the pathogenetic mechanism of ischemia remained uncertain in the majority of the patients. Nevertheless, none of the above 6 patients showed occlusion or significant degree of stenosis of the basilar artery, and abnormal vertebrobasilar flow void signal, observed in patients with large or multifocal brain stem infarction,23 24 was not detected in any of our patients. Helgason and Wilbur25 also found that none of their 10 patients with unilateral pontine infarction presenting prominent sensory signs showed abnormal vertebral flow void signal. Therefore, unilateral pontine base ischemia seems to be most often caused by small arterial (lacunar) occlusion of paramedian or circumferential branches rather than large-vessel atherothrombosis or cardiogenic embolism. However, some of the large lesions widely involving the ventral surface (patients 1, 4 through 10, 14, 15, 18, 20, 28, 29, 33, and 34) may have been related to atheromatous branch occlusion.26 27 28 29

Spectrum of Clinical Syndromes
In patients with PMH, the motor weakness was usually progressive and unresponsive to anticoagulation. The progressive mode of onset and unresponsiveness to anticoagulation were previously described in patients with lacunar stroke.30 31 32 The weakness tended to be more marked in the upper than lower extremity and in distal (hand or foot) than proximal parts of the limbs. These features are in accordance with the previous studies with pontine infarction,6 33 although dominant leg weakness was also reported.6 34 In agreement with previous studies with unilateral brain stem infarction,6 33 35 36 the prognosis was relatively good in our series. However, some degree of motor weakness remained in patients with initially severe hemiparesis. Despite frequently severe limb weakness, facial paresis and dysarthria were often mild or even absent in occasional cases. Distinct lingual, palatal-lingual, or palatal-lingual-laryngeal hemipareses were observed in 6 patients, which resembled the clinical features of so-called capsular genu syndrome.37

In the literature, the differentiation between AH and DA-CH has not always been clear. Fisher20 stated that the latter may be a variant of the former. After analyzing 337 patients with lacunar stroke, Chamorro et al38 stated that syndromes of AH and DA-CH may be viewed as one entity. Glass et al19 reported that DA-CH seen in their 6 patients with pontine infarction had characteristics of cerebellar ataxia and suggested that some of the cases previously reported as having AH should be reclassified as having DA-CH syndrome. However, Fisher's17 original description of DA-CH referred to "clumsiness, awkwardness, slowness of fine manipulations, wavering ataxia on finger to nose test which is not clearly cerebellar in type." Therefore, in our study patients with obvious ataxia and definitive weakness (grade IV) were classified as having AH.

Several cases described here deserve attention. Patient 27 showed dysarthria and hemiataxia but without hemiparesis or hemihypesthesia. A few patients with similar symptoms were previously described: dysarthria–facial paresis–hemiataxia (second cases of Glass et al19 and Hopf et al39 ) and isolated hemiataxia (second case of Nabatame et al14 ). They were variously classified as AH,14 DA-CH,19 and pontine supranuclear facial palsy.39 However, cerebellar hemiataxia without hemiparesis is distinguished from the original description of AH40 and may be described as dysarthria-hemiataxia syndrome as a variant of AH. Hemiataxia without hemiparesis has also been described in patients with thalamic stroke, usually with accompanying sensory symptoms,41 42 although hemiataxia without sensory dysfunction can also be caused by thalamic43 or capsular44 lesions.

We found 2 patients with AH and additional ataxia on the side ipsilateral to the lesion. Van Gijn and Vermeulen45 described bilateral AH (ataxic tetraplegia) due to recurrent pontine infarctions. Recent reports also described bilateral ataxia following unilateral pontine lesions,25 35 46 which may be attributable to an involvement of the crossing corticopontocerebellar tracts.46 Our patients had ataxia that was more marked in the lower extremities and subjectively felt a sense of heaviness or weakness in both legs. The marked gait difficulty seen in these patients was reminiscent of astasia or gait ataxia caused by unilateral thalamic47 or midbrain48 49 strokes.

We examined 6 patients with DA-CH syndrome. We also observed 3 patients with dysarthria and facial paresis and 1 with dysarthria only but without involvement of the limbs. This clinical feature may be designated as dysarthria–facial paresis syndrome as a variant of DA-CH.50 Pure dysarthria or dysarthria–facial paresis syndrome has previously been reported to be produced by capsular–corona radiata, cortical, or pontine strokes.50 51 52 53 54

Clinical-Radiological Correlation
In the patients with PMH or SMS, the lesions causing severe hemiparesis were usually large and widely involved the ventral surface of the paramedian caudal or middle pons (patients 1, 4, 6, 7, 8, 10, 14, and 15), whereas small, median lesions (patients 2, 11, and 12) correlated with mild limb weakness. However, patients without or with minimal limb weakness (DA-CH and its variants) frequently had large lesions in the paramedian rostral pons (patients 28 through 30 and 33 through 35). The lack of correlation between the size of lesion and the degree of hemiparesis was noted by previous authors,33 55 who speculated that a large part of the infarct seen on MRI may implicate edema rather than destructive lesions. This assumption may be supported by an observation that a large pontine infarct was significantly reduced in size on follow-up MRI.33 However, this is hardly a satisfactory explanation given our observation that the paramedian lesions at the level of the caudal or middle pons large enough to cause severe hemiparesis did not produce a corresponding degree of symptoms when they are located in the rostral pons.

Therefore, other explanations should be considered. First, the corticospinal tracts in the midbrain are located in the middle of the cerebral peduncle as compact bundles. In the upper pons, however, they run along with the corticopontine fibers in a loosely dispersed manner within abundant and heavily traversing nonpyramidal fibers.20 Therefore, the impact on the pyramidal tracts by a focal infarct in the upper pons may not be as severe as in the lower pons, where pyramidal fibers again become compact. Second and more importantly, the corticospinal tracts are situated in the dorsolateral part of the pontine base at the level of the upper pons and are converged into the anteromedial surface of the upper medulla to form compact bundles.56 Therefore, the pontine base lesions, usually situated in the paramedian-ventral area, may more effectively damage the corticospinal tracts when they are located in the lower rather than upper part of the pons (Fig 4Down). This topographic characteristic may explain why the lesions located (patients 13 and 17) or extending (patient 18) into the lateral part of the upper pons produced relatively more severe motor weakness (PMH) than paramedian lesions (DA-CH).



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  		Figure 4. Schematic drawing of large infarcts located on the caudal (A) and rostral (B) pons producing pure motor hemiplegia and dysarthria–clumsy hand syndrome, respectively.

Also noteworthy was that dysarthria was usually more marked in patients with upper pontine lesions (patients 5, 8, 13, 16 through 18, and 20 with PMH and patients with DA-CH syndrome) compared with the patients with severe hemiparesis (PMH) without upper pontine lesions (patients 3, 4, 9, 10, 14, and 15). In the midbrain and upper pons, the corticobulbar tracts are located medial to the corticospinal fibers.57 At the pontine level, there are multiple connections between both corticobulbar tracts except for the fibers subserving the lower facial muscles.58 59 The presence of these connections or aberrant fibers at multiple levels of the pons may explain the paucity or transience of palatal and lingual weakness in patients with unilateral strokes. The aberrant fibers of the nucleus ambiguus or hypoglossal nuclei are given off at the level of the upper pons, although they are reinforced by the bulbopontine fibers emerging at the level of the pontomedullary junction.60 The rostral pontine lesions therefore may effectively involve the multiple crossing fibers as well as the medial part of the corticospinal tracts (Fig 4Up), thus easily producing bulbar symptoms.

Fisher20 stated that pontine base infarctions at the junction of the upper one third and inferior two thirds may produce AH. Bogousslavsky et al13 and Nabatame et al,14 after analyzing MRI findings of their patients with AH, found that the lesions were located in the dorsomedial area, sparing the ventral part. Our patients with AH showed lesions in various areas, suggesting that in the pontine base, pontocerebellar fibers are widespread and may easily be involved. The disappearance and reappearance of limb ataxia after the progression or recovery of severe motor weakness in some of the patients with PMH suggested that it is the balance of the involvement of the pyramidal and pontocerebellar tracts that determines the clinical subtypes. Relatively laterally (patients 17, 18, 20, and 22) or far ventrally (patients 20 and 21) situated midcaudal pontine lesions may have involved the corticospinal tracts less markedly, thus producing AH or dysarthria-hemiataxia syndrome. The rostral pontine lesions of patients 23 and 24 were similar in location to that producing DA-CH, further suggesting that clinical differentiation of DA-CH and AH may not be absolute. The lesions of patients 25 and 26 producing bilateral ataxia and marked gait disturbance might have predominantly involved pontovermis or fastigiopontine fibers, both of which are bilaterally connected between the pons and the cerebellar vermis.61

Finally, 5 patients presented with transient pathological crying, laughter, depression, or psychotic behaviors. Pathological crying or laughter, classically seen in patients with bilateral cerebral lesions as a component of pseudobulbar palsy,62 63 is known to occur in patients with unilateral strokes.64 Transient crying,65 uncontrollable laughter,25 mania,66 or psychotic symptoms67 were also reported in patients with brain stem stroke. Andersen et al68 suggested that some of these symptoms may be attributed to altered serotonin neurotransmission. Presumably, the pontine serotonergic center or the superior projection from this structure might have been involved in the above 5 patients.

Note: Some of the patients in this study were included in our previous articles.50 69


*    Acknowledgments
 
We wish to thank S. Yoon, RN, for help in preparing the manuscript.

Received January 25, 1995; revision received March 14, 1995; accepted March 14, 1995.


*    References
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 up arrowSubjects and Methods
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 *References
 

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